PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 9863180-5 1996 injection of apomorphine (Apo) 5 mg.kg-1, the levodopa content was decreased below that of BL group (P < 0.05). Levodopa 46-54 aminopeptidase O Rattus norvegicus 26-29 9863180-6 1996 The Apo inhibition on levodopa content was completely reversed by CSL (40 mg.kg-1, i.p.) Levodopa 22-30 aminopeptidase O Rattus norvegicus 4-7 8783836-4 1996 The purified PPO was found to be a doublet of M(r) 60,000 and 69,000 when analysed by SDS-PAGE with a Km 4.3 +/- 0.3 mM for L-dihydroxyphenylalanine. Levodopa 124-148 catechol oxidase B, chloroplastic Solanum tuberosum 13-16 18624322-0 1996 L-DOPA production from tyrosinase immobilized on nylon 6,6. Levodopa 0-6 tyrosinase Homo sapiens 23-33 8699255-0 1996 Double transduction with GTP cyclohydrolase I and tyrosine hydroxylase is necessary for spontaneous synthesis of L-DOPA by primary fibroblasts. Levodopa 113-119 GTP cyclohydrolase 1 Rattus norvegicus 25-45 8699255-0 1996 Double transduction with GTP cyclohydrolase I and tyrosine hydroxylase is necessary for spontaneous synthesis of L-DOPA by primary fibroblasts. Levodopa 113-119 tyrosine hydroxylase Rattus norvegicus 50-70 8817341-1 1996 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to L-dihydroxyphenylalanine (L-DOPA), the rate-limiting step in the biosynthesis of dopamine. Levodopa 68-92 tyrosine hydroxylase Homo sapiens 0-20 8842399-0 1996 Dopaminergic transplants suppress L-DOPA-induced Fos expression in the dopamine-depleted striatum in a rat model of Parkinson"s disease. Levodopa 34-40 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 49-52 8842399-9 1996 The stimulatory effect of L-DOPA on c-Fos expression observed within the lesioned striatum was suppressed by fetal VM transplants. Levodopa 26-32 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 36-41 8842399-11 1996 Taken together, these findings suggest that glutamatergic modulation is involved in the L-DOPA-induced c-Fos expression in the denervated striatum which is normalized by fetal VM transplants. Levodopa 88-94 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 103-108 8804732-4 1996 In MPTP-treated monkeys that received L-DOPA, a significant increase in both GAD67 and GAD65 mRNA levels was measured in the putamen when compared to control or MPTP-treated monkeys. Levodopa 38-44 glutamate decarboxylase 1 Homo sapiens 77-82 8804732-4 1996 In MPTP-treated monkeys that received L-DOPA, a significant increase in both GAD67 and GAD65 mRNA levels was measured in the putamen when compared to control or MPTP-treated monkeys. Levodopa 38-44 glutamate decarboxylase 2 Homo sapiens 87-92 8817341-1 1996 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to L-dihydroxyphenylalanine (L-DOPA), the rate-limiting step in the biosynthesis of dopamine. Levodopa 68-92 tyrosine hydroxylase Homo sapiens 22-24 8817341-1 1996 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to L-dihydroxyphenylalanine (L-DOPA), the rate-limiting step in the biosynthesis of dopamine. Levodopa 94-100 tyrosine hydroxylase Homo sapiens 0-20 8817341-1 1996 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to L-dihydroxyphenylalanine (L-DOPA), the rate-limiting step in the biosynthesis of dopamine. Levodopa 94-100 tyrosine hydroxylase Homo sapiens 22-24 8836986-4 1996 On the other hand, by administration of L-DOPA combined with L-threo-DOPS, the levels of monoamines increased in general, whereas the monoamine metabolites by catechol-O-methyltransferase were reduced compared with those in the patients treated with L-DOPA alone. Levodopa 40-46 catechol-O-methyltransferase Homo sapiens 159-187 8836986-4 1996 On the other hand, by administration of L-DOPA combined with L-threo-DOPS, the levels of monoamines increased in general, whereas the monoamine metabolites by catechol-O-methyltransferase were reduced compared with those in the patients treated with L-DOPA alone. Levodopa 250-256 catechol-O-methyltransferase Homo sapiens 159-187 8675685-7 1996 In rats given L-DOPA in the drinking water for 5 d, there were decreases in both proximal tubule AT1 receptor mRNA expression (80 +/- 5%; n = 6; P < 0.005) and specific [125I] Ang II binding (control: 0.74 +/- 0.13 fmol/mg pro vs. 0.40 +/- 0.63 fmol/mg pro; n = 5; P < 0.05). Levodopa 14-20 angiotensinogen Rattus norvegicus 179-185 8710082-2 1996 In MPTP-treated monkeys, the expression of GAD67 mRNA was increased in cells from the internal pallidum, and this effect was abolished by L-dopa treatment. Levodopa 138-144 glutamate decarboxylase 1 Homo sapiens 43-48 8710082-4 1996 These results indicate that the level of GAD67 mRNA is increased in the cells of the internal pallidum after nigrostriatal dopaminergic denervation and that this increase can be reversed by L-dopa therapy. Levodopa 190-196 glutamate decarboxylase 1 Homo sapiens 41-46 8703564-43 1996 Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. Levodopa 32-40 parkin RBR E3 ubiquitin protein ligase Homo sapiens 128-133 8726541-0 1996 Effect of one month"s treatment with peripherally acting catechol-O-methyltransferase inhibitor, entacapone, on pharmacokinetics and motor response to levodopa in advanced parkinsonian patients. Levodopa 151-159 catechol-O-methyltransferase Homo sapiens 57-85 8726541-8 1996 Peripheral COMT inhibition with entacapone increased significantly the bioavailability of levodopa and prolonged its antiparkinsonian effect after a single dose and after repeated dosing for 4 weeks. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 11-15 8783276-1 1996 L-3,4-Dihydroxyphenylalanine (L-DOPA) inhibits the activity of tryptophan hydroxylase (TRH) and thus serotonin synthesis. Levodopa 0-28 thyrotropin releasing hormone Rattus norvegicus 63-85 8807664-1 1996 Catechol-O-methyltransferase (COMT) inactivates catecholamines and catechol drugs such as L-DOPA. Levodopa 90-96 catechol-O-methyltransferase Homo sapiens 0-28 8807664-1 1996 Catechol-O-methyltransferase (COMT) inactivates catecholamines and catechol drugs such as L-DOPA. Levodopa 90-96 catechol-O-methyltransferase Homo sapiens 30-34 8783276-1 1996 L-3,4-Dihydroxyphenylalanine (L-DOPA) inhibits the activity of tryptophan hydroxylase (TRH) and thus serotonin synthesis. Levodopa 0-28 thyrotropin releasing hormone Rattus norvegicus 87-90 8783276-1 1996 L-3,4-Dihydroxyphenylalanine (L-DOPA) inhibits the activity of tryptophan hydroxylase (TRH) and thus serotonin synthesis. Levodopa 30-36 thyrotropin releasing hormone Rattus norvegicus 63-85 8813364-6 1996 These findings suggest that the newly produced dopamine from L-DOPA in serotonin neurons of the rat DR is degraded by endogenous MAO. Levodopa 61-67 monoamine oxidase A Rattus norvegicus 129-132 8783276-1 1996 L-3,4-Dihydroxyphenylalanine (L-DOPA) inhibits the activity of tryptophan hydroxylase (TRH) and thus serotonin synthesis. Levodopa 30-36 thyrotropin releasing hormone Rattus norvegicus 87-90 8813364-0 1996 Dopamine produced from L-DOPA is degraded by endogenous monoamine oxidase in neurons of the dorsal raphe nucleus of the rat: an immunohistochemical study. Levodopa 23-29 monoamine oxidase A Rattus norvegicus 56-73 8813364-1 1996 The aim of the present study is to examine by immunohistochemistry whether dopamine produced from L-DOPA in serotonin neurons of the rat brain is degraded by endogenous monoamine oxidase (MAO). Levodopa 98-104 monoamine oxidase A Rattus norvegicus 169-186 8813364-1 1996 The aim of the present study is to examine by immunohistochemistry whether dopamine produced from L-DOPA in serotonin neurons of the rat brain is degraded by endogenous monoamine oxidase (MAO). Levodopa 98-104 monoamine oxidase A Rattus norvegicus 188-191 8813364-3 1996 In L-DOPA/carbidopa-injected rats that were pretreated with an intraperitoneal injection of a MAO inhibitor, pargyline, when compared with the L-DOPA/carbidopa-injected rats without the pargyline pretreatment, neurons of the cluster of the DR became much darker in dopamine staining. Levodopa 3-9 monoamine oxidase A Rattus norvegicus 94-97 8791174-0 1996 Potentiation of L-dopa-induced behavioral excitement by histamine H1-receptor antagonists in mice. Levodopa 16-22 histamine receptor H1 Mus musculus 56-77 8635567-11 1996 With future improvement in the gene transduction procedure for more efficient, sustained expression of the TH transgene in vivo, genetically engineered DOPA-producing astrocytes hold great promise as a tool to explore the potential of ex vivo gene therapy in Parkinson"s disease. Levodopa 152-156 tyrosine hydroxylase Rattus norvegicus 107-109 8626863-6 1996 It is concluded that the inhibitory potency of GHRH-Ant on GHRH(1-44)NH2 is relatively weak (about 1/60 in molar base), and that L-dopa- or clonidine-induced GH release seems to be mediated by the release of hypothalamic GHRH. Levodopa 129-135 growth hormone releasing hormone Homo sapiens 47-51 8626863-6 1996 It is concluded that the inhibitory potency of GHRH-Ant on GHRH(1-44)NH2 is relatively weak (about 1/60 in molar base), and that L-dopa- or clonidine-induced GH release seems to be mediated by the release of hypothalamic GHRH. Levodopa 129-135 solute carrier family 25 member 6 Homo sapiens 52-55 8626863-6 1996 It is concluded that the inhibitory potency of GHRH-Ant on GHRH(1-44)NH2 is relatively weak (about 1/60 in molar base), and that L-dopa- or clonidine-induced GH release seems to be mediated by the release of hypothalamic GHRH. Levodopa 129-135 growth hormone releasing hormone Homo sapiens 59-63 8791174-1 1996 Effects of histamine H1-receptor antagonists on L-dopa-induced behavioral excitement were examined in mice to confirm behaviorally the inhibition of dopamine uptake by these compounds. Levodopa 48-54 histamine receptor H1 Mus musculus 11-32 8741130-5 1996 They were not influenced significantly by antiparkinsonian drugs in patients, although there was a trend for CSF nitrate levels to be higher in patients treated with levodopa or with dopamine agonists. Levodopa 166-174 colony stimulating factor 2 Homo sapiens 109-112 8699535-7 1996 However, [14C]dopamine (DA) was also detected in both rat and mouse astrocytes after 30 min L-DOPA incubation, indicating the existence of aromatic L-amino acid decarboxylase (AADC). Levodopa 92-98 dopa decarboxylase Mus musculus 176-180 8670114-1 1996 L-Aromatic amino acid decarboxylase (dopa decarboxylase; DDC) is a pyridoxal 5"-phosphate (PLP)-dependent homodimeric enzyme that catalyses the decarboxylation of L-dopa and other L-aromatic amino acids. Levodopa 163-169 dopa decarboxylase Sus scrofa 37-55 8727690-0 1996 Effects of intravenous L-dopa on P300 and regional cerebral blood flow in parkinsonism. Levodopa 23-29 E1A binding protein p300 Homo sapiens 33-37 8618687-2 1996 In MPTP-intoxicated monkeys, the expression of GAD67 mRNA was increased in the SNpr neurons, and the increase was reversed by L-dopa treatment. Levodopa 126-132 glutamate decarboxylase 1 Homo sapiens 47-52 8618687-6 1996 GAD67 mRNA expression was reduced in both MPTP-intoxicated monkeys, whether or not they received L-dopa therapy, and PD patients, compared to their respective controls. Levodopa 97-103 glutamate decarboxylase 1 Homo sapiens 0-5 8592137-9 1996 In the CD-1 mice estrogen also produced a significant increase in L-DOPA-evoked dopamine release; however, this response was unaltered by MPTP treatment. Levodopa 66-72 CD1 antigen complex Mus musculus 7-11 8867520-5 1996 At the beginning of the study, basal hormonal levels were within normal limits, and levodopa administration induced a significant suppression in PRL and TSH levels (both p < 0.01)) and a significant increase in GH (p < 0.01). Levodopa 84-92 prolactin Homo sapiens 145-148 8867520-5 1996 At the beginning of the study, basal hormonal levels were within normal limits, and levodopa administration induced a significant suppression in PRL and TSH levels (both p < 0.01)) and a significant increase in GH (p < 0.01). Levodopa 84-92 growth hormone 1 Homo sapiens 211-213 8867520-10 1996 The dopaminergic effects of levodopa on TSH, GH, and IGF-I secretion were unchanged by terguride treatment. Levodopa 28-36 growth hormone 1 Homo sapiens 45-47 8867520-10 1996 The dopaminergic effects of levodopa on TSH, GH, and IGF-I secretion were unchanged by terguride treatment. Levodopa 28-36 insulin like growth factor 1 Homo sapiens 53-58 8592137-10 1996 A significant increase in L-DOPA-evoked DOPAC output was obtained only for estrogen-treated CD-1 mice. Levodopa 26-32 CD1 antigen complex Mus musculus 92-96 8592137-11 1996 Both strains show very similar responses to the estrogen treatment, but differential responses of dopamine release to L-DOPA between the C57Bl and CD-1 mice were obtained with regard to the interactive effects of estrogen and MPTP. Levodopa 118-124 CD1 antigen complex Mus musculus 147-151 8761620-8 1996 The movements around the hip, knee and ankle joints that were initially reduced, poorly increased after L-Dopa intake. Levodopa 104-110 hedgehog interacting protein Homo sapiens 25-28 8632348-7 1996 The utilization of L-tyrosine or L-dopa as the substrate suggests a mechanism involving competition with arbutin for the L-tyrosine binding site at the active site of tyrosinase. Levodopa 33-39 tyrosinase Homo sapiens 167-177 8615170-0 1996 Effects of catechol-O-methyltransferase (COMT) inhibition on the pharmacokinetics of L-DOPA. Levodopa 85-91 catechol-O-methyltransferase Homo sapiens 11-39 8615170-0 1996 Effects of catechol-O-methyltransferase (COMT) inhibition on the pharmacokinetics of L-DOPA. Levodopa 85-91 catechol-O-methyltransferase Homo sapiens 41-45 8522954-1 1996 The tyrosine hydroxylase (TH) gene is expressed exclusively in cells and neurons that synthesize and release L-DOPA or catecholamines. Levodopa 109-115 tyrosine hydroxylase Mus musculus 4-24 8772480-3 1996 To determine whether the PRL elevation was due to a decrease in hypothalamic generation of DA, we measured the inhibition of PRL by L-dopa before and after inhibition of peripheral decarboxylase activity with carbidopa. Levodopa 132-138 prolactin Homo sapiens 125-128 8772480-4 1996 Without verapamil, L-dopa alone and carbidopa-L-dopa caused similar maximum decreases in PRL levels of 83.2 +/- 2.5 and 80.3 +/- 2.0%, respectively. Levodopa 19-25 prolactin Homo sapiens 89-92 8772480-5 1996 With verapamil, the PRL maximum decrement with L-dopa was 85.2 +/- 2.7% and with carbidopa-L-dopa was 76.3 +/- 1.9% (P < 0.01). Levodopa 47-53 prolactin Homo sapiens 20-23 8964257-11 1996 There is a marked TR difference between patients receiving and not receiving L-DOPA. Levodopa 77-83 coagulation factor II thrombin receptor Homo sapiens 18-20 8836934-6 1996 As expected, LD/carbidopa increased the concentration of GH and decreased that of PRL. Levodopa 13-15 growth hormone 1 Homo sapiens 57-59 8522954-1 1996 The tyrosine hydroxylase (TH) gene is expressed exclusively in cells and neurons that synthesize and release L-DOPA or catecholamines. Levodopa 109-115 tyrosine hydroxylase Mus musculus 26-28 8836934-6 1996 As expected, LD/carbidopa increased the concentration of GH and decreased that of PRL. Levodopa 13-15 prolactin Homo sapiens 82-85 8761019-2 1996 TH activity was determined in tissue extracts by measuring the accumulation of L-DOPA following administration of the dopa decarboxylase inhibitor, NSD-1015. Levodopa 79-85 tyrosine 3-monooxygenase Mesocricetus auratus 0-2 9029407-10 1996 These results indicate that long-term treatment with clozapine, sulpiride and L-DOPA may modify the reactivity of D4-like DA receptors regulating NAT activity of chick retina. Levodopa 78-84 arylamine N-acetyltransferase, liver isozyme Gallus gallus 146-149 8988460-3 1996 The MAO-B inhibition could result in a potentiation of the effect and the reduction of the dose of L-dopa, including the restoration of the sensitivity to L-dopa treatment, when the response to the drug has already been diminished or lost. Levodopa 99-105 monoamine oxidase B Homo sapiens 4-9 8988460-3 1996 The MAO-B inhibition could result in a potentiation of the effect and the reduction of the dose of L-dopa, including the restoration of the sensitivity to L-dopa treatment, when the response to the drug has already been diminished or lost. Levodopa 155-161 monoamine oxidase B Homo sapiens 4-9 8988463-1 1996 Selegiline is a relatively selective inhibitor of monoamine oxidase type B that has been used in Parkinson"s disease as an adjunct to levodopa and as putative neuroprotective therapy. Levodopa 134-142 monoamine oxidase B Homo sapiens 50-74 8602107-5 1996 However, only SKF38393 and levodopa increased AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. Levodopa 27-35 cAMP responsive element binding protein 1 Rattus norvegicus 55-59 8602107-7 1996 Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa. Levodopa 156-164 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 34-39 8652014-8 1996 At 25-30 days of age, levodopa-induced motor activity was decreased in comparison with that of the 18- to 20-day-old rats, possibly due to changing patterns of D1/D2-dopamine receptor subtype interactions. Levodopa 22-30 dopamine receptor D2 Rattus norvegicus 160-183 8950311-3 1996 This effect of alpha-MT, an inhibitor of tyrosine hydroxylase (TH), is partially reversible by co-administration of L-dihydroxyphenylalanine, the product of TH. Levodopa 116-140 pale Drosophila melanogaster 41-61 8950311-3 1996 This effect of alpha-MT, an inhibitor of tyrosine hydroxylase (TH), is partially reversible by co-administration of L-dihydroxyphenylalanine, the product of TH. Levodopa 116-140 pale Drosophila melanogaster 63-65 8750961-2 1995 Although the site of this conversion in the DA-denervated striatum has yet to be identified, it has been proposed that L-DOPA could be converted to DA at non-dopaminergic sites containing AADC. Levodopa 119-125 dopa decarboxylase Rattus norvegicus 188-192 8555803-12 1995 During the trial the dose of levodopa required to produce optimum motor control steadily increased in arm 1 (median daily dose 375 mg at 1 year and 625 mg at 4 years), but median dose in arm 2 did not change (375 mg). Levodopa 29-37 kallikrein related peptidase 4 Homo sapiens 102-107 8548806-4 1995 Within a few minutes of being injected with L-dihdroxyphenylalanine (L-DOPA), the product of TH, the DA-/- mice became more active and consumed more food than control mice. Levodopa 69-75 tyrosine hydroxylase Mus musculus 93-95 8530477-6 1995 The apparent Km value of the enzyme (designated the Dopa/tyrosine sulfotransferase) for L-Dopa, determined at a constant 14 microM of 3"-phosphoadenosine 5"-phosphosulfate, was 0.76 mM. Levodopa 88-94 sulfotransferase family 1B member 1 Rattus norvegicus 52-82 8750961-1 1995 The efficacy of L-dihydroxyphenylalanine (L-DOPA) in ameliorating the symptoms of Parkinson"s disease (PD) is attributed to its conversion to dopamine (DA) by the enzyme aromatic L-amino-acid decarboxylase (AADC) in the striatum. Levodopa 16-40 dopa decarboxylase Rattus norvegicus 170-205 8750961-6 1995 Acute administration of L-DOPA to DA-denervated animals elicited contralateral rotational behavior as well as a pronounced c-fos protein immunoreactivity in the striatum ipsilateral to the lesion. Levodopa 24-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 123-128 8750961-1 1995 The efficacy of L-dihydroxyphenylalanine (L-DOPA) in ameliorating the symptoms of Parkinson"s disease (PD) is attributed to its conversion to dopamine (DA) by the enzyme aromatic L-amino-acid decarboxylase (AADC) in the striatum. Levodopa 16-40 dopa decarboxylase Rattus norvegicus 207-211 8750961-9 1995 These results strongly suggest the existence of a class of AADC-containing striatal cells that can form DA from exogenous L-DOPA in the rat. Levodopa 122-128 dopa decarboxylase Rattus norvegicus 59-63 8750961-1 1995 The efficacy of L-dihydroxyphenylalanine (L-DOPA) in ameliorating the symptoms of Parkinson"s disease (PD) is attributed to its conversion to dopamine (DA) by the enzyme aromatic L-amino-acid decarboxylase (AADC) in the striatum. Levodopa 42-48 dopa decarboxylase Rattus norvegicus 170-205 8750961-1 1995 The efficacy of L-dihydroxyphenylalanine (L-DOPA) in ameliorating the symptoms of Parkinson"s disease (PD) is attributed to its conversion to dopamine (DA) by the enzyme aromatic L-amino-acid decarboxylase (AADC) in the striatum. Levodopa 42-48 dopa decarboxylase Rattus norvegicus 207-211 7595534-1 1995 Aromatic L-amino acid decarboxylase (AADC) is expressed in a wide variety of tissues, including those where it is known to convert L-DOPA and 5-hydroxytryptophan to dopamine and serotonin, respectively. Levodopa 131-137 dopa decarboxylase Homo sapiens 0-35 8787797-6 1995 The proposed pharmacokinetic model and the evaluation of carbidopa in this study will provide useful information for the development of drug delivery systems for levodopa or catechol-O-methyltransferase inhibitors, for further stabilization of plasma concentrations of levodopa in parkinsonian patients. Levodopa 269-277 catechol-O-methyltransferase Homo sapiens 174-202 7595534-1 1995 Aromatic L-amino acid decarboxylase (AADC) is expressed in a wide variety of tissues, including those where it is known to convert L-DOPA and 5-hydroxytryptophan to dopamine and serotonin, respectively. Levodopa 131-137 dopa decarboxylase Homo sapiens 37-41 8748929-16 1995 L-dopa, the precursor of DA, also blocked the AdoMet-induced motor effects. Levodopa 0-6 methionine adenosyltransferase 1A Rattus norvegicus 46-52 7556145-7 1995 Upon incubation of a melanosome-rich fraction with the melanin precursor L-3,4-dihydroxyphenylalanine (Dopa) followed by immunoblot analysis, the si locus protein, the p locus protein, and other putative matrix constituents became rapidly insoluble in SDS when compared with the members of the tyrosinase-related family of melanosomal membrane proteins. Levodopa 73-101 tyrosinase Homo sapiens 294-304 8747120-6 1995 In response to L-dopa and arginine hydrochloride stimulation, serum GH rose to above 7 mg/ml in all patients. Levodopa 15-21 growth hormone 1 Homo sapiens 68-70 7574470-2 1995 We have demonstrated expansion of the CAG trinucleotide repeat of the MJD1 gene located on chromosome 14q32.1 in 2 patients of Azorean descent who presented with levodopa-responsive atypical parkinsonism. Levodopa 162-170 ataxin 3 Homo sapiens 70-74 8726116-0 1995 Levodopa induces AP-1 and CREB DNA-binding activities in the rat striatum. Levodopa 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 8726116-1 1995 In order to elucidate the effect of levodopa and bromocriptine on the DNA-binding activities of transcription factors, AP-1 and CREB DNA-binding activities were investigated using gel-shift assay. Levodopa 36-44 cAMP responsive element binding protein 1 Rattus norvegicus 128-132 8726116-2 1995 Intraperitoneal administration of 100 mg/kg levodopa with 50 mg/kg benserazide in rats increased both AP-1 and CREB DNA-binding activities in the dorsolateral aspect of the striatum. Levodopa 44-52 cAMP responsive element binding protein 1 Rattus norvegicus 111-115 8583216-8 1995 IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p < 0.002) with amantadine uptake. Levodopa 67-75 interleukin 2 Homo sapiens 0-4 7567987-5 1995 Aromatic L-amino acid decarboxylase catalyzes the decarboxylation of L-5-hydroxytryptophan to serotonin and that of L-3,4-dihydroxyphenylalanine to dopamine. Levodopa 116-144 dopa decarboxylase Homo sapiens 0-35 8527287-0 1995 Pharmacokinetic-pharmacodynamic interaction between the COMT inhibitor tolcapone and single-dose levodopa. Levodopa 97-105 catechol-O-methyltransferase Homo sapiens 56-60 7643100-0 1995 Influence of selective inhibition of monoamine oxidase A or B on striatal metabolism of L-DOPA in hemiparkinsonian rats. Levodopa 88-94 monoamine oxidase A Rattus norvegicus 37-56 7644493-1 1995 Clones encoding pro-phenol oxidase [pro-PO; zymogen of phenol oxidase (monophenol, L-dopa:oxygen oxidoreductase, EC 1.14.18.1)] A1 were isolated from a lambda gt10 library that originated from Drosophila melanogaster strain Oregon-R male adults. Levodopa 83-89 Prophenoloxidase 1 Drosophila melanogaster 36-42 8665546-0 1995 Acute effects of COMT inhibition on L-DOPA pharmacokinetics in patients treated with carbidopa and selegiline. Levodopa 36-42 catechol-O-methyltransferase Homo sapiens 17-21 8665546-1 1995 The effects of acute catechol-O-methyltransferase (COMT) inhibition on L-DOPA pharmacokinetics were studied in 10 parkinsonian subjects on stable doses of L-DOPA/carbidopa and selegiline. Levodopa 71-77 catechol-O-methyltransferase Homo sapiens 51-55 8578949-5 1995 Whereas the oxidation of L-dopa catalysed by tyrosinase ws inhibited by L-tyrosine, the non-specific oxidation of D-dopa was not. Levodopa 25-31 tyrosinase Homo sapiens 45-55 7603406-3 1995 Growth hormone (GH) reserve was assessed by two different provocative stimuli (Clonidine and L-Dopa). Levodopa 93-99 growth hormone 1 Homo sapiens 0-14 7603406-3 1995 Growth hormone (GH) reserve was assessed by two different provocative stimuli (Clonidine and L-Dopa). Levodopa 93-99 growth hormone 1 Homo sapiens 16-18 7651438-1 1995 Recent experimental reports concerning L-dihydroxyphenylalanine (L-DOPA) and aromatic L-amino acid decarboxylase (AADC, L-DOPA decarboxylase) are reviewed in this article. Levodopa 120-126 dopa decarboxylase Homo sapiens 86-112 7494810-9 1995 CONCLUSIONS: This tripeptide, a potential prodrug of L-Dopa, is absorbed by the intestinal peptide transporter, is relatively stable in the gut wall, and is converted to L-Dopa by peptidases with the cleavage by pyroglutamyl aminopeptidase I to L-Dopa-Pro as the rate limiting step. Levodopa 53-59 pyroglutamyl-peptidase I Rattus norvegicus 212-241 7494810-9 1995 CONCLUSIONS: This tripeptide, a potential prodrug of L-Dopa, is absorbed by the intestinal peptide transporter, is relatively stable in the gut wall, and is converted to L-Dopa by peptidases with the cleavage by pyroglutamyl aminopeptidase I to L-Dopa-Pro as the rate limiting step. Levodopa 170-176 pyroglutamyl-peptidase I Rattus norvegicus 212-241 7582093-0 1995 Effects of nigrostriatal denervation and L-dopa therapy on the GABAergic neurons in the striatum in MPTP-treated monkeys and Parkinson"s disease: an in situ hybridization study of GAD67 mRNA. Levodopa 41-47 glutamate decarboxylase 1 Homo sapiens 180-185 7582093-4 1995 L-Dopa therapy significantly reduced GAD67 mRNA expression in the putamen and caudate nucleus to levels similar to those found in control monkeys. Levodopa 0-6 glutamate decarboxylase 1 Homo sapiens 37-42 7582093-8 1995 In parkinsonian patients who had been chronically treated with L-dopa, GAD67 mRNA expression was significantly decreased in all GABAergic neurons, in the caudate nucleus (by 44%), putamen (by 43.5%) and ventral striatum (by 26%). Levodopa 63-69 glutamate decarboxylase 1 Homo sapiens 71-76 7582093-9 1995 The opposite variation of GAD67 mRNA in patients with Parkinson"s disease, compared with MPTP-treated monkeys, might be explained by the combination of chronic nigrostriatal denervation and long-term L-dopa therapy. Levodopa 200-206 glutamate decarboxylase 1 Homo sapiens 26-31 7791123-0 1995 Rotation and striatal c-fos expression after repeated, daily treatment with selective dopamine receptor agonists and levodopa. Levodopa 117-125 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 22-27 8635184-1 1995 Tolcapone, a catechol-O-methyltransferase inhibitor, can interfere with the metabolism of levodopa and dopamine and could prolong the motor effect induced by levodopa in parkinsonian patients. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 13-41 8635184-1 1995 Tolcapone, a catechol-O-methyltransferase inhibitor, can interfere with the metabolism of levodopa and dopamine and could prolong the motor effect induced by levodopa in parkinsonian patients. Levodopa 158-166 catechol-O-methyltransferase Homo sapiens 13-41 7663983-10 1995 A significant increase of [3H]FNZ binding in the GPi only of dyskinetic monkeys, namely those treated with pulsatile U91356A or levodopa was seen compared to untreated MPTP or naive controls. Levodopa 128-136 glucose-6-phosphate isomerase Macaca fascicularis 49-52 7651438-3 1995 Administration of exogenous L-DOPA affects dopamine receptor status, AADC activity, and mitochondrial oxidation in experimental animals. Levodopa 28-34 dopa decarboxylase Homo sapiens 69-73 7651456-7 1995 The acute inhibition of amino acid decarboxylase, monoamine oxidase-B, and COMT is well tolerated and prolongs the L-DOPA response in PD patients. Levodopa 115-121 monoamine oxidase B Homo sapiens 50-69 7651456-7 1995 The acute inhibition of amino acid decarboxylase, monoamine oxidase-B, and COMT is well tolerated and prolongs the L-DOPA response in PD patients. Levodopa 115-121 catechol-O-methyltransferase Homo sapiens 75-79 7715703-5 1995 Administration of L-DOPA (dihydroxyphenylalanine), the product of the tyrosine hydroxylase reaction, to pregnant females results in complete rescue of mutant mice in utero. Levodopa 18-24 tyrosine hydroxylase Mus musculus 70-90 7637869-0 1995 Chronic L-DOPA treatment differentially regulates gene expression of glutamate decarboxylase, preproenkephalin and preprotachykinin in the striatum of 6-hydroxydopamine-lesioned rat. Levodopa 8-14 glutamate-ammonia ligase Rattus norvegicus 69-92 7637869-3 1995 Treatment with L-DOPA (200 mg/kg/24 h) for eight weeks reduced but did not abolish the 6-hydroxydopamine lesion-induced elevation of preproenkephalin messenger RNA and slightly reduced the elevation of glutamate decarboxylase (M(r) 67,000) messenger RNA in denervated striatum relative to intact side and control groups. Levodopa 15-21 glutamate-ammonia ligase Rattus norvegicus 202-225 7637869-5 1995 The effect of L-DOPA on the gene expression of preproenkephalin and glutamate decarboxylase (M(r) 67,000) differs from the increase in striatal enkephalin content and glutamate decarboxylase activity previously found following L-DOPA treatment. Levodopa 14-20 glutamate-ammonia ligase Rattus norvegicus 68-91 7637869-5 1995 The effect of L-DOPA on the gene expression of preproenkephalin and glutamate decarboxylase (M(r) 67,000) differs from the increase in striatal enkephalin content and glutamate decarboxylase activity previously found following L-DOPA treatment. Levodopa 14-20 proenkephalin Rattus norvegicus 53-63 7637869-5 1995 The effect of L-DOPA on the gene expression of preproenkephalin and glutamate decarboxylase (M(r) 67,000) differs from the increase in striatal enkephalin content and glutamate decarboxylase activity previously found following L-DOPA treatment. Levodopa 227-233 glutamate-ammonia ligase Rattus norvegicus 68-91 7637869-5 1995 The effect of L-DOPA on the gene expression of preproenkephalin and glutamate decarboxylase (M(r) 67,000) differs from the increase in striatal enkephalin content and glutamate decarboxylase activity previously found following L-DOPA treatment. Levodopa 227-233 proenkephalin Rattus norvegicus 53-63 7542537-6 1995 Furthermore, this MPTP-induced decrease in CCK-8 persisted with repeated levodopa administration; therefore, the ineffectiveness of the levodopa treatment may have been be due to the degeneration of the nigrostriatal DA neurons. Levodopa 73-81 cholecystokinin Mus musculus 43-46 7542537-8 1995 The CCK-8 level decreased in the thalamus+midbrain, hippocampus and hindbrain of the MPTP+levodopa-treated group, although there were no changes in the MPTP-treated controls. Levodopa 90-98 cholecystokinin Mus musculus 4-7 7830076-6 1995 Catalase or superoxide dismutase each partially protected against L-DOPA toxicity in PC12 cells. Levodopa 66-72 catalase Rattus norvegicus 0-8 7884499-1 1995 UNLABELLED: The goal of this study was to examine the relationship between D2 dopamine receptor density and levodopa dosage, disease duration and dyskinesia in Parkinson"s disease (PD). Levodopa 108-116 dopamine receptor D2 Homo sapiens 75-95 7768276-4 1995 Catechol-O-methyltransferase inhibitors could be beneficial as adjunct drugs of L-DOPA not only in Parkinson"s disease but also in the coincident depressive illness. Levodopa 80-86 catechol-O-methyltransferase Rattus norvegicus 0-28 8665534-1 1995 We studied the effect of entacapone, a catechol-O-methyltransferase (COMT) inhibitor, on the pharmacokinetics and metabolism of levodopa after administration of a controlled-release (CR) levodopa-carbidopa preparation (Sinemet CR) in an open, randomized trial in 12 healthy male volunteers. Levodopa 128-136 catechol-O-methyltransferase Homo sapiens 69-73 7830050-1 1995 L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B. Levodopa 0-28 monoamine oxidase B Homo sapiens 243-267 7830050-1 1995 L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B. Levodopa 30-36 monoamine oxidase B Homo sapiens 243-267 7766285-5 1995 It is suggested that 5-HT2A receptor blockade is the most likely basis for the effectiveness of clozapine in L-DOPA psychosis. Levodopa 109-115 5-hydroxytryptamine receptor 2A Homo sapiens 21-36 8785021-0 1995 Synergistic interactions between COMT-/MAO-inhibitors and L-Dopa in MPTP-treated mice. Levodopa 58-64 catechol-O-methyltransferase Mus musculus 33-37 7826365-5 1995 When L-dopa is substrate, 6-BH4 does not inhibit the enzyme implicating separate binding sites for L-dopa and L-tyrosine on tyrosinase. Levodopa 99-105 tyrosinase Homo sapiens 124-134 8728769-2 1995 Inactivation of lipoamide dehydrogenase (LipDH) by the Cu(II)/H2O2 Fenton system (SF-Cu(II): (5.0 microM Cu(II), 3.0 mM H2O2) was enhanced by catecholamines (CAs), namely, epinephrine, levoDOPA (DOPA), DOPAMINE, 6-hydroxyDOPAMINE (OH-DOPAMINE) and related compounds (DOPAC, CATECHOL, etc.). Levodopa 185-193 dihydrolipoamide dehydrogenase Homo sapiens 16-39 9620056-0 1995 In vivo comparison of the effects of inhibition of MAO-A versus MAO-B on striatal L-DOPA and dopamine metabolism. Levodopa 82-88 monoamine oxidase A Rattus norvegicus 51-56 9620056-0 1995 In vivo comparison of the effects of inhibition of MAO-A versus MAO-B on striatal L-DOPA and dopamine metabolism. Levodopa 82-88 monoamine oxidase B Rattus norvegicus 64-69 9620056-3 1995 Extracellular levels of dopamine were enhanced and DA metabolite levels strongly inhibited both under basal conditions and following L-DOPA administration by pretreatment with the nonselective MAO inhibitor pargyline and the MAO-A selective inhibitors clorgyline and Ro 41-1049. Levodopa 133-139 monoamine oxidase A Rattus norvegicus 225-230 9620056-7 1995 In contrast, both MAO-A and MAO-B mediate DA formation when L-DOPA is administered exogenously. Levodopa 60-66 monoamine oxidase A Rattus norvegicus 18-23 9620056-7 1995 In contrast, both MAO-A and MAO-B mediate DA formation when L-DOPA is administered exogenously. Levodopa 60-66 monoamine oxidase B Rattus norvegicus 28-33 7475917-1 1995 The peripheral decarboxylase inhibitors benserazide and carbidopa, often administered in combination with L-dopa in the treatment of Parkinson"s disease, are also very good inhibitors of semicarbazide-sensitive amine oxidase (SSAO). Levodopa 106-112 amine oxidase copper containing 2 Homo sapiens 187-224 7475917-2 1995 In untreated patients and in patients treated with L-dopa alone, plasma SSAO activity is normal. Levodopa 51-57 amine oxidase copper containing 2 Homo sapiens 72-76 7475917-3 1995 In patients treated with L-dopa plus benserazide or carbidopa (Madopar or Sinemnet), however, plasma SSAO activity is strongly inhibited, contrary to the paradoxical 3-fold increase in plasma aromatic-L-amino acid decarboxylase activity we reported previously. Levodopa 25-31 amine oxidase copper containing 2 Homo sapiens 101-105 7669403-3 1995 The patients had a delayed plasma thyroid stimulating hormone (TSH) response and plasma PRL excessive response to thyrotropin releasing hormone (TRH), and a low plasma growth hormone releasing hormone (GRF) response to L-dopa. Levodopa 219-225 growth hormone releasing hormone Homo sapiens 168-200 7669403-3 1995 The patients had a delayed plasma thyroid stimulating hormone (TSH) response and plasma PRL excessive response to thyrotropin releasing hormone (TRH), and a low plasma growth hormone releasing hormone (GRF) response to L-dopa. Levodopa 219-225 growth hormone releasing hormone Homo sapiens 202-205 7874502-10 1994 These results suggest that the reduced striatal DA peak in the gliotic striatum after L-dopa administration was due to accelerated DA catabolism through enhanced MAO activity. Levodopa 86-92 monoamine oxidase A Rattus norvegicus 162-165 8584678-4 1995 In Parkinson"s disease AAAD is the rate-controlling enzyme for the synthesis of DA when L-DOPA is administered and any change of AAAD activity could have clinical consequences. Levodopa 88-94 dopa decarboxylase Homo sapiens 23-27 8584678-4 1995 In Parkinson"s disease AAAD is the rate-controlling enzyme for the synthesis of DA when L-DOPA is administered and any change of AAAD activity could have clinical consequences. Levodopa 88-94 dopa decarboxylase Homo sapiens 129-133 7697371-1 1994 The aim of the present study is to examine whether aromatic L-amino acid decarboxylase (AADC) catalyzes the conversion of exogenous L-3,4-dihydroxyphenylalanine (L-DOPA) to dopamine in serotonin neurons of the rat dorsal raphe nucleus. Levodopa 132-160 dopa decarboxylase Rattus norvegicus 60-86 7697371-1 1994 The aim of the present study is to examine whether aromatic L-amino acid decarboxylase (AADC) catalyzes the conversion of exogenous L-3,4-dihydroxyphenylalanine (L-DOPA) to dopamine in serotonin neurons of the rat dorsal raphe nucleus. Levodopa 132-160 dopa decarboxylase Rattus norvegicus 88-92 7697371-1 1994 The aim of the present study is to examine whether aromatic L-amino acid decarboxylase (AADC) catalyzes the conversion of exogenous L-3,4-dihydroxyphenylalanine (L-DOPA) to dopamine in serotonin neurons of the rat dorsal raphe nucleus. Levodopa 162-168 dopa decarboxylase Rattus norvegicus 60-86 7697371-1 1994 The aim of the present study is to examine whether aromatic L-amino acid decarboxylase (AADC) catalyzes the conversion of exogenous L-3,4-dihydroxyphenylalanine (L-DOPA) to dopamine in serotonin neurons of the rat dorsal raphe nucleus. Levodopa 162-168 dopa decarboxylase Rattus norvegicus 88-92 7697371-4 1994 The present result suggests that AADC decarboxylating L-5-hydroxytryptophan to serotonin in physiological conditions is also able to catalyze the in vivo decarboxylation of exogenous L-DOPA. Levodopa 183-189 dopa decarboxylase Rattus norvegicus 33-37 7867755-1 1994 It has been suggested that levodopa (L-dopa), a dopamine precursor used to treat Parkinson"s disease, may be toxic to grafted fetal neuroblasts; if so, the use of the monoamine oxidase B inhibitor selegiline might prevent such toxicity. Levodopa 27-35 monoamine oxidase B Rattus norvegicus 167-186 7867755-1 1994 It has been suggested that levodopa (L-dopa), a dopamine precursor used to treat Parkinson"s disease, may be toxic to grafted fetal neuroblasts; if so, the use of the monoamine oxidase B inhibitor selegiline might prevent such toxicity. Levodopa 37-43 monoamine oxidase B Rattus norvegicus 167-186 7886620-0 1994 Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats. Levodopa 77-83 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 49-54 7886620-2 1994 Combined D1/D2 receptor stimulation by L-dopa activates c-fos in a manner not additive with muscarinic receptor blockade by scopolamine. Levodopa 39-45 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 56-61 7886620-3 1994 On the other hand, blockade of NMDA receptors by MK 801 reduced c-fos expression induced by L-dopa while, depending on the dose of L-dopa, differentially affecting contralateral turning behavior. Levodopa 92-98 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 64-69 7931332-5 1994 Moreover, the threonine phosphorylation of DARPP-32 produced by maximally effective doses of either forskolin (in striatum) or L-3,4-dihydroxyphenylalanine (in substantia nigra) was increased further by GABA. Levodopa 127-155 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 43-51 7914399-3 1994 The reduced expression of tyrosine hydroxylase may be due to either the evolving neurodegenerative process or its downregulation, possibly secondary to chronic levodopa treatment. Levodopa 160-168 tyrosine 3-monooxygenase Macaca fascicularis 26-46 7957769-7 1994 In conclusion, the inhibitory effect of tolcapone on the O-methylation of levodopa to 3-OMD by COMT is largely due to improved levodopa and dopamine availability in the brain, and to the reduced formation of 3-OMD. Levodopa 74-82 catechol-O-methyltransferase Mus musculus 95-99 7957769-7 1994 In conclusion, the inhibitory effect of tolcapone on the O-methylation of levodopa to 3-OMD by COMT is largely due to improved levodopa and dopamine availability in the brain, and to the reduced formation of 3-OMD. Levodopa 127-135 catechol-O-methyltransferase Mus musculus 95-99 7729088-11 1994 2) After L-dopa treatment, rCBF was significantly increased only in the striatum as compared with the pretreatment level (51.9 +/- 9.3-->63.1 +/- 9.9 ml/100 g/min, p < 0.01). Levodopa 9-15 CCAAT/enhancer binding protein zeta Rattus norvegicus 27-31 7834959-8 1994 On the other hand, the metabolites of NA and DA by catechol-O-methyltransferase (COMT), normetanephrine (NMN) and 3-methoxytyramine (3-MT), decreased in the patients treated with droxidopa and L-DOPA compared with the patients administered with L-DOPA alone and control patients. Levodopa 193-199 catechol-O-methyltransferase Homo sapiens 81-85 7834959-8 1994 On the other hand, the metabolites of NA and DA by catechol-O-methyltransferase (COMT), normetanephrine (NMN) and 3-methoxytyramine (3-MT), decreased in the patients treated with droxidopa and L-DOPA compared with the patients administered with L-DOPA alone and control patients. Levodopa 245-251 catechol-O-methyltransferase Homo sapiens 81-85 7937819-8 1994 L-Dopa produced marked CREB phosphorylation in striatal neurons in rats ipsilateral, but not contralateral, to a 6-hydroxydopamine lesion. Levodopa 0-6 cAMP responsive element binding protein 1 Rattus norvegicus 23-27 7984527-4 1994 This illustrates the potential use of IBZM tomoscintigraphy to identify Parkinson-like"s disease presenting with decreased dopamine D2 receptor density; and hence to predict L-Dopa effectiveness. Levodopa 174-180 dopamine receptor D2 Homo sapiens 123-143 7839669-3 1994 It may be suggested that madopare withdrawal-induced decreases in MAO activity might be, to a certain extent, a cause of dyskinesias occurring after discontinuation of L-DOPA drugs. Levodopa 168-174 monoamine oxidase A Rattus norvegicus 66-69 7993663-3 1994 Two patients with propionic acidemia had decreased growth hormone secretion in response to provocative stimuli (intravenous L-arginine and oral levodopa or clonidine); the remaining subjects had sufficient growth hormone secretion. Levodopa 144-152 growth hormone 1 Homo sapiens 51-65 7952244-3 1994 Clinical studies show that COMT inhibitors prolong the action of levodopa in patients with the "wearing off" phenomenon. Levodopa 65-73 catechol-O-methyltransferase Homo sapiens 27-31 8079344-4 1994 Exposure of wild-type (CHO/WT) or CHO/AADC cultures to L-dopa (62 to 500 microM) resulted in intracellular accumulation of L-dopa or L-dopa and dopamine, respectively, that was concentration-dependent. Levodopa 55-61 dopa decarboxylase Bos taurus 38-42 8079344-4 1994 Exposure of wild-type (CHO/WT) or CHO/AADC cultures to L-dopa (62 to 500 microM) resulted in intracellular accumulation of L-dopa or L-dopa and dopamine, respectively, that was concentration-dependent. Levodopa 123-129 dopa decarboxylase Bos taurus 38-42 8079344-4 1994 Exposure of wild-type (CHO/WT) or CHO/AADC cultures to L-dopa (62 to 500 microM) resulted in intracellular accumulation of L-dopa or L-dopa and dopamine, respectively, that was concentration-dependent. Levodopa 123-129 dopa decarboxylase Bos taurus 38-42 8079344-9 1994 Although CHO/AADC cultures were more sensitive than CHO/WT to L-dopa and Mn, this was completely accounted for by the differences in intracellular catechol levels between the two cell lines. Levodopa 62-68 dopa decarboxylase Bos taurus 13-17 7952244-6 1994 Thus, COMT inhibitors and clozapine provide new opportunities for the treatment of patients with longstanding PD and fluctuating responses to levodopa. Levodopa 142-150 catechol-O-methyltransferase Homo sapiens 6-10 8027058-13 1994 The DHICA oxidase activity of LEMT displayed a Km for DHICA of about 0.8 mM, as compared to 1.9 mM for L-DOPA and 0.23 nM for L-tyrosine. Levodopa 103-109 tyrosinase-related protein 1 Mus musculus 4-17 8058159-4 1994 This study suggests that beta 2-adrenergic agonists as adjunct therapy to levodopa may be beneficial in PD. Levodopa 74-82 ATPase H+ transporting V0 subunit a2 Homo sapiens 25-31 7945976-7 1994 Both COMT inhibitors suppressed the L-dopa induced increase of 3-OMD plasma levels, OR-486 being more effective than OR-462. Levodopa 36-42 catechol-O-methyltransferase Rattus norvegicus 5-9 7920871-0 1994 Reduced growth hormone response to L-dopa and pyridostigmine in obesity. Levodopa 35-41 growth hormone 1 Homo sapiens 8-22 8035323-1 1994 Catechol-O-methyltransferase (COMT) catalyzes the O-methylation of catecholamine and catechol drugs such as levodopa and methyldopa. Levodopa 108-116 catechol-O-methyltransferase Homo sapiens 0-28 7920871-5 1994 Growth hormone responses and GH area under the response curve (AUC) to L-dopa were significantly lower in obese subjects than those in controls. Levodopa 71-77 growth hormone 1 Homo sapiens 29-31 7920871-6 1994 Pyridostigmine significantly enhanced the GH response to L-dopa in both obese and control subjects. Levodopa 57-63 growth hormone 1 Homo sapiens 42-44 7920871-7 1994 However, enhanced GH responses in obese subjects were attenuated biologically and lower than those in controls with L-dopa only. Levodopa 116-122 growth hormone 1 Homo sapiens 18-20 8207420-0 1994 L-3,4-dihydroxyphenylalanine-induced dopamine release in the striatum of intact and 6-hydroxydopamine-treated rats: differential effects of monoamine oxidase A and B inhibitors. Levodopa 0-28 monoamine oxidase A Rattus norvegicus 140-159 8207420-10 1994 The present findings indicate that deamination by monoamine oxidase A is the primary mechanism for catabolism of striatal dopamine, both under basal conditions and after administration of exogenous L-DOPA. Levodopa 198-204 monoamine oxidase A Rattus norvegicus 50-69 8035323-1 1994 Catechol-O-methyltransferase (COMT) catalyzes the O-methylation of catecholamine and catechol drugs such as levodopa and methyldopa. Levodopa 108-116 catechol-O-methyltransferase Homo sapiens 30-34 7937580-6 1994 Fetal skin samples incubated with L-DOPA solution indicated a lack of tyrosinase activity and showed that the melanosomes had not progressed beyond stage II. Levodopa 34-40 tyrosinase Homo sapiens 70-80 8075859-16 1994 In conclusion, the present results show that both L-DOPA and GluDOPA give origin to substantial amounts of dopamine and the newly-formed amine undergoes considerable deamination to DOPAC.However, dopamine originating from GluDOPA was less deaminated than that resulting from L-DOPA;it appears that this different behaviour may concern aspects related to the formation of the amine and also those related to its deamination and disposition, namely the processes involved in the access of newly-formed dopamine to MAO. Levodopa 50-56 monoamine oxidase A Rattus norvegicus 512-515 7518301-7 1994 In the presence of L-dopa/carbidopa, a peripherally active inhibitor of catechol O-methyltransferase (COMT) entacapone had a short-lasting increasing effect on L-dopa efflux. Levodopa 19-25 catechol-O-methyltransferase Rattus norvegicus 72-100 7971745-1 1994 Human TRP-1 has been immunopurified from normal human melanocytes cultured from black neonatal subjects and used to investigate the catalytic function of TRP-1 for the two substrates, L-tyrosine and L-DOPA. Levodopa 199-205 tRNA-Pro (anticodon AGG) 2-5 Homo sapiens 6-11 7971745-1 1994 Human TRP-1 has been immunopurified from normal human melanocytes cultured from black neonatal subjects and used to investigate the catalytic function of TRP-1 for the two substrates, L-tyrosine and L-DOPA. Levodopa 199-205 tRNA-Pro (anticodon AGG) 2-5 Homo sapiens 154-159 7971745-4 1994 However, there was apparent TH activity exhibited by immunopurified TRP-1 under conditions with low tyrosine concentration (< or = 0.8 microCi/ml of 3H-tyrosine), prolonged incubation time (i.e., overnight) and in the absence of the cofactor L-DOPA. Levodopa 245-251 tRNA-Pro (anticodon AGG) 2-5 Homo sapiens 68-73 8197131-1 1994 Dark-eyed albino (C44H) is a recessive allele at the mouse albino (c) locus, which encodes tyrosinase (monophenol,L-dopa:oxygen oxidoreductase, EC 1.14.18.1), the key enzyme in melanin synthesis. Levodopa 114-120 tyrosinase Mus musculus 91-101 7912958-9 1994 The steroid also significantly increased TH activity in the lateral retrochiasmatic area as assessed by the formation of L-3-4 dihydroxyphenylalanine (L-DOPA). Levodopa 121-149 tyrosine hydroxylase Homo sapiens 41-43 7912958-9 1994 The steroid also significantly increased TH activity in the lateral retrochiasmatic area as assessed by the formation of L-3-4 dihydroxyphenylalanine (L-DOPA). Levodopa 151-157 tyrosine hydroxylase Homo sapiens 41-43 7518301-7 1994 In the presence of L-dopa/carbidopa, a peripherally active inhibitor of catechol O-methyltransferase (COMT) entacapone had a short-lasting increasing effect on L-dopa efflux. Levodopa 19-25 catechol-O-methyltransferase Rattus norvegicus 102-106 7518301-7 1994 In the presence of L-dopa/carbidopa, a peripherally active inhibitor of catechol O-methyltransferase (COMT) entacapone had a short-lasting increasing effect on L-dopa efflux. Levodopa 160-166 catechol-O-methyltransferase Rattus norvegicus 72-100 7518301-7 1994 In the presence of L-dopa/carbidopa, a peripherally active inhibitor of catechol O-methyltransferase (COMT) entacapone had a short-lasting increasing effect on L-dopa efflux. Levodopa 160-166 catechol-O-methyltransferase Rattus norvegicus 102-106 8064113-2 1994 The assay measures the pink pigment formed by the reaction of Besthorn"s hydrazone (3-methyl-2-benzothiazoninone hydrazone, or MBTH) with dopaquinone, the product of oxidation of L-dopa by tyrosinase. Levodopa 179-185 tyrosinase Homo sapiens 189-199 8190296-0 1994 Effect of peripheral catechol-O-methyltransferase inhibition on the pharmacokinetics and pharmacodynamics of levodopa in parkinsonian patients. Levodopa 109-117 catechol-O-methyltransferase Homo sapiens 21-49 8190296-1 1994 Catechol-O-methyltransferase (COMT) metabolizes a portion of administered levodopa and thus makes it unavailable for conversion to dopamine in the brain. Levodopa 74-82 catechol-O-methyltransferase Homo sapiens 0-28 8190296-1 1994 Catechol-O-methyltransferase (COMT) metabolizes a portion of administered levodopa and thus makes it unavailable for conversion to dopamine in the brain. Levodopa 74-82 catechol-O-methyltransferase Homo sapiens 30-34 8190296-9 1994 We conclude that inhibition of COMT by entacapone increases the plasma half-life of levodopa and augments the antiparkinsonian effects of single and repeated doses of levodopa. Levodopa 84-92 catechol-O-methyltransferase Homo sapiens 31-35 8190296-9 1994 We conclude that inhibition of COMT by entacapone increases the plasma half-life of levodopa and augments the antiparkinsonian effects of single and repeated doses of levodopa. Levodopa 167-175 catechol-O-methyltransferase Homo sapiens 31-35 8004447-0 1994 The effects of chronic continuous versus intermittent levodopa treatments on striatal and extrastriatal D1 and D2 dopamine receptors and dopamine uptake sites in the 6-hydroxydopamine lesioned rat--an autoradiographic study. Levodopa 54-62 dopamine receptor D2 Rattus norvegicus 104-132 8207328-1 1994 In melanocytes, the biosynthesis of L-dopa derived indole polymer, melanin, is accelerated by tyrosinase and related enzymes. Levodopa 36-42 tyrosinase Homo sapiens 94-104 8127373-3 1994 COMT also inactivates catechol-type compounds such as L-DOPA. Levodopa 54-60 catechol-O-methyltransferase Homo sapiens 0-4 7638039-4 1994 Nadir plasma PRL levels during levodopa tests were significantly increased before and during treatment. Levodopa 31-39 prolactin Homo sapiens 13-16 8305475-6 1994 In the presence of tyrosinase, the binding of L-Dopa-derived intermediates to BSA was also decreased by DCT and the percentage of decrease was even higher than using L-DC as initial melanin precursor. Levodopa 46-52 dopachrome tautomerase Homo sapiens 104-107 7638039-6 1994 Peak plasma PRL levels during TRH tests and nadir plasma PRL levels during levodopa tests were also significantly increased. Levodopa 75-83 prolactin Homo sapiens 57-60 27520516-6 1994 COMT inhibitors also decrease the levels of COMT-dependent metabolites of adrenaline (epinephrine) and noradrenaline (norepinephrine) in plasma.Entacapone, to1capone and CGP 28014 improve the bioavailability of levodopa and inhibit the formation of 3-0-methyldopa in human volunteers. Levodopa 211-219 catechol-O-methyltransferase Homo sapiens 0-4 27520516-6 1994 COMT inhibitors also decrease the levels of COMT-dependent metabolites of adrenaline (epinephrine) and noradrenaline (norepinephrine) in plasma.Entacapone, to1capone and CGP 28014 improve the bioavailability of levodopa and inhibit the formation of 3-0-methyldopa in human volunteers. Levodopa 211-219 catechol-O-methyltransferase Homo sapiens 44-48 8126502-0 1994 Effect of entacapone, a peripherally acting catechol-O-methyltransferase inhibitor, on the motor response to acute treatment with levodopa in patients with Parkinson"s disease. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 44-72 8126502-1 1994 Catechol-O-methyltransferase (COMT) inhibitors may be useful in the treatment of Parkinson"s disease by improving the bioavailability of levodopa and by prolonging its effects. Levodopa 137-145 catechol-O-methyltransferase Homo sapiens 0-28 8126502-1 1994 Catechol-O-methyltransferase (COMT) inhibitors may be useful in the treatment of Parkinson"s disease by improving the bioavailability of levodopa and by prolonging its effects. Levodopa 137-145 catechol-O-methyltransferase Homo sapiens 30-34 8126502-5 1994 Plasma levodopa concentrations were increased with both doses of the COMT inhibitor. Levodopa 7-15 catechol-O-methyltransferase Homo sapiens 69-73 7893372-0 1994 Role of D1 receptor mechanisms in the potentiation of motor responses to L-dopa and apomorphine by MK 801 in the reserpine-treated mouse. Levodopa 73-79 dopamine receptor D1 Mus musculus 8-19 8070503-3 1994 High red blood cell (RBC) COMT activity has been correlated with a poor response to levodopa treatment in Parkinson"s disease. Levodopa 84-92 catechol-O-methyltransferase Homo sapiens 26-30 9160587-0 1994 Growth hormone response to clonidine and L-dopa in normal volunteers. Levodopa 41-47 growth hormone 1 Homo sapiens 0-14 7893380-0 1994 Effect of a selective MAO-A inhibitor (Ro 41-1049) on striatal L-dopa and dopamine metabolism: an in vivo study. Levodopa 63-69 monoamine oxidase A Rattus norvegicus 22-27 8263548-4 1994 In animals treated with MPTP, L-DOPA-evoked DA release was reduced significantly in CD-1 mice, but not in C57/B1 mice, treated with testosterone. Levodopa 30-36 CD1 antigen complex Mus musculus 84-88 7893380-4 1994 We conclude that inhibition of central MAO-A activity promotes synaptic accumulation of dopamine following administration of pharmacological doses of L-dopa. Levodopa 150-156 monoamine oxidase A Rattus norvegicus 39-44 8263548-8 1994 More interestingly, they show an important differential modulatory effect of testosterone upon L-DOPA-evoked DA release as a function of MPTP treatment and indicate that testosterone significantly alters the neurotoxic effects of MPTP in the CD-1 mouse. Levodopa 95-101 CD1 antigen complex Mus musculus 242-246 8579765-12 1994 In fact, after levodopa plus benserazide, naloxone-induced ACTH, cortisol and LH increments in parkinsonian patients were significantly higher than before therapy and were indistinguishable from those observed in the normal controls. Levodopa 15-23 proopiomelanocortin Homo sapiens 59-63 8239566-9 1993 Reduced glutathione, ascorbate, superoxide dismutase, and catalase prevented the effect of levodopa and dopamine on complex I. Levodopa 91-99 catalase Homo sapiens 58-66 7900446-3 1994 It is suggested that a decrease in MAO activity after madapar cessation may be responsible for dyskinesia arising after cessation of L-DOPA preparations treatment. Levodopa 133-139 monoamine oxidase A Rattus norvegicus 35-38 8243704-0 1993 Diminished growth hormone responses to L-dopa in polycystic ovarian disease. Levodopa 39-45 growth hormone 1 Homo sapiens 11-25 8255478-0 1993 Catechol-O-methyltransferase inhibitor tolcapone prolongs levodopa/carbidopa action in parkinsonian patients. Levodopa 58-66 catechol-O-methyltransferase Homo sapiens 0-28 8119326-6 1993 We conclude that L-dopa-induced circling behaviour is enhanced and prolonged by all types of catechol O-methyltransferase inhibitors regardless of their brain penetration. Levodopa 17-23 catechol-O-methyltransferase Rattus norvegicus 93-121 8112501-0 1993 Specific increase of L-dopa levels in plasma upon infusion of tyrosinase containing liposomes. Levodopa 21-27 tyrosinase Rattus norvegicus 62-72 8112501-6 1993 From the experiments, evidence has been obtained that liposome-entrapped tyrosinase is able to affect specifically L-3,4-dihydroxyphenylalanine (L-DOPA) levels which increase dramatically. Levodopa 115-143 tyrosinase Rattus norvegicus 73-83 8112501-6 1993 From the experiments, evidence has been obtained that liposome-entrapped tyrosinase is able to affect specifically L-3,4-dihydroxyphenylalanine (L-DOPA) levels which increase dramatically. Levodopa 145-151 tyrosinase Rattus norvegicus 73-83 8112501-8 1993 The possible use of liposome-entrapped tyrosinase to raise L-DOPA levels in catecholamine related disorders is discussed. Levodopa 59-65 tyrosinase Rattus norvegicus 39-49 8246167-6 1993 Superfusion with the aromatic L-amino acid decarboxylase (AADC) inhibitor NSD-1055 (250 microM) abolished the inhibitory effects of L-DOPA, as did L-sulpiride (1 microM), an inhibitor of DA receptors of the D2 subtype. Levodopa 132-138 dopa decarboxylase Rattus norvegicus 21-56 8301021-4 1993 Methyl dopa (MD), levodopa (LD) or methyl catechol (MC) were conjugated to rabbit serum albumin (RSA) under high pH (base) conditions or by a tyrosinase (tyr) catalyzed reaction. Levodopa 18-26 tyrosinase Oryctolagus cuniculus 142-152 8123719-1 1993 An enzyme-amperometric method is proposed for the analysis of total phenols and L-dopa; the method is based on the enzyme tyrosinase, which is immobilized in a Nylon membrane and coupled to an oxygen gas-diffusion amperometric electrode. Levodopa 80-86 tyrosinase Homo sapiens 122-132 8246167-6 1993 Superfusion with the aromatic L-amino acid decarboxylase (AADC) inhibitor NSD-1055 (250 microM) abolished the inhibitory effects of L-DOPA, as did L-sulpiride (1 microM), an inhibitor of DA receptors of the D2 subtype. Levodopa 132-138 dopa decarboxylase Rattus norvegicus 58-62 7901010-8 1993 The tyrosinase activity of control and theophylline-treated extracts displayed several kinetic differences, including different Km values for both substrates and requirements for the cofactor L-dopa. Levodopa 192-198 tyrosinase Homo sapiens 4-14 7903989-1 1993 HPD is a clinical entity characterized by childhood-onset postural dystonia, which shows marked diurnal fluctuation (aggravation of symptoms towards evening and their alleviation in the morning after sleep), and dramatic and sustained response to levodopa without any adverse effects, such as wearing-off or dyskinesia. Levodopa 247-255 4-hydroxyphenylpyruvate dioxygenase Homo sapiens 0-3 8513959-0 1993 Growth hormone response to L-dopa and pyridostigmine in women with polycystic ovarian syndrome. Levodopa 27-33 growth hormone 1 Homo sapiens 0-14 8270948-2 1993 After incubation with 5 mM L-DOPA for several hours the endogenous tyrosinase of the haemolymph forms an electron dense reaction product. Levodopa 27-33 tyrosinase Homo sapiens 67-77 8108317-4 1993 When the dopa decarboxylase inhibitor alpha-methyldopa is added to the incubation medium, it reduces DA levels and conversely increases the amount of L-DOPA in a dose-dependent manner. Levodopa 150-156 dopa decarboxylase Rattus norvegicus 9-27 8237142-1 1993 Aromatic L-amino acid decarboxylase (AADC) decarboxylates both L-5-hydroxytryptophan to serotonin in serotonergic neurons and pineal cells, and L-dopa to dopamine in catecholaminergic neurons and adrenal medullary cells. Levodopa 144-150 dopa decarboxylase Homo sapiens 0-35 8237142-1 1993 Aromatic L-amino acid decarboxylase (AADC) decarboxylates both L-5-hydroxytryptophan to serotonin in serotonergic neurons and pineal cells, and L-dopa to dopamine in catecholaminergic neurons and adrenal medullary cells. Levodopa 144-150 dopa decarboxylase Homo sapiens 37-41 8237142-5 1993 We expressed a recombinant human AADC in COS cells and proved that the expressed enzyme decarboxylated both L-5-hydroxytryptophan to serotonin and L-dopa to dopamine. Levodopa 147-153 dopa decarboxylase Homo sapiens 33-37 8221117-0 1993 L-dopa stimulates c-fos expression in dopamine denervated striatum by combined activation of D-1 and D-2 receptors. Levodopa 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 18-23 8221117-1 1993 Administration of L-dopa to unilaterally 6-hydroxydopamine-lesioned rats, activates the early gene c-fos in the lesioned caudate-putamen. Levodopa 18-24 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-104 8221117-2 1993 D-1 receptor blockade by SCH 23390, prevented L-dopa-induced Fos-like immunoreactivity in the whole caudate-putamen, while D-2 receptor blockade by raclopride reduced Fos-like immunoreactivity only in the dorso-lateral portion. Levodopa 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 61-64 8221117-3 1993 The results suggest that L-dopa induces c-fos primarily through an activation of D-1 receptors, while D-2 receptor stimulation plays a facilitatory influence on D-1-mediated c-fos expression. Levodopa 25-31 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 40-45 7901395-0 1993 Differential effect of selective D-1 and D-2 dopamine receptor agonists on levodopa-induced dyskinesia in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- exposed monkeys. Levodopa 75-83 dopamine receptor D2 Homo sapiens 41-62 7682705-1 1993 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to 3,4-dihydroxy-L-phenylalanine, the first and rate-limiting step in catecholamine biosynthesis. Levodopa 68-97 tyrosine hydroxylase Rattus norvegicus 0-20 8507669-6 1993 On the basis of these results, it is proposed that the influence of ferrous ions on tyrosinase is due to the formation of dopa in the chemical hydroxylation of tyrosine. Levodopa 122-126 tyrosinase Homo sapiens 84-94 8492125-7 1993 In contrast, administration of L-DOPA, quinpirole, or SKF 23390 for 7 days lowers AAAD activity in the striatum. Levodopa 31-37 dopa decarboxylase Mus musculus 82-86 8097235-2 1993 TH activity (determined by L-3,4-dihydroxyphenylalanine accumulation in the median eminence after blockade of decarboxylase with NSD 1055) showed a 30-40% decrease within 1 h of incubation with estradiol. Levodopa 27-55 tyrosine hydroxylase Rattus norvegicus 0-2 8510830-1 1993 Aromatic L-amino acid decarboxylase (AADC) decarboxylates L-DOPA and 5-hydroxytryptophan into dopamine and serotonin, respectively. Levodopa 58-64 dopa decarboxylase Rattus norvegicus 0-35 8510830-1 1993 Aromatic L-amino acid decarboxylase (AADC) decarboxylates L-DOPA and 5-hydroxytryptophan into dopamine and serotonin, respectively. Levodopa 58-64 dopa decarboxylase Rattus norvegicus 37-41 8341294-1 1993 L-Dopa is metabolized to 3-O-methyldopa (3OMD) by catechol-O-methyltransferase (COMT). Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 50-78 8341294-1 1993 L-Dopa is metabolized to 3-O-methyldopa (3OMD) by catechol-O-methyltransferase (COMT). Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 80-84 8210606-0 1993 Growth hormone response after administration of L-dopa, clonidine, and growth hormone releasing hormone in children with Down syndrome. Levodopa 48-54 growth hormone 1 Homo sapiens 0-14 8210606-1 1993 We studied the response of growth hormone secretion after the administration of L-dopa, clonidine, and growth hormone releasing hormone in eight growth-retarded children with Down syndrome aged 1 to 6.5 years. Levodopa 80-86 growth hormone 1 Homo sapiens 27-41 8321428-0 1993 A selective MAOB inhibitor Ro19-6327 potentiates the effects of levodopa on parkinsonism induced by MPTP in the common marmoset. Levodopa 64-72 amine oxidase [flavin-containing] B Callithrix jacchus 12-16 7682705-1 1993 Tyrosine hydroxylase (TH) catalyzes the conversion of L-tyrosine to 3,4-dihydroxy-L-phenylalanine, the first and rate-limiting step in catecholamine biosynthesis. Levodopa 68-97 tyrosine hydroxylase Rattus norvegicus 22-24 8477410-0 1993 The effect of catechol-O-methyl transferase inhibition by entacapone on the pharmacokinetics and metabolism of levodopa in healthy volunteers. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 14-43 8472357-0 1993 Measuring L-dopa in plasma and urine to monitor therapy of elderly patients with Parkinson disease treated with L-dopa and a dopa decarboxylase inhibitor. Levodopa 10-16 dopa decarboxylase Homo sapiens 125-143 8477410-1 1993 We studied the effect of inhibiting the enzyme catechol-O-methyltransferase (COMT) by a novel COMT inhibitor, entacapone, on the pharmacokinetics and metabolism of levodopa in 12 healthy male volunteers. Levodopa 164-172 catechol-O-methyltransferase Homo sapiens 47-75 8477410-1 1993 We studied the effect of inhibiting the enzyme catechol-O-methyltransferase (COMT) by a novel COMT inhibitor, entacapone, on the pharmacokinetics and metabolism of levodopa in 12 healthy male volunteers. Levodopa 164-172 catechol-O-methyltransferase Homo sapiens 77-81 8100096-3 1993 In contrast to this generally accepted idea, Yoshimi Misu and Yoshio Goshima propose, in this Viewpoint article, that L-dopa itself is an endogenous neurotransmitter or neuromodulator in the CNS. Levodopa 118-124 NOP2/Sun RNA methyltransferase 2 Homo sapiens 53-57 8491280-0 1993 Levodopa induction of Fos immunoreactivity in rat brain following partial and complete lesions of the substantia nigra. Levodopa 0-8 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 22-25 8491280-3 1993 We have investigated the potential effects of L-DOPA in early PD by analyzing its influence on the activity of the immediate early gene Fos in the partially lesioned rat. Levodopa 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 136-139 8491280-4 1993 Fos has been used to examine neuronal response to a variety of stimuli in vivo, and L-DOPA is known to increase Fos-like immunoreactivity (FosLI) in striatal neurons after complete lesions of the SN. Levodopa 84-90 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 112-115 8491280-10 1993 Therefore L-DOPA induces Fos in the striatum after partial as well as complete SN lesions. Levodopa 10-16 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 25-28 8491280-11 1993 This result suggests that L-DOPA-induced Fos expression may occur in the early stages of PD and may not require dopamine receptor upregulation, which is believed to develop only in completely lesioned rats and in later stages of PD. Levodopa 26-32 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 41-44 8491280-12 1993 The unexpected induction of Fos activity in brain regions besides the striatum suggests that L-DOPA therapy in patients with PD may have more widespread effects than previously anticipated. Levodopa 93-99 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-31 8491280-13 1993 Since Fos is known to regulate gene transcription, potential alterations in its activity may contribute to the complications associated with L-DOPA therapy in PD. Levodopa 141-147 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 6-9 8426360-2 1993 Aromatic L-amino acid decarboxylase (AADC) is the enzyme responsible for the final step in the biosynthesis of both dopamine and serotonin via decarboxylation of L-dopa and 5-hydroxy-L-tryptophan, respectively. Levodopa 162-168 dopa decarboxylase Mus musculus 0-35 8479601-2 1993 Since SAM causes PD-like symptoms in rodents, the decreased efficacy of chronic L-dopa administered to PD patients may result from a rebound increase in SAM via methionine adenosyl transferase (MAT), which produces SAM from methionine and ATP. Levodopa 80-86 methionine adenosyltransferase 1A Homo sapiens 161-192 8479601-2 1993 Since SAM causes PD-like symptoms in rodents, the decreased efficacy of chronic L-dopa administered to PD patients may result from a rebound increase in SAM via methionine adenosyl transferase (MAT), which produces SAM from methionine and ATP. Levodopa 80-86 methionine adenosyltransferase 1A Homo sapiens 194-197 8479601-6 1993 These results show that short interval, chronic L-dopa treatments significantly increases MAT activity, which increases the production of SAM. Levodopa 48-54 methionine adenosyltransferase I, alpha Mus musculus 90-93 8479601-8 1993 Thus, an increase in MAT may be related to the decreased efficacy of chronic L-dopa therapy in PD. Levodopa 77-83 methionine adenosyltransferase I, alpha Mus musculus 21-24 8097025-3 1993 Since Purkinje cells in such cerebellar regions displayed no immunoreactivity to dopamine-beta-hydroxylase, the TH-immunoreactive Purkinje cells identified in the present study might contain dopamine or L-DOPA. Levodopa 203-209 tyrosine hydroxylase Rattus norvegicus 112-114 8426360-2 1993 Aromatic L-amino acid decarboxylase (AADC) is the enzyme responsible for the final step in the biosynthesis of both dopamine and serotonin via decarboxylation of L-dopa and 5-hydroxy-L-tryptophan, respectively. Levodopa 162-168 dopa decarboxylase Mus musculus 37-41 8422386-6 1993 On the reaction of AADC with L-3,4-dihydroxyphenylalanine (L-dopa), the absorption of PLP showed biphasic changes before reaching a steady-state. Levodopa 29-57 dopa decarboxylase Rattus norvegicus 19-23 8422386-6 1993 On the reaction of AADC with L-3,4-dihydroxyphenylalanine (L-dopa), the absorption of PLP showed biphasic changes before reaching a steady-state. Levodopa 59-65 dopa decarboxylase Rattus norvegicus 19-23 8370570-3 1993 The synthesis of dopamine in tissues incubated with 500 microM L-dopa for 20 min in conditions of catechol-O-methyltransferase (Comt) inhibition was found to be in the duodenum, jejunum and ileum 2-fold that in the proximal colon, 6-fold that in the glandular stomach and 120-fold that in the non-glandular stomach and distal colon. Levodopa 63-69 catechol-O-methyltransferase Rattus norvegicus 98-126 8440292-1 1993 The paper reports plasma levels of levodopa (LD), its main metabolites [dopamine, dihydroxyphenylacetic acid, homovanillic acid, 3-O-methyldopa (3-O-MD)] and carbidopa in 14 parkinsonian patients first treated with Sinemet and thereafter with Sinemet-CR4. Levodopa 35-43 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 251-254 8112370-3 1993 A small decrease in the AUC of homovanillic acid (HVA), the COMT dependent metabolite of levodopa, was observed (from 455 to 303 h.ng.ml-1). Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 60-64 8458598-1 1993 L-Dopa is converted to dopamine by aromatic-L-amino acid decarboxylase (AADC). Levodopa 0-6 dopa decarboxylase Homo sapiens 35-70 8458598-1 1993 L-Dopa is converted to dopamine by aromatic-L-amino acid decarboxylase (AADC). Levodopa 0-6 dopa decarboxylase Homo sapiens 72-76 8370570-3 1993 The synthesis of dopamine in tissues incubated with 500 microM L-dopa for 20 min in conditions of catechol-O-methyltransferase (Comt) inhibition was found to be in the duodenum, jejunum and ileum 2-fold that in the proximal colon, 6-fold that in the glandular stomach and 120-fold that in the non-glandular stomach and distal colon. Levodopa 63-69 catechol-O-methyltransferase Rattus norvegicus 128-132 1358675-2 1992 BDNF mRNA expression in the striatum, which was quantified with the reverse transcriptase polymerase chain reaction, was up-regulated from 2 h after oral administration of levodopa, a precursor of dopamine. Levodopa 172-180 brain derived neurotrophic factor Mus musculus 0-4 8406335-7 1993 This suggests a specific but as yet undetermined effect of L-dopa on urinary GH secretion. Levodopa 59-65 growth hormone 1 Homo sapiens 77-79 8417137-13 1993 These in vivo data show that the new COMT inhibitors markedly inhibit the O-methylation of L-dopa and increase its availability to brain, which is reflected as increased DA formation. Levodopa 91-97 catechol-O-methyltransferase Rattus norvegicus 37-41 1465439-1 1992 Aromatic L-amino acid decarboxylase (AADC, EC 4.1.1.28) catalyzes the decarboxylation of L-dopa to dopamine in catecholamine cells and 5-hydroxytryptophan to serotonin in serotonin-producing neurons. Levodopa 89-95 dopa decarboxylase Rattus norvegicus 0-35 1465439-1 1992 Aromatic L-amino acid decarboxylase (AADC, EC 4.1.1.28) catalyzes the decarboxylation of L-dopa to dopamine in catecholamine cells and 5-hydroxytryptophan to serotonin in serotonin-producing neurons. Levodopa 89-95 dopa decarboxylase Rattus norvegicus 37-41 1429711-1 1992 Tyrosinase (EC 1.14.18.1) is a copper-containing metalloglycoprotein that catalyzes several steps in the melanin pigment biosynthetic pathway; the hydroxylation of tyrosine to L-3,4-dihydroxyphenylalanine (dopa) and the subsequent oxidation of dopa to dopaquinone. Levodopa 176-204 tyrosinase Homo sapiens 0-10 1429711-1 1992 Tyrosinase (EC 1.14.18.1) is a copper-containing metalloglycoprotein that catalyzes several steps in the melanin pigment biosynthetic pathway; the hydroxylation of tyrosine to L-3,4-dihydroxyphenylalanine (dopa) and the subsequent oxidation of dopa to dopaquinone. Levodopa 206-210 tyrosinase Homo sapiens 0-10 1429711-1 1992 Tyrosinase (EC 1.14.18.1) is a copper-containing metalloglycoprotein that catalyzes several steps in the melanin pigment biosynthetic pathway; the hydroxylation of tyrosine to L-3,4-dihydroxyphenylalanine (dopa) and the subsequent oxidation of dopa to dopaquinone. Levodopa 244-248 tyrosinase Homo sapiens 0-10 8262472-4 1993 GH secretion in response to pharmacological stimuli (insulin, arginine and/or L-Dopa) was evaluated when growth failure occurred. Levodopa 78-84 growth hormone 1 Homo sapiens 0-2 1336046-1 1992 The photo-induction of free radicals in synthetic L-dihydroxyphenylalanine (L-DOPA) melanin in the presence of bovine serum albumin (BSA) was studied by electron paramagnetic resonance (EPR) spectroscopy. Levodopa 50-76 albumin Homo sapiens 118-131 1405340-2 1992 Proximal tubule cells produce dopamine after decarboxylation of L-DOPA via the enzyme aromatic L-amino acid decarboxylase (AADC). Levodopa 64-70 dopa decarboxylase Rattus norvegicus 95-121 1332473-0 1992 Effects of calcium channel blockade with verapamil on the prolactin responses to TRH, L-dopa, and bromocriptine. Levodopa 86-92 prolactin Homo sapiens 58-67 1332473-6 1992 In these same volunteers, PRL levels decreased from 13.2 +/- 2.5 ng/ml to a nadir of 5.5 +/- 1.6 ng/ml in response to L-dopa. Levodopa 118-124 prolactin Homo sapiens 26-29 1332473-8 1992 The percentage decreased in PRL in response to L-dopa (60 +/- 5% versus 62 +/- 3%) were not significantly different (p > 0.05). Levodopa 47-53 prolactin Homo sapiens 28-31 1300941-0 1992 Neurochemical and psychomotor interactions of new selective COMT inhibitors with clorgyline and nomifensine in levodopa-treated rats and mice. Levodopa 111-119 catechol-O-methyltransferase Rattus norvegicus 60-64 1300941-6 1992 All COMT inhibitors (30 mg/kg) slightly enhanced levodopa/carbidopa (15/30 mg/kg)-induced hypoactivity in rats. Levodopa 49-57 catechol-O-methyltransferase Rattus norvegicus 4-8 1405340-2 1992 Proximal tubule cells produce dopamine after decarboxylation of L-DOPA via the enzyme aromatic L-amino acid decarboxylase (AADC). Levodopa 64-70 dopa decarboxylase Rattus norvegicus 123-127 1385171-4 1992 Administration of L-DOPA to sham-operated rats bilaterally increased SP levels in striatum and substantia nigra, and [Met5]enkephalin and CCK content in substantia nigra. Levodopa 18-24 proenkephalin Rattus norvegicus 123-133 1303156-2 1992 The expressed enzyme activity was stereoselective for L-5-hydroxytryptophan and L-DOPA and blocked by NSD-1015 an inhibitor of AADC. Levodopa 80-86 dopa decarboxylase Bos taurus 127-131 1385171-5 1992 L-DOPA treatment of 6-OHDA-lesioned rats increased [Met5]- and [Leu5]enkephalin and CCK levels in the striatum ipsilateral to the lesion but not on the intact side. Levodopa 0-6 proenkephalin Rattus norvegicus 69-79 1385171-5 1992 L-DOPA treatment of 6-OHDA-lesioned rats increased [Met5]- and [Leu5]enkephalin and CCK levels in the striatum ipsilateral to the lesion but not on the intact side. Levodopa 0-6 cholecystokinin Rattus norvegicus 84-87 1385171-6 1992 In the substantia nigra, the lesion-induced decrease in [Leu5]enkephalin and SP was reversed by L-DOPA treatment, [Met5]enkephalin and CCK levels ipsilateral to the lesion were further enhanced, and there was an increase in NT ipsilateral to the lesion. Levodopa 96-102 proenkephalin Rattus norvegicus 62-72 1519417-1 1992 The function of the growth hormone-releasing hormone (GHRH)-growth hormone (GH) axis in Cushing"s disease was studied by monitoring (a) the GH responses to GHRH loading and L-dopa loading, (b) the GHRH response to L-dopa loading, and (c) the daytime profiles of plasma GH concentration. Levodopa 173-179 growth hormone releasing hormone Homo sapiens 20-52 1511683-5 1992 Moreover, using L-3,4-dihydroxyphenylalanine (dopa) and related compounds, it was shown that the presence of dopachrome tautomerase mediates an initial acceleration of melanogenesis since L-dopachrome is rapidly transformed to DHICA, but that melanin formation is inhibited because of the stability of this carboxylated indole compared to 5,6-dihydroxyindole (DHI), its decarboxylated counterpart obtained by spontaneous decarboxylation of L-dopachrome. Levodopa 16-44 dopachrome tautomerase Homo sapiens 109-131 1511683-5 1992 Moreover, using L-3,4-dihydroxyphenylalanine (dopa) and related compounds, it was shown that the presence of dopachrome tautomerase mediates an initial acceleration of melanogenesis since L-dopachrome is rapidly transformed to DHICA, but that melanin formation is inhibited because of the stability of this carboxylated indole compared to 5,6-dihydroxyindole (DHI), its decarboxylated counterpart obtained by spontaneous decarboxylation of L-dopachrome. Levodopa 46-50 dopachrome tautomerase Homo sapiens 109-131 1519417-1 1992 The function of the growth hormone-releasing hormone (GHRH)-growth hormone (GH) axis in Cushing"s disease was studied by monitoring (a) the GH responses to GHRH loading and L-dopa loading, (b) the GHRH response to L-dopa loading, and (c) the daytime profiles of plasma GH concentration. Levodopa 173-179 growth hormone releasing hormone Homo sapiens 54-58 1519417-1 1992 The function of the growth hormone-releasing hormone (GHRH)-growth hormone (GH) axis in Cushing"s disease was studied by monitoring (a) the GH responses to GHRH loading and L-dopa loading, (b) the GHRH response to L-dopa loading, and (c) the daytime profiles of plasma GH concentration. Levodopa 214-220 growth hormone releasing hormone Homo sapiens 20-52 1519417-1 1992 The function of the growth hormone-releasing hormone (GHRH)-growth hormone (GH) axis in Cushing"s disease was studied by monitoring (a) the GH responses to GHRH loading and L-dopa loading, (b) the GHRH response to L-dopa loading, and (c) the daytime profiles of plasma GH concentration. Levodopa 214-220 growth hormone releasing hormone Homo sapiens 54-58 1519417-3 1992 However, GHRH release following L-dopa was similar in patients and controls. Levodopa 32-38 growth hormone releasing hormone Homo sapiens 9-13 1613509-10 1992 The results of the present study suggest that metabolism through COMT regulates extracellular concentrations of DA formed from exogenously administered L-DOPA but not of endogenous DA. Levodopa 152-158 catechol-O-methyltransferase Rattus norvegicus 65-69 1584187-7 1992 Another approach is the use of selegiline (deprenyl), MAO-B inhibitor slowing the breakdown of dopamine and thereby extending the duration of levodopa effect. Levodopa 142-150 monoamine oxidase B Homo sapiens 54-59 1356793-9 1992 These findings suggest that the transport of aromatic amino acids across the blood-brain barrier may be regulated through beta 2-adrenoceptors and that co-administration of beta 2-adrenoceptor agonists with L-DOPA may enhance the therapeutic efficacy of L-DOPA. Levodopa 254-260 adrenoceptor beta 2 Rattus norvegicus 122-141 1401748-1 1992 We have evaluated baseline and l-dopa-stimulated peripheral growth hormone releasing hormone (pGHRH) secretion in 6 obese pre-pubertal children and in 7 age-matched controls. Levodopa 31-37 growth hormone releasing hormone Homo sapiens 60-92 1595643-4 1992 In both controls and treated patients, TRH did not influence GH secretion, whereas L-dopa significantly increased GH levels. Levodopa 83-89 growth hormone 1 Homo sapiens 114-116 1595643-6 1992 Because L-dopa would stimulate hypothalamic GH-releasing hormone (GHRH) secretion, four untreated patients, unresponsive to L-dopa, received GHRH, and GH levels rose markedly. Levodopa 8-14 growth hormone releasing hormone Homo sapiens 44-64 1595643-6 1992 Because L-dopa would stimulate hypothalamic GH-releasing hormone (GHRH) secretion, four untreated patients, unresponsive to L-dopa, received GHRH, and GH levels rose markedly. Levodopa 8-14 growth hormone releasing hormone Homo sapiens 66-70 1595643-6 1992 Because L-dopa would stimulate hypothalamic GH-releasing hormone (GHRH) secretion, four untreated patients, unresponsive to L-dopa, received GHRH, and GH levels rose markedly. Levodopa 8-14 growth hormone 1 Homo sapiens 44-46 1584187-9 1992 Clinical trials are planned with levodopa pro-drugs and inhibitors of catechol-O-methyltransferase to learn if these approaches can improve problems of long-term levodopa therapy. Levodopa 162-170 catechol-O-methyltransferase Homo sapiens 70-98 1518496-0 1992 [The effects of l-dopa administration on the prolactin levels in short-stature subjects]. Levodopa 16-22 prolactin Homo sapiens 45-54 1388592-1 1992 The influence of bioisosteric replacement of catechol moiety of L-Dopa and alpha-Methyldopa with benzimidazole and benzotriazole ring has been examined on dopamine beta-hydroxylase and tyrosinase, in order to evidentiate an inhibitory activity on the synthesis of catecholamines and a possible antihypertensive action. Levodopa 64-70 dopamine beta-hydroxylase Homo sapiens 155-180 1388592-1 1992 The influence of bioisosteric replacement of catechol moiety of L-Dopa and alpha-Methyldopa with benzimidazole and benzotriazole ring has been examined on dopamine beta-hydroxylase and tyrosinase, in order to evidentiate an inhibitory activity on the synthesis of catecholamines and a possible antihypertensive action. Levodopa 64-70 tyrosinase Homo sapiens 185-195 1350073-1 1992 Studies indicate that selegiline, a monoamine oxidase type B inhibitor, slows progression of Parkinson"s disease (PD) and delays the need for levodopa. Levodopa 142-150 monoamine oxidase B Homo sapiens 36-60 1350074-1 1992 The major neuropathology of Parkinson"s disease (PD) is the degeneration of nigrostriatal dopamine (DA), resulting in a deficiency of DA, and of the enzyme tyrosine hydroxylase (TH), which catalyzes the synthesis of L-dopa. Levodopa 216-222 tyrosine hydroxylase Mus musculus 156-176 1350074-1 1992 The major neuropathology of Parkinson"s disease (PD) is the degeneration of nigrostriatal dopamine (DA), resulting in a deficiency of DA, and of the enzyme tyrosine hydroxylase (TH), which catalyzes the synthesis of L-dopa. Levodopa 216-222 tyrosine hydroxylase Mus musculus 178-180 1350074-3 1992 The increase of TH activity by modification of the enzyme leads to an increased synthesis of striatal L-dopa, and thereby replenishes the missing DA more efficiently. Levodopa 102-108 tyrosine hydroxylase Mus musculus 16-18 1540578-1 1992 Aromatic L-amino acid decarboxylase (AADC) catalyzes the decarboxylation of both L-3,4-dihydroxyphenylalanine and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are major mammalian neurotransmitters and hormones belonging to catecholamines and indoleamines. Levodopa 81-109 dopa decarboxylase Homo sapiens 0-35 1540578-1 1992 Aromatic L-amino acid decarboxylase (AADC) catalyzes the decarboxylation of both L-3,4-dihydroxyphenylalanine and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are major mammalian neurotransmitters and hormones belonging to catecholamines and indoleamines. Levodopa 81-109 dopa decarboxylase Homo sapiens 37-41 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 210-216 prolactin Homo sapiens 165-168 1518496-5 1992 PRL levels significantly decreased in all groups, also in those with a deficient response to l-dopa (1 and 2a); furthermore no significant correlation between PRL and GH levels was demonstrated. Levodopa 93-99 prolactin Homo sapiens 0-3 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 56-62 prolactin Homo sapiens 81-90 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 56-62 prolactin Homo sapiens 92-95 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 56-62 prolactin Homo sapiens 165-168 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 56-62 growth hormone 1 Homo sapiens 389-403 1518496-1 1992 In this study, on the basis of the inhibiting action of l-dopa administration on prolactin (PRL) secretion, we evaluated in a number of short children the levels of PRL during the provocative stimuli test with l-dopa in order to identify an index able to give reliability to the test and to investigate whether some differences may exist among the subjects showing a different response in growth hormone (GH) secretion to l-dopa. Levodopa 210-216 prolactin Homo sapiens 165-168 1575457-5 1992 Mean caudate and putamen: cerebellar RAC uptake ratios of the group with PD and a fluctuating response to L-dopa were significantly reduced by 30% and 18%, respectively. Levodopa 106-112 AKT serine/threonine kinase 1 Homo sapiens 37-40 1537368-7 1992 Treatment with L-dopa up to 800 mg/day (along with carbidopa 200 mg/day) corrected the low CSF homovanillic acid levels and produced some improvement in the Parkinsonism but no other obvious clinical benefit. Levodopa 15-21 colony stimulating factor 2 Homo sapiens 91-94 1346143-5 1992 Our data showed a significant increase (P less than 0.001) in GH, GHRH, and SRIH levels (peak vs. basal values) in response to L-dopa administration in all groups. Levodopa 127-133 growth hormone 1 Homo sapiens 62-64 1346143-5 1992 Our data showed a significant increase (P less than 0.001) in GH, GHRH, and SRIH levels (peak vs. basal values) in response to L-dopa administration in all groups. Levodopa 127-133 growth hormone releasing hormone Homo sapiens 66-70 1549240-0 1992 Catechol-O-methyltransferase inhibition increases striatal L-dopa and dopamine: an in vivo study in rats. Levodopa 59-65 catechol-O-methyltransferase Rattus norvegicus 0-28 1549240-1 1992 We administered Ro 40-7592, an inhibitor of the enzyme catechol-O-methyltransferase (COMT) that crosses the blood-brain barrier, to rats and monitored extracellular catecholamine levels in the corpus striatum before and after the intraperitoneal administration of a bolus of l-dopa. Levodopa 275-281 catechol-O-methyltransferase Rattus norvegicus 85-89 1549240-4 1992 We conclude that inhibition of COMT activity promotes central dopamine synthesis and release following administration of pharmacologic doses of l-dopa. Levodopa 144-150 catechol-O-methyltransferase Rattus norvegicus 31-35 1533556-4 1992 GH was evaluated by levodopa (125 mg up to 15 kg, and 250 mg between 15-30 kg), clonidine (0.15 mg m-2) stimulation tests and hGH secretory patterns by the integrated 24 h. GH concentration (IC-GH) using a constant withdrawal pump with continuous blood collection every 30 min. Levodopa 20-28 growth hormone 1 Homo sapiens 0-2 1533556-6 1992 Peak serum GH after levodopa and clonidine was found to be below 10 ng ml-1 for both stimulatory tests in seven out of the 20 children studied. Levodopa 20-28 growth hormone 1 Homo sapiens 11-13 1345575-4 1992 TRH 0.2 mg iv blunted GH response to L-dopa 0.5 g p.o. Levodopa 37-43 thyrotropin releasing hormone Homo sapiens 0-3 1345575-4 1992 TRH 0.2 mg iv blunted GH response to L-dopa 0.5 g p.o. Levodopa 37-43 growth hormone 1 Homo sapiens 22-24 1571080-3 1992 While a majority (15 patients, 7 on Madopar HBS and 8 on Sinemet CR4) showed a favourable response after 2 months of slow-release L-dopa treatment the clinical benefit remained stable in only 2 patients on Madopar HBS and 3 patients on Sinemet CR4 over the entire follow-up period of 12 months. Levodopa 130-136 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 65-68 1285949-0 1992 Muscarinic cholinergic receptor-mediated modulation on striatal c-fos mRNA expression induced by levodopa in rat brain. Levodopa 97-105 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 64-69 1285949-3 1992 Levodopa given alone increase the expression of c-fos mRNA. Levodopa 0-8 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 48-53 1285949-4 1992 Although carbachol or trihexyphenidyl alone was ineffective in inducing c-fos mRNA, the combination of levodopa and carbachol (> or = to 0.1 mg/kg) significantly suppressed the induction of c-fos mRNA as compared with levodopa given alone. Levodopa 103-111 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 193-198 1285949-4 1992 Although carbachol or trihexyphenidyl alone was ineffective in inducing c-fos mRNA, the combination of levodopa and carbachol (> or = to 0.1 mg/kg) significantly suppressed the induction of c-fos mRNA as compared with levodopa given alone. Levodopa 221-229 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 193-198 1285949-5 1992 The combined administration of levodopa and trihexyphenidyl showed a trend toward an additive effect on the induction of c-fos mRNA vs levodopa alone. Levodopa 31-39 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 121-126 1557063-5 1992 Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase. Levodopa 87-95 monoamine oxidase B Homo sapiens 41-65 1285949-5 1992 The combined administration of levodopa and trihexyphenidyl showed a trend toward an additive effect on the induction of c-fos mRNA vs levodopa alone. Levodopa 135-143 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 121-126 1285949-6 1992 These findings suggest that the muscarinic cholinergic system may modulate the levodopa-induced c-fos mRNA expression which then regulates the expression of other mRNAs. Levodopa 79-87 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 96-101 1609114-16 1992 In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities. Levodopa 77-83 monoamine oxidase B Homo sapiens 41-46 1734304-7 1992 In addition, COMT inhibition may have clinical advantages by improving levodopa treatment in PD. Levodopa 71-79 catechol-O-methyltransferase Homo sapiens 13-17 1609114-16 1992 In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities. Levodopa 109-115 monoamine oxidase B Homo sapiens 41-46 1915732-6 1991 These data suggest that denervation of the striatum enhances the production of a striatally derived neurotrophic factor, the production of which is sensitive to levodopa. Levodopa 161-169 neurotrophin 3 Rattus norvegicus 100-119 1961117-0 1991 Age-related decrease in plasma growth hormone: response to growth hormone-releasing hormone, arginine, and L-dopa in obesity. Levodopa 107-113 growth hormone 1 Homo sapiens 31-45 1961117-5 1991 The mean peak levels of plasma GH in response to GRH, arginine, and L-dopa in obese subjects were 11.3 +/- 2.1, 21.9 +/- 4.4, and 5.2 +/- 0.3 ng/mL in adolescents, 8.2 +/- 1.6, 9.1 +/- 1.5, and 3.1 +/- 0.6 ng/mL in those in their 20s, and 4.5 +/- 0.4, 7.3 +/- 1.4, and 2.8 +/- 0.3 ng/mL in those 30 years or older, respectively, showing a significant decrease in peak GH level with advancing age (P less than .05 to P less than .01). Levodopa 68-74 growth hormone 1 Homo sapiens 31-33 1939384-1 1991 Characterization of peripheral and cerebral L-3,4-dihydroxy-6-[18F]fluorophenylalanine (FDOPA) metabolism in humans and monkeys has shown FDOPA to be an analogue of L-DOPA for the study of the dopaminergic system with positron emission tomography (PET). Levodopa 165-171 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 44-47 1953749-1 1991 The early enzyme-mediated reaction sequence in the biosynthesis of melanin from L-tyrosine involves an initial hydroxylation (monophenol oxidase activity, MPO) of the aromatic amino acid precursor to form L-dopa (3,4-dihydroxyphenylalanine), and the ensuing oxidation (diphenol oxidase activity, DPO) of the resultant diphenol to form dopaquinone. Levodopa 205-211 Prophenoloxidase 1 Drosophila melanogaster 126-144 1801681-8 1991 These results suggest that fetal plasma L-dopa may be converted to dopamine by fetal kidney DDC, and that the dopamine is voided into the amniotic cavity in fetal urine. Levodopa 40-46 dopa decarboxylase Rattus norvegicus 92-95 1915732-7 1991 Chronic levodopa treatment in Parkinson"s disease may therefore contribute to disease progression by reducing the compensating effects of this neurotrophic factor on remaining mesencephalic neurons. Levodopa 8-16 neurotrophin 3 Rattus norvegicus 143-162 1684735-3 1991 In this study, the cerebrospinal fluid content of a proenkephalin derivative, Met5 enkephalin-Arg6-Gly7-Leu8 (MERGL), was found in significantly low concentrations in parkinsonian patients following overnight withdrawal of all medications compared with control subjects, and failed to change after at least 16 h of steady-state, optimal doses of levodopa infusion intravenously. Levodopa 346-354 selectin L Homo sapiens 104-108 1922797-3 1991 Peak CSF levodopa and dopamine sulfate levels occurred 1 to 1.5 hours after peak plasma concentration of levodopa. Levodopa 9-17 colony stimulating factor 2 Homo sapiens 5-8 1922797-3 1991 Peak CSF levodopa and dopamine sulfate levels occurred 1 to 1.5 hours after peak plasma concentration of levodopa. Levodopa 105-113 colony stimulating factor 2 Homo sapiens 5-8 1922797-4 1991 The time course of clinical improvement and worsening correlated precisely with the appearance and disappearance of both levodopa and dopamine sulfate in the CSF. Levodopa 121-129 colony stimulating factor 2 Homo sapiens 158-161 1922797-5 1991 The precise correlation between CSF dopamine sulfate and levodopa indicates that in patients with advanced PD the brain retains some capacity to convert levodopa to dopamine. Levodopa 57-65 colony stimulating factor 2 Homo sapiens 32-35 1922797-5 1991 The precise correlation between CSF dopamine sulfate and levodopa indicates that in patients with advanced PD the brain retains some capacity to convert levodopa to dopamine. Levodopa 153-161 colony stimulating factor 2 Homo sapiens 32-35 1922797-6 1991 The transient nature of the correlation between motor fluctuations, CSF levodopa, and CSF dopamine sulfate is consistent with suggestions that in patients with advanced PD there is a diminished capacity to store dopamine synthesized from exogenous levodopa. Levodopa 72-80 colony stimulating factor 2 Homo sapiens 68-71 1766471-6 1991 In the striatum, all COMT inhibitors (with levodopa/carbidopa) blocked 3-OMD formation but elevated neither dopamine nor DOPAC levels. Levodopa 43-51 catechol-O-methyltransferase Rattus norvegicus 21-25 1766471-9 1991 All three COMT inhibitors decreased high 3-OMD levels evoked by MAO inhibitors (+ levodopa/carbidopa). Levodopa 82-90 catechol-O-methyltransferase Rattus norvegicus 10-14 1766471-9 1991 All three COMT inhibitors decreased high 3-OMD levels evoked by MAO inhibitors (+ levodopa/carbidopa). Levodopa 82-90 monoamine oxidase A Rattus norvegicus 64-67 1766471-12 1991 In the hypothalamus, COMT inhibitors decreased 3-OMD levels to 1/5-1/30 of those after levodopa/carbidopa alone. Levodopa 87-95 catechol-O-methyltransferase Rattus norvegicus 21-25 1766471-13 1991 COMT inhibitors suppressed 3-OMD formation also in clorgyline and pargyline (+ levodopa/carbidopa) treated rats. Levodopa 79-87 catechol-O-methyltransferase Rattus norvegicus 0-4 1906272-1 1991 Melanin biosynthesis is a multistep process with the first step being the conversion of L-tyrosine to L-Dopa catalyzed by the enzyme tyrosinase. Levodopa 102-108 tyrosinase Homo sapiens 133-143 1653610-8 1991 Bis-cysteinate tyrosinase activity is down-regulated to 30% of native enzyme activity in the L-dopa assay; suggesting a true regulatory role for dithiols. Levodopa 93-99 tyrosinase Homo sapiens 15-25 1782731-11 1991 Standardized exercise is as effective as L-DOPA/P as a stimulation test for growth hormone response in very short children with abnormal growth velocities. Levodopa 41-47 growth hormone 1 Homo sapiens 76-90 1928809-4 1991 The plasma renin activity and prolactin decreased as a result of L-dopa administration. Levodopa 65-71 renin Homo sapiens 11-16 1928809-6 1991 These results suggest that the blood pressure-lowering effect of L-dopa may be mediated through multiple sites involving D1 dopamine receptors, the central nervous system, and the renin-angiotensin system. Levodopa 65-71 renin Homo sapiens 180-185 1831841-3 1991 Before treatment, peak serum growth hormone concentrations were less than 10 micrograms/L after levodopa and clonidine stimulation tests in five patients, after clonidine in three patients, and after levodopa in three patients. Levodopa 96-104 growth hormone 1 Homo sapiens 29-43 1865161-2 1991 Sinemet CR4 offers a theoretically attractive method of achieving gradual sustained release of levodopa over time which may be more physiological to striatal dopamine receptors in the early stages of the disease. Levodopa 95-103 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 8-11 1787777-4 1991 Treatment with levodopa induced an increase in interleukin-1 synthesis, and in IgM and IgA levels in plasma, which suggest a possible selective action on cells of the immune system. Levodopa 15-23 interleukin 1 alpha Homo sapiens 47-60 1921938-7 1991 In patients treated with L-Dopa, there is a negative correlation between the changes in amplitude and the changes in clinical rating for NS1, N1 and MP components. Levodopa 25-31 influenza virus NS1A binding protein Homo sapiens 137-140 1647691-4 1991 LLC-PK1 cells contained high levels of aromatic L-amino acid decarboxylase (AADC) (Km 0.19 +/- 0.08 mM, Vmax 3.69 +/- 0.57 nmol.mg-1.min-1) and converted L-dopa to DA in a nonsaturable fashion up to 1 mM L-dopa. Levodopa 154-160 dopa decarboxylase Sus scrofa 76-80 1647691-4 1991 LLC-PK1 cells contained high levels of aromatic L-amino acid decarboxylase (AADC) (Km 0.19 +/- 0.08 mM, Vmax 3.69 +/- 0.57 nmol.mg-1.min-1) and converted L-dopa to DA in a nonsaturable fashion up to 1 mM L-dopa. Levodopa 204-210 dopa decarboxylase Sus scrofa 48-74 1647691-4 1991 LLC-PK1 cells contained high levels of aromatic L-amino acid decarboxylase (AADC) (Km 0.19 +/- 0.08 mM, Vmax 3.69 +/- 0.57 nmol.mg-1.min-1) and converted L-dopa to DA in a nonsaturable fashion up to 1 mM L-dopa. Levodopa 204-210 dopa decarboxylase Sus scrofa 76-80 1829645-0 1991 D1/D2 dopamine receptor stimulation by L-dopa. Levodopa 39-45 dopamine receptor D2 Rattus norvegicus 0-23 1717109-5 1991 Intermittent levodopa treatment further increased GAD activity, decreased CAT activity, restored substance P to control levels, markedly increased dynorphin content, and had no effect on enkephalin. Levodopa 13-21 choline O-acetyltransferase Rattus norvegicus 74-77 1717109-6 1991 In contrast, continuous levodopa elevated globus pallidus enkephalin beyond the levels occurring with denervation, but had no effect on any of the other neurochemical measures. Levodopa 24-32 proenkephalin Rattus norvegicus 58-68 1717109-8 1991 With the exception of substance P, levodopa did not reverse the effects of the 6-OHDA lesion but, rather, either exacerbated the lesion-induced changes (e.g. GAD and enkephalin) or altered neurochemical markers which had been unaffected by the lesion (e.g. CAT and dynorphin). Levodopa 35-43 proenkephalin Rattus norvegicus 166-176 24194105-1 1991 In rats with unilateral lesion of the nigrostriatal dopaminergic pathway, L-DOPA induces contralateral turning through activation of denervated D-1 and D-2 receptors. Levodopa 74-80 solute carrier family 3 member 1 Rattus norvegicus 144-155 1921938-9 1991 After L-Dopa therapy, the NS1 component from de novo patients was increased in amplitude. Levodopa 6-12 influenza virus NS1A binding protein Homo sapiens 26-29 2049250-8 1991 By contrast, the AUC for levodopa following the low protein meal (193.9 +/- 15.7 micrograms ml-1 min) was significantly lower compared with administration in the fasted state (216.5 +/- 26.1 micrograms ml-1 min). Levodopa 25-33 interleukin 17F Homo sapiens 92-96 1688340-1 1991 Monoaminergic neurons use dopa decarboxylase (DDC; aromatic-L-amino-acid carboxy-lyase, EC 4.1.1.28) to form dopamine from L-3,4-dihydroxyphenylalanine (L-dopa). Levodopa 153-159 dopa decarboxylase Homo sapiens 26-44 1826481-6 1991 In contrast, intermittent levodopa therapy (50 mg/kg, ip, bid) produced a noticeable down regulation of the dopamine receptor system and also contributed to some region-specific recovery of the morphochemical pattern of D1 receptor binding site reaggregation with the postsynaptic cyclic AMP second messenger transduction system. Levodopa 26-34 BH3 interacting domain death agonist Homo sapiens 58-61 1822766-8 1991 The presence of a methyl group at the alpha-carbon of L-Tyr and L-dopa also increases the affinity of the ASC system for these agents. Levodopa 64-70 steroid sulfatase Mus musculus 106-109 1688340-1 1991 Monoaminergic neurons use dopa decarboxylase (DDC; aromatic-L-amino-acid carboxy-lyase, EC 4.1.1.28) to form dopamine from L-3,4-dihydroxyphenylalanine (L-dopa). Levodopa 153-159 dopa decarboxylase Homo sapiens 46-49 2033120-1 1991 Aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-dopa to dopamine, displayed species-specific differences in both activity and immunoreactivity in the cerebellum, olfactory bulb, and adrenal glands of three rodent species, the hamster, rat, and mouse. Levodopa 69-75 dopa decarboxylase Rattus norvegicus 0-35 2033120-1 1991 Aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-dopa to dopamine, displayed species-specific differences in both activity and immunoreactivity in the cerebellum, olfactory bulb, and adrenal glands of three rodent species, the hamster, rat, and mouse. Levodopa 69-75 dopa decarboxylase Mus musculus 37-41 1900435-2 1991 Tyrosinase catalyzes the oxidation by molecular oxygen of L-dopa to o-dopaquinone, which evolves non-enzymatically through a branched pathway with cyclization or hydroxylation reactions. Levodopa 58-64 tyrosinase Homo sapiens 0-10 1672072-4 1991 TH synthesized by the implanted fibroblasts appeared to convert tyrosine to L-dopa actively, as observed in vitro, and to affect the host brain, as assessed through a behavioral measurement. Levodopa 76-82 tyrosine hydroxylase Rattus norvegicus 0-2 1672072-5 1991 These results suggest that primary fibroblasts genetically altered to express TH have the capacity to deliver L-dopa locally to the striatum in quantities sufficient to compensate partially for the loss of intrinsic striatal dopaminergic input. Levodopa 110-116 tyrosine hydroxylase Rattus norvegicus 78-80 1674920-4 1991 Br or L-Dopa was considered to be effective when serum GH or PRL levels were suppressed more than 50% of the basal value. Levodopa 6-12 growth hormone 1 Homo sapiens 55-57 1842116-5 1991 After TRH, prolactin levels increased to 13.8 ng/ml in controls and 15.2 ng/ml in patients treated with levo-DOPA. Levodopa 104-113 thyrotropin releasing hormone Homo sapiens 6-9 1842116-5 1991 After TRH, prolactin levels increased to 13.8 ng/ml in controls and 15.2 ng/ml in patients treated with levo-DOPA. Levodopa 104-113 prolactin Homo sapiens 11-20 1842116-7 1991 We postulate that low basal levels of prolactin in patients treated with levo-DOPA reveal a residual suppressing effect of the drug. Levodopa 73-82 prolactin Homo sapiens 38-47 1899328-3 1991 We have investigated the oxidation chemistry of a low molecular weight peptidyl DOPA analog, N-acetylDOPA ethyl ester (NAcDEE), and have shown that a major product of oxidation is an unsaturated DOPA derivative, N-acetyl-alpha,beta-dehydroDOPA ethyl ester (NAc delta DEE) (see companion paper, Rzepecki et al., Arch. Levodopa 80-84 synuclein alpha Homo sapiens 119-122 1899328-3 1991 We have investigated the oxidation chemistry of a low molecular weight peptidyl DOPA analog, N-acetylDOPA ethyl ester (NAcDEE), and have shown that a major product of oxidation is an unsaturated DOPA derivative, N-acetyl-alpha,beta-dehydroDOPA ethyl ester (NAc delta DEE) (see companion paper, Rzepecki et al., Arch. Levodopa 101-105 synuclein alpha Homo sapiens 119-122 1674920-4 1991 Br or L-Dopa was considered to be effective when serum GH or PRL levels were suppressed more than 50% of the basal value. Levodopa 6-12 prolactin Homo sapiens 61-64 1709847-6 1991 Levodopa (L-dopa) [125 to 500mg orally], the physiological precursor of the catecholamines, administered either alone or in combination with carbidopa (50mg orally), to prevent its peripheral decarboxylation to dopamine, and/or the beta-adrenoceptor antagonist propranolol (0.75 mg/kg orally), and the alpha 2-adrenoceptor agonist clonidine (0.15 mg/m2 orally), are a fairly reliable stimulus of GH release. Levodopa 0-8 growth hormone 1 Homo sapiens 396-398 1674920-9 1991 Suppression of serum GH level by L-Dopa was also observed in the Ss group. Levodopa 33-39 growth hormone 1 Homo sapiens 21-23 1674920-10 1991 In contrast to the difference in the response of GH, serum PRL level was equally suppressed by Br or L-Dopa in each group. Levodopa 101-107 prolactin Homo sapiens 59-62 2000699-4 1991 The AUCs for the plasma GHRH and GH responses in the L-dopa test in young and elderly men were 32.0 +/- 2.7 vs 20.3 +/- 1.8 ng.h-1.l-1 (p less than 0.001), and 21.8 +/- 4.6 vs 5.4 +/- 1.1 micrograms.h-1.l-1 (p less than 0.01), respectively, indicating decreased releases of GHRH and GH in the elderly. Levodopa 53-59 growth hormone releasing hormone Homo sapiens 24-28 1867054-2 1991 AChE-positive cells were first observed at gestational day 12, and AChE-positive neurons which take up L-DOPA were found at gestational day 14, while VIP-like immunoreactive neurons were not seen until gestational day 16. Levodopa 103-109 acetylcholinesterase Mus musculus 67-71 1986445-5 1991 Impaired growth hormone (GH) secretion was present in 6 patients after insulin-induced hypoglycaemia and L-dopa administration. Levodopa 105-111 growth hormone 1 Homo sapiens 9-23 1986445-5 1991 Impaired growth hormone (GH) secretion was present in 6 patients after insulin-induced hypoglycaemia and L-dopa administration. Levodopa 105-111 growth hormone 1 Homo sapiens 25-27 2000699-5 1991 Correlations between the AUCs for plasma GHRH and GH responses in L-dopa were found in both groups, but the ratio of the AUCs for GH/GHRH was lower in the elderly group. Levodopa 66-72 growth hormone releasing hormone Homo sapiens 41-45 2000699-6 1991 The elderly group showed a significant correlation between the basal plasma IGF-I level and the AUCs for plasma GH in the GHRH and L-dopa tests. Levodopa 131-137 insulin like growth factor 1 Homo sapiens 76-81 1653780-5 1991 The growth of neuroblastoma tumours was inhibited by different mechanisms: L-dopa and its metabolite dopamine reduced the activity of tyrosinase, BSO reduced glutathione levels, and L-dopa and tamoxifen raised cAMP concentrations. Levodopa 75-81 tyrosinase Homo sapiens 134-144 1884738-11 1991 New COMT inhibitors may provide a valuable approach to the treatment of Parkinson"s disease in combination with L-dopa and dopa decarboxylase inhibitor therapy. Levodopa 112-118 catechol-O-methyltransferase Homo sapiens 4-8 1916649-5 1991 The baseline peak serum GH response to L-dopa/arginine stimulation for the study population as a whole, was in the hyposecretory range (9.6 +/- 1.9 ng/ml), accompanied by a low level of circulating IGF-I (0.56 +/- 0.09 U/ml). Levodopa 39-45 insulin like growth factor 1 Homo sapiens 198-203 1761075-1 1991 The influence of age on the kinetics of a standard oral dose of levodopa administered with an inhibitor of peripheral dopa decarboxylase enzymes (benserazide) has been evaluated in 40 patients with Parkinson"s disease (age 34-78 y) on chronic therapy. Levodopa 64-72 dopa decarboxylase Homo sapiens 118-136 1958292-2 1991 The inhibition of dopa decarboxylase and monoamine oxidase B resulting from this combination suggests that there may be a counter-regulatory increase in the activity of the third main enzyme in the catabolism of levodopa, i.e. catecholamine-O-methyl transferase (COMT). Levodopa 212-220 dopa decarboxylase Homo sapiens 18-36 1958292-2 1991 The inhibition of dopa decarboxylase and monoamine oxidase B resulting from this combination suggests that there may be a counter-regulatory increase in the activity of the third main enzyme in the catabolism of levodopa, i.e. catecholamine-O-methyl transferase (COMT). Levodopa 212-220 monoamine oxidase B Homo sapiens 41-60 1958292-2 1991 The inhibition of dopa decarboxylase and monoamine oxidase B resulting from this combination suggests that there may be a counter-regulatory increase in the activity of the third main enzyme in the catabolism of levodopa, i.e. catecholamine-O-methyl transferase (COMT). Levodopa 212-220 catechol-O-methyltransferase Homo sapiens 227-261 1958292-2 1991 The inhibition of dopa decarboxylase and monoamine oxidase B resulting from this combination suggests that there may be a counter-regulatory increase in the activity of the third main enzyme in the catabolism of levodopa, i.e. catecholamine-O-methyl transferase (COMT). Levodopa 212-220 catechol-O-methyltransferase Homo sapiens 263-267 1958292-3 1991 The current study on 36 patients with Parkinson"s disease under long-term treatment with levodopa/dopadecarboxylase inhibitor showed, however, that the erythrocyte-COMT was unaffected by additional (-)-deprenyl medication. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 164-168 1666709-5 1991 In the NST, L-DOPA produces a decrease of CAT and ACE activity and of protein content in the D fraction, which corresponds with inhibition of the function of the parasympathetic (AC-ergic) system in response to activation of the peripheral adrenergic system. Levodopa 12-18 angiotensin I converting enzyme Rattus norvegicus 50-53 1899117-5 1991 This hypothesis is supported by the observation that the administration of the dopamine precursor, L-dopa, with MDMA reverses the protective effects of 5-HT2 receptor antagonists. Levodopa 99-105 5-hydroxytryptamine receptor 2A Homo sapiens 152-166 1875781-2 1991 The mean soluble COMT activities with 3,4-dihydroxybenzoic acid (DBA) and 3,4-dihydroxyphenylalanine (L-DOPA) as substrate were 70-242 and 70-174 pmol/min mg, respectively. Levodopa 102-108 catechol-O-methyltransferase Homo sapiens 17-21 1875781-4 1991 The AADC activities, measured with L-DOPA as the substrate, increased from 114 pmol/min mg in the corpus to 3488 pmol/min mg in the jejunum. Levodopa 35-41 dopa decarboxylase Homo sapiens 4-8 1875781-5 1991 The affinity of the soluble COMT was approximately 20 times higher for DBA (Km 15-19 microM) than for L-DOPA (Km 300-600 microM). Levodopa 102-108 catechol-O-methyltransferase Homo sapiens 28-32 1875781-6 1991 The Km-values for L-DOPA of AADC and COMT were of the same order of magnitude. Levodopa 18-24 dopa decarboxylase Homo sapiens 28-32 1875781-6 1991 The Km-values for L-DOPA of AADC and COMT were of the same order of magnitude. Levodopa 18-24 catechol-O-methyltransferase Homo sapiens 37-41 1901390-4 1991 The stimulatory effect of clonidine and L-dopa on GH release is mediated via GHRH. Levodopa 40-46 growth hormone releasing hormone Homo sapiens 77-81 1797228-1 1991 Aromatic L-amino acid decarboxylase (AADC) is responsible for the conversion of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are important neurotransmitters. Levodopa 80-108 dopa decarboxylase Rattus norvegicus 0-35 1797228-1 1991 Aromatic L-amino acid decarboxylase (AADC) is responsible for the conversion of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are important neurotransmitters. Levodopa 80-108 dopa decarboxylase Rattus norvegicus 37-41 1797228-1 1991 Aromatic L-amino acid decarboxylase (AADC) is responsible for the conversion of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are important neurotransmitters. Levodopa 110-116 dopa decarboxylase Rattus norvegicus 0-35 1797228-1 1991 Aromatic L-amino acid decarboxylase (AADC) is responsible for the conversion of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan to dopamine and serotonin, respectively, which are important neurotransmitters. Levodopa 110-116 dopa decarboxylase Rattus norvegicus 37-41 1843006-2 1991 The secretion of GH was studied by means of insulin (ITT), glucose (GTT), lysine-vasopressin (LVP), and L-Dopa administrations. Levodopa 104-110 growth hormone 1 Homo sapiens 17-19 1843006-5 1991 Contrarily, after L-Dopa administration, GH elevations were normal in the two younger and absent in the oldest case. Levodopa 18-24 growth hormone 1 Homo sapiens 41-43 2279968-0 1990 Growth hormone response to L-dopa and clonidine in autistic children. Levodopa 27-33 growth hormone 1 Homo sapiens 0-14 2081822-1 1990 By indirect immunohistochemistry, the present study examined the distribution of neuronal structures in the cat medulla oblongata, pons, and midbrain, showing immunoreactivity to aromatic L-amino acid decarboxylase (AADC), which catalyzes the conversion of L-3, 4-dihydroxyphenylalanine (L-DOPA) to dopamine, and 5-hydroxytryptophan to serotonin (5HT). Levodopa 288-294 dopa decarboxylase Rattus norvegicus 188-214 2081822-1 1990 By indirect immunohistochemistry, the present study examined the distribution of neuronal structures in the cat medulla oblongata, pons, and midbrain, showing immunoreactivity to aromatic L-amino acid decarboxylase (AADC), which catalyzes the conversion of L-3, 4-dihydroxyphenylalanine (L-DOPA) to dopamine, and 5-hydroxytryptophan to serotonin (5HT). Levodopa 288-294 dopa decarboxylase Rattus norvegicus 216-220 2083366-2 1990 The results indicate that agonists 5-HT1A like receptors largely than 5-HT2,3 agonists, 5-HT2 antagonists and nondirect 5-HT agonists promote restoration of the L-DOPA disturbed escape behaviour in acute stress situation. Levodopa 161-167 5-hydroxytryptamine receptor 1A Rattus norvegicus 35-41 2279968-8 1990 In the autistic subjects, the L-Dopa-stimulated growth hormone peak was delayed and the clonidine growth hormone peak was premature. Levodopa 30-36 growth hormone 1 Homo sapiens 48-62 2099784-0 1990 Short- and long-term effects of L-dopa administration on striatal acetylcholinesterase activity. Levodopa 32-38 acetylcholinesterase Rattus norvegicus 66-86 1708406-5 1990 In the striatum, the decreased concentration of SRIF recovered to the normal level with levodopa injections. Levodopa 88-96 somatostatin Mus musculus 48-52 1708406-8 1990 In the hippocampus, the decreased SRIF levels were still low after levodopa treatment. Levodopa 67-75 somatostatin Mus musculus 34-38 1708406-9 1990 Since it has been reported that SRIF concentrations are significantly reduced in the frontal cortex and hippocampus of demented parkinsonians and patients with senile dementia of the Alzheimer type and that levodopa treatment induced various psychiatric side effects, the results of the present study suggest some relationship among levodopa treatment, SRIF depletion and the demented state. Levodopa 207-215 somatostatin Mus musculus 32-36 1708406-9 1990 Since it has been reported that SRIF concentrations are significantly reduced in the frontal cortex and hippocampus of demented parkinsonians and patients with senile dementia of the Alzheimer type and that levodopa treatment induced various psychiatric side effects, the results of the present study suggest some relationship among levodopa treatment, SRIF depletion and the demented state. Levodopa 207-215 somatostatin Mus musculus 353-357 2124622-6 1990 It is concluded that both MAO-A and MAO-B are important in the metabolism of newly formed DA in kidney slices incubated with exogenous L-dopa. Levodopa 135-141 monoamine oxidase A Rattus norvegicus 26-31 2124622-6 1990 It is concluded that both MAO-A and MAO-B are important in the metabolism of newly formed DA in kidney slices incubated with exogenous L-dopa. Levodopa 135-141 monoamine oxidase B Rattus norvegicus 36-41 2099784-2 1990 The aim of the present work was to study the effect of L-dopa administration on acetylcholinesterase (EC 3.1.1.7) activity in rat (Wistar) brain striatum. Levodopa 55-61 acetylcholinesterase Rattus norvegicus 80-100 2099784-3 1990 Short-term administration of a mixture of L-dopa (10 mg/kg) and carbidopa (1 mg/kg) resulted in an increase in dopamine content and a decrease in acetylcholinesterase activity of the tissue. Levodopa 42-48 acetylcholinesterase Rattus norvegicus 146-166 2289048-0 1990 L-dopa as substrate for human duodenal catechol-O-methyltransferase and aromatic L-amino acid decarboxylase. Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 39-67 2289048-0 1990 L-dopa as substrate for human duodenal catechol-O-methyltransferase and aromatic L-amino acid decarboxylase. Levodopa 0-6 dopa decarboxylase Homo sapiens 72-107 2272023-0 1990 Effect of a novel catechol-O-methyltransferase inhibitor, nitecapone, on the metabolism of L-dopa in healthy volunteers. Levodopa 91-97 catechol-O-methyltransferase Homo sapiens 18-46 2084146-10 1990 Challenge with either L-dopa or clonidine produced a peak GH response of 2.3 ng/ml (normals = greater than 7 ng/ml). Levodopa 22-28 growth hormone 1 Homo sapiens 58-60 2270318-1 1990 We sought to clarify the mechanisms of growth hormone (GH) secretion induced by insulin hypoglycemia, L-dopa, and arginine in man. Levodopa 102-108 growth hormone 1 Homo sapiens 39-53 2272023-11 1990 The changes in L-Dopa metabolism by COMT inhibitor warrant further clinical studies in Parkinson"s disease. Levodopa 15-21 catechol-O-methyltransferase Homo sapiens 36-40 2118219-3 1990 GH response to GRH, arginine, and L-dopa in obese subjects was markedly impaired before weight reduction, whereas significantly increased responses were noted after weight reduction (P less than .01). Levodopa 34-40 growth hormone 1 Homo sapiens 0-2 2282937-4 1990 The MAC-reducing effect of L-DOPA was attenuated by selective antagonism of the D2 dopamine receptor with YM-09151-2 while selective blockade of the D1 dopamine receptor with SCH-23390 did not alter L-DOPA"s effect on the MAC for halothane. Levodopa 27-33 dopamine receptor D2 Mus musculus 80-100 2118219-4 1990 Impaired integrated GH response to GRH, arginine, and L-dopa in obese subjects was significantly restored after weight reduction (P less than .01). Levodopa 54-60 growth hormone 1 Homo sapiens 20-22 2118219-0 1990 Very-low-calorie diet-induced weight reduction reverses impaired growth hormone secretion response to growth hormone-releasing hormone, arginine, and L-dopa in obesity. Levodopa 150-156 growth hormone 1 Homo sapiens 65-79 2243617-2 1990 Trp-P-2 inhibited the enzyme activity toward L-DOPA more markedly than that toward 5-hydroxytryptophan. Levodopa 45-51 polycystin 2, transient receptor potential cation channel Homo sapiens 0-7 2243617-5 1990 Among a series of heterocyclic amines examined for their effects on the activity toward L-DOPA, Trp-P-2 was the most potent inhibitor, followed by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, then Trp-P-1. Levodopa 88-94 polycystin 2, transient receptor potential cation channel Homo sapiens 96-103 2243617-5 1990 Among a series of heterocyclic amines examined for their effects on the activity toward L-DOPA, Trp-P-2 was the most potent inhibitor, followed by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, then Trp-P-1. Levodopa 88-94 polycystin 1, transient receptor potential channel interacting Homo sapiens 201-208 1697660-4 1990 In 8 children, PD and L-dopa when administered alone induced an equivalent GH rise (area under the response curve, mean +/- SEM: 241.4 +/- 31.1 vs. 202.9 +/- 38.6 micrograms/l/h) while their coadministration had an additive effect (435.4 +/- 41.4 micrograms/l/h; p less than 0.02 vs. PD and L-dopa alone). Levodopa 22-28 growth hormone 1 Homo sapiens 75-77 2119841-8 1990 The most striking effect of chronic treatment with levodopa plus benserazide was the appearance of large quantities of 3-MT in plasma, CSF and brain. Levodopa 51-59 colony stimulating factor 2 Rattus norvegicus 135-138 1976043-2 1990 These neurons have an uptake mechanism for L-DOPA, and contain the enzymes for converting L-DOPA (but not D-DOPA) to dopamine and noradrenaline, i.e. aromatic L-aminoacid decarboxylase and dopamine beta-hydroxylase. Levodopa 90-96 dopamine beta-hydroxylase Cavia porcellus 189-214 1697660-7 1990 These data show that the enhancement of the cholinergic activity by PD increases the L-dopa-induced GH release but fails to modify both Arg- and GAL-induced GH release in short children. Levodopa 85-91 growth hormone 1 Homo sapiens 100-102 2318945-0 1990 Blindness impairs plasma growth hormone response to L-dopa but not to arginine. Levodopa 52-58 growth hormone 1 Homo sapiens 25-39 2116809-2 1990 In inactin-anesthesized rats, L-dopa increased natriuresis, diuresis and renal blood flow; these effects were linked to endorenal DA synthesis and to DA-1 receptor stimulation since they were suppressed by both carbidopa and SCH 23390. Levodopa 30-36 RT1 class II, locus Da Rattus norvegicus 150-154 1972967-9 1990 Metabolic conversion of L-dopa by AADC is thus preserved in the case of an approach via the basolateral side of the proximal tubular cells. Levodopa 24-30 dopa decarboxylase Rattus norvegicus 34-38 1979968-1 1990 MIF-1, a synthetic tripeptide with MSH-release inhibitory properties, has been reported to improve symptoms of Parkinson"s disease, attenuate levodopa-related dyskinesias and diminish the dyskinetic movements of Tardive dyskinesia. Levodopa 142-150 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 0-5 1979968-3 1990 There is evidence to suggest that MIF-1 increases nigro-striatal dopaminergic activity, but its ability to improve symptoms in patients with Parkinson"s disease, levodopa-related dyskinesias and Tardive dyskinesia cannot be explained solely on the basis of the drug"s effect on striatal dopaminergic neurons. Levodopa 162-170 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 34-39 2166532-2 1990 The enzyme L-amino acid decarboxylase (L-AADC) that converts L-dopa to DA has been localized to the proximal tubule cells with immunocytochemistry. Levodopa 61-67 dopa decarboxylase Homo sapiens 41-45 2318945-4 1990 Because L-dopa is believed to release GH by stimulating endogenous GHRH, whereas arginine may act by suppressing endogenous somatostatin secretion, we propose that blindness may impair GH release by inhibiting GHRH secretion. Levodopa 8-14 growth hormone releasing hormone Homo sapiens 67-71 2320253-0 1990 CCK-8S inhibits L-dopa-induced dyskinesias in parkinsonian squirrel monkeys. Levodopa 16-22 cholecystokinin Homo sapiens 0-3 2320253-1 1990 Systemic administration of CCK-8S (1 or 10 micrograms/kg IP) markedly inhibited L-dopa-induced dyskinesias in parkinsonian monkeys, but did not interfere with locomotor stimulation by L-dopa. Levodopa 80-86 cholecystokinin Homo sapiens 27-30 2300246-6 1990 Age and disease severity were the most significant predictors of survival after initiation of levodopa treatment. Levodopa 94-102 renin binding protein Homo sapiens 0-3 1970430-0 1990 Tetrahydrobiopterin-dependent production of L-dopa in NRK fibroblasts transfected with tyrosine hydroxylase cDNA: future use for intracerebral grafting. Levodopa 44-50 tyrosine hydroxylase Rattus norvegicus 87-107 1970430-1 1990 In the present study, tyrosine hydroxylase (TH; EC 1.14.16.2) cDNA was transfected into cultured fibroblasts and the production of L-3,4-dihydroxyphenylalanine (L-DOPA) was determined. Levodopa 131-159 tyrosine hydroxylase Rattus norvegicus 22-42 1970430-1 1990 In the present study, tyrosine hydroxylase (TH; EC 1.14.16.2) cDNA was transfected into cultured fibroblasts and the production of L-3,4-dihydroxyphenylalanine (L-DOPA) was determined. Levodopa 131-159 tyrosine hydroxylase Rattus norvegicus 44-46 1970430-1 1990 In the present study, tyrosine hydroxylase (TH; EC 1.14.16.2) cDNA was transfected into cultured fibroblasts and the production of L-3,4-dihydroxyphenylalanine (L-DOPA) was determined. Levodopa 161-167 tyrosine hydroxylase Rattus norvegicus 22-42 1970430-1 1990 In the present study, tyrosine hydroxylase (TH; EC 1.14.16.2) cDNA was transfected into cultured fibroblasts and the production of L-3,4-dihydroxyphenylalanine (L-DOPA) was determined. Levodopa 161-167 tyrosine hydroxylase Rattus norvegicus 44-46 2106792-6 1990 3,4-Dihydroxyphenylacetic acid (DOPAC) is detectable in the adrenal cortex but not in the adrenal medulla, and DOPAC levels increased significantly after L-dopa, which indicates monoamine oxidase (MAO) activity within the adrenal cortex. Levodopa 154-160 monoamine oxidase A Rattus norvegicus 178-195 2106792-6 1990 3,4-Dihydroxyphenylacetic acid (DOPAC) is detectable in the adrenal cortex but not in the adrenal medulla, and DOPAC levels increased significantly after L-dopa, which indicates monoamine oxidase (MAO) activity within the adrenal cortex. Levodopa 154-160 monoamine oxidase A Rattus norvegicus 197-200 2113389-12 1990 In these animals levodopa/carbidopa increased brain L-dopa 2.4-4-fold, those of 3-OMD 1.2-1.7-fold compared to intact animals, but the synthesis and metabolism of dopamine and the effects of COMT and MAO inhibitors were not significantly changed. Levodopa 17-25 catechol-O-methyltransferase Rattus norvegicus 191-195 2340838-9 1990 The mean dose of levodopa in Sinemet CR4 was 1,186 +/- 458 mg and the mean dose of carbidopa was 797 +/- 115 mg. Levodopa 17-25 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 37-40 2340841-0 1990 Steady plasma levodopa concentrations required for good clinical response to CR-4 in patients with "on-off". Levodopa 14-22 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 77-81 1983011-13 1990 Based upon some additional studies with levodopa, the results suggest that a combination of DA-1 and DA-2 agonistic activity is a desirable feature of a new drug, since it appears suitable to provide vasodilation while counteracting the neurohumoral abnormality of congestive heart failure. Levodopa 40-48 immunoglobulin heavy diversity 4-11 (non-functional) Homo sapiens 92-96 2113389-12 1990 In these animals levodopa/carbidopa increased brain L-dopa 2.4-4-fold, those of 3-OMD 1.2-1.7-fold compared to intact animals, but the synthesis and metabolism of dopamine and the effects of COMT and MAO inhibitors were not significantly changed. Levodopa 17-25 monoamine oxidase A Rattus norvegicus 200-203 2154126-1 1990 The enzyme L-amino acid decarboxylase (L-AADC), found in abundance in rat proximal tubule cell cytosol, converts L-dopa to dopamine. Levodopa 113-119 dopa decarboxylase Rattus norvegicus 41-45 2154126-8 1990 Carbidopa, an inhibitor of L-AADC, abolished the L-dopa-induced inhibition of nystatin-stimulated QO2 in cells from HS rats and was without significant effect in cells from LS rats. Levodopa 49-55 dopa decarboxylase Rattus norvegicus 29-33 2138080-3 1990 Both dopamine D1 and D2 receptors are consistently elevated in Parkinson"s diseased striata from patients who have not been medicated with L-dopa pre-mortem. Levodopa 139-145 dopamine receptor D1 Homo sapiens 5-33 2089083-5 1990 It is concluded that both MAO-A and MAO-B are important in the metabolism of newly-formed dopamine in kidney slices incubated with exogenous L-DOPA. Levodopa 141-147 monoamine oxidase A Rattus norvegicus 26-31 2089083-5 1990 It is concluded that both MAO-A and MAO-B are important in the metabolism of newly-formed dopamine in kidney slices incubated with exogenous L-DOPA. Levodopa 141-147 monoamine oxidase B Rattus norvegicus 36-41 2291808-0 1990 Prolactin release and milk removal induced by suckling and milking in lactating ewes is prevented by L-dopa treatment. Levodopa 101-107 prolactin Homo sapiens 0-9 2303915-7 1990 Hearts and spleens from -Cu mice appeared to have higher tyrosine 3-monooxygenase activity as judged by increasing rates of L-dihydroxyphenylalanine accumulation following injection of m-hydroxybenzylhydrazine (NSD-1015), an inhibitor of aromatic amino acid decarboxylase. Levodopa 124-148 tyrosine hydroxylase Mus musculus 57-81 2128510-0 1990 Effects of the COMT inhibitor, CGP 28014, on plasma homovanillic acid and O-methylation of exogenous L-dopa in the rat. Levodopa 101-107 catechol-O-methyltransferase Rattus norvegicus 15-19 2291808-7 1990 The inhibitory effect of 200 mg of L-DOPA on the secretion of prolactin after milking lasted for about 120 min, and thereafter a significant increase in serum prolactin level occurred. Levodopa 35-41 prolactin Homo sapiens 62-71 2291808-7 1990 The inhibitory effect of 200 mg of L-DOPA on the secretion of prolactin after milking lasted for about 120 min, and thereafter a significant increase in serum prolactin level occurred. Levodopa 35-41 prolactin Homo sapiens 159-168 2291808-9 1990 Doses of 25 or 50 mg of L-DOPA prevented the surge of prolactin observed immediately after milking, but a long-lasting release of prolactin was obtained thereafter. Levodopa 24-30 prolactin Homo sapiens 54-63 2291808-10 1990 The inhibitory effect of L-DOPA on prolactin release could be overridden by the suckling or milking stimuli according to the dose administered. Levodopa 25-31 prolactin Homo sapiens 35-44 876212-0 1977 [Stimulation of the secretion of somatotropin by administration of Nacom (L-dopa and L-carbidopa) in ambulatory patients with retarded growth]. Levodopa 74-80 growth hormone 1 Homo sapiens 33-45 778710-0 1976 The effect of L-dopa and clomiphene citrate on peripheral plasma levels of luteinizing hormone-releasing factor. Levodopa 14-20 CREB3 regulatory factor Homo sapiens 75-111 778710-1 1976 Response of luteinizing hormone-releasing factor (LRF) and gonadotropin levels to orally administered L-dopa and clomiphene citrate were measured in 13 healthy female volunteers. Levodopa 102-108 CREB3 regulatory factor Homo sapiens 12-48 778710-1 1976 Response of luteinizing hormone-releasing factor (LRF) and gonadotropin levels to orally administered L-dopa and clomiphene citrate were measured in 13 healthy female volunteers. Levodopa 102-108 CREB3 regulatory factor Homo sapiens 50-53 778710-3 1976 The results indicated a suggestive but statistically nonsignificant elevation of peripheral plasma LRF following L-dopa administration but no response following clomiphene ingestion. Levodopa 113-119 CREB3 regulatory factor Homo sapiens 99-102 33824605-9 2021 Oral levodopa/dopa decarboxylase inhibitor application is inevitably necessary with advance of PD. Levodopa 5-13 dopa decarboxylase Homo sapiens 14-32 33971218-0 2021 The p75 neurotrophin receptor as a novel intermediate in L-dopa-induced dyskinesia in experimental Parkinson"s disease. Levodopa 57-63 nerve growth factor receptor Rattus norvegicus 4-29 33821889-1 2021 To inculcate biocatalytic activity in the oxygen-storage protein myoglobin (Mb), a genetically engineered myoglobin mutant H64DOPA (DOPA = L-3,4-dihydroxyphenylalanine) has been created. Levodopa 139-167 myoglobin Homo sapiens 65-74 33821889-1 2021 To inculcate biocatalytic activity in the oxygen-storage protein myoglobin (Mb), a genetically engineered myoglobin mutant H64DOPA (DOPA = L-3,4-dihydroxyphenylalanine) has been created. Levodopa 139-167 myoglobin Homo sapiens 76-78 33821889-1 2021 To inculcate biocatalytic activity in the oxygen-storage protein myoglobin (Mb), a genetically engineered myoglobin mutant H64DOPA (DOPA = L-3,4-dihydroxyphenylalanine) has been created. Levodopa 139-167 myoglobin Homo sapiens 106-115 29185545-3 2017 A community service-based longitudinal study showed that dopamine transporter imaging could help identify subgroups of patients with parkinsonism associated with antipsychotics with a progressive course, potentially manageable with l-dopa. Levodopa 232-238 solute carrier family 6 member 3 Homo sapiens 57-77 33808712-1 2021 Aromatic amino acid decarboxylase (AADC) deficiency is a rare, autosomal recessive neurometabolic disorder caused by mutations in the DDC gene, leading to a deficit of AADC, a pyridoxal 5"-phosphate requiring enzyme that catalyzes the decarboxylation of L-Dopa and L-5-hydroxytryptophan in dopamine and serotonin, respectively. Levodopa 254-260 dopa decarboxylase Homo sapiens 35-39 33808712-1 2021 Aromatic amino acid decarboxylase (AADC) deficiency is a rare, autosomal recessive neurometabolic disorder caused by mutations in the DDC gene, leading to a deficit of AADC, a pyridoxal 5"-phosphate requiring enzyme that catalyzes the decarboxylation of L-Dopa and L-5-hydroxytryptophan in dopamine and serotonin, respectively. Levodopa 254-260 dopa decarboxylase Homo sapiens 168-172 33809767-11 2021 We also include our own studies, highlighting the possible protective cardiac effects induced by L-DOPA treatment through the enhancement of HSP27 levels and activity. Levodopa 97-103 heat shock protein family B (small) member 1 Homo sapiens 141-146 32795166-1 2021 In this study, the interaction of Fe3O4@CaAl-LDH@L-Dopa nanoparticles (NPs) with human serum albumin (HSA) was investigated in simulated physiological conditions applying UV-visible, fluorescence, and circular dichroism (CD) spectroscopic techniques. Levodopa 49-55 albumin Homo sapiens 87-100 33033739-0 2020 SPG15: A Rare Correlation with Atypical Juvenile Parkinsonism Responsive to Levodopa. Levodopa 76-84 zinc finger FYVE-type containing 26 Homo sapiens 0-5 29120065-0 2018 Biallelic mutations in mitochondrial tryptophanyl-tRNA synthetase cause Levodopa-responsive infantile-onset Parkinsonism. Levodopa 72-80 tryptophanyl-tRNA synthetase 1 Homo sapiens 37-65 29120065-5 2018 Here, we report the case of a 17-year-old boy with compound heterozygous mutations in WARS2 (p.Trp13Gly, p.Ser228Trp) who presented with infantile-onset, Levodopa-responsive Parkinsonism at the age of 2 years. Levodopa 154-162 tryptophanyl tRNA synthetase 2, mitochondrial Homo sapiens 86-91 23152595-0 2012 Nociceptin/orphanin FQ receptor agonists attenuate L-DOPA-induced dyskinesias. Levodopa 51-57 prepronociceptin Rattus norvegicus 0-10 27006626-7 2015 Detected PRKN variants moderately correlated with PD course and response to L-dopa. Levodopa 76-82 parkin RBR E3 ubiquitin protein ligase Homo sapiens 9-13 23811734-7 2013 Enhancing the physiological activity of 5-HT1A receptors with 5-HT1A agonists might alleviate anxiety, dyskinesia and tremor, although a deleterious effect on the anti-parkinsonian efficacy of L-DOPA may ultimately limit the use of this class of compounds. Levodopa 193-199 5-hydroxytryptamine receptor 1A Homo sapiens 40-46 24687255-7 2014 Moreover, results from phase II and III trials also demonstrate that A2A antagonists are effective in reducing off-time, without worsening troublesome dyskinesia, and in increasing on-time with a mild increase of non-troublesome dyskinesia, in patients at an advanced stage of PD treated with L-DOPA. Levodopa 293-299 immunoglobulin kappa variable 2D-29 Homo sapiens 69-72 23152595-0 2012 Nociceptin/orphanin FQ receptor agonists attenuate L-DOPA-induced dyskinesias. Levodopa 51-57 opioid related nociceptin receptor 1 Rattus norvegicus 11-31 23152595-1 2012 In the present study we investigated whether the neuropeptide nociceptin/orphanin FQ (N/OFQ), previously implicated in the pathogenesis of Parkinson"s disease, also affects L-DOPA-induced dyskinesia. Levodopa 173-179 prepronociceptin Rattus norvegicus 62-72 23152595-1 2012 In the present study we investigated whether the neuropeptide nociceptin/orphanin FQ (N/OFQ), previously implicated in the pathogenesis of Parkinson"s disease, also affects L-DOPA-induced dyskinesia. Levodopa 173-179 prepronociceptin Rattus norvegicus 73-84 34582053-7 2022 Cutaneous P-SYN and abnormal DAT scans were noted in the 4 levodopa-responsive patients and 1 asymptomatic patient. Levodopa 59-67 solute carrier family 6 member 3 Homo sapiens 29-32 34876467-5 2022 L-Dopa treatment of gch1-/- larvae improved survival without ameliorating the motor phenotype. Levodopa 0-6 GTP cyclohydrolase 1 Danio rerio 20-24 34939797-0 2022 Surface Plasmon Resonance Identifies High-Affinity Binding of l-DOPA to Siderocalin/Lipocalin-2 through Iron-Siderophore Action: Implications for Parkinson"s Disease Treatment. Levodopa 62-68 lipocalin 2 Homo sapiens 84-95 34986438-7 2022 Upon glucose binding, GBP undergoes a significant conformational change that is manifested as a change in the electrochemistry of L-DOPA. Levodopa 130-136 transmembrane protein 132A Homo sapiens 22-25 34882402-2 2022 Herein, we identified S05014 (l-Tyr, IC50 = 6.25 +- 1.43 nM; l-Dopa, IC50 = 0.64 +- 0.40 muM) as a highly effective tyrosinase inhibitor. Levodopa 61-67 tyrosinase Homo sapiens 116-126 34838844-13 2022 Lastly, systemically treating Opn4-/- mice with the dopamine precursor L-DOPA reduced their form-deprivation myopia by half compared to non-treated mice. Levodopa 71-77 opsin 4 (melanopsin) Mus musculus 30-34 34984873-8 2021 In shake-flask fermentation, the DOPA decarboxylase gene from Homo sapiens (Hsddc) showed the highest dopamine production (3.33 g/L), while the DOPA decarboxylase gene from Drosophila Melanogaster (Dmddc) showed the least residual L-DOPA concentration (0.02 g/L). Levodopa 231-237 dopa decarboxylase Homo sapiens 33-51 34962574-3 2022 Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD. Levodopa 253-261 monoamine oxidase B Homo sapiens 155-179 34962574-3 2022 Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD. Levodopa 253-261 monoamine oxidase B Homo sapiens 181-186 34962574-3 2022 Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD. Levodopa 253-261 catechol-O-methyltransferase Homo sapiens 203-231 34962574-3 2022 Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD. Levodopa 253-261 catechol-O-methyltransferase Homo sapiens 233-237 34984873-5 2021 In this study, DOPA decarboxylase gene from Sus scrofa (Ssddc) was cloned into plasmids with different copy numbers, and transformed into a previously developed L-DOPA producing strain Escherichia coli T004. Levodopa 161-167 dopa decarboxylase Sus scrofa 15-33 34984873-8 2021 In shake-flask fermentation, the DOPA decarboxylase gene from Homo sapiens (Hsddc) showed the highest dopamine production (3.33 g/L), while the DOPA decarboxylase gene from Drosophila Melanogaster (Dmddc) showed the least residual L-DOPA concentration (0.02 g/L). Levodopa 231-237 dopa decarboxylase Homo sapiens 144-162 34935105-7 2022 By inhibiting COMT, opicapone slows levodopa metabolism and increases its availability. Levodopa 36-44 catechol-O-methyltransferase Homo sapiens 14-18 34767786-0 2021 Analysis of L-DOPA and Droxidopa binding to Human beta2-Adrenergic Receptor. Levodopa 12-18 adrenoceptor beta 2 Homo sapiens 50-75 34767786-3 2021 We show that molecular docking of L-DOPA and Droxidopa into rigid and flexible beta2 AR models leads for both ligands to binding anchor sites comparable to those experimentally reported for adrenaline, namely D113/N312 and S203/S204/S207 side chains. Levodopa 34-40 adenosine A2a receptor Homo sapiens 79-87 34915449-8 2022 RESULTS: Therapeutic effect of GPi DBS on FOG were correlated with the disease duration of PD before DBS surgery, preoperative improvement in FOG severity by levodopa medication, and the distance from active contact of DBS electrode to the prefrontal region of GPi anatomical site. Levodopa 158-166 zinc finger protein, FOG family member 1 Homo sapiens 42-45 34297092-9 2021 In an additional set of experiments, we were able to rescue alpha-synuclein-induced alterations of motor function, striatal synaptic plasticity, and increased spontaneous excitatory synaptic currents by a sub-chronic treatment with L-Dopa, a precursor of dopamine widely used in the therapy of Parkinson"s disease, clearly demonstrating that a dysfunctional dopamine system plays a critical role in the early phases of the disease. Levodopa 232-238 synuclein alpha Homo sapiens 60-75 34915449-8 2022 RESULTS: Therapeutic effect of GPi DBS on FOG were correlated with the disease duration of PD before DBS surgery, preoperative improvement in FOG severity by levodopa medication, and the distance from active contact of DBS electrode to the prefrontal region of GPi anatomical site. Levodopa 158-166 zinc finger protein, FOG family member 1 Homo sapiens 142-145 34915449-9 2022 CONCLUSIONS: Our study results suggest that the effect of GPi DBS on FOG is correlated with disease duration, levodopa responsiveness on FOG before DBS surgery and DBS electrode location, providing useful information to predict FOG outcome after GPi DBS in PD patients. Levodopa 110-118 zinc finger protein, FOG family member 1 Homo sapiens 69-72 34915449-9 2022 CONCLUSIONS: Our study results suggest that the effect of GPi DBS on FOG is correlated with disease duration, levodopa responsiveness on FOG before DBS surgery and DBS electrode location, providing useful information to predict FOG outcome after GPi DBS in PD patients. Levodopa 110-118 zinc finger protein, FOG family member 1 Homo sapiens 137-140 34915449-9 2022 CONCLUSIONS: Our study results suggest that the effect of GPi DBS on FOG is correlated with disease duration, levodopa responsiveness on FOG before DBS surgery and DBS electrode location, providing useful information to predict FOG outcome after GPi DBS in PD patients. Levodopa 110-118 zinc finger protein, FOG family member 1 Homo sapiens 228-231 34313482-3 2021 Treatment with L-dihydroxyphenylalanine, not tyrosine, caused the production of dopamine in the incubation of INS-1 cells (rat islet beta cell line) and primary isolated islets, which was blocked by AADC inhibitor NSD-1015. Levodopa 15-39 dopa decarboxylase Rattus norvegicus 199-203 34956087-8 2021 The peak value of growth hormone was 10.26 ng/ml in the levodopa provocation test. Levodopa 56-64 growth hormone 1 Homo sapiens 18-32 34550406-11 2021 CONCLUSION: Our results suggest that combining 5-HT2AR antagonism with mGluR2 activation results in greater reduction of L-DOPA-induced dyskinesia and PD psychosis. Levodopa 121-127 glutamate receptor, ionotropic, AMPA2 (alpha 2) Mus musculus 71-77 34125397-0 2021 Liposomal Form of L-Dopa and SH-Sy5y Cell-Derived Exosomes Modulate the Tyrosine Hydroxylase/Dopamine Receptor D2 Signaling Pathway in Parkinson"s Rat Models. Levodopa 18-24 tyrosine hydroxylase Homo sapiens 72-92 34125397-0 2021 Liposomal Form of L-Dopa and SH-Sy5y Cell-Derived Exosomes Modulate the Tyrosine Hydroxylase/Dopamine Receptor D2 Signaling Pathway in Parkinson"s Rat Models. Levodopa 18-24 dopamine receptor D2 Homo sapiens 93-113 33907036-1 2021 Growing evidence has highlighted that angiotensin-converting enzyme (ACE)-inhibitors (ACEi)/AT1 receptor blockers (ARBs) may influence the complex interplay between dopamine and the renin-angiotensin system in the nigrostriatal pathway, thus affecting the development of levodopa-induced dyskinesia in Parkinson"s disease (PD). Levodopa 271-279 angiotensin I converting enzyme Homo sapiens 38-67 34757293-4 2021 The congener proteins treated with tyrosinase convert 3, 4-dihydroxy-l-phenylalanine to dopaquinone for strain-promoted click chemistry. Levodopa 54-84 tyrosinase Homo sapiens 35-45 33907036-1 2021 Growing evidence has highlighted that angiotensin-converting enzyme (ACE)-inhibitors (ACEi)/AT1 receptor blockers (ARBs) may influence the complex interplay between dopamine and the renin-angiotensin system in the nigrostriatal pathway, thus affecting the development of levodopa-induced dyskinesia in Parkinson"s disease (PD). Levodopa 271-279 angiotensin I converting enzyme Homo sapiens 69-72 34992971-2 2021 Classic GTP cyclohydrolase 1 (GCH-1)-associated DRD consists of early-onset lower limb asymmetrical dystonia, with sleep benefit, diurnal variation, and excellent and sustained response to low l-dopa doses. Levodopa 193-199 GTP cyclohydrolase 1 Homo sapiens 8-28 34992971-2 2021 Classic GTP cyclohydrolase 1 (GCH-1)-associated DRD consists of early-onset lower limb asymmetrical dystonia, with sleep benefit, diurnal variation, and excellent and sustained response to low l-dopa doses. Levodopa 193-199 GTP cyclohydrolase 1 Homo sapiens 30-35 34992971-4 2021 We describe a GCH-1-associated late-onset DRD case with a family history of parkinsonism and cervical dystonia whose response to levodopa was poor and complicated with dyskinesia, blepharospasm, and severe nonmotor symptoms. Levodopa 129-137 GTP cyclohydrolase 1 Homo sapiens 14-19 34992971-6 2021 Summary: GCH-1-related dystonia may exhibit wide intrafamilial phenotypic variability, no diurnal fluctuation, poor response to l-dopa, and such complications as dyskinesia, epilepsy, sleep disorders, autonomic dysfunction, oculogyric crisis, myoclonus, or tics. Levodopa 128-134 GTP cyclohydrolase 1 Homo sapiens 9-14 34806120-0 2022 Interactions of a boron-containing levodopa derivative on D2 dopamine receptor and its effects in a Parkinson disease model. Levodopa 35-43 dopamine receptor D2 Mus musculus 58-78 34806120-4 2022 Theoretical results yielded higher affinity of the compound DPBX, a Dopaboroxazolidone, than levodopa on D2DR. Levodopa 93-101 dopamine receptor D2 Mus musculus 105-109 34830228-0 2021 L-dopa-Dependent Effects of GLP-1R Agonists on the Survival of Dopaminergic Cells Transplanted into a Rat Model of Parkinson Disease. Levodopa 0-6 glucagon-like peptide 1 receptor Rattus norvegicus 28-34 34830228-11 2021 The co-administration of L-dopa and exendin-4 also led to indicators of insulin resistance not seen with liraglutide, which may underpin the differential effects observed between the two GLP1-R agonists. Levodopa 25-31 glucagon-like peptide 1 receptor Rattus norvegicus 187-193 34767639-9 2021 Unilateral dopamine depletion caused bilateral reduction of RGS4 levels, which was reversed by L-Dopa. Levodopa 95-101 regulator of G-protein signaling 4 Mus musculus 60-64 34767639-0 2021 RGS4 negatively modulates Nociceptin/Orphanin FQ opioid receptor signaling: implication for L-Dopa-induced dyskinesia. Levodopa 92-98 regulator of G-protein signaling 4 Rattus norvegicus 0-4 34767639-10 2021 L-Dopa acutely upregulated RGS4 in the lesioned striatum. Levodopa 0-6 regulator of G-protein signaling 4 Mus musculus 27-31 34469756-3 2021 The aim of the present study was to examine the influence of 7-{5,8-dimethyl-(1,2,4)triazolo(1,5-a)pyrazin-2-yl}-2-phenylimidazo(1,2-a)pyrimidine (CPL500036), a novel selective inhibitor of PDE10A, on sensorimotor deficits and therapeutic effects of L-DOPA in hemiparkinsonian rats. Levodopa 250-256 phosphodiesterase 10A Rattus norvegicus 190-196 34750479-1 2021 In Parkinson"s disease (PD), the effects of both Ldopa and subthalamic deep brain stimulation (STN-DBS) are known to change cost-valuation. Levodopa 49-54 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 95-98 34776935-10 2021 Prolonged L-DOPA treatment further increased GFAP levels. Levodopa 10-16 glial fibrillary acidic protein Rattus norvegicus 45-49 34474045-8 2021 Expression of 5HT1B mRNA was elevated in the lesioned striatum of intermittently levodopa-treated rats, but this elevation was normalized by concomitant use of ZNS. Levodopa 81-89 5-hydroxytryptamine receptor 1B Rattus norvegicus 14-19 34834946-1 2021 A bidirectional negative relationship between Hepatitis C virus (HCV) replication and gene expression of the catecholamine biosynthetic enzyme L-Dopa decarboxylase (DDC) was previously shown in the liver and attributed at least to an association of DDC with phosphatidylinositol 3-kinase (PI3K). Levodopa 143-149 dopa decarboxylase Homo sapiens 165-168 34834946-1 2021 A bidirectional negative relationship between Hepatitis C virus (HCV) replication and gene expression of the catecholamine biosynthetic enzyme L-Dopa decarboxylase (DDC) was previously shown in the liver and attributed at least to an association of DDC with phosphatidylinositol 3-kinase (PI3K). Levodopa 143-149 dopa decarboxylase Homo sapiens 249-252 34474045-9 2021 The severity of AIMs was correlated with the ratio of 5HT1B to 5HT1A mRNA expression in the lesioned striatum, indicating that the anti-LID effect of ZNS is based on inhibition via 5HT1B receptors to direct pathway MSNs sensitized by intermittent levodopa treatment. Levodopa 247-255 5-hydroxytryptamine receptor 1B Rattus norvegicus 54-59 34474045-9 2021 The severity of AIMs was correlated with the ratio of 5HT1B to 5HT1A mRNA expression in the lesioned striatum, indicating that the anti-LID effect of ZNS is based on inhibition via 5HT1B receptors to direct pathway MSNs sensitized by intermittent levodopa treatment. Levodopa 247-255 5-hydroxytryptamine receptor 1A Rattus norvegicus 63-68 34474045-9 2021 The severity of AIMs was correlated with the ratio of 5HT1B to 5HT1A mRNA expression in the lesioned striatum, indicating that the anti-LID effect of ZNS is based on inhibition via 5HT1B receptors to direct pathway MSNs sensitized by intermittent levodopa treatment. Levodopa 247-255 5-hydroxytryptamine receptor 1B Rattus norvegicus 181-186 34346015-3 2021 Thus, we performed a meta-analysis to assess whether COMT and MAO-B genetic variants are associated with an increased incidence of levodopa-induced dyskinesia (LID) in PD patients. Levodopa 131-139 monoamine oxidase B Homo sapiens 62-67 34284020-0 2021 L-DOPA promotes striatal dopamine release through D1 receptors and reversal of dopamine transporter. Levodopa 0-6 solute carrier family 6 member 3 Homo sapiens 79-99 34371144-2 2021 CDGI is strongly down-regulated in two hyperkinetic conditions related to striatal dysfunction: Huntington"s disease and levodopa-induced dyskinesia in Parkinson"s disease. Levodopa 121-129 RAS, guanyl releasing protein 2 Mus musculus 0-4 34346015-0 2021 Association of COMT rs4680 and MAO-B rs1799836 polymorphisms with levodopa-induced dyskinesia in Parkinson"s disease-a meta-analysis. Levodopa 66-74 catechol-O-methyltransferase Homo sapiens 15-19 34346015-0 2021 Association of COMT rs4680 and MAO-B rs1799836 polymorphisms with levodopa-induced dyskinesia in Parkinson"s disease-a meta-analysis. Levodopa 66-74 monoamine oxidase B Homo sapiens 31-36 34346015-3 2021 Thus, we performed a meta-analysis to assess whether COMT and MAO-B genetic variants are associated with an increased incidence of levodopa-induced dyskinesia (LID) in PD patients. Levodopa 131-139 catechol-O-methyltransferase Homo sapiens 53-57 34638785-5 2021 We observed that in SARS-CoV2-infected enterocytes, ACE2 co-regulates not only with DDC but also with a specific group of genes involved in (i) the dopamine/trace amines metabolic pathway, (ii) the absorption of microbiota-derived L-DOPA and (iii) the absorption of neutral amino acids serving as precursors to neurotransmitters. Levodopa 231-237 angiotensin converting enzyme 2 Homo sapiens 52-56 34641332-0 2021 Role of 5-HT1A Receptor in Vilazodone-Mediated Suppression of L-DOPA-Induced Dyskinesia and Increased Responsiveness to Cortical Input in Striatal Medium Spiny Neurons in an Animal Model of Parkinson"s Disease. Levodopa 62-68 5-hydroxytryptamine receptor 1A Homo sapiens 8-23 34630283-2 2021 The current levodopa treatment requires the addition of other drugs, such as catechol-O-methyl transferase (COMT) inhibitors, to alleviate motor fluctuations in advanced PD. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 77-106 34630283-2 2021 The current levodopa treatment requires the addition of other drugs, such as catechol-O-methyl transferase (COMT) inhibitors, to alleviate motor fluctuations in advanced PD. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 108-112 34552196-0 2021 Dopaminergic co-transmission with sonic hedgehog inhibits abnormal involuntary movements in models of Parkinson"s disease and L-Dopa induced dyskinesia. Levodopa 126-132 sonic hedgehog Mus musculus 34-48 34638567-6 2021 In addition, the Nogo A pathway was significantly downregulated in rats treated with levodopa (LD) compared to vehicle-treated animals subjected to tMCAO. Levodopa 85-93 reticulon 4 Rattus norvegicus 17-23 34552196-8 2021 These findings indicate that augmenting Shh signaling in the L-Dopa treated brain may be a promising therapeutic approach for mitigating the dyskinetic side effects of long-term treatment with L-Dopa. Levodopa 61-67 sonic hedgehog Mus musculus 40-43 34552196-8 2021 These findings indicate that augmenting Shh signaling in the L-Dopa treated brain may be a promising therapeutic approach for mitigating the dyskinetic side effects of long-term treatment with L-Dopa. Levodopa 193-199 sonic hedgehog Mus musculus 40-43 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 allograft inflammatory factor 1 Rattus norvegicus 322-327 34498463-1 2021 In living organisms, tyrosinase selectively produces l-DOPA from l-tyrosine. Levodopa 53-59 tyrosinase Homo sapiens 21-31 34498463-2 2021 Here, a bicomponent hydrogel is used as a template for tyrosinase-catalyzed selective generation of l-DOPA from tyrosine. Levodopa 100-106 tyrosinase Homo sapiens 55-65 34229013-0 2021 Neuroinflammation and L-dopa-induced abnormal involuntary movements in 6-hydroxydopamine-lesioned rat model of Parkinson"s disease are counteracted by combined administration of a 5-HT1A/1B receptor agonist and A2A receptor antagonist. Levodopa 22-28 5-hydroxytryptamine receptor 1A Rattus norvegicus 180-186 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 glial fibrillary acidic protein Rattus norvegicus 157-161 34229013-6 2021 Evaluation of immediate-early-gene zif-268 (index of neuronal activation) after l-dopa challenge, showed an increase in its expression in denervated CPu of rats pretreated with l-dopa or l-dopa plus preladenant compared with vehicle, whereas rats pretreated with eltoprazine, with or without preladenant, had lower zif-268-expression. Levodopa 80-86 early growth response 1 Rattus norvegicus 35-42 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 allograft inflammatory factor 1 Rattus norvegicus 166-171 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 interleukin 1 alpha Rattus norvegicus 248-256 34229013-6 2021 Evaluation of immediate-early-gene zif-268 (index of neuronal activation) after l-dopa challenge, showed an increase in its expression in denervated CPu of rats pretreated with l-dopa or l-dopa plus preladenant compared with vehicle, whereas rats pretreated with eltoprazine, with or without preladenant, had lower zif-268-expression. Levodopa 80-86 early growth response 1 Rattus norvegicus 315-322 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 allograft inflammatory factor 1 Rattus norvegicus 260-265 34229013-6 2021 Evaluation of immediate-early-gene zif-268 (index of neuronal activation) after l-dopa challenge, showed an increase in its expression in denervated CPu of rats pretreated with l-dopa or l-dopa plus preladenant compared with vehicle, whereas rats pretreated with eltoprazine, with or without preladenant, had lower zif-268-expression. Levodopa 177-183 early growth response 1 Rattus norvegicus 35-42 34229013-4 2021 The combined subchronic pretreatment with l-dopa plus eltoprazine and preladenant reduced AIMs induced by acute l-dopa challenge in these rats and decreased GFAP and IBA-1 immunoreactivity induced by the drug in both CPu and SNc, with reduction in IL-1beta in IBA-1-positive cells in both CPu and SNc, and in TNF-alpha in IBA-1-positive cells in SNc. Levodopa 42-48 tumor necrosis factor Rattus norvegicus 309-318 34229013-6 2021 Evaluation of immediate-early-gene zif-268 (index of neuronal activation) after l-dopa challenge, showed an increase in its expression in denervated CPu of rats pretreated with l-dopa or l-dopa plus preladenant compared with vehicle, whereas rats pretreated with eltoprazine, with or without preladenant, had lower zif-268-expression. Levodopa 187-193 early growth response 1 Rattus norvegicus 35-42 34514401-0 2021 Levodopa-responsive dystonia caused by biallelic PRKN exon inversion invisible to exome sequencing. Levodopa 0-8 parkin RBR E3 ubiquitin protein ligase Homo sapiens 49-53 34328686-6 2021 We have identified plasma miR-19b as a possible biomarker for LevoDopa therapy and validated this result in human differentiated dopaminergic neurons exposed to LevoDopa. Levodopa 62-70 microRNA 19b-1 Homo sapiens 26-33 34140181-1 2021 A series of aryl phenoxy methyl triazole conjugated with thiosemicarbazides were designed, synthesized, and evaluated for their tyrosinase inhibitory activities in the presence of l-dopa and l-tyrosine as substrates. Levodopa 180-186 tyrosinase Homo sapiens 128-138 34140181-3 2021 Among the derivatives, compound 9j bearing benzyl displayed exceptionally high potency against tyrosinase with IC50 value of 0.11 muM and 0.17 muM in the presence of l-tyrosine and l-dopa as substrates which is significantly lower than that of kojic acid as the positive control with an IC50 value of 9.28 muM for l-tyrosine and 9.30 muM for l-dopa. Levodopa 181-187 tyrosinase Homo sapiens 95-105 34140181-3 2021 Among the derivatives, compound 9j bearing benzyl displayed exceptionally high potency against tyrosinase with IC50 value of 0.11 muM and 0.17 muM in the presence of l-tyrosine and l-dopa as substrates which is significantly lower than that of kojic acid as the positive control with an IC50 value of 9.28 muM for l-tyrosine and 9.30 muM for l-dopa. Levodopa 342-348 tyrosinase Homo sapiens 95-105 34525893-2 2021 AREAS COVERED: Peripheral inhibition of dopa-decarboxylase has long been considered an essential component of levodopa treatment at every stage of illness. Levodopa 110-118 dopa decarboxylase Homo sapiens 40-58 34525893-3 2021 In contrast, only relatively recently have catechol-O-methyltransferase (COMT) inhibitors been utilized to block the other major pathway of degradation and optimize levodopa delivery to the brain. Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 43-71 34525893-3 2021 In contrast, only relatively recently have catechol-O-methyltransferase (COMT) inhibitors been utilized to block the other major pathway of degradation and optimize levodopa delivery to the brain. Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 73-77 34225162-2 2021 COMT inhibitors enhance the bioavailability of levodopa to the brain, and therefore are combined with levodopa for the treatment of motor fluctuations in PD. Levodopa 47-55 catechol-O-methyltransferase Homo sapiens 0-4 34225162-3 2021 Inhibitors of the MAO-B isoform, in turn, are used as monotherapy or in conjunction with levodopa in PD, and function by reducing the central degradation of dopamine. Levodopa 89-97 monoamine oxidase B Homo sapiens 18-23 34328686-7 2021 In silico analysis suggests that the LevoDopa-induced miR-19b regulates ubiquitin-mediated proteolysis. Levodopa 37-45 microRNA 19b-1 Homo sapiens 54-61 34161592-3 2021 OBJECTIVE: To test whether bilateral stimulation centered at the fields of Forel improves levodopa unresponsive freezing of gait (FOG), balance problems, postural instability, and falls in PD. Levodopa 90-98 zinc finger protein, FOG family member 1 Homo sapiens 130-133 34489685-0 2021 L-3,4-Dihydroxyphenylalanine Recovers Circadian Rhythm Disturbances in the Rat Models of Parkinson"s Disease by Regulating the D1R-ERK1/2-mTOR Pathway. Levodopa 0-28 mitogen activated protein kinase 3 Rattus norvegicus 131-137 34489685-0 2021 L-3,4-Dihydroxyphenylalanine Recovers Circadian Rhythm Disturbances in the Rat Models of Parkinson"s Disease by Regulating the D1R-ERK1/2-mTOR Pathway. Levodopa 0-28 mechanistic target of rapamycin kinase Rattus norvegicus 138-142 34489685-3 2021 This study aims to explore the L-dopa effects on the rhythmic expression of core clock proteins (brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor cycle kaput (CLOCK)), in the striatum of the rat model of PD and its underlying molecular mechanisms. Levodopa 31-37 clock circadian regulator Rattus norvegicus 81-86 34489685-3 2021 This study aims to explore the L-dopa effects on the rhythmic expression of core clock proteins (brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor cycle kaput (CLOCK)), in the striatum of the rat model of PD and its underlying molecular mechanisms. Levodopa 31-37 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 97-133 34489685-3 2021 This study aims to explore the L-dopa effects on the rhythmic expression of core clock proteins (brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor cycle kaput (CLOCK)), in the striatum of the rat model of PD and its underlying molecular mechanisms. Levodopa 31-37 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 135-140 34489685-3 2021 This study aims to explore the L-dopa effects on the rhythmic expression of core clock proteins (brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor cycle kaput (CLOCK)), in the striatum of the rat model of PD and its underlying molecular mechanisms. Levodopa 31-37 clock circadian regulator Rattus norvegicus 179-184 34489685-10 2021 The expressions of BMAL1 and CLOCK protein were rhythmic fluctuated without significant phase alterations when 6-OHDA or L-dopa was applied. Levodopa 121-127 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 19-24 34489685-12 2021 The CV of the expressions of both BMAL1 and CLOCK was decreased in the 6-OHDA group; this process was reversed by L-dopa. Levodopa 114-120 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 34-39 34489685-12 2021 The CV of the expressions of both BMAL1 and CLOCK was decreased in the 6-OHDA group; this process was reversed by L-dopa. Levodopa 114-120 clock circadian regulator Rattus norvegicus 44-49 34489685-13 2021 Moreover, the CV of BMAL1 and CLOCK was elevated in the L-dopa rats. Levodopa 56-62 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 20-25 34489685-13 2021 Moreover, the CV of BMAL1 and CLOCK was elevated in the L-dopa rats. Levodopa 56-62 clock circadian regulator Rattus norvegicus 30-35 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 101-107 mitogen activated protein kinase 3 Rattus norvegicus 30-36 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 101-107 ribosomal protein S6 kinase B1 Rattus norvegicus 38-42 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 101-107 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 276-281 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 101-107 clock circadian regulator Rattus norvegicus 286-291 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 192-198 mitogen activated protein kinase 3 Rattus norvegicus 30-36 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 192-198 ribosomal protein S6 kinase B1 Rattus norvegicus 38-42 34489685-14 2021 The phosphorylation levels of ERK1/2, S6K1, and 4E-BP1 in 6-OHDA-lesioned striatum were increased by L-dopa or D1 receptor agonist SKF38393 (p < 0.05, respectively), not by the combination of L-dopa and D1 receptor antagonist SCH23390, which was similar to the expressions of BMAL1 and CLOCK. Levodopa 192-198 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 276-281 34489685-15 2021 Conclusion: L-dopa recovers the circadian rhythm disturbances in PD rats by regulating the D1R-ERK1/2-mTOR pathway. Levodopa 12-18 mitogen activated protein kinase 3 Rattus norvegicus 95-101 34489685-15 2021 Conclusion: L-dopa recovers the circadian rhythm disturbances in PD rats by regulating the D1R-ERK1/2-mTOR pathway. Levodopa 12-18 mechanistic target of rapamycin kinase Rattus norvegicus 102-106 34443532-1 2021 The aim of the present work was to develop a green multi-platform methodology for the quantification of l-DOPA in solid-state mixtures by means of MIR and NIR spectroscopy. Levodopa 104-110 membrane associated ring-CH-type finger 8 Homo sapiens 147-150 34443532-6 2021 The multi-platform approach provided a higher accuracy than the individual block analysis, indicating that the association of MIR and NIR spectral data, especially by means of SO-PLS, represents a valid solution for the quantification of the l-DOPA excess in enantiomeric mixtures. Levodopa 242-248 membrane associated ring-CH-type finger 8 Homo sapiens 126-129 34306611-0 2021 Time until Need for Levodopa among New Users of Dopamine Agonists or MAO-B Inhibitors. Levodopa 20-28 monoamine oxidase B Homo sapiens 69-74 34306611-2 2021 Our primary endpoint was time until need for levodopa among new monotherapy users of dopamine agonists and MAO-B inhibitors. Levodopa 45-53 monoamine oxidase B Homo sapiens 107-112 34392713-7 2022 Drug delivery efficiency by oral dosing was directly compared to IP injection by collecting plasma and analyzing L-DOPA levels with HPLC. Levodopa 113-119 succinate dehydrogenase complex iron sulfur subunit B Rattus norvegicus 65-67 34392713-9 2022 HPLC showed that oral administration of the compound at the same dose as IP injection yielded significantly lower plasma levels, and that higher oral L-DOPA doses yield higher plasma L-DOPA content. Levodopa 183-189 succinate dehydrogenase complex iron sulfur subunit B Rattus norvegicus 73-75 34434108-5 2021 Moreover, the increases of dopamine D1-receptor, p-DARPP-32, DeltaFosB, p-ERK1/2, and p-c-Jun ser63, along with the decrease in p-c-Jun ser73, induced by L-dopa in 6-OHDA-treated rats were significantly reversed by pretreatment with CA. Levodopa 154-160 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 51-59 34434108-5 2021 Moreover, the increases of dopamine D1-receptor, p-DARPP-32, DeltaFosB, p-ERK1/2, and p-c-Jun ser63, along with the decrease in p-c-Jun ser73, induced by L-dopa in 6-OHDA-treated rats were significantly reversed by pretreatment with CA. Levodopa 154-160 mitogen activated protein kinase 3 Rattus norvegicus 74-80 34434108-5 2021 Moreover, the increases of dopamine D1-receptor, p-DARPP-32, DeltaFosB, p-ERK1/2, and p-c-Jun ser63, along with the decrease in p-c-Jun ser73, induced by L-dopa in 6-OHDA-treated rats were significantly reversed by pretreatment with CA. Levodopa 154-160 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-93 34434108-5 2021 Moreover, the increases of dopamine D1-receptor, p-DARPP-32, DeltaFosB, p-ERK1/2, and p-c-Jun ser63, along with the decrease in p-c-Jun ser73, induced by L-dopa in 6-OHDA-treated rats were significantly reversed by pretreatment with CA. Levodopa 154-160 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 130-135 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 BCL2, apoptosis regulator Rattus norvegicus 37-42 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 caspase 3 Rattus norvegicus 99-108 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 poly (ADP-ribose) polymerase 1 Rattus norvegicus 118-146 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 mitogen-activated protein kinase 3 Homo sapiens 150-156 34434108-9 2021 By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. Levodopa 202-208 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-165 34175496-0 2021 DNAJC6 mutation causing cranial-onset dystonia with tremor dominant levodopa non-responsive parkinsonism: A novel phenotype. Levodopa 68-76 DnaJ heat shock protein family (Hsp40) member C6 Homo sapiens 0-6 34175496-1 2021 DNAJC6 mutation causes two types of phenotypes: slowly progressive parkinsonism with levodopa response and rapidly progressive parkinsonism with additional manifestations like intellectual disability, epilepsy etc. Levodopa 85-93 DnaJ heat shock protein family (Hsp40) member C6 Homo sapiens 0-6 34131032-0 2021 Subregion-specific regulation of dopamine D1 receptor signaling in the striatum: implication for L-DOPA-induced dyskinesia. Levodopa 97-103 dopamine receptor D1 Mus musculus 33-53 34131032-9 2021 When L-DOPA-induced dyskinesia (LID) was developed, D1 receptor signaling in the IC was upregulated and correlated with the severity of LID. Levodopa 5-11 dopamine receptor D1 Mus musculus 52-63 34131032-13 2021 Aberrant activation of D1 receptor signaling in the IC is involved in L-DOPA-induced dyskinesia (LID). Levodopa 70-76 dopamine receptor D1 Mus musculus 23-34 34288271-2 2021 The relatively common (prevalence about one in three) and protein-altering rs6265 single nucleotide polymorphism (C > T) in the gene BDNF has been associated with different clinical outcomes with levodopa. Levodopa 196-204 brain derived neurotrophic factor Homo sapiens 133-137 34306611-9 2021 The mean number of days until the first prescription of levodopa was dispensed was higher among the dopamine agonist users (621 days) compared to the MAO-B inhibitor users (352 days). Levodopa 56-64 monoamine oxidase B Homo sapiens 150-155 33269743-1 2021 Entacapone, a catechol-O-methyltransferase inhibitor, can strengthen the therapeutic effects of levodopa on the treatment of Parkinson"s disease. Levodopa 96-104 catechol-O-methyltransferase Mus musculus 14-42 34185793-0 2021 Alteration of L-Dopa decarboxylase expression in SARS-CoV-2 infection and its association with the interferon-inducible ACE2 isoform. Levodopa 14-20 angiotensin converting enzyme 2 Homo sapiens 120-124 34185793-1 2021 L-Dopa decarboxylase (DDC) is the most significantly co-expressed gene with ACE2, which encodes for the SARS-CoV-2 receptor angiotensin-converting enzyme 2 and the interferon-inducible truncated isoform dACE2. Levodopa 0-6 dopa decarboxylase Homo sapiens 22-25 34185793-1 2021 L-Dopa decarboxylase (DDC) is the most significantly co-expressed gene with ACE2, which encodes for the SARS-CoV-2 receptor angiotensin-converting enzyme 2 and the interferon-inducible truncated isoform dACE2. Levodopa 0-6 angiotensin converting enzyme 2 Homo sapiens 124-155 34185793-1 2021 L-Dopa decarboxylase (DDC) is the most significantly co-expressed gene with ACE2, which encodes for the SARS-CoV-2 receptor angiotensin-converting enzyme 2 and the interferon-inducible truncated isoform dACE2. Levodopa 0-6 Acetylcholine esterase Drosophila melanogaster 203-208 34221698-0 2021 A Case of GCH-1 Mutation Dopa-Responsive Dystonia Requiring High Doses of Levodopa for Treatment. Levodopa 74-82 GTP cyclohydrolase 1 Homo sapiens 10-15 34221698-5 2021 Highlights: Mutations in the GCH-1 gene are associated with Autosomal Dominant Dopamine Responsive Dystonia which is typically defined by dramatic responses to low doses of levodopa. Levodopa 173-181 GTP cyclohydrolase 1 Homo sapiens 29-34 34099487-0 2021 Fyn knockdown prevents levodopa-induced dyskinesia in a mouse model of Parkinson"s disease. Levodopa 23-31 Fyn proto-oncogene Mus musculus 0-3 34078477-1 2021 BACKGROUND: Freezing of gait (FOG) is a particularly debilitating motor deficit seen in a subset of Parkinson"s disease (PD) patients that is poorly responsive to standard levodopa therapy or deep brain stimulation (DBS) of established PD targets such as the subthalamic nucleus and the globus pallidus interna. Levodopa 172-180 zinc finger protein, FOG family member 1 Homo sapiens 30-33 34073856-4 2021 This paper provides a proof-of-concept method for enzymatically creating levodopa-containing proteins using the enzyme tyrosinase and provides spectral evidence of in vitro incorporation in addition to the induction of the unfolded protein response due to levodopa. Levodopa 73-81 tyrosinase Homo sapiens 119-129 34070217-6 2021 Rhes protein binds to and activates striatal mTORC1, and modulates L-DOPA-induced dyskinesia in PD rodent models. Levodopa 67-73 RASD family member 2 Homo sapiens 0-4 34394914-5 2021 The dystonic symptoms responded very well to levodopa treatment, and genetic analysis identified a novel heterozygous mutation in the C-terminal catalytic domain of GCH1. Levodopa 45-53 GTP cyclohydrolase 1 Homo sapiens 165-169 35535012-5 2022 RESULTS: The altered phenotypes of SCIN of parkinsonian mice during the "off levodopa" state resulting from aberrant Kir/leak and Kv1.3 currents can be rapidly reverted by acute inhibition of cAMP-ERK1/2 signaling. Levodopa 77-85 potassium voltage-gated channel, shaker-related subfamily, member 3 Mus musculus 130-135 35500310-0 2022 A selective dual-response biosensor for tyrosinase monophenolase activity based on lanthanide metal-organic frameworks assisted boric acid-levodopa polymer dots. Levodopa 139-147 tyrosinase Homo sapiens 40-50 35331847-9 2022 However, D2 receptor-mediated inhibition of firing (by quinpirole or L-DOPA) was blunted in DAT-KO rats, while GABAB-mediated inhibition was preserved. Levodopa 69-75 solute carrier family 6 member 3 Rattus norvegicus 92-95 35546556-9 2022 The second explanation relates to the systemic induction of the enzyme aromatic L-amino acid decarboxylase (AADC), leading to premature conversion of levodopa into dopamine, again limiting the bioavailability within the brain. Levodopa 150-158 dopa decarboxylase Homo sapiens 71-106 35546556-9 2022 The second explanation relates to the systemic induction of the enzyme aromatic L-amino acid decarboxylase (AADC), leading to premature conversion of levodopa into dopamine, again limiting the bioavailability within the brain. Levodopa 150-158 dopa decarboxylase Homo sapiens 108-112 35603896-0 2022 Association of Catechol-O-Methyltransferase Gene rs4680 Polymorphism and Levodopa Induced Dyskinesia in Parkinson"s Disease: A Meta-Analysis and Systematic Review. Levodopa 73-81 catechol-O-methyltransferase Homo sapiens 15-43 35331847-7 2022 Basal extracellular DA concentration measured with fast-scan controlled-adsorption voltammetry was higher in DAT-KO rats both in the striatum and SNc and was enhanced by L-DOPA (particularly after pharmacological block of monoamine oxidase), confirming that DA release after L-DOPA is not due to DAT reversal. Levodopa 170-176 solute carrier family 6 member 3 Rattus norvegicus 109-112 35331847-7 2022 Basal extracellular DA concentration measured with fast-scan controlled-adsorption voltammetry was higher in DAT-KO rats both in the striatum and SNc and was enhanced by L-DOPA (particularly after pharmacological block of monoamine oxidase), confirming that DA release after L-DOPA is not due to DAT reversal. Levodopa 170-176 solute carrier family 6 member 3 Rattus norvegicus 296-299 35331847-7 2022 Basal extracellular DA concentration measured with fast-scan controlled-adsorption voltammetry was higher in DAT-KO rats both in the striatum and SNc and was enhanced by L-DOPA (particularly after pharmacological block of monoamine oxidase), confirming that DA release after L-DOPA is not due to DAT reversal. Levodopa 275-281 solute carrier family 6 member 3 Rattus norvegicus 109-112 35150767-4 2022 Cabergoline co-treatment with L-dopa reduced LID, striatal preprodynorphin mRNA expression, and hypertrophy of the entopeduncular nucleus, indicating that cabergoline has an anti-LID effect independent of the L-dopa-sparing effect. Levodopa 30-36 prodynorphin Rattus norvegicus 59-74 35508570-0 2022 Marked response to levodopa in a patient with multiple system atrophy presenting with orthostatic hypotension: should reduced DAT uptake on DaTSCAN be a criterion for response to levodopa? Levodopa 19-27 solute carrier family 6 member 3 Homo sapiens 126-129 35508570-0 2022 Marked response to levodopa in a patient with multiple system atrophy presenting with orthostatic hypotension: should reduced DAT uptake on DaTSCAN be a criterion for response to levodopa? Levodopa 179-187 solute carrier family 6 member 3 Homo sapiens 126-129 35378500-8 2022 Significant improvement in inner retina thickness (*p < 0.05) was observed when L-Dopa was given alone and/or with IGF-1. Levodopa 80-86 insulin like growth factor 1 Homo sapiens 115-120 35378500-11 2022 Western studies suggest that L-Dopa+IGF-1 modulates its effects via Akt/ERK dependent pathway. Levodopa 29-35 insulin like growth factor 1 Homo sapiens 36-41 35378500-11 2022 Western studies suggest that L-Dopa+IGF-1 modulates its effects via Akt/ERK dependent pathway. Levodopa 29-35 AKT serine/threonine kinase 1 Homo sapiens 68-71 35378500-11 2022 Western studies suggest that L-Dopa+IGF-1 modulates its effects via Akt/ERK dependent pathway. Levodopa 29-35 mitogen-activated protein kinase 1 Homo sapiens 72-75 35378500-12 2022 CONCLUSION: First ever report on synergistic effect of L-Dopa+IGF-1 in a rat model of diabetic retinopathy. Levodopa 55-61 insulin-like growth factor 1 Rattus norvegicus 62-67 35398727-10 2022 Independent predictors of FOG were: disease duration of more than ten years, levodopa daily dose higher than 500 mg/day, motor status, and COMT AA genotype. Levodopa 77-85 zinc finger protein, FOG family member 1 Homo sapiens 26-29 35466956-7 2022 RESULTS: Baseline plasma NfL was a significant predictor of psychotic symptoms longitudinally across the study adjusted for age, Hoehn and Yahr stage, duration of follow up, duration of disease, baseline levodopa and dopamine agonist medication, and baseline cognition: (OR 8.15 (95% CI 1.40-47.4), p = 0.020). Levodopa 204-212 neurofilament light chain Homo sapiens 25-28 35563817-1 2022 The catechol-O-methyltransferase inhibitors entacapone and opicapone prolong the efficacy of conventional oral levodopa/dopa decarboxylase inhibitor formulations through an increase in levodopa plasma bioavailability. Levodopa 111-119 dopa decarboxylase Homo sapiens 120-138 35563817-1 2022 The catechol-O-methyltransferase inhibitors entacapone and opicapone prolong the efficacy of conventional oral levodopa/dopa decarboxylase inhibitor formulations through an increase in levodopa plasma bioavailability. Levodopa 185-193 catechol-O-methyltransferase Homo sapiens 4-32 35563817-1 2022 The catechol-O-methyltransferase inhibitors entacapone and opicapone prolong the efficacy of conventional oral levodopa/dopa decarboxylase inhibitor formulations through an increase in levodopa plasma bioavailability. Levodopa 185-193 dopa decarboxylase Homo sapiens 120-138 35563817-2 2022 Catechol-O-methyltransferase inhibitors influence the homocysteine metabolism associated with levodopa/dopa decarboxylase application. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 0-28 35563817-2 2022 Catechol-O-methyltransferase inhibitors influence the homocysteine metabolism associated with levodopa/dopa decarboxylase application. Levodopa 94-102 dopa decarboxylase Homo sapiens 103-121 35466951-7 2022 Furthermore, L-DOPA had no effect on overall survival (HuNu) or dopaminergic neuron content of the graft (TH positive cells) but did lead to an increase in the number of GIRK2 positive neurons. Levodopa 13-19 potassium inwardly rectifying channel subfamily J member 6 Homo sapiens 170-175 35361840-5 2022 We confirmed a high overlap between the identified highly predictive molecular pathways and determinants of levodopa clinical responsiveness, including well-known (Wnt signaling, angiogenesis, dopaminergic activity) and recently discovered (immune markers, gonadotropin-releasing hormone receptor) pathways/components. Levodopa 108-116 gonadotropin releasing hormone receptor Homo sapiens 257-296 35257824-1 2022 BACKGROUND: Recent studies have reported an association between PPP2R5D mutations and early-onset levodopa-responsive parkinsonism, but this gene has yet to be analyzed comprehensively in a large Parkinson"s disease (PD) cohort. Levodopa 98-106 protein phosphatase 2 regulatory subunit B'delta Homo sapiens 64-71 35462702-9 2022 Conclusion: FOG is a common symptom in MSA patients and it is correlated with poor quality of life, disease progression and severity, levodopa-equivalent dose, and cerebellum impairment. Levodopa 134-142 zinc finger protein, FOG family member 1 Homo sapiens 12-15 35131711-8 2022 We also show that the combination of doxorubicin and L-DOPA drugs impedes the alpha-synuclein aggregation. Levodopa 53-59 synuclein alpha Homo sapiens 78-93 35447917-0 2022 Fucoxanthin Prevents Long-Term Administration l-DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells. Levodopa 46-52 mitogen-activated protein kinase 1 Mus musculus 87-90 35447917-0 2022 Fucoxanthin Prevents Long-Term Administration l-DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells. Levodopa 46-52 mitogen-activated protein kinase 8 Mus musculus 91-94 35447917-0 2022 Fucoxanthin Prevents Long-Term Administration l-DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells. Levodopa 46-52 jun proto-oncogene Mus musculus 95-100 35447917-5 2022 In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l-DA (200 muM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. Levodopa 111-115 Eph receptor B1 Rattus norvegicus 310-313 35447917-5 2022 In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l-DA (200 muM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. Levodopa 111-115 mitogen-activated protein kinase 8 Rattus norvegicus 314-317 35447917-5 2022 In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l-DA (200 muM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. Levodopa 111-115 jun proto-oncogene Mus musculus 318-323 35447917-5 2022 In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l-DA (200 muM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. Levodopa 111-115 caspase 3 Rattus norvegicus 349-358 35329915-1 2022 PLA2G6-dystonia-parkinsonism (PLAN-DP) is characterized by levodopa responsive parkinsonism and dystonia. Levodopa 59-67 phospholipase A2 group VI Homo sapiens 0-6 35257172-0 2022 L-DOPA-Induced Neurogenesis in the Hippocampus Is Mediated Through GPR143, a Distinct Mechanism of Dopamine. Levodopa 0-6 G protein-coupled receptor 143 Mus musculus 67-73 35257172-3 2022 Here, we show that L-DOPA and its receptor, GPR143, the gene product of ocular albinism 1, regulate neurogenesis in the dentate gyrus (DG) in a dopamine-independent manner. Levodopa 19-25 G protein-coupled receptor 143 Mus musculus 44-50 35257172-4 2022 L-DOPA at concentrations far lower than that of dopamine promoted proliferation of neural stem and progenitor cells in wild-type mice under the inhibition of its conversion to dopamine; this effect was abolished in GPR143 gene-deficient (Gpr143-/y) mice. Levodopa 0-6 G protein-coupled receptor 143 Mus musculus 238-244 35257172-7 2022 Our findings suggest that L-DOPA through GPR143 modulates hippocampal neurogenesis, thereby playing a role in mood regulation in the hippocampus. Levodopa 26-32 G protein-coupled receptor 143 Mus musculus 41-47 35532631-0 2022 The Influence of ADORA2A on Levodopa-Induced Dyskinesia. Levodopa 28-36 adenosine A2a receptor Homo sapiens 17-24 35264705-10 2022 The relative amount of improvement in tap amplitude and stride length with levodopa was correlated. Levodopa 75-83 nuclear RNA export factor 1 Homo sapiens 38-41 35532631-4 2022 Objective: The aim of this study was to study the polymorphisms of rs2298383, rs35060421, and rs5751876 in the ADORA2A in patients diagnosed as PD and describe their possible relationships with levodopa-induced dyskinesias (LID). Levodopa 194-202 adenosine A2a receptor Homo sapiens 111-118 35203338-0 2022 Prevention of L-Dopa-Induced Dyskinesias by MPEP Blockade of Metabotropic Glutamate Receptor 5 Is Associated with Reduced Inflammation in the Brain of Parkinsonian Monkeys. Levodopa 14-20 glutamate metabotropic receptor 5 Homo sapiens 61-94 35217995-3 2022 Catechol-O-methyl transferase inhibitors (COMT-Is) are one of the recommended first-line levodopa add-on therapies for the amelioration of end-of dose motor fluctuations in patient with advanced Parkinson"s disease. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 42-46 35080852-10 2022 Incorporation of DOPA into the ELP increased adhesive strength by 2.5 times and reduced failure rates. Levodopa 17-21 nuclear receptor subfamily 5 group A member 1 Homo sapiens 31-34 35203338-7 2022 The L-Dopa-treated dyskinetic MPTP monkeys had increased Iba1 content in the putamen, substantia nigra, and globus pallidus, which was prevented by MPEP cotreatment; similar findings were observed for CD68 contents in the putamen and globus pallidus. Levodopa 4-10 allograft inflammatory factor 1 Homo sapiens 57-61 35203338-9 2022 GFAP contents were elevated in MPTP + L-Dopa-treated monkeys among these brain regions and prevented by MPEP in the putamen and subthalamic nucleus. Levodopa 38-44 glial fibrillary acidic protein Homo sapiens 0-4 35172843-9 2022 RESULTS: We show in primary human microglia that dopamine, L-DOPA, and high extracellular K+, but not norepinephrine and epinephrine, block canonical, non-canonical, and alpha-syn-mediated NLRP3 inflammasome-driven IL-1beta secretion. Levodopa 59-65 synuclein alpha Homo sapiens 170-179 35172843-9 2022 RESULTS: We show in primary human microglia that dopamine, L-DOPA, and high extracellular K+, but not norepinephrine and epinephrine, block canonical, non-canonical, and alpha-syn-mediated NLRP3 inflammasome-driven IL-1beta secretion. Levodopa 59-65 NLR family pyrin domain containing 3 Homo sapiens 189-194 35185524-4 2022 Methods: We examined the effect of acute levodopa treatment on striatal c-Fos expression in LID using D1-Cre PD rats with dyskinetic symptoms induced by chronic levodopa administration. Levodopa 41-49 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 72-77 35172843-9 2022 RESULTS: We show in primary human microglia that dopamine, L-DOPA, and high extracellular K+, but not norepinephrine and epinephrine, block canonical, non-canonical, and alpha-syn-mediated NLRP3 inflammasome-driven IL-1beta secretion. Levodopa 59-65 interleukin 1 alpha Homo sapiens 215-223 35185418-3 2022 NaOH method was used for melanin content assay, cellular tyrosinase (TYR) activity was determined by 3,4-Dihydroxy-L-phenylalanine (L-DOPA) oxidation to dopachrome, premature senescence was analyzed by senescence-associated beta-galactosidase (SA-beta-gal) staining kit, and the levels of p21, p16, p62, and GATA4 proteins were detected by Western blotting. Levodopa 132-138 tyrosinase Homo sapiens 69-72 35185418-3 2022 NaOH method was used for melanin content assay, cellular tyrosinase (TYR) activity was determined by 3,4-Dihydroxy-L-phenylalanine (L-DOPA) oxidation to dopachrome, premature senescence was analyzed by senescence-associated beta-galactosidase (SA-beta-gal) staining kit, and the levels of p21, p16, p62, and GATA4 proteins were detected by Western blotting. Levodopa 132-138 tyrosinase Homo sapiens 57-67 35185524-7 2022 Results: Striatal D1 + neurons in LID rats showed increased expression of c-Fos, a widely used marker for neuronal activation, following levodopa injection. Levodopa 137-145 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 74-79 35180134-1 2022 BACKGROUND: Long-term levodopa administration for treating Parkinson"s disease (PD) may shorten the duration of effect and cause dyskinesias, inducing the need for catechol-O-methyltransferase (COMT) inhibitors as adjuvant therapy. Levodopa 22-30 catechol-O-methyltransferase Homo sapiens 164-192 35063136-0 2022 Right ventricular overloading is attenuated in monocrotaline-induced pulmonary hypertension model rats with a disrupted Gpr143 gene, the gene that encodes the 3,4-l-dihydroxyphenyalanine (l-DOPA) receptor. Levodopa 188-194 G protein-coupled receptor 143 Rattus norvegicus 120-126 35063136-3 2022 We previously showed that 3,4-l-dihydroxylphenyalanine (DOPA) sensitizes vasomotor response to sympathetic tone via coupling between the adrenergic receptor alpha1 (ADRA1) and a G protein-coupled receptor 143 (GPR143), a DOPA receptor. Levodopa 56-60 G protein-coupled receptor 143 Rattus norvegicus 178-208 35063136-3 2022 We previously showed that 3,4-l-dihydroxylphenyalanine (DOPA) sensitizes vasomotor response to sympathetic tone via coupling between the adrenergic receptor alpha1 (ADRA1) and a G protein-coupled receptor 143 (GPR143), a DOPA receptor. Levodopa 56-60 G protein-coupled receptor 143 Rattus norvegicus 210-216 35063136-5 2022 Pretreating the isolated pulmonary arteries with DOPA 1 muM enhanced vasoconstriction in response to phenylephrine, an ADRA1 agonist, but not to U-46619, a thromboxane A2 agonist or endothelin-1. Levodopa 49-53 endothelin 1 Rattus norvegicus 182-194 34602499-11 2022 The strongest association with surgical outcome was detected between a reduction in levodopa equivalent daily dose and common variations tagging two linkage disequilibrium blocks with SH3GL2. Levodopa 84-92 SH3 domain containing GRB2 like 2, endophilin A1 Homo sapiens 184-190 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 184-192 synemin Homo sapiens 6-9 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 184-192 tyrosine hydroxylase Homo sapiens 102-122 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 184-192 tyrosine hydroxylase Homo sapiens 124-126 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 194-200 synemin Homo sapiens 6-9 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 194-200 tyrosine hydroxylase Homo sapiens 102-122 35090325-8 2022 alpha-Syn aggregation also results in the disruption of dopamine synthesis through phosphorylation of tyrosine hydroxylase (TH), a key enzyme involved in the conversion of tyrosine to levodopa (L-DOPA), the amino acid precursor to dopamine. Levodopa 194-200 tyrosine hydroxylase Homo sapiens 124-126 35180134-1 2022 BACKGROUND: Long-term levodopa administration for treating Parkinson"s disease (PD) may shorten the duration of effect and cause dyskinesias, inducing the need for catechol-O-methyltransferase (COMT) inhibitors as adjuvant therapy. Levodopa 22-30 catechol-O-methyltransferase Homo sapiens 194-198 2685650-2 1989 The most effective is Sinemet CR (Sinemet CR4), with an erodible polymer matrix that retards release of levodopa. Levodopa 104-112 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 42-45 2532558-1 1989 L-Dopa and dopaminergic agonists selective for the D1- or D2-dopamine receptor subtype induce contraversive rotation in rats which have been unilaterally lesioned with injections of 6-hydroxydopamine (6-OHDA) into the substantia nigra. Levodopa 0-6 dopamine receptor D2 Rattus norvegicus 58-78 2532558-4 1989 In unilaterally lesioned animals, L-dopa and the D1-selective agonists SKF 38393 and CY 208-243 produce contralateral rotation and induction of the nuclear proto-oncogene c-fos in the lesioned striatum. Levodopa 34-40 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 156-176 2559014-3 1989 The administration of L-dopa produced a decrease of serum prolactin in all. Levodopa 22-28 prolactin Homo sapiens 58-67 2511222-8 1989 The mean decrement in serum PRL level after L-dopa ingestion was greater in group 1 than in group 3 (P less than 0.05). Levodopa 44-50 prolactin Homo sapiens 28-31 2515218-1 1989 To determine how L-dopa stimulates GH secretion, we investigated its interaction with GHRH in vivo. Levodopa 17-23 growth hormone releasing hormone Homo sapiens 86-90 2515218-5 1989 After L-dopa-GHRH-TRH the GH-increase was significantly higher (45.7 +/- 11.1 micrograms/l) compared to L-dopa-TRH alone. Levodopa 6-12 growth hormone releasing hormone Homo sapiens 13-17 2669475-4 1989 GH levels did not increase after TRH or LHRH administration but decreased after L-Dopa and glucose. Levodopa 80-86 growth hormone 1 Homo sapiens 0-2 2573533-8 1989 The dissociation between the effects of both continuous and intermittent levodopa on D-1 and D-2 agonist-induced rotation indicates that D-1 and D-2 dopamine receptor-mediated mechanisms respond differently to chronic levodopa treatment. Levodopa 73-81 dopamine receptor D2 Rattus norvegicus 145-166 2573533-8 1989 The dissociation between the effects of both continuous and intermittent levodopa on D-1 and D-2 agonist-induced rotation indicates that D-1 and D-2 dopamine receptor-mediated mechanisms respond differently to chronic levodopa treatment. Levodopa 218-226 dopamine receptor D2 Rattus norvegicus 145-166 2817390-2 1989 The assay is based on the decarboxylation of L-3,4-dihydroxyphenylalanine using Streptococcus tyrosine decarboxylase apoenzyme, which requires PLP as cofactor. Levodopa 45-73 pyridoxal phosphatase Homo sapiens 143-146 2503796-14 1989 Administration of L-dopa decreased the serum PRL of subject 1 from 33 to 7 ng/mL, but had no clinically significant effect in subject 2. Levodopa 18-24 prolactin Homo sapiens 45-48 2559840-6 1989 Patients with idiopathic and postpartum hypopituitarism showed low response to 4RHs or none at all, but L-dopa evoked a normal GHRH response in 2 of the 4 cases having no GH response. Levodopa 104-110 growth hormone releasing hormone Homo sapiens 127-131 2559840-7 1989 In the patients with hypopituitarism due to resection of a pituitary tumor, the response of anterior pituitary hormones to 4RHs was low, and L-dopa administration induced a normal GHRH and low GH response in 5 out of the 7 cases. Levodopa 141-147 growth hormone releasing hormone Homo sapiens 180-184 2559840-10 1989 These results indicate that the combination of the 4RHs test and L-dopa test is a simple and useful means for evaluating hypothalamic-pituitary function by measuring the response of plasma GHRH and six anterior pituitary hormones in the patients with endocrine disorders. Levodopa 65-71 growth hormone releasing hormone Homo sapiens 189-193 2765910-6 1989 For each of the 3 doses of L-DOPA, maximal DA output was observed for animals tested under the EB + P-4-6 h hormonal condition, with statistically significant differences in the areas under the L-DOPA-stimulated DA response curves obtained following the 10(-6) and 10(-5) M doses of L-DOPA infusion. Levodopa 27-33 protein disulfide isomerase family A, member 6 Rattus norvegicus 100-105 2765910-6 1989 For each of the 3 doses of L-DOPA, maximal DA output was observed for animals tested under the EB + P-4-6 h hormonal condition, with statistically significant differences in the areas under the L-DOPA-stimulated DA response curves obtained following the 10(-6) and 10(-5) M doses of L-DOPA infusion. Levodopa 194-200 protein disulfide isomerase family A, member 6 Rattus norvegicus 100-105 2765910-6 1989 For each of the 3 doses of L-DOPA, maximal DA output was observed for animals tested under the EB + P-4-6 h hormonal condition, with statistically significant differences in the areas under the L-DOPA-stimulated DA response curves obtained following the 10(-6) and 10(-5) M doses of L-DOPA infusion. Levodopa 194-200 protein disulfide isomerase family A, member 6 Rattus norvegicus 100-105 2475587-2 1989 L-DOPA administration, consisting of a daily dosage of 600 mg plus 150 mg aromatic L-amino acid decarboxylase inhibitor was continued in all cases for at least 3 months. Levodopa 0-6 dopa decarboxylase Homo sapiens 74-109 2501597-4 1989 The effect of catechol-O-methyltransferase (COMT) inhibitor, OR-611, on the potentiation of L-dopa-induced contralateral rotation in 6-OHDA-lesioned rats was also studied. Levodopa 92-98 catechol-O-methyltransferase Rattus norvegicus 44-48 2742363-1 1989 We evaluated the effect of administration of L-dopa, alone or in combination with a peripheral decarboxylase inhibitor, on plasma levels of aromatic-L-amino acid decarboxylase (ALAAD). Levodopa 45-51 dopa decarboxylase Homo sapiens 140-175 2577249-8 1989 These cells showed TH activity and the product, L-DOPA, was detected intracellularly due to the absence of L-amino acid decarboxylase (AADC, EC 4. Levodopa 48-54 dopa decarboxylase Homo sapiens 107-133 2570369-9 1989 The mass of TH was determined using an immunoblot assay, and the in situ activity of TH was calculated from the rate of intracellular accumulation of L-dihydroxyphenylalanine (DOPA) after administration of an inhibitor of DOPA decarboxylase activity. Levodopa 150-174 tyrosine hydroxylase Rattus norvegicus 85-87 2570369-9 1989 The mass of TH was determined using an immunoblot assay, and the in situ activity of TH was calculated from the rate of intracellular accumulation of L-dihydroxyphenylalanine (DOPA) after administration of an inhibitor of DOPA decarboxylase activity. Levodopa 176-180 tyrosine hydroxylase Rattus norvegicus 85-87 2775615-12 1989 In the presence of carbidopa, the plasma clearance of intravenous levodopa (50 mg) was reduced in both age groups but remained lower in the elderly (5.8 +/- 0.9 ml min-1 kg-1 compared with 9.3 +/- 1.0 ml min-1 kg-1; P less than 0.01). Levodopa 66-74 CD59 molecule (CD59 blood group) Homo sapiens 164-174 2775615-12 1989 In the presence of carbidopa, the plasma clearance of intravenous levodopa (50 mg) was reduced in both age groups but remained lower in the elderly (5.8 +/- 0.9 ml min-1 kg-1 compared with 9.3 +/- 1.0 ml min-1 kg-1; P less than 0.01). Levodopa 66-74 CD59 molecule (CD59 blood group) Homo sapiens 204-214 2677320-9 1989 Endothelial cell transport of L-leucine was markedly inhibited during perfusion with 1 mM-BCH (beta-2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid, system L analogue), L-leucine, D-leucine, L-phenylalanine, L-methionine and L-DOPA. Levodopa 226-232 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 95-101 2760634-1 1989 The effect of levodopa (L-dopa), alone or in combination with a peripheral decarboxylase inhibitor (PDI), on plasma levels of aromatic-L-amino acid decarboxylase (ALAAD, = dopa decarboxylase), L-dopa, 3-O-methyl-dopa (3-OMD), dopamine (DA), noradrenaline, adrenaline and dopamine beta-hydroxylase has been studied. Levodopa 14-22 dopa decarboxylase Homo sapiens 126-161 2760634-1 1989 The effect of levodopa (L-dopa), alone or in combination with a peripheral decarboxylase inhibitor (PDI), on plasma levels of aromatic-L-amino acid decarboxylase (ALAAD, = dopa decarboxylase), L-dopa, 3-O-methyl-dopa (3-OMD), dopamine (DA), noradrenaline, adrenaline and dopamine beta-hydroxylase has been studied. Levodopa 24-30 dopa decarboxylase Homo sapiens 126-161 2497615-0 1989 Influence of estrogen administration on growth hormone response to GHRH and L-Dopa in patients with Turner"s syndrome. Levodopa 76-82 growth hormone 1 Homo sapiens 40-54 2567051-1 1989 Levodopa (+ dopa decarboxylase inhibitor) is the most active of all drugs used in the treatment of Parkinson"s disease. Levodopa 0-8 dopa decarboxylase Homo sapiens 12-30 2500649-5 1989 Of the tested methods (tests with TRH, L-DOPA and bromocriptine) STH reserves are better revealed with L-DOPA and TRH tests, gonadotropic reserves, especially LH,--with TRH and bromocriptine tests. Levodopa 39-45 saitohin Homo sapiens 65-68 2495972-0 1989 L-dopa activates c-fos in the striatum ipsilateral to a 6-hydroxydopamine lesion of the substantia nigra. Levodopa 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 17-22 2645703-7 1989 Of 53 patients, 23 were able to discontinue prednisone and be maintained on monodrug cyclosporine therapy, and 21 of the 53 patients had growth hormone measured using L-dopa stimulation. Levodopa 167-173 growth hormone 1 Homo sapiens 137-151 2645703-11 1989 Based on these data we suggest that (1) discontinuation of even very small doses of prednisone may be essential for normalizing growth hormone response to L-dopa and (2) further studies are needed to exploit the growth stimulation effect of recombinant growth hormone in transplanted children. Levodopa 155-161 growth hormone 1 Homo sapiens 128-142 2555090-1 1989 The results of a six month open-label study comparing the efficacy of controlled-release levodopa-carbidopa (Sinemet CR-4 200 mg/50 mg) with standard levodopa/carbidopa (250 mg/25 mg) in 17 patients with idiopathic Parkinson"s disease and severe response fluctuations, are reported. Levodopa 89-97 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 98-108 2711918-4 1989 Past and present L-dopa side-effects are more likely to be caused by disease progression than by L-dopa therapy. Levodopa 97-103 EH domain containing 1 Homo sapiens 0-4 2555090-5 1989 Delayed onset of antiparkinsonian effect of CR-4, resulting from an increase of Tmax for levodopa, was one of the major complaints and required additional small amounts of standard levodopa in three patients. Levodopa 89-97 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 44-48 2555090-5 1989 Delayed onset of antiparkinsonian effect of CR-4, resulting from an increase of Tmax for levodopa, was one of the major complaints and required additional small amounts of standard levodopa in three patients. Levodopa 181-189 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 44-48 2565377-1 1989 It has been suggested that a form of inherited dystonia responsive to levodopa might be due to an abnormality of tyrosine hydroxylase gene. Levodopa 70-78 tyrosine hydroxylase Homo sapiens 113-133 2495961-4 1989 The treatment significantly increased growth hormone (GH) response to L-dopa administration (P less than 0.025) as well as sleep GH secretion (P less than 0.025). Levodopa 70-76 growth hormone 1 Homo sapiens 38-52 2495961-6 1989 Prior to treatment, baseline and peak values of plasma growth hormone releasing hormone (GH-RH) following L-dopa were low. Levodopa 106-112 growth hormone releasing hormone Homo sapiens 55-87 2495961-6 1989 Prior to treatment, baseline and peak values of plasma growth hormone releasing hormone (GH-RH) following L-dopa were low. Levodopa 106-112 growth hormone releasing hormone Homo sapiens 89-94 2495961-7 1989 After HCG therapy, GH-RH response to L-dopa increased significantly (from 9.2 +/- 5.6 to 20.2 +/- 6.2 pg/ml; P less than 0.05), but remained (P less than 0.001) lower than in normal prepubertal children. Levodopa 37-43 growth hormone releasing hormone Homo sapiens 19-24 2709040-9 1989 Both subgroups required a significantly higher daily dose of levodopa while on CR4. Levodopa 61-69 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 79-82 2682215-2 1989 More sustained plasma levodopa levels may be achieved with a new controlled-release formulation of carbidopa/levodopa, Sinemet CR4. Levodopa 22-30 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 127-130 2682215-10 1989 Sinemet CR4 seems to offer a new and effective strategy for the management of levodopa-related fluctuations. Levodopa 78-86 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 8-11 3141449-1 1988 Plasma GH responses to human GHRH, arginine, L-dopa, and insulin-induced hypoglycemia were determined in seven myotonic dystrophy (MD) patients. Levodopa 45-51 growth hormone 1 Homo sapiens 7-9 3177326-4 1988 Growth hormone release was evaluated by arginine and levodopa tests after the end of treatment. Levodopa 53-61 growth hormone 1 Homo sapiens 0-14 3141449-7 1988 These findings suggest that 1) the impaired GH release after GHRH, arginine, and L-dopa administration in MD patients is not due to somatotroph deficiency, since the GH response to hypoglycemia is well preserved; and 2) insulin-induced hypoglycemia may stimulate GH release at least in part via inhibition of somatostatin release. Levodopa 81-87 growth hormone 1 Homo sapiens 44-46 3243205-0 1988 Diminished growth hormone secretion in blind males after L-dopa stimulation. Levodopa 57-63 growth hormone 1 Homo sapiens 11-25 3243205-1 1988 Growth hormone secretion after L-dopa administration (1000 mg p.o.) Levodopa 31-37 growth hormone 1 Homo sapiens 0-14 3243205-3 1988 The average increment of plasma growth hormone after L-dopa stimulation in the blind was below the criterion for a positive response (less than 5 ng ml-1). Levodopa 53-59 growth hormone 1 Homo sapiens 32-46 3243205-5 1988 After L-dopa stimulation there was a significantly diminished growth hormone response in the young adult blind compared to control volunteers. Levodopa 6-12 growth hormone 1 Homo sapiens 62-76 3243342-1 1988 Basal and L-dopa-stimulated secretion of growth hormone (GH) was investigated in 10 patients with beta-thalassaemia major. Levodopa 10-16 growth hormone 1 Homo sapiens 41-55 3243342-1 1988 Basal and L-dopa-stimulated secretion of growth hormone (GH) was investigated in 10 patients with beta-thalassaemia major. Levodopa 10-16 growth hormone 1 Homo sapiens 57-59 3243342-6 1988 In contrast, the pituitary responsiveness to L-dopa, expressed as the relative maximum response for GH (GH delta %), was significantly higher in the latter two groups (8.5-fold, p less than 0.05, and 10.9-fold, p less than 0.02, respectively). Levodopa 45-51 growth hormone 1 Homo sapiens 100-102 3243342-6 1988 In contrast, the pituitary responsiveness to L-dopa, expressed as the relative maximum response for GH (GH delta %), was significantly higher in the latter two groups (8.5-fold, p less than 0.05, and 10.9-fold, p less than 0.02, respectively). Levodopa 45-51 growth hormone 1 Homo sapiens 104-106 2907999-3 1988 The in situ molar activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-dihydroxyphenylalanine in the median eminence following the administration of a L-dihydroxiphenylalanine decarboxylase inhibitor. Levodopa 138-162 tyrosine hydroxylase Rattus norvegicus 30-50 2907999-3 1988 The in situ molar activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-dihydroxyphenylalanine in the median eminence following the administration of a L-dihydroxiphenylalanine decarboxylase inhibitor. Levodopa 138-162 tyrosine hydroxylase Rattus norvegicus 52-54 3141449-5 1988 The plasma GH responses to a 30-min iv infusion of arginine (0.5 g/kg BW) and oral ingestion of L-dopa (0.5 g) were attenuated to a similar extent, whereas insulin-induced hypoglycemia caused a significant increase in plasma GH in all seven MD patients [mean peak, 17.4 +/- 4.1 (+/- SE) microgram/L]. Levodopa 96-102 growth hormone 1 Homo sapiens 11-13 3141449-5 1988 The plasma GH responses to a 30-min iv infusion of arginine (0.5 g/kg BW) and oral ingestion of L-dopa (0.5 g) were attenuated to a similar extent, whereas insulin-induced hypoglycemia caused a significant increase in plasma GH in all seven MD patients [mean peak, 17.4 +/- 4.1 (+/- SE) microgram/L]. Levodopa 96-102 growth hormone 1 Homo sapiens 225-227 3171977-1 1988 A selective catechol-O-methyltransferase inhibitor, OR-462, was studied for its ability to affect pharmacokinetic properties of L-dopa after the p.o. Levodopa 128-134 catechol-O-methyltransferase Rattus norvegicus 12-40 3138280-0 1988 Variable plasma growth hormone (GH)-releasing hormone and GH responses to clonidine, L-dopa, and insulin in normal men. Levodopa 85-91 growth hormone 1 Homo sapiens 32-34 3138280-0 1988 Variable plasma growth hormone (GH)-releasing hormone and GH responses to clonidine, L-dopa, and insulin in normal men. Levodopa 85-91 growth hormone 1 Homo sapiens 58-60 3138280-7 1988 L-Dopa increased plasma ir-GHRH at 60 min (P less than 0.05) and GH at 60-120 min (P less than 0.05). Levodopa 0-6 growth hormone releasing hormone Homo sapiens 27-31 3138280-7 1988 L-Dopa increased plasma ir-GHRH at 60 min (P less than 0.05) and GH at 60-120 min (P less than 0.05). Levodopa 0-6 growth hormone 1 Homo sapiens 27-29 3170408-9 1988 After treatment with met-hGH, five of seven subjects had a suppressed GH response to stimulation from either L-dopa/arginine or submaximal exercise. Levodopa 109-116 growth hormone 1 Homo sapiens 26-28 3140237-1 1988 Tyrosinase (monophenol monooxygenase; monophenol, L-dopa:oxygen oxidoreductase, EC 1.14.18.1) is a key enzyme in the synthesis of melanin. Levodopa 50-56 tyrosinase Mus musculus 0-10 3145820-0 1988 Growth hormone (GH) responses to arginine and L-dopa alone and after GHRH pretreatment. Levodopa 46-52 growth hormone 1 Homo sapiens 0-14 2837907-8 1988 Benserazide (Bz), an inhibitor of the enzyme L-aromatic amino acid decarboxylase (AADC) that converts L-dopa to DA, significantly attenuated the natriuresis in HS rats but had no effect on GFR. Levodopa 102-108 dopa decarboxylase Rattus norvegicus 82-86 3145820-8 1988 L-dopa alone induced a rise in GH levels maximal at 90 min (17.6 +/- 7.4 mU/l, mean +/- SEM) but this rise was abolished by pretreatment with GHRH. Levodopa 0-6 growth hormone 1 Homo sapiens 31-33 3145820-8 1988 L-dopa alone induced a rise in GH levels maximal at 90 min (17.6 +/- 7.4 mU/l, mean +/- SEM) but this rise was abolished by pretreatment with GHRH. Levodopa 0-6 growth hormone releasing hormone Homo sapiens 142-146 3291893-7 1988 Tyrosine hydroxylase is probably induced in this syndrome, since plasma levels of L-DOPA were also elevated. Levodopa 82-88 tyrosine hydroxylase Homo sapiens 0-20 3290706-5 1988 Plasma levodopa levels with CR4-Sinemet were smoother than with Sinemet. Levodopa 7-15 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 28-31 3393296-6 1988 Infusion of the DOPA decarboxylase inhibitor carbidopa (5 micrograms in 1 microliter) 30 min prior to peripheral L-DOPA injection not only reduced contralateral circling but reversed the direction of turning 20 min after the L-DOPA injection. Levodopa 225-231 dopa decarboxylase Rattus norvegicus 16-34 3145820-0 1988 Growth hormone (GH) responses to arginine and L-dopa alone and after GHRH pretreatment. Levodopa 46-52 growth hormone 1 Homo sapiens 16-18 2896121-2 1988 The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME) after the administration of a DOPA decarboxylase inhibitor. Levodopa 132-160 tyrosine hydroxylase Rattus norvegicus 24-44 2896121-2 1988 The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME) after the administration of a DOPA decarboxylase inhibitor. Levodopa 132-160 tyrosine hydroxylase Rattus norvegicus 46-48 2896121-2 1988 The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME) after the administration of a DOPA decarboxylase inhibitor. Levodopa 162-166 tyrosine hydroxylase Rattus norvegicus 24-44 2896121-2 1988 The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME) after the administration of a DOPA decarboxylase inhibitor. Levodopa 162-166 tyrosine hydroxylase Rattus norvegicus 46-48 3145820-1 1988 In order to investigate the mechanisms by which arginine and L-dopa cause GH release in humans we measured the GH response to GHRH 1-44 (200 micrograms i.v. Levodopa 61-67 growth hormone 1 Homo sapiens 74-76 2897907-1 1988 This article summarizes the existing neuroendocrine literature and reports the growth hormone response to stimulation with L-dopa and clonidine in male children and adolescents with attention deficit hyperactivity disorder. Levodopa 123-129 growth hormone 1 Homo sapiens 79-93 2897232-3 1988 In situ TH activity was calculated from the rate of intracellular accumulation of L-dihydroxyphenylalanine (DOPA). Levodopa 82-106 tyrosine hydroxylase Rattus norvegicus 8-10 2897232-3 1988 In situ TH activity was calculated from the rate of intracellular accumulation of L-dihydroxyphenylalanine (DOPA). Levodopa 108-112 tyrosine hydroxylase Rattus norvegicus 8-10 2897232-5 1988 mol of DOPA.h-1.mol of TH-1, respectively, compared to 30 +/- 2 for rats that drank water. Levodopa 7-11 tyrosine hydroxylase Rattus norvegicus 23-25 2897232-6 1988 The activity of TH in the SCG of animals that drank 10 mM, 30 mM, and 100 mM NaCl was 143 +/- 24, 167 +/- 12, and 272 +/- 13 mol DOPA.h-1.mol TH-1, respectively, compared to 119 +/- 10 for animals that drank water. Levodopa 129-133 tyrosine hydroxylase Rattus norvegicus 16-18 2839820-3 1988 The use of L-dopa reducing the levels of ACTH and prolactin led to the improvement of indices of cellular immunity and the patients" clinical status. Levodopa 11-17 proopiomelanocortin Homo sapiens 41-45 2839820-3 1988 The use of L-dopa reducing the levels of ACTH and prolactin led to the improvement of indices of cellular immunity and the patients" clinical status. Levodopa 11-17 prolactin Homo sapiens 50-59 2830786-2 1988 Prolactin (PRL) secretory dynamics were evaluated by several stimulation (thyrotropin-releasing hormone [TRH], sulpiride) and suppression (L-dopa) tests. Levodopa 139-145 prolactin Homo sapiens 0-9 3285599-3 1988 The occurrence of long-term complications such as fluctuations of mobility (on/off phenomena) and dyskinesias caused the use of lower levodopa doses and the simultaneous application of other antiparkinson drugs, e. g. anticholinergics, amantadines, dopamine agonists and MAO-B-inhibitors. Levodopa 134-142 monoamine oxidase B Homo sapiens 271-276 2830786-5 1988 L-dopa administration resulted in normal PRL suppression. Levodopa 0-6 prolactin Homo sapiens 41-44 3379830-0 1988 Activities of aromatic L-amino acid decarboxylase with L-dopa as substrate in brush-border- and basolateral membranes and cytoplasm obtained from rat renal cortex. Levodopa 55-61 dopa decarboxylase Rattus norvegicus 23-49 2963016-6 1988 Domperidone (10 mg iv), a DA antagonist which does not cross the blood brain barrier, increased only plasma beta EP levels, an effect inhibited both by L-dopa and DA. Levodopa 152-158 proopiomelanocortin Homo sapiens 108-115 3379830-1 1988 Activities of aromatic L-amino acid decarboxylase (AADC) with L-dopa as its substrate were determined in the plasma membranes and other cellular components isolated from rat renal cortex. Levodopa 62-68 dopa decarboxylase Rattus norvegicus 14-49 3379830-1 1988 Activities of aromatic L-amino acid decarboxylase (AADC) with L-dopa as its substrate were determined in the plasma membranes and other cellular components isolated from rat renal cortex. Levodopa 62-68 dopa decarboxylase Rattus norvegicus 51-55 3247497-6 1988 MAO-A and MAO-B of human liver mitochondria were also inhibited by L-DOPA (Ki = 152 microM and 275 microM, respectively). Levodopa 67-73 monoamine oxidase A Homo sapiens 0-5 3380074-1 1988 This article summarizes the existing neuroendocrine literature and reports the growth hormone response to stimulation with L-dopa and clonidine in male children and adolescents with attention deficit hyperactivity disorder. Levodopa 123-129 growth hormone 1 Homo sapiens 79-93 2908321-0 1988 Do tyrosine hydroxylase-immunoreactive neurons in the ventrolateral arcuate nucleus produce dopamine or only L-dopa? Levodopa 109-115 tyrosine hydroxylase Homo sapiens 3-23 2907130-1 1988 This work describes a comparative study of the tyrosinase activity determined using three methods which are the most extensively employed; two radiometric assays using L-tyrosine as substrate (tyrosine hydroxylase and melanin formation activities) and one spectrophotometric assay using L-dopa (dopa oxidase activity). Levodopa 287-293 tyrosinase Homo sapiens 47-57 2907130-4 1988 The results show that mammalian tyrosinase has a greater turnover number for L-dopa than for L-tyrosine. Levodopa 77-83 tyrosinase Homo sapiens 32-42 3056728-1 1988 L-dopa 7 micrograms.kg-1.min-1 was given intravenously over 2 h to six healthy subjects, controlled by an infusion of saline on a separate occasion, with measurement of plasma renin activity (PRA), urinary sodium and potassium excretion, effective renal plasma flow (ERPF), glomerular filtration rate (GFR), blood pressure, and pulse rate. Levodopa 0-6 renin Homo sapiens 176-181 3247497-6 1988 MAO-A and MAO-B of human liver mitochondria were also inhibited by L-DOPA (Ki = 152 microM and 275 microM, respectively). Levodopa 67-73 monoamine oxidase B Homo sapiens 10-15 3188768-1 1988 L-DOPA effects on the activities of enzymes controlling the neurotransmitters utilization: monoamine oxidases (MAO) A and B and acetylcholinesterase (AChE) were demonstrated in synaptosomes and mitochondria of the cells in sensorimotor cortex and caudate nucleus. Levodopa 0-6 acetylcholinesterase (Cartwright blood group) Homo sapiens 150-154 3188768-2 1988 Sixty minutes after a single dose of L-DOPA the MAO and AChE activities were virtually unchanged in subfractions of both brain regions. Levodopa 37-43 acetylcholinesterase (Cartwright blood group) Homo sapiens 56-60 3448711-7 1987 The administration of a single injection of L-dopa led to decreases of plasma PRL and GH levels in both grafted and control rats, but while marked increases in hypothalamic and anterior pituitary contents of DA were shown in both groups, the hypothalamic content of NE was only increased in control animals. Levodopa 44-50 prolactin Rattus norvegicus 78-81 3125836-7 1987 These results show that the effect of polyamines on mammalian tyrosinase is due to direct enzyme-oligoamine interactions rather than to a nonspecific action on L-dopa oxidation products, and suggest that physiological polyamines might play a modulatory role on mammalian melanogenesis. Levodopa 160-166 tyrosinase Homo sapiens 62-72 3448711-7 1987 The administration of a single injection of L-dopa led to decreases of plasma PRL and GH levels in both grafted and control rats, but while marked increases in hypothalamic and anterior pituitary contents of DA were shown in both groups, the hypothalamic content of NE was only increased in control animals. Levodopa 44-50 gonadotropin releasing hormone receptor Rattus norvegicus 86-88 3658164-5 1987 At the end of 6 weeks CR4 treatment, there was an increase in percent "on" time and mean interdose interval; the number of daily doses and "off" periods were diminished and a slight reduction in the variability of plasma levodopa levels was observed. Levodopa 221-229 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 22-25 2823263-1 1987 Screening of a lambda gt11 human melanocyte cDNA library with antibodies against hamster tyrosinase (monophenol, L-dopa:oxygen oxidoreductase, EC 1.14.18.1) resulted in the isolation of 16 clones. Levodopa 113-119 tyrosinase Mus musculus 89-99 3118729-1 1987 The growth hormone (GH) responses to (A) GRF 1-44, 1 microgram/kg i.v., (B) L-dopa and either arginine, insulin, or glucagon, and (C) exercise were evaluated in 10 children (3 girls, 7 boys; ages 10 years to 15 years, 8 months), 2-10.75 years following cranial irradiation for medulloblastoma (8 patients), pineoblastoma (1 patient), and a fourth ventricular ependymoma (1 patient). Levodopa 76-82 growth hormone 1 Homo sapiens 4-18 3118729-1 1987 The growth hormone (GH) responses to (A) GRF 1-44, 1 microgram/kg i.v., (B) L-dopa and either arginine, insulin, or glucagon, and (C) exercise were evaluated in 10 children (3 girls, 7 boys; ages 10 years to 15 years, 8 months), 2-10.75 years following cranial irradiation for medulloblastoma (8 patients), pineoblastoma (1 patient), and a fourth ventricular ependymoma (1 patient). Levodopa 76-82 growth hormone 1 Homo sapiens 20-22 3632371-3 1987 In a double-blind, crossover clinical trial, one such preparation, CR-5 (Merck, Sharp & Dohme), produced significantly less plasma levodopa variations and substantially improved motor performance over Sinemet in 15 patients with mild to moderate fluctuations, all but one of whom chose to continue on CR-5 therapy after the study. Levodopa 131-139 teratocarcinoma-derived growth factor 1 pseudogene 5 Homo sapiens 67-71 3658164-6 1987 Overall benefit waned over the next 6 months, despite addition of standard levodopa or Sinemet to overcome the delayed onset of antiparkinsonian effect of CR4 which resulted from prolongation in the Tmax for levodopa. Levodopa 208-216 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 155-158 3658164-7 1987 The major benefits of CR4 were reduction in off time and in the number of daily off periods, with fewer levodopa doses per day and prolongation of the interdose interval. Levodopa 104-112 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 22-25 3670563-3 1987 A dose-dependent and often complete blockade of all three signs was obtained with L-DOPA plus carbidopa (10:1) as well as with other classes of pharmacological agents that are used in the treatment of Parkinson"s disease, i.e. direct or indirect dopamine (DA) agonists (amantadine, pergolide, lisuride) and inhibitors of monoamine oxidase (MAO) (clorgyline, pargyline, deprenyl, tranylcypromine). Levodopa 82-88 monoamine oxidase A Rattus norvegicus 321-338 3118233-5 1987 The CDP-choline did not modify the apomorphine-induced stimulant effect but potentiated the circling behaviour produced by L-DOPA and amphetamine. Levodopa 123-129 cut-like homeobox 1 Rattus norvegicus 4-7 3118233-6 1987 The data show that the effects of CDP-choline were mediated by a presynaptic mechanism: the potentiation of the effects of L-DOPA cannot be explained by an activation of tyrosine hydroxylase, but seems to be related to an improvement of release of newly synthesized dopamine from exogenous L-DOPA. Levodopa 123-129 cut-like homeobox 1 Rattus norvegicus 34-37 3670563-3 1987 A dose-dependent and often complete blockade of all three signs was obtained with L-DOPA plus carbidopa (10:1) as well as with other classes of pharmacological agents that are used in the treatment of Parkinson"s disease, i.e. direct or indirect dopamine (DA) agonists (amantadine, pergolide, lisuride) and inhibitors of monoamine oxidase (MAO) (clorgyline, pargyline, deprenyl, tranylcypromine). Levodopa 82-88 monoamine oxidase A Rattus norvegicus 340-343 3118233-6 1987 The data show that the effects of CDP-choline were mediated by a presynaptic mechanism: the potentiation of the effects of L-DOPA cannot be explained by an activation of tyrosine hydroxylase, but seems to be related to an improvement of release of newly synthesized dopamine from exogenous L-DOPA. Levodopa 290-296 cut-like homeobox 1 Rattus norvegicus 34-37 3120620-3 1987 5-S-Glutathione-L-dopa is first synthesized by the tyrosinase-catalyzed reaction between L-dopa and glutathione. Levodopa 16-22 tyrosinase Homo sapiens 51-61 3123283-0 1987 [Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases]. Levodopa 34-40 growth hormone releasing hormone Homo sapiens 65-97 3123283-2 1987 In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. Levodopa 340-346 growth hormone releasing hormone Homo sapiens 31-35 3123283-0 1987 [Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases]. Levodopa 34-40 growth hormone releasing hormone Homo sapiens 99-103 3123283-2 1987 In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. Levodopa 340-346 growth hormone 1 Homo sapiens 31-33 3123283-4 1987 In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. Levodopa 85-91 growth hormone releasing hormone Homo sapiens 50-54 3123283-1 1987 The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. Levodopa 114-120 growth hormone releasing hormone Homo sapiens 24-56 3123283-4 1987 In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. Levodopa 85-91 growth hormone 1 Homo sapiens 50-52 3123283-1 1987 The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. Levodopa 114-120 growth hormone releasing hormone Homo sapiens 58-62 3123283-5 1987 In subjects with simple obesity, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). Levodopa 123-129 growth hormone releasing hormone Homo sapiens 57-61 3123283-5 1987 In subjects with simple obesity, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). Levodopa 123-129 growth hormone 1 Homo sapiens 57-59 3123283-1 1987 The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. Levodopa 114-120 growth hormone 1 Homo sapiens 24-38 3123283-9 1987 These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states. Levodopa 55-61 growth hormone 1 Homo sapiens 28-30 3123283-9 1987 These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states. Levodopa 55-61 growth hormone releasing hormone Homo sapiens 91-95 3123283-9 1987 These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states. Levodopa 55-61 growth hormone releasing hormone Homo sapiens 270-274 3123283-9 1987 These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states. Levodopa 55-61 growth hormone releasing hormone Homo sapiens 270-274 3123283-9 1987 These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states. Levodopa 324-330 growth hormone 1 Homo sapiens 28-30 3123284-5 1987 The plasma PRL responses to dopaminergic agents (L-dopa, CB-154, dopamine) were greater in responders than in non-responders (% of basal: L-dopa, 33.7 +/- 3.7% vs 51.6 +/- 5.6% at 150 min, P less than 0.05; CB-154, 16.5 +/- 2.6% vs 30.9 +/- 2.8% at 6 hr, P less than 0.05; dopamine, 31.7 +/- 5.6% vs 44.9 +/- 4.3% at 90 min, P less than 0.05). Levodopa 49-55 prolactin Homo sapiens 11-14 3123283-1 1987 The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. Levodopa 114-120 growth hormone 1 Homo sapiens 58-60 3123284-5 1987 The plasma PRL responses to dopaminergic agents (L-dopa, CB-154, dopamine) were greater in responders than in non-responders (% of basal: L-dopa, 33.7 +/- 3.7% vs 51.6 +/- 5.6% at 150 min, P less than 0.05; CB-154, 16.5 +/- 2.6% vs 30.9 +/- 2.8% at 6 hr, P less than 0.05; dopamine, 31.7 +/- 5.6% vs 44.9 +/- 4.3% at 90 min, P less than 0.05). Levodopa 138-144 prolactin Homo sapiens 11-14 3123283-2 1987 In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. Levodopa 205-211 growth hormone releasing hormone Homo sapiens 31-35 3123283-2 1987 In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. Levodopa 205-211 growth hormone 1 Homo sapiens 31-33 3119181-1 1987 The local concentration of 6-[18F]fluoro-L-dopa(18F) reflects the activity of aromatic acid decarboxylase (AADC), the enzyme that generates dopamine from its precursor amino acid, L-dopa. Levodopa 41-47 dopa decarboxylase Homo sapiens 78-105 3119181-1 1987 The local concentration of 6-[18F]fluoro-L-dopa(18F) reflects the activity of aromatic acid decarboxylase (AADC), the enzyme that generates dopamine from its precursor amino acid, L-dopa. Levodopa 41-47 dopa decarboxylase Homo sapiens 107-111 3109490-1 1987 The actions of glutathione S-transferase and tyrosinase on the in vitro production of glutathionyl-3,4-dihydroxyphenylalanine and the dopachrome level in the presence of GSH and L-3,4-dihydroxyphenylalanine were studied. Levodopa 178-206 glutathione S-transferase kappa 1 Homo sapiens 15-40 3119696-1 1987 We have investigated the importance of the dopaminergic control of gonadotropin secretion by studying LH, FSH and PRL responses to L-dopa and bromocriptine in patients with polycystic ovary syndrome (PCOS). Levodopa 131-137 prolactin Homo sapiens 114-117 3119696-5 1987 Prolactin sensitivity to the inhibitory effect of bromocriptine and L-dopa showed a significant correlation with the basal PRL level (p less than 0.01). Levodopa 68-74 prolactin Homo sapiens 123-126 2884996-0 1987 Phosphorylated isomers of L-dopa stimulate MSH binding capacity and responsiveness to MSH in cultured melanoma cells. Levodopa 26-32 msh homeobox 2 Homo sapiens 43-46 2884996-0 1987 Phosphorylated isomers of L-dopa stimulate MSH binding capacity and responsiveness to MSH in cultured melanoma cells. Levodopa 26-32 msh homeobox 2 Homo sapiens 86-89 2884996-8 1987 Thus dopa phosphates and/or L-dopa can act as regulators of the MSH receptor system. Levodopa 28-34 msh homeobox 2 Homo sapiens 64-67 2888776-6 1987 Our results also suggest that the L-dopa treatment results in a decrease in tyrosinase activity per melanosome. Levodopa 34-40 tyrosinase Mus musculus 76-86 2887537-7 1987 Loss of dopamine (30-40%) in the hypothalamus of affected patients has been shown in recent studies, and is compatible with the reported abnormalities of growth hormone release in response to L-dopa administration, elevated plasma levels of MSH, and reduced CSF levels of somatostatin and beta-endorphins in these patients. Levodopa 192-198 growth hormone 1 Homo sapiens 154-168 3106726-7 1987 Chlorpromazine injections failed to elevate serum prolactin in all patients, and administration of levodopa caused a partial reduction in serum prolactin; thus, the hypothalamus may be an important locus of endocrine malfunction in these patients. Levodopa 99-107 prolactin Homo sapiens 144-153 3793848-0 1987 Growth hormone inhibitory and stimulatory actions of L-dopa in patients with acromegaly. Levodopa 53-59 growth hormone 1 Homo sapiens 0-14 3572026-4 1987 The mechanism of action may involve interaction with the melanocyte-specific enzyme, tyrosinase, for which the cysteinylcatechols could become a better substrate than L-dopa itself. Levodopa 167-173 tyrosinase Homo sapiens 85-95 3574696-0 1987 Parkinson"s disease and motor fluctuations: long-acting carbidopa/levodopa (CR-4-Sinemet). Levodopa 66-74 teratocarcinoma-derived growth factor 1 pseudogene 4 Homo sapiens 76-80 3585225-7 1987 Plasma prolactin concentrations were decreased by L-DOPA in both pituitary grafted and control rats. Levodopa 50-56 prolactin Rattus norvegicus 7-16 3109206-0 1987 Impaired response of growth hormone-releasing hormone (GHRH) measured in plasma after L-dopa stimulation in patients with idiopathic delayed puberty. Levodopa 86-92 growth hormone releasing hormone Homo sapiens 21-53 3109206-0 1987 Impaired response of growth hormone-releasing hormone (GHRH) measured in plasma after L-dopa stimulation in patients with idiopathic delayed puberty. Levodopa 86-92 growth hormone releasing hormone Homo sapiens 55-59 3109206-6 1987 The peak of GHRH after L-Dopa was 41 +/- 10 pg/ml in IDP and 96 +/- 25 pg/ml in CSS (p less than 0.02). Levodopa 23-29 growth hormone releasing hormone Homo sapiens 12-16 2946308-6 1986 NAC or N-methyl NAM appeared to extend the period of elevated brain DA levels with L-dopa treatment. Levodopa 83-89 X-linked Kx blood group Homo sapiens 0-3 3104183-3 1987 The oral administration of 500 mg of levodopa (Dopa) also suppressed the concentration of plasma LH to 73.0 +/- 3.5%, but the pretreatment with two doses of 100 mg each of carbidopa (CD), a peripheral dopa decarboxylase inhibitor, attenuated this suppressing effect of Dopa on LH levels (nadir 82.4 +/- 4.1). Levodopa 37-45 dopa decarboxylase Homo sapiens 201-219 3668521-3 1987 The response of MAO-inhibited rats to L-dopa contrasted sharply with those not treated with the MAO inhibitor; the latter showed no change in NE, NMN and 3-MT after similar administration of L-dopa. Levodopa 38-44 monoamine oxidase A Rattus norvegicus 16-19 2879287-4 1986 The in situ activity of the enzyme was assayed by measuring the rate of synthesis of L-3,4-dihydroxyphenylalanine (dopa), and the results were expressed as mol of dopa per hr per mol of TyrOHase. Levodopa 163-167 tyrosine hydroxylase Rattus norvegicus 186-194 2881450-1 1987 PLG potentiates the action of levodopa in 6-OH-DA-treated rats. Levodopa 30-38 plasminogen Rattus norvegicus 0-3 2881450-2 1987 PLG plus levodopa is more effective than levodopa alone. Levodopa 41-49 plasminogen Rattus norvegicus 0-3 2950731-0 1987 Dopamine D2 receptor density in parkinsonian brain is constant for duration of disease, age, and duration of L-dopa therapy. Levodopa 109-115 dopamine receptor D2 Homo sapiens 0-20 2960778-0 1987 Potentiation of central effects of L-dopa by an inhibitor of catechol-O-methyltransferase. Levodopa 35-41 catechol-O-methyltransferase Rattus norvegicus 61-89 2960778-5 1987 Thus inhibition of COMT, like inhibition of MAO, is able to enhance the central effects of L-dopa. Levodopa 91-97 catechol-O-methyltransferase Rattus norvegicus 19-23 2960778-5 1987 Thus inhibition of COMT, like inhibition of MAO, is able to enhance the central effects of L-dopa. Levodopa 91-97 monoamine oxidase A Rattus norvegicus 44-47 3792452-3 1986 Administration of L-DOPA plus carbidopa, bromocriptine or pergolide for 12 months decreased [Met5]enkephalin (except bromocriptine) and neurotensin, but not [Leu5]enkephalin, levels in striatum. Levodopa 18-24 proenkephalin Rattus norvegicus 98-108 3792452-3 1986 Administration of L-DOPA plus carbidopa, bromocriptine or pergolide for 12 months decreased [Met5]enkephalin (except bromocriptine) and neurotensin, but not [Leu5]enkephalin, levels in striatum. Levodopa 18-24 neurotensin Rattus norvegicus 136-147 3122863-1 1986 Plasma prolactin and GH responses following TRH, sulpiride, L-dopa, and bromocriptine administration. Levodopa 60-66 prolactin Homo sapiens 7-16 2946308-6 1986 NAC or N-methyl NAM appeared to extend the period of elevated brain DA levels with L-dopa treatment. Levodopa 83-89 SH3 and cysteine rich domain 3 Homo sapiens 16-19 3122863-1 1986 Plasma prolactin and GH responses following TRH, sulpiride, L-dopa, and bromocriptine administration. Levodopa 60-66 gamma-glutamyl hydrolase Homo sapiens 21-23 2875946-1 1986 Elevation of brain catecholamine levels by systemic administration of L-dopa in dogs pretreated with the dopa decarboxylase inhibitor carbidopa inhibits the secretion of vasopressin and adrenocorticotropic hormone (ACTH) and decreases arterial blood pressure. Levodopa 70-76 dopa decarboxylase Canis lupus familiaris 105-123 2875946-1 1986 Elevation of brain catecholamine levels by systemic administration of L-dopa in dogs pretreated with the dopa decarboxylase inhibitor carbidopa inhibits the secretion of vasopressin and adrenocorticotropic hormone (ACTH) and decreases arterial blood pressure. Levodopa 70-76 proopiomelanocortin Canis lupus familiaris 186-213 2875946-1 1986 Elevation of brain catecholamine levels by systemic administration of L-dopa in dogs pretreated with the dopa decarboxylase inhibitor carbidopa inhibits the secretion of vasopressin and adrenocorticotropic hormone (ACTH) and decreases arterial blood pressure. Levodopa 70-76 proopiomelanocortin Canis lupus familiaris 215-219 3530616-10 1986 The mainstay of therapy is levodopa, which is used in combination with dopa decarboxylase inhibitors to decrease the peripheral conversion of levodopa to dopamine. Levodopa 27-35 dopa decarboxylase Homo sapiens 71-89 3019241-2 1986 It has been reported that native catalase can peroxidatically oxidize larger organic molecules (e.g. L-dopa) and that catalase maintained at alkaline pH for various lengths of time demonstrates an increase in peroxidase activity using guaiacol as substrate. Levodopa 101-107 catalase Homo sapiens 33-41 3019241-2 1986 It has been reported that native catalase can peroxidatically oxidize larger organic molecules (e.g. L-dopa) and that catalase maintained at alkaline pH for various lengths of time demonstrates an increase in peroxidase activity using guaiacol as substrate. Levodopa 101-107 catalase Homo sapiens 118-126 3530616-10 1986 The mainstay of therapy is levodopa, which is used in combination with dopa decarboxylase inhibitors to decrease the peripheral conversion of levodopa to dopamine. Levodopa 142-150 dopa decarboxylase Homo sapiens 71-89 3490854-5 1986 PIR also facilitated the effect of L-dopa and L-5-HTP on the hind limb flexor reflex of the spinal rat. Levodopa 35-41 pirin Rattus norvegicus 0-3 3748387-1 1986 In five patients with parkinsonism, the optimal dosage of a controlled-release levodopa/carbidopa preparation (CR-3) was three times higher than the dosage of Sinemet and produced higher plasma levodopa concentrations, but did not reduce the fluctuations in plasma levodopa or clinical response. Levodopa 79-87 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 111-115 3748387-1 1986 In five patients with parkinsonism, the optimal dosage of a controlled-release levodopa/carbidopa preparation (CR-3) was three times higher than the dosage of Sinemet and produced higher plasma levodopa concentrations, but did not reduce the fluctuations in plasma levodopa or clinical response. Levodopa 194-202 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 111-115 3748387-1 1986 In five patients with parkinsonism, the optimal dosage of a controlled-release levodopa/carbidopa preparation (CR-3) was three times higher than the dosage of Sinemet and produced higher plasma levodopa concentrations, but did not reduce the fluctuations in plasma levodopa or clinical response. Levodopa 194-202 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 111-115 3748387-2 1986 Plasma levodopa concentrations were higher and clinical responses better before the first dose of the day with CR-3. Levodopa 7-15 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 111-115 3748387-5 1986 CR-3 could benefit a few severely affected patients, but it is necessary to understand the factors that affect absorption of levodopa from sustained-release preparations, as well as the consequences of prolonged elevation of plasma levodopa levels. Levodopa 232-240 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 0-4 3086358-1 1986 Contrary to a previous report, pretreatment of normal men with carbidopa plus L-dopa (Sinemet 25/250) markedly inhibited the PRL response to TRH, a stimulus that acts directly on the pituitary. Levodopa 78-84 prolactin Homo sapiens 125-128 3086358-1 1986 Contrary to a previous report, pretreatment of normal men with carbidopa plus L-dopa (Sinemet 25/250) markedly inhibited the PRL response to TRH, a stimulus that acts directly on the pituitary. Levodopa 78-84 thyrotropin releasing hormone Homo sapiens 141-144 3086358-0 1986 Carbidopa plus L-dopa pretreatment inhibits the prolactin (PRL) response to thyrotropin-releasing hormone and thus cannot distinguish central from pituitary sites of prolactin stimulation. Levodopa 15-21 prolactin Homo sapiens 48-57 3086358-0 1986 Carbidopa plus L-dopa pretreatment inhibits the prolactin (PRL) response to thyrotropin-releasing hormone and thus cannot distinguish central from pituitary sites of prolactin stimulation. Levodopa 15-21 prolactin Homo sapiens 59-62 3956487-1 1986 Dihydropteridine reductase (DHPR) was irreversibly inactivated in a time-dependent way by incubation with 3,4-dihydroxyphenylalanine (L-dopa). Levodopa 134-140 quinoid dihydropteridine reductase Homo sapiens 28-32 3086358-0 1986 Carbidopa plus L-dopa pretreatment inhibits the prolactin (PRL) response to thyrotropin-releasing hormone and thus cannot distinguish central from pituitary sites of prolactin stimulation. Levodopa 15-21 thyrotropin releasing hormone Homo sapiens 76-105 2872094-3 1986 The in situ activity of TH was assayed by the accumulation of L-dihydroxyphenylalanine (DOPA) in the median eminence of hypothalamic fragments incubated in the presence of NSD 1015. Levodopa 62-86 tyrosine hydroxylase Rattus norvegicus 24-26 2872094-3 1986 The in situ activity of TH was assayed by the accumulation of L-dihydroxyphenylalanine (DOPA) in the median eminence of hypothalamic fragments incubated in the presence of NSD 1015. Levodopa 88-92 tyrosine hydroxylase Rattus norvegicus 24-26 2872094-4 1986 When hypothalamic fragments were incubated with veratridine (0-10(-3) M), maximal stimulation of TH activity was observed at 10(-4) M. The mean concentration of DOPA in the median eminence of hypothalamic fragments incubated with 10(-4) M veratridine was 3 times that seen in its absence. Levodopa 161-165 tyrosine hydroxylase Rattus norvegicus 97-99 3725825-2 1986 The present study investigated the possibility that intraperitoneal injections of the dopamine agonists l-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. Levodopa 104-110 neurotensin Rattus norvegicus 191-202 3725825-6 1986 Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of l-dopa or bromocriptine which, when given alone, had no effect on food intake. Levodopa 130-136 neurotensin Rattus norvegicus 61-72 3091296-5 1986 The GHRH data in these patients are in agreement with those in older literature on hGH responsiveness to stimuli such as L-dopa, arginine and insulin induced hypoglycaemia. Levodopa 121-127 growth hormone releasing hormone Homo sapiens 4-8 2424323-3 1986 Patients were given an overnight dexamethasone suppression test, and the effects of thyrotropin-releasing hormone and L-dopa on plasma growth hormone and prolactin were examined. Levodopa 118-124 growth hormone 1 Homo sapiens 135-149 2424323-3 1986 Patients were given an overnight dexamethasone suppression test, and the effects of thyrotropin-releasing hormone and L-dopa on plasma growth hormone and prolactin were examined. Levodopa 118-124 prolactin Homo sapiens 154-163 2420928-8 1986 These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA). Levodopa 192-198 monoamine oxidase B Homo sapiens 102-107 3956487-0 1986 The time-dependent inactivation of human brain dihydropteridine reductase by the oxidation products of L-dopa. Levodopa 103-109 quinoid dihydropteridine reductase Homo sapiens 47-73 3956487-1 1986 Dihydropteridine reductase (DHPR) was irreversibly inactivated in a time-dependent way by incubation with 3,4-dihydroxyphenylalanine (L-dopa). Levodopa 134-140 quinoid dihydropteridine reductase Homo sapiens 0-26 3956487-4 1986 L-Dopa itself was not an inhibitor of DHPR although dopachrome, the aminochrome formed following oxidation of L-dopa, was a reversible inhibitor of DHPR with an I50 of 0.60 mM. Levodopa 0-6 quinoid dihydropteridine reductase Homo sapiens 148-152 3956487-4 1986 L-Dopa itself was not an inhibitor of DHPR although dopachrome, the aminochrome formed following oxidation of L-dopa, was a reversible inhibitor of DHPR with an I50 of 0.60 mM. Levodopa 110-116 quinoid dihydropteridine reductase Homo sapiens 148-152 3956487-5 1986 The quinone products of oxidation of L-dopa were responsible for the time-dependent inactivation of DHPR. Levodopa 37-43 quinoid dihydropteridine reductase Homo sapiens 100-104 3093352-3 1986 L-Dopa induced a 2-fold increase in circulating GHRH 30-45 min before the elevation of GH. Levodopa 0-6 growth hormone releasing hormone Homo sapiens 48-52 3080462-9 1986 Oral administration of L-dopa (0.5 g) caused a significant increase in both plasma hGHRH-LI and GH levels in normal subjects, and the plasma hGHRH-LI peak slightly preceded or coincided with that of plasma GH in individual subjects. Levodopa 23-29 growth hormone releasing hormone Homo sapiens 83-88 3080462-9 1986 Oral administration of L-dopa (0.5 g) caused a significant increase in both plasma hGHRH-LI and GH levels in normal subjects, and the plasma hGHRH-LI peak slightly preceded or coincided with that of plasma GH in individual subjects. Levodopa 23-29 growth hormone releasing hormone Homo sapiens 141-146 3080462-10 1986 There was also a significant correlation between plasma hGHRH-LI and the GH rises after L-dopa administration when their net increments were compared. Levodopa 88-94 growth hormone releasing hormone Homo sapiens 56-61 2871516-0 1986 Differential effect of repeated treatment with L-dopa on dopamine-D1 or -D2 receptors. Levodopa 47-53 dopamine receptor D1 Homo sapiens 57-85 3517886-1 1986 The influence of L-DOPA on the behavioral effects of LHRH was studied in male rats. Levodopa 17-23 gonadotropin releasing hormone 1 Rattus norvegicus 53-57 3517886-4 1986 L-DOPA (100 mg/kg, IP), administered after LHRH, stimulated SMA, RB and HSB. Levodopa 0-6 gonadotropin releasing hormone 1 Rattus norvegicus 43-47 3517886-5 1986 In addition L-DOPA antagonized the effect of LHRH on acquisition of CARs and counteracted the antagonism between LHRH and amphetamine in acquisition of CARs and SMA. Levodopa 12-18 gonadotropin releasing hormone 1 Rattus norvegicus 45-49 3517886-5 1986 In addition L-DOPA antagonized the effect of LHRH on acquisition of CARs and counteracted the antagonism between LHRH and amphetamine in acquisition of CARs and SMA. Levodopa 12-18 gonadotropin releasing hormone 1 Rattus norvegicus 113-117 2431571-1 1986 The dopa oxidase activity of tyrosinase in the skin from albino and black mice was assayed using a technique based on the formation of two diastereomers of 5-S-cysteinyldopa when incubating tissue extracts with both L-dopa and D-dopa as substrates in the presence of cysteine. Levodopa 216-222 tyrosinase Mus musculus 29-39 2431571-4 1986 This stereospecific dopa-oxidation is indicative of the presence of tyrosinase and corresponds well with earlier determinations of the rates of oxidation for human tyrosinase, using L-dopa and D-dopa as substrates. Levodopa 182-188 tyrosinase Homo sapiens 68-78 2431571-4 1986 This stereospecific dopa-oxidation is indicative of the presence of tyrosinase and corresponds well with earlier determinations of the rates of oxidation for human tyrosinase, using L-dopa and D-dopa as substrates. Levodopa 182-188 tyrosinase Homo sapiens 164-174 3082400-0 1986 Selective inhibition of monoamine oxidase type B by MDL 72145 increases the central effects of L-dopa without modifying its cardiovascular effects. Levodopa 95-101 monoamine oxidase B Rattus norvegicus 24-48 3082400-1 1986 The potential of a new, potent, irreversible and selective inhibitor of monoamine oxidase type B, (E)-2-(3,4-dimethoxyphenyl)-3-fluorallyamine (MDL 72145), to augment the effects of L-DOPA in an animal model which reproduces the biochemical defect of Parkinson"s disease has been evaluated. Levodopa 182-188 monoamine oxidase B Rattus norvegicus 72-96 3082400-2 1986 In rats bearing unilateral 6-hydroxydopamine lesions of the nigro-striatal dopamine pathways, both MDL 72145 and clorgyline, a selective inhibitor of MAO A, augmented the contralateral turning response to L-DOPA combined with carbidopa. Levodopa 205-211 monoamine oxidase A Rattus norvegicus 150-155 3097257-2 1986 LTS could depend on the chronic overload of L-dopa + ID and could be due to a consequent "receptor disease" and derangement of the neuronal functionality mainly in regard to the enzymatic chains, storage mechanisms and hyperactivity of the monoamine oxidase type B (MAO B). Levodopa 44-50 monoamine oxidase B Homo sapiens 240-264 2946813-5 1986 These results suggest that DA-D1 and DA-D2 receptors are differently affected by prolonged L-dopa treatment. Levodopa 91-97 defender against cell death 1 Homo sapiens 27-32 2946813-7 1986 The increased supersensitivity of the DA-D1 receptors may play a role in the clinical changes seen in parkinsonian patients following chronic use of L-dopa. Levodopa 149-155 defender against cell death 1 Homo sapiens 38-43 3097257-3 1986 Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response. Levodopa 163-169 monoamine oxidase B Homo sapiens 24-29 3097263-1 1986 The selective monoamine oxidase (MAO) type B inhibitor has proven to be a useful adjunct to L-dopa therapy of Parkinson"s disease. Levodopa 92-98 monoamine oxidase B Homo sapiens 14-44 2998505-1 1985 Experiments on alert rats have shown that, with pre-inhibition of peripheral DOPA-decarboxylase, L-DOPA suppresses behavioral nociceptive reactions without changing hemodynamic ones. Levodopa 97-103 dopa decarboxylase Rattus norvegicus 77-95 3713989-8 1986 This agrees with in vivo results of Alper and his colleagues who found an increased accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in neuro-intermediate lobes of dehydrated rats after inhibition of DOPA-decarboxylase. Levodopa 100-128 dopa decarboxylase Rattus norvegicus 203-221 3713989-8 1986 This agrees with in vivo results of Alper and his colleagues who found an increased accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in neuro-intermediate lobes of dehydrated rats after inhibition of DOPA-decarboxylase. Levodopa 130-134 dopa decarboxylase Rattus norvegicus 203-221 4091266-3 1985 Purified AADC showed a single band with an Mr of 50,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and decarboxylated L-3,4-dihydroxyphenylalanine, L-5-hydroxytryptophan, and L-threo-3,4-dihydroxyphenylserine (a synthetic precursor of natural norepinephrine). Levodopa 137-165 dopa decarboxylase Homo sapiens 9-13 4056323-6 1985 These data indicate that (a) there is diminished capacity by skeletal muscle of old rats to synthesize protein; (b) this decrease is related to the reduced GH secretion because protein synthesis can be restored by GH administration; and (c) the dose of L-dopa given, although it increased the levels of circulating GH, did not completely restore protein synthetic capacity. Levodopa 253-259 gonadotropin releasing hormone receptor Rattus norvegicus 156-158 4056323-6 1985 These data indicate that (a) there is diminished capacity by skeletal muscle of old rats to synthesize protein; (b) this decrease is related to the reduced GH secretion because protein synthesis can be restored by GH administration; and (c) the dose of L-dopa given, although it increased the levels of circulating GH, did not completely restore protein synthetic capacity. Levodopa 253-259 gonadotropin releasing hormone receptor Rattus norvegicus 214-216 4056323-6 1985 These data indicate that (a) there is diminished capacity by skeletal muscle of old rats to synthesize protein; (b) this decrease is related to the reduced GH secretion because protein synthesis can be restored by GH administration; and (c) the dose of L-dopa given, although it increased the levels of circulating GH, did not completely restore protein synthetic capacity. Levodopa 253-259 gonadotropin releasing hormone receptor Rattus norvegicus 214-216 3003588-7 1985 The dopaminergic agents L-dopa and bromocriptine antagonized the R-PIA and NECA-induced increase in serum prolactin. Levodopa 24-30 ribose 5-phosphate isomerase A Rattus norvegicus 65-70 3930664-3 1985 However, in rats previously treated with the MAO inhibitors pargyline or tranylcypromine, the same L-DOPA or free DA treatment resulted in significant increases in both 3-MT and DA sulfate in the hypothalamus, brainstem, and striatum. Levodopa 99-105 monoamine oxidase A Rattus norvegicus 45-48 3934058-2 1985 The stimulation of growth hormone (GH) release by hypoglycemia, the decline of elevated GH by hyperglycemia and a little lower somatostatin like immunoreactivity (SLI) may support abnormalities of hypothalamic function, but the existence of pituitary microadenoma cannot be ruled out because of the paradoxical suppression of GH release by oral administration of bromocriptine (CB-154) and L-DOPA and the stimulation of GH release by intravenous administration of TRH. Levodopa 390-396 SHC adaptor protein 2 Homo sapiens 163-166 4054700-5 1985 Basal gastrin concentrations were increased after L-dopa and after L-dopa plus carbidopa. Levodopa 50-56 gastrin Homo sapiens 6-13 4054700-5 1985 Basal gastrin concentrations were increased after L-dopa and after L-dopa plus carbidopa. Levodopa 67-73 gastrin Homo sapiens 6-13 3935892-5 1985 This effect was not potentiated by L-deprenyl, although L-dopa-induced growth hormone secretion was increased after L-deprenyl premedication. Levodopa 56-62 growth hormone 1 Homo sapiens 71-85 2996509-1 1985 We measured the activity of aromatic L-amino acid decarboxylase with L-dihydroxyphenylalanine as a substrate (DOPA decarboxylase) in normal lung tissues and lung tumors obtained fresh at surgery. Levodopa 69-93 dopa decarboxylase Homo sapiens 110-128 3936450-4 1985 L-Dopa induced a two fold increase in circulating GHRH levels 30 to 45 minutes before the elevation of GH. Levodopa 0-6 growth hormone releasing hormone Homo sapiens 50-54 3935892-6 1985 There was negative correlation between growth hormone secretion and the increase of plasma homovanillic acid after L-dopa. Levodopa 115-121 growth hormone 1 Homo sapiens 39-53 3935351-0 1985 [Plasma prolactin and GH response after thyrotropin-releasing hormone (TRH), L-DOPA and sulpiride in patients with senile dementia of Alzheimer type]. Levodopa 77-83 gamma-glutamyl hydrolase Homo sapiens 22-24 2858860-4 1985 Pretreatment with L-dopa (100 mg/kg body wt) completely blocked the PP-induced stimulation of prolactin release, indicating that antidopaminergic action of PP either at the hypothalamic or anterior pituitary level was responsible for its effects on the release of prolactin. Levodopa 18-24 prolactin Rattus norvegicus 94-103 3997747-0 1985 Plasma growth hormone response to oral l-dopa in infantile autism. Levodopa 39-45 growth hormone 1 Homo sapiens 7-21 3997747-2 1985 The results indicate a high incidence (at least 30%) of blunted plasma growth hormone (GH) responses following oral administration of l-dopa in this sample. Levodopa 134-140 growth hormone 1 Homo sapiens 71-85 3997747-2 1985 The results indicate a high incidence (at least 30%) of blunted plasma growth hormone (GH) responses following oral administration of l-dopa in this sample. Levodopa 134-140 growth hormone 1 Homo sapiens 87-89 3927772-0 1985 A spectrophotometric assay for mammalian tyrosinase utilizing the formation of melanochrome from L-dopa. Levodopa 97-103 tyrosinase Homo sapiens 41-51 2858860-4 1985 Pretreatment with L-dopa (100 mg/kg body wt) completely blocked the PP-induced stimulation of prolactin release, indicating that antidopaminergic action of PP either at the hypothalamic or anterior pituitary level was responsible for its effects on the release of prolactin. Levodopa 18-24 prolactin Rattus norvegicus 264-273 3924793-8 1985 Furthermore, TRH, DN-1417 or methamphetamine caused a dose-related climbing behavior in mice pretreated with L-DOPA and Ro 4-4602. Levodopa 109-115 thyrotropin releasing hormone Mus musculus 13-16 3977547-2 1985 Serum prolactin (PRL) level was assessed after challenges with apomorphine hydrochloride, saline, dopamine hydrochloride, or levodopa-carbidopa (Sinemet) in 19 control and 38 chronic schizophrenic subjects. Levodopa 125-133 prolactin Homo sapiens 6-15 3921593-3 1985 On the contrary, levodopa administration was able to reduce PRL secretion in all the subjects studied. Levodopa 17-25 prolactin Homo sapiens 60-63 2995954-1 1985 New syntheses of three thyrotropin releasing hormone (TRH) analogues ([Dopa2]THR, [Nic1]TRH, and [Tyr(30NO2)2]TRH) have been reported (Dopa stands for L-3,4-dihydroxyphenylalanine, Nic--for nicotinic acid and Tyr(3-NO2)--for L-3-nitrotyrosine). Levodopa 151-179 thyrotropin releasing hormone Rattus norvegicus 23-52 2995954-1 1985 New syntheses of three thyrotropin releasing hormone (TRH) analogues ([Dopa2]THR, [Nic1]TRH, and [Tyr(30NO2)2]TRH) have been reported (Dopa stands for L-3,4-dihydroxyphenylalanine, Nic--for nicotinic acid and Tyr(3-NO2)--for L-3-nitrotyrosine). Levodopa 151-179 thyrotropin releasing hormone Rattus norvegicus 54-57 3990445-2 1985 Levodopa antagonizes the oxotremorine-induced cerebral symptoms (akinesia + tremor); however this antagonism disappears when mice are chronically pretreated orally with CDP-choline, confirming the action of CDP-choline on dopaminergic pathways. Levodopa 0-8 cut-like homeobox 1 Mus musculus 169-172 3976351-0 1985 Autonomic cardiovascular responses in parkinsonism: effect of levodopa with dopa-decarboxylase inhibition. Levodopa 62-70 dopa decarboxylase Homo sapiens 76-94 4091838-5 1985 However, under the influence of alpha-methyl-dopa, an inhibitor of the dopadecarboxylase (aromatic L-amino acid decarboxylase, EC 4.1.1.28) the stimulatory effect of L-dopa on protein fucosylation was attenuated. Levodopa 166-172 dopa decarboxylase Rattus norvegicus 71-88 4091838-5 1985 However, under the influence of alpha-methyl-dopa, an inhibitor of the dopadecarboxylase (aromatic L-amino acid decarboxylase, EC 4.1.1.28) the stimulatory effect of L-dopa on protein fucosylation was attenuated. Levodopa 166-172 dopa decarboxylase Rattus norvegicus 90-125 2984490-11 1985 Behaviorally, GABA receptor agonists diminish the stereotypies induced by apomorphine or L-DOPA suggesting that GABAergic stimulation results also in an antidopaminergic action which is exerted beyond the dopamine synapse. Levodopa 89-95 GABA type A receptor-associated protein Homo sapiens 14-27 3990445-2 1985 Levodopa antagonizes the oxotremorine-induced cerebral symptoms (akinesia + tremor); however this antagonism disappears when mice are chronically pretreated orally with CDP-choline, confirming the action of CDP-choline on dopaminergic pathways. Levodopa 0-8 cut-like homeobox 1 Mus musculus 207-210 6437227-8 1984 After gonadotropin-releasing hormone stimulation, delta max serum luteinizing hormone was elevated in patients with polycystic ovary syndrome but decreased to control levels after treatment with L-dopa. Levodopa 195-201 gonadotropin releasing hormone 1 Homo sapiens 6-36 3870537-5 1985 Although the estrogen receptor assay is a fundamental procedure to know hormone dependency in breast cancer, the changes produced in the serum prolactin level after administering L-dopa is a simple and reproducible method that can be used as alternative predictive test in some cases. Levodopa 179-185 prolactin Homo sapiens 143-152 3870537-6 1985 This work shows that a 65 per 100 decrease or more in the L-dopa induced prolactin level prognosticates the existence of a hormone responsive tumor. Levodopa 58-64 prolactin Homo sapiens 73-82 3991364-2 1985 Although hypermotility induced by methamphetamine was not potentiated by central administration of VIP, L-DOPA-induced hypermotility in pargyline-pretreated rats was markedly enhanced by VIP and this hypermotility was suppressed by simultaneous administration of cholecystokinin octapeptide (CCK-8) in a dose-related manner. Levodopa 104-110 vasoactive intestinal peptide Rattus norvegicus 187-190 6504328-0 1984 Suppression of L-dopa-induced circling in rats with nigral lesions by blockade of central dopa-decarboxylase: implications for mechanism of action of L-dopa in parkinsonism. Levodopa 15-21 dopa decarboxylase Rattus norvegicus 90-108 6504328-0 1984 Suppression of L-dopa-induced circling in rats with nigral lesions by blockade of central dopa-decarboxylase: implications for mechanism of action of L-dopa in parkinsonism. Levodopa 150-156 dopa decarboxylase Rattus norvegicus 90-108 6504328-1 1984 Dopamine (DA) elevations in rat striatum produced by combined administration of L-dopa and carbidopa were abolished when L-dopa was injected with NSD-1015, an inhibitor of central dopa-decarboxylase. Levodopa 80-86 dopa decarboxylase Rattus norvegicus 180-198 6504328-1 1984 Dopamine (DA) elevations in rat striatum produced by combined administration of L-dopa and carbidopa were abolished when L-dopa was injected with NSD-1015, an inhibitor of central dopa-decarboxylase. Levodopa 121-127 dopa decarboxylase Rattus norvegicus 180-198 6437857-4 1984 To reduce peaks and rapid fluctuations of L-DOPA plasma levels (possibly responsible for peak-dose dyskinesias and end-of-dose deterioration) a slow-release formulation of L-DOPA in combination with benserazide or with benserazide plus catechol-O-methyltransferase inhibitors should be developed. Levodopa 172-178 catechol-O-methyltransferase Homo sapiens 236-264 6437857-5 1984 In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc. Levodopa 41-47 monoamine oxidase B Homo sapiens 93-98 6150877-4 1984 The dopamine precursor, L-dopa (20 mg/kg), reduced pituitary PRL content. Levodopa 24-30 prolactin Oncorhynchus mykiss 61-64 18551654-1 1984 Frog epidermis tyrosinase has been immobilized on Enzacryl-AA (a polyacrylamide-based support) and CPG(zirclad)-Arylamine (a controlled pore glass support) in order to stabilize the tyrosine hydroxylase activity of the enzyme; in this way, the immobilized enzyme could be used to synthesize L-dopa from L-tyrosine. Levodopa 291-297 tyrosinase Homo sapiens 15-25 18551654-3 1984 The results showed a noticeable improvement (in immobilization yield, coupling efficiency, and storage and operational stabilities) over previous reports in which tyrosinase was immobilized for L-dopa production. Levodopa 194-200 tyrosinase Homo sapiens 163-173 6499233-0 1984 Inhibitory effect of cimetidine on L-dopa-stimulated growth hormone release in normal man. Levodopa 35-41 growth hormone 1 Homo sapiens 53-67 6431057-2 1984 After phenytoin treatment, growth hormone response to levodopa increased. Levodopa 54-62 growth hormone 1 Homo sapiens 27-41 6435675-1 1984 The inhibition by m-coumaric acid of oxidation of L-dopa by epidermis tyrosinase (monophenol,dihydroxy-L-phenylalanine:oxygen oxidoreductase, EC 1.14.18.1) is characterized by a prolonged transient phase. Levodopa 50-56 thioredoxin reductase 1 Homo sapiens 126-140 6745164-2 1984 Drugs that increase DA in hypophysial portal blood (amphetamine, methylphenidate and L-dopa) increased DA content, decreased PRL secretion, and had no effect on lysosomal enzyme activity. Levodopa 85-91 prolactin Rattus norvegicus 125-128 6745164-8 1984 Furthermore, pretreatment with bromocriptine and L-dopa blocked both the increase in serum PRL concentration and the decrease in anterior pituitary DA content induced by alpha-methyltyrosine and gamma-butyrolactone. Levodopa 49-55 prolactin Rattus norvegicus 91-94 6745164-9 1984 On the other hand, bromocriptine and L-dopa blocked the increase in serum PRL concentration but not the reduction in anterior pituitary DA content caused by reserpine, indicating that reserpine has a direct action on DA storage mechanisms in the anterior pituitary. Levodopa 37-43 prolactin Rattus norvegicus 74-77 6333583-4 1984 After this treatment AADC activities could be detected in the monkey serum by using both L-DOPA and L-5-HTP as substrates. Levodopa 89-95 dopa decarboxylase Rattus norvegicus 21-25 6333583-6 1984 Serum AADC was partially purified from monkey and compared with that of rat using both L-DOPA and L-5-HTP as substrates, but the ratio of the activities for the two substrates did not change significantly in each fraction during purification from either monkey or rat serum. Levodopa 87-93 dopa decarboxylase Rattus norvegicus 6-10 6431057-0 1984 Phenytoin-induced increase in growth hormone response to levodopa in adult males. Levodopa 57-65 growth hormone 1 Homo sapiens 30-44 6431057-3 1984 There was a close relationship between growth hormone response to levodopa and plasma phenytoin concentrations. Levodopa 66-74 growth hormone 1 Homo sapiens 39-53 6432894-0 1984 The growth hormone responses to L-dopa and TRH in acromegaly. Levodopa 32-38 growth hormone 1 Homo sapiens 4-18 6205316-3 1984 It has been assumed, based on indirect evidence, that aromatic L-amino acid decarboxylase (L-AAD), the enzyme responsible for the conversion of L-5-hydroxytryptophan (5-HTP) to 5-HT as well as L-3,4-dihydroxyphenylalanine (L-dopa) to dopamine (DA), is ubiquitously distributed in most tissues of the body including the AP. Levodopa 223-229 dopa decarboxylase Rattus norvegicus 54-89 6734032-3 1984 Since Caucasians with Parkinson"s disease who had high RBC-COMT activity appeared to have more adverse effects from levodopa (L-dopa) than had those with low RBC-COMT activity, L-dopa doses and adverse responses in Filipinos with parkinsonism were compared to those of Caucasians with parkinsonism. Levodopa 116-124 catechol-O-methyltransferase Homo sapiens 59-63 6734032-5 1984 The possible association of the clinical differences in L-dopa tolerance and response between Filipinos and Caucasians with Parkinson"s disease, with the racial differences in RBC-COMT activity is discussed. Levodopa 56-62 catechol-O-methyltransferase Homo sapiens 180-184 6735152-14 1984 Plasma concentrations of GH were reduced by the peripheral administration of NE, which might be expected not to cross the blood-brain-barrier (BBB), alpha 1/alpha 2 agonists clonidine and p-amino clonidine (which does not cross BBB), NE/E precursors L-DOPA and DOPS, and the beta agonist, isoproterenol. Levodopa 250-256 growth hormone 1 Homo sapiens 25-27 6714437-5 1984 The genetically controlled level of COMT activity in the RBC reflects the level of enzyme activity in other tissues and is significantly correlated with individual variations in the methyl conjugation of catechol drugs such as L-dopa and methyldopa. Levodopa 227-233 catechol-O-methyltransferase Homo sapiens 36-40 6539375-5 1984 Both parents were heterozygous for the hGH-N gene deletion and had a low hGH response to arginine and L-dopa tolerance tests, but had normal basal somatomedin-C levels and normal somatomedin-C generation tests. Levodopa 102-108 growth hormone 1 Homo sapiens 39-44 6374488-2 1984 Oral administration of L-dopa plus propranolol induced a potent and sustained GH release in the subjects tested (26 +/- 6 ng/ml). Levodopa 23-29 growth hormone 1 Homo sapiens 78-80 6145774-0 1984 Effect of L-dopa on glutamate decarboxylase activity in the hypothalamic and amygdaloid nuclei. Levodopa 10-16 glutamate-ammonia ligase Homo sapiens 20-43 6145774-1 1984 Repeated administration of L-dopa methylester produced a significant increase in glutamate decarboxylase (GAD) activity without pyridoxal-5"-phosphate in the lateral hypothalamic area and medial amygdaloid nucleus. Levodopa 27-33 glutamate-ammonia ligase Homo sapiens 81-104 6145774-1 1984 Repeated administration of L-dopa methylester produced a significant increase in glutamate decarboxylase (GAD) activity without pyridoxal-5"-phosphate in the lateral hypothalamic area and medial amygdaloid nucleus. Levodopa 27-33 glutamate-ammonia ligase Homo sapiens 106-109 6145774-2 1984 The effect of L-dopa on GAD activity was opposite to that of haloperidol in the lateral hypothalamic area. Levodopa 14-20 glutamate-ammonia ligase Homo sapiens 24-27 6374488-5 1984 completely suppressed the L-dopa-induced GH secretion (2 +/- 09.5 ng/ml). Levodopa 26-32 growth hormone 1 Homo sapiens 41-43 6545817-1 1984 In addition to beta-adrenergic receptor agonists, L-dopa and dopamine have been also shown to activate the production of melatonin and its synthesizing enzyme, serotonin N-acetyltransferase. Levodopa 50-56 serotonin N-acetyltransferase Bos taurus 160-189 6420440-15 1984 The growth increments during L-dopa therapy occurred in the three children who had significant increases in hGH and somatomedin-C; of the three children with significant growth increments during bromocriptine therapy, two had increases in somatomedin-C, and one achieved a normal peak hGH value. Levodopa 29-35 insulin like growth factor 1 Homo sapiens 116-129 6141712-2 1984 However, decrease in AADC with L-DOPA as substrate was not statistically significant. Levodopa 31-37 dopa decarboxylase Homo sapiens 21-25 6141712-5 1984 Changes in AADC with L-DOPA or L-5-HTP as substrates varied in parkinsonian brains. Levodopa 21-27 dopa decarboxylase Homo sapiens 11-15 6441736-2 1984 The enzyme activity was detected by staining the gels with L-3,4-dihydroxyphenylalanine, dopamine and 5,6-dihydroxyindole as substrates for tyrosinase (EC 1.14.18.1). Levodopa 59-87 tyrosinase Homo sapiens 140-150 6657127-1 1983 The changes in prolactin release induced by acute doses of L-Dopa + benserazide (250 mg) were analysed in Parkinson disease patients undergoing various drug treatments. Levodopa 59-65 prolactin Homo sapiens 15-24 6523351-1 1984 The authors studied the basal and L-DOPA-stimulated levels of STH and basal level of prolactin in blood serum of 128 patients presenting with acromegaly. Levodopa 34-40 saitohin Homo sapiens 62-65 6523351-1 1984 The authors studied the basal and L-DOPA-stimulated levels of STH and basal level of prolactin in blood serum of 128 patients presenting with acromegaly. Levodopa 34-40 prolactin Homo sapiens 85-94 6688812-0 1983 Cholinergic receptor control mechanisms for L-dopa, apomorphine, and clonidine-induced growth hormone secretion in man. Levodopa 44-50 growth hormone 1 Homo sapiens 87-101 6649642-0 1983 [The L-DOPA-propranolol test for the evaluation of reserves in secretory growth hormone]. Levodopa 5-11 growth hormone 1 Homo sapiens 73-87 6359046-0 1983 Age-dependent depressor effect of L-dopa in dogs with inhibition of extracerebral dopa decarboxylase. Levodopa 34-40 dopa decarboxylase Canis lupus familiaris 82-100 6634874-4 1983 Conversely, L-DOPA produced significant stimulation only when MAO-A was inhibited. Levodopa 12-18 monoamine oxidase A Mus musculus 62-67 6626185-9 1983 Serum growth hormone was found to be 8.44 +/- 1.4(SE) ng/ml in the L-Dopa group and 4.6 +/- 0.9 ng/ml in the control group. Levodopa 67-73 gonadotropin releasing hormone receptor Rattus norvegicus 6-20 6626185-10 1983 It is concluded that the continuous administration of L-Dopa produces an increase of circulating serum growth hormone levels, and this in turn enhances growth. Levodopa 54-60 gonadotropin releasing hormone receptor Rattus norvegicus 103-117 6414103-7 1983 It is concluded 1) that even in hypophysectomized normoprolactinemic patients the circulating PRL may originate mainly from the residual tumor cells, and 2) that the sulpiride test is useful to detect the abnormalities of hypothalamo-pituitary axis in operated patients with PRL-secreting adenomas, whereas TRH, arginine, and L-dopa tests are less useful for such purposes. Levodopa 326-332 prolactin Homo sapiens 94-97 6409113-9 1983 Catalase reduced the cytotoxicity of L-dopa by half, while it had no inhibitory effect on the strong cytotoxicity of 5-S-cysteaminyldopamine. Levodopa 37-43 catalase Homo sapiens 0-8 6861440-3 1983 The highest dose was as effective as 500 mg L-dopa, although the duration of action was shorter, with a decrease to below 50% of basal PRL values in all patients. Levodopa 44-50 prolactin Homo sapiens 135-138 6861440-4 1983 Serum GH did not rise in nonacromegalic subjects, but it fell after 400 mg ibopamine in the L-dopa-sensitive acromegalic patients. Levodopa 92-98 growth hormone 1 Homo sapiens 6-8 6889295-0 1983 [Effect of acute levodopa load on blood prolactin concentration in patients with thyroid diseases]. Levodopa 17-25 prolactin Homo sapiens 40-49 6889295-1 1983 In 14 thyrotoxic patients and 5 persons with endemic euthyroid goiter the blood plasma prolactin content was studied under the action of an acute oral load of levodopa in a dose of 0.5 g. It was found that the basal prolactin level was significantly higher in the blood of patients of both sexes with thyrotoxicosis and endemic euthyroid goiter than that in the control group (10 healthy humans). Levodopa 159-167 prolactin Homo sapiens 87-96 6889295-1 1983 In 14 thyrotoxic patients and 5 persons with endemic euthyroid goiter the blood plasma prolactin content was studied under the action of an acute oral load of levodopa in a dose of 0.5 g. It was found that the basal prolactin level was significantly higher in the blood of patients of both sexes with thyrotoxicosis and endemic euthyroid goiter than that in the control group (10 healthy humans). Levodopa 159-167 prolactin Homo sapiens 216-225 6889295-2 1983 The blood plasma prolactin content markedly decreased in thyrotoxic patients under levodopa effect, regardless of the sex, whereas in patients with endemic euthyroid goiter the drug exhibited no considerable action on the prolactin level. Levodopa 83-91 prolactin Homo sapiens 17-26 6135575-0 1983 A comparison of the effects of reversible and irreversible inhibitors of aromatic L-amino acid decarboxylase on the half-life and other pharmacokinetic parameters of oral L-3,4-dihydroxyphenylalanine. Levodopa 171-199 dopa decarboxylase Rattus norvegicus 73-108 6135575-8 1983 Although AADC inhibition reduced the magnitude of the increases in serum dopamine levels following L-DOPA administration, no reduction in serum 3,4-dihydroxyphenylacetic acid levels was observed. Levodopa 99-105 dopa decarboxylase Rattus norvegicus 9-13 6404691-2 1983 Harding-Passey mouse-melanoma tyrosinase (EC 1.14.18.1) is inhibited during L-3,4-dihydroxyphenylalanine oxidation by reaction products. Levodopa 76-104 tyrosinase Mus musculus 30-40 6634455-0 1983 [Growth hormone secretion in patients with various types of diabetes mellitus and in healthy persons after L-dopa stimulation]. Levodopa 107-113 growth hormone 1 Homo sapiens 1-15 6401764-7 1983 Five patients responded with significant reduction in the serum hPRL concentration after L-dopa, and in three patients, no change was observed. Levodopa 89-95 prolactin Homo sapiens 64-68 6305147-9 1983 In addition, TRH (2.5-20 mg/kg) markedly enhanced the circling behavior induced by L-DOPA or apomorphine in mice with unilateral caudate nucleus lesions induced by injection of 6-OHDA. Levodopa 83-89 thyrotropin releasing hormone Mus musculus 13-16 6343098-0 1983 Effect of l-dopa on growth hormone, glucose, insulin, and cortisol response in obese subjects. Levodopa 10-16 growth hormone 1 Homo sapiens 20-34 6343098-3 1983 The obese subjects displayed a lack of growth hormone responsiveness to L-dopa and a diminished GH responsiveness to hypoglycemia. Levodopa 72-78 growth hormone 1 Homo sapiens 39-53 6222183-4 1983 Following L-dopa, plasma prolactin concentrations decreased by greater than 50%, with the nadir noted within 90 minutes. Levodopa 10-16 prolactin Homo sapiens 25-34 6860117-3 1983 In the subsequent 3 h, the ERG recordings, blood levels and clinical ratings of extrapyramidal symptoms significantly dropped after a delay of 60 min in relation to the occurrence of the peak plasma L DOPA level. Levodopa 199-205 ETS transcription factor ERG Homo sapiens 27-30 6132624-4 1983 In addition the administration of L-DOPA and morphine facilitated the effect of MIF while preliminary administration of MIF blocked the effect of morphine given in threshold doses. Levodopa 34-40 macrophage migration inhibitory factor Rattus norvegicus 80-83 6413305-1 1983 The prolactin responses to an oral challenge of L-dopa (0.5 g) and bromocriptine (2.5 mg) were studied in 31 hyperprolactinemic females without radiological abnormalities of pituitary fossa, in 12 hyperprolactinemic patients with minor radiological evidence suggesting the presence of a pituitary adenoma and in 16 normal volunteers in the early puerperium with physiological hyperprolactinemia. Levodopa 48-54 prolactin Homo sapiens 4-13 6413305-4 1983 These results suggest that the L-dopa suppression test might serve as a reliable indicator to detect prolactin-secreting microadenomas in patients with persistent hyperprolactinemia and radiologically normal pituitary fossae. Levodopa 31-37 prolactin Homo sapiens 101-110 6642424-6 1983 On the other hand, the administration of L-dopa resulted in a significant decrease in growth hormone level from 74.25 +/- 22 ng/ml (mean +/- SEM) at zero time to a level of 52.8 +/- 21 and 58.77 +/- 22.7 ng/ml at the 60- and 90-min intervals, respectively (p less than 0.05), and a significant decrease in prolactin level from a baseline of 56.18 +/- 17 to 25.5 +/- 8.4 ng/ml (p less than 0.001) at the 60-min interval. Levodopa 41-47 prolactin Homo sapiens 306-315 6407880-2 1983 The rate of tyrosinase formation has been calculated by coupling the activatory process of frog epidermis pro-tyrosinase by trypsin to the oxidation of L-DOPA to dopachrome. Levodopa 152-158 tyrosinase Homo sapiens 12-22 6308150-3 1983 The antagonism of the neuroleptic-induced increase in dopamine receptor sensitivity and the decrease in dopamine synthesis and release may be responsible for the effectiveness of the GABA receptor agonists in the treatment of neuroleptic- and L-DOPA-induced dyskinesia. Levodopa 243-249 GABA type A receptor-associated protein Homo sapiens 183-196 6402812-4 1983 The latter reacted to both the specific L-Dopa test and to the non-specific TRH test with an increase in GH serum concentration. Levodopa 40-46 growth hormone 1 Homo sapiens 105-107 7153475-1 1982 After oral administration of l-dihydroxyphenylalanine (L-dopa) to calves, plasma concentrations of L-dopa, dopamine, norepinephrine and parathyroid hormone increased whereas prolactin and calcium decreased while epinephrine remained unchanged. Levodopa 55-61 prolactin Bos taurus 174-183 7130339-3 1982 Preoperatively, the PRL inhibitory responses to L-dopa cured, 4 .3 +/- 3.8%; uncured, 50.1 +/- 5.5% of baseline) was blunted by pretreatment with the decarboxylase inhibitor carbidopa (cured, 79.1 +/- 4.1%; uncured, 76.8 +/- 9.2%). Levodopa 48-54 prolactin Homo sapiens 20-23 6757593-0 1982 [Response of growth hormone (HGH) to L-dopa, L-arginine and their combination in normal individuals]. Levodopa 37-43 growth hormone 1 Homo sapiens 13-27 6983619-4 1982 AADC activities towards L-DOPA and L-5-HTP as substrates were also decreased significantly in almost all tissues of SC-treated rats. Levodopa 24-30 dopa decarboxylase Rattus norvegicus 0-4 6983619-7 1982 Serum AADC activities were decreased drastically using both L-DOPA and L-5-HTP as substrates. Levodopa 60-66 dopa decarboxylase Rattus norvegicus 6-10 7137962-8 1982 The data presented here indicate that use of catechol-O-methyltransferase inhibitors with L-dopa may be of value in the treatment of parkinsonian patients. Levodopa 90-96 catechol-O-methyltransferase Homo sapiens 45-73 7153475-1 1982 After oral administration of l-dihydroxyphenylalanine (L-dopa) to calves, plasma concentrations of L-dopa, dopamine, norepinephrine and parathyroid hormone increased whereas prolactin and calcium decreased while epinephrine remained unchanged. Levodopa 29-53 prolactin Bos taurus 174-183 6621850-0 1983 Prolactin and growth hormone response to levodopa in affective illness. Levodopa 41-49 growth hormone 1 Homo sapiens 14-28 6621850-1 1983 Prolactin (PRL) and growth hormone (GH) response to L-Dopa have been studied in 51 affectively ill women (26 unipolar and 25 bipolar) before and after amitriptyline treatment and in 14 normal female controls. Levodopa 52-58 growth hormone 1 Homo sapiens 36-38 6621850-2 1983 There was no difference in GH response to L-dopa in all groups studied except for bipolar postmenopausal women, who showed a blunted GH response to L-Dopa compared to bipolar premenopausal women. Levodopa 148-154 growth hormone 1 Homo sapiens 133-135 6983619-0 1982 Effect of pyridoxal phosphate deficiency on aromatic L-amino acid decarboxylase activity with L-DOPA and L-5-hydroxytryptophan as substrates in rats. Levodopa 94-100 dopa decarboxylase Rattus norvegicus 53-79 7049677-7 1982 Peak levels of LH after L-dopa treatment coincided with increased DA levels in the ME, no change in NE, and a clear drop in LHRH. Levodopa 24-30 gonadotropin releasing hormone 1 Rattus norvegicus 124-128 7102764-3 1982 In puerperal hyperprolactinemic subjects, the basal PRL (116.8 +/- 16.4 ng/ml) was suppressed 77% +/- 2% after administration of L-dopa and 51% +/- 7% after L-dopa plus carbidopa, significantly different from that of L-dopa alone (p less than 0.005), but similar to that observed in normal subjects. Levodopa 129-135 prolactin Homo sapiens 52-55 7102764-3 1982 In puerperal hyperprolactinemic subjects, the basal PRL (116.8 +/- 16.4 ng/ml) was suppressed 77% +/- 2% after administration of L-dopa and 51% +/- 7% after L-dopa plus carbidopa, significantly different from that of L-dopa alone (p less than 0.005), but similar to that observed in normal subjects. Levodopa 157-163 prolactin Homo sapiens 52-55 7102764-3 1982 In puerperal hyperprolactinemic subjects, the basal PRL (116.8 +/- 16.4 ng/ml) was suppressed 77% +/- 2% after administration of L-dopa and 51% +/- 7% after L-dopa plus carbidopa, significantly different from that of L-dopa alone (p less than 0.005), but similar to that observed in normal subjects. Levodopa 157-163 prolactin Homo sapiens 52-55 7102764-4 1982 In the patients with idiopathic hyperprolactinemia, the baseline PRL (131 +/- 38 ng/ml) decreased 56.3% after the administration of L-dopa. Levodopa 132-138 prolactin Homo sapiens 65-68 7102764-5 1982 In the presence of peripheral dopa decarboxylase inhibition, the administration of L-dopa decreased plasma PRL values 30%, a drop significantly different from that of L-dopa alone (p less than 0.02). Levodopa 83-89 prolactin Homo sapiens 107-110 7102764-8 1982 The increased pituitary sensitivity to L-dopa observed in puerperal women may be due to alterations in PRL receptors or vascularity. Levodopa 39-45 prolactin Homo sapiens 103-106 6799584-1 1982 Tyrosinase activity (Monophenol, dihydroxyphenylalanine: oxygen oxidoreductase EC 1.14.18.1) in vitiligo and normal epidermal homogenates of skin from human beings was measured by estimating beta 3,4-dihydroxyphenylalanine (dopa) by a highly sensitive fluorometric method described in this paper. Levodopa 191-222 tyrosinase Homo sapiens 0-10 6749630-0 1982 Effect of L-dopa administration on insulin binding: possible role of growth hormone in regulation of insulin receptor affinity. Levodopa 10-16 insulin Homo sapiens 35-42 6749630-0 1982 Effect of L-dopa administration on insulin binding: possible role of growth hormone in regulation of insulin receptor affinity. Levodopa 10-16 insulin receptor Homo sapiens 101-117 6749630-1 1982 We have investigated changes in insulin binding to erythrocytes in response to the oral administration of 500 mg of L-Dopa in ten healthy subjects. Levodopa 116-122 insulin Homo sapiens 32-39 6749630-2 1982 L-Dopa administration increases insulin binding from 5.18 +/- 0.14% (mean +/- SEM) to 6.18 +/- 0.34% (P less than 0.05) with concomitant increase in basal plasma growth hormone from 1.3 +/- 0.1 ng/ml to 14.4 +/- 4.8 ng/ml (P less than 0.05). Levodopa 0-6 insulin Homo sapiens 32-39 6749630-2 1982 L-Dopa administration increases insulin binding from 5.18 +/- 0.14% (mean +/- SEM) to 6.18 +/- 0.34% (P less than 0.05) with concomitant increase in basal plasma growth hormone from 1.3 +/- 0.1 ng/ml to 14.4 +/- 4.8 ng/ml (P less than 0.05). Levodopa 0-6 growth hormone 1 Homo sapiens 162-176 7121609-0 1982 Catechol-O-methyltransferase inhibition by U-0521 increases striatal utilization of levodopa. Levodopa 84-92 catechol-O-methyltransferase Rattus norvegicus 0-28 7121609-7 1982 U-0521, a potent COMT inhibitor, enhances the availability and utilization of levodopa in the brain and may thus be helpful in future treatment of parkinsonian patients. Levodopa 78-86 catechol-O-methyltransferase Homo sapiens 17-21 7044409-0 1982 Inhibition of the renin--aldosterone axis and of prolactin secretion during pregnancy by L-dopa. Levodopa 89-95 renin Homo sapiens 18-23 7044409-0 1982 Inhibition of the renin--aldosterone axis and of prolactin secretion during pregnancy by L-dopa. Levodopa 89-95 prolactin Homo sapiens 49-58 7044409-5 1982 The decreased activity of the renin-aldosterone axis after administration of L-dopa may be attributed to an accumulation of dopamine and catecholamines in the brain, resulting in a diminution of sympathetic outflow from the central nervous system. Levodopa 77-83 renin Homo sapiens 30-35 7044409-6 1982 The simultaneous and comparable changes of both PRA and PA after L-dopa treatment, as well as the reversibility of aldosterone suppression by infusion of angiotensin II, suggest that the inhibition of aldosterone secretion by L-dopa is mediated by a decrease of renin release. Levodopa 226-232 angiotensinogen Homo sapiens 154-168 7044409-6 1982 The simultaneous and comparable changes of both PRA and PA after L-dopa treatment, as well as the reversibility of aldosterone suppression by infusion of angiotensin II, suggest that the inhibition of aldosterone secretion by L-dopa is mediated by a decrease of renin release. Levodopa 226-232 renin Homo sapiens 262-267 7096047-0 1982 Growth hormone response to L-dopa in the thinned obese. Levodopa 27-33 growth hormone 1 Homo sapiens 0-14 7096047-1 1982 The response of plasma growth hormone (GH) to 0.5 g L-dopa was studied in 17 obese nondiabetic subjects and in 6 normal-weight subjects, aged 16 to 46 yr. Levodopa 52-58 growth hormone 1 Homo sapiens 23-37 6805079-8 1982 One patient in whom the fasting GH level was not increased had progressed to the stage of panhypopituitarism, in the remaining patient challenge with thyrotrophin-releasing hormone (TRH) led to increased GH levels and L-dopa challenge resulted in a paradoxical decrease in GH levels. Levodopa 218-224 thyrotropin releasing hormone Homo sapiens 182-185 6805079-9 1982 Seven patients with increased GH levels who were challenged with L-dopa showed the typical decrease in GH levels found in this condition; in 5 of these patients, challenged with TRH, GH levels increased. Levodopa 65-71 growth hormone 1 Homo sapiens 30-32 6805079-9 1982 Seven patients with increased GH levels who were challenged with L-dopa showed the typical decrease in GH levels found in this condition; in 5 of these patients, challenged with TRH, GH levels increased. Levodopa 65-71 growth hormone 1 Homo sapiens 103-105 6805079-9 1982 Seven patients with increased GH levels who were challenged with L-dopa showed the typical decrease in GH levels found in this condition; in 5 of these patients, challenged with TRH, GH levels increased. Levodopa 65-71 growth hormone 1 Homo sapiens 103-105 6953463-4 1982 After levodopa treatment, only patients with left symptomatology responded to the attention task with an enlargement of EP components, largely in the noninvolved hemisphere. Levodopa 6-14 epiregulin Homo sapiens 120-122 6122169-0 1982 L-dopa restores amplitude of growth hormone pulses in old male rats to that observed in young male rats. Levodopa 0-6 gonadotropin releasing hormone receptor Rattus norvegicus 29-43 7084415-3 1982 Pretreatment with fusaric acid, an inhibitor of dopamine-beta-hydroxylase, also antagonizes the mydriatic effect of L-dopa. Levodopa 116-122 dopamine beta hydroxylase Mus musculus 48-73 6978249-2 1982 To evaluate the possible involvement of prolactin in the regulation of testosterone secretion during exercise, the influence of prolactin inhibition by oral L-dopa (1 g) pretreatment was also studied. Levodopa 157-163 prolactin Homo sapiens 128-137 6978249-6 1982 Pharmacological blockade of prolactin release by L-dopa pretreatment failed to modify the response of testosterone to bicycle ergometer exercise. Levodopa 49-55 prolactin Homo sapiens 28-37 6799584-3 1982 The activity of tyrosinase in normal human skin from different individuals and from different regions of the body was in the range of 4 to 140 picomoles of beta 3,4-dihydroxyphenylalanine formed per min/mg protein of epidermal homogenate. Levodopa 156-187 tyrosinase Homo sapiens 16-26 6122169-3 1982 Treatment of old rats with L-dopa increased the number of animals showing elevated GH pulses to 53%. Levodopa 27-33 gonadotropin releasing hormone receptor Rattus norvegicus 83-85 6122169-5 1982 Treatment of old animals with L-dopa increased mean plasma GH concentrations to 132.9 +/- 11.2 ng/ml (p less than 0.05) which was not significantly different from GH values in young rats. Levodopa 30-36 gonadotropin releasing hormone receptor Rattus norvegicus 59-61 6803810-8 1982 A DOPA decarboxylase inhibitor in clinical use, benserazide, is, however, a much superior catechol-O-methyltransferase substrate and may have the therapeutic advantage of decreasing methylation of L-DOPA [2]. Levodopa 197-203 dopa decarboxylase Sus scrofa 2-20 6122169-7 1982 L-Dopa increased pituitary GH concentrations in old rats to 318 +/- 32.2 micrograms/mg protein, which was not significantly different from that in either young or old vehicle-treated animals. Levodopa 0-6 gonadotropin releasing hormone receptor Rattus norvegicus 27-29 6122169-9 1982 These data indicate that L-dopa can increase the amplitude of GH pulses and elevate mean plasma GH in old male rats to levels present in young male rats, probably by increasing hypothalamic catecholamines. Levodopa 25-31 gonadotropin releasing hormone receptor Rattus norvegicus 62-64 6122169-9 1982 These data indicate that L-dopa can increase the amplitude of GH pulses and elevate mean plasma GH in old male rats to levels present in young male rats, probably by increasing hypothalamic catecholamines. Levodopa 25-31 gonadotropin releasing hormone receptor Rattus norvegicus 96-98 6278076-6 1982 However, prolactin levels were significantly lower in the Parkinsonian patients treated with levodopa versus the untreated group. Levodopa 93-101 prolactin Homo sapiens 9-18 6812398-4 1982 L-Dopa induced a statistically significant suppression of TRH, caused PRL release; such suppression appears to be lower when TRH plus pyridoxine were administered simultaneously. Levodopa 0-6 thyrotropin releasing hormone Homo sapiens 58-61 6812398-4 1982 L-Dopa induced a statistically significant suppression of TRH, caused PRL release; such suppression appears to be lower when TRH plus pyridoxine were administered simultaneously. Levodopa 0-6 thyrotropin releasing hormone Homo sapiens 125-128 6807859-4 1982 Although L-dopa suppresses prolactin normally, the ability of thyrotropin releasing hormone (TRH) to stimulate the release of prolactin and thyroid stimulating hormone (TSH) is blunted. Levodopa 9-15 prolactin Homo sapiens 27-36 6127638-2 1982 This is documented by observations that in humans, especially in subjects with primary hypothyroidism, the dopamine precursor l-Dopa, dopamine receptor agonist bromocryptine, and dopamine itself decrease plasma levels of TSH and in some instances inhibit TSH secretory response to thyrotropin-releasing hormone (TRH). Levodopa 126-132 thyrotropin releasing hormone Homo sapiens 281-310 7162583-7 1982 The positive effect of CDP-choline on parkinsonian patients already treated with L-dopa + dopa decarboxylase inhibitor stands for a possible action on the DA receptor through an activation of the phospholipid metabolism. Levodopa 81-87 cut like homeobox 1 Homo sapiens 23-26 20487843-0 1982 Demonstration of aromatic l-amino acid decarboxylase activity in human brain with l-dopa and l-5-hydroxytryptophan as substrates by high-performance liquid chromatography with electrochemical detection. Levodopa 82-88 dopa decarboxylase Homo sapiens 17-52 7070643-0 1982 Prolactin response to acute administration of different L-dopa plus decarboxylase inhibitors in Parkinson"s disease. Levodopa 56-62 prolactin Homo sapiens 0-9 20487843-1 1982 The enzymatic decarboxylations of l-DOPA and l-5-hydroxytryptophan (l-5-HTP) by aromatic l-amino acid decarboxylase (AADC) were measured with homogenates from human brain regions, caduate nucleus and hypothalamus, using our new and highly sensitive methods for l-DOPA decarboxylase and l-5-HTP decarboxylase by high-performance liquid chromatography with electrochemical detection (HPLC-ED). Levodopa 34-40 dopa decarboxylase Homo sapiens 89-115 7251816-0 1981 Dopaminergic regulation of growth hormone (GH) secretion in normal man: correlation of L-dopa and dopamine levels with the GH response. Levodopa 87-93 growth hormone 1 Homo sapiens 123-125 20487843-1 1982 The enzymatic decarboxylations of l-DOPA and l-5-hydroxytryptophan (l-5-HTP) by aromatic l-amino acid decarboxylase (AADC) were measured with homogenates from human brain regions, caduate nucleus and hypothalamus, using our new and highly sensitive methods for l-DOPA decarboxylase and l-5-HTP decarboxylase by high-performance liquid chromatography with electrochemical detection (HPLC-ED). Levodopa 34-40 dopa decarboxylase Homo sapiens 117-121 20487843-1 1982 The enzymatic decarboxylations of l-DOPA and l-5-hydroxytryptophan (l-5-HTP) by aromatic l-amino acid decarboxylase (AADC) were measured with homogenates from human brain regions, caduate nucleus and hypothalamus, using our new and highly sensitive methods for l-DOPA decarboxylase and l-5-HTP decarboxylase by high-performance liquid chromatography with electrochemical detection (HPLC-ED). Levodopa 34-40 dopa decarboxylase Homo sapiens 263-281 20487843-2 1982 Dopamine formed from l-DOPA as substrate was measured for DOPA decarboxylase activity using d-DOPA for the blank. Levodopa 21-27 dopa decarboxylase Homo sapiens 58-76 20487843-6 1982 AADC activities in human brains were found to be widely variable for both l-DOPA and l-5-HTP as substrates. Levodopa 74-80 dopa decarboxylase Homo sapiens 0-4 20487843-8 1982 AADC activity for l-DOPA in the brain was found to be linear up to 40 min of incubation, while that for l-5-HTP was found to be linear up to 240 min of incubation. Levodopa 18-24 dopa decarboxylase Homo sapiens 0-4 6173137-0 1981 Inhibition of reverse transcriptase by tyrosinase generated quinones related to levodopa and dopamine. Levodopa 80-88 tyrosinase Homo sapiens 39-49 6810204-3 1981 Levodopa elicited a normal suppression of prolactin concentrations in parkinsonian subjects; the major abnormality to emerge was attenuation of the response to thyrotropin-releasing hormone (TRH) in the parkinsonian patients following administration of Sinemet (levodopa plus carbidopa) or bromocriptine. Levodopa 262-270 thyrotropin releasing hormone Homo sapiens 160-189 6810204-3 1981 Levodopa elicited a normal suppression of prolactin concentrations in parkinsonian subjects; the major abnormality to emerge was attenuation of the response to thyrotropin-releasing hormone (TRH) in the parkinsonian patients following administration of Sinemet (levodopa plus carbidopa) or bromocriptine. Levodopa 262-270 thyrotropin releasing hormone Homo sapiens 191-194 6810204-5 1981 Since the addition of carbidopa enhanced the suppression of prolactin induced by levodopa, exogenous levodopa probably acts predominantly through the formation of dopamine in the hypothalamus, but inside the blood-brain barrier, rather than as a direct effect of circulating dopamine on the anterior pituitary or areas of the hypothalamus outside the blood-brain barrier. Levodopa 81-89 prolactin Homo sapiens 60-69 6810204-5 1981 Since the addition of carbidopa enhanced the suppression of prolactin induced by levodopa, exogenous levodopa probably acts predominantly through the formation of dopamine in the hypothalamus, but inside the blood-brain barrier, rather than as a direct effect of circulating dopamine on the anterior pituitary or areas of the hypothalamus outside the blood-brain barrier. Levodopa 101-109 prolactin Homo sapiens 60-69 7021041-0 1981 Inhibition of the renin-angiotensin-aldosterone system by L-dopa with and without inhibition of extracerebral dopa decarboxylase in man. Levodopa 58-64 renin Homo sapiens 18-23 7334406-2 1981 In subjects on chronic therapy with levodopa and carbidopa (Sinemet), the growth hormone releasing effect of Madopar was blunted. Levodopa 36-44 growth hormone 1 Homo sapiens 74-88 6810204-3 1981 Levodopa elicited a normal suppression of prolactin concentrations in parkinsonian subjects; the major abnormality to emerge was attenuation of the response to thyrotropin-releasing hormone (TRH) in the parkinsonian patients following administration of Sinemet (levodopa plus carbidopa) or bromocriptine. Levodopa 0-8 prolactin Homo sapiens 42-51 7296879-0 1981 Determination of free and conjugated catecholamines and L-3,4-dihydroxyphenylalanine in plasma and urine: evidence for a catechol-O-methyltransferase inhibitor in uraemia. Levodopa 56-84 catechol-O-methyltransferase Homo sapiens 121-149 6790560-0 1981 Calcium and calcium-antagonistic effects on prolactin and growth hormone responses to thyrotropin-releasing hormone and L-dopa in man. Levodopa 120-126 growth hormone 1 Homo sapiens 58-72 6790560-5 1981 Five hundred milligrams of L-dopa increased the GH level from 2.2 +/- 0.7 to 16.7 +/- 2.2 ng/ml in 60 min (P less than 0.002) and reduced the PRL level from 11.6 +/- 2.9 to 3.1 +/- 0.4 ng/ml in 150 min (P less than 0.05). Levodopa 27-33 prolactin Homo sapiens 142-145 6792273-5 1981 This result seems to suggest that it is cytochemically appropriate to use DOPA as the substrate of tyrosinase. Levodopa 74-78 tyrosinase Mus musculus 99-109 6792292-4 1981 With this technique, tyrosinase from normally pigmented brown, black, blond, and red hairbulbs gives a single band when the gel is stained with L-dopa for enzyme activity. Levodopa 144-150 tyrosinase Homo sapiens 21-31 7258240-1 1981 In 27 pregnant subjects (21 treated women and six control subjects), the effect of L-dopa (500 to 1,000 mg orally) on vascular sensitivity to angiotensin II amide (Hypertensin, Ciba) was examined in 16 of these women, 1,000 mg of L-dopa resulted in a significant decrease in vascular responsiveness to angiotensin, i.e., an increase in angiotensin pressor dose from 16.9 +/- 5.0 to 19.6 +/- 4.5 ng . Levodopa 83-89 angiotensinogen Homo sapiens 142-156 7301038-5 1981 Injections of L-DOPA lowered prolactin in young but not in old rats, while apomorphine reduced prolactin levels in both groups. Levodopa 14-20 prolactin Rattus norvegicus 29-38 7030527-3 1981 L-dopa diminished the rise in renin following tilt and this effect of L-dopa was abolished by carbidopa. Levodopa 0-6 renin Homo sapiens 30-35 7030527-3 1981 L-dopa diminished the rise in renin following tilt and this effect of L-dopa was abolished by carbidopa. Levodopa 70-76 renin Homo sapiens 30-35 7195482-0 1981 Aromatic L-amino acid decarboxylase in rat corpus striatum: implications for action of L-dopa in parkinsonism. Levodopa 87-93 dopa decarboxylase Rattus norvegicus 0-35 6785431-0 1981 Serum prolactin concentrations in mangabey (Cercocebus atys lunulatus) and patas (Erythrocebus patas) monkeys in response to stress, ketamine, TRH, sulpiride and levodopa. Levodopa 162-170 prolactin Homo sapiens 6-15 6785431-8 1981 Oral administration of levodopa was followed by a significant fall in serum prolactin. Levodopa 23-31 prolactin Homo sapiens 76-85 6785431-11 1981 The variations in serum prolactin levels observed in these monkeys under the influence of stress, TRH, sulpiride and levodopa are similar to those observed in man to the same stimuli, although the experimental conditions were quite different. Levodopa 117-125 prolactin Homo sapiens 24-33 7205652-2 1981 L-Dopa administration increased DA concentrations in both lesioned and unlesioned sides; absolute increases were higher in control striata and pretreatment with carbidopa (an inhibitor of peripheral DDC) amplified the increases on both sides. Levodopa 0-6 dopa decarboxylase Rattus norvegicus 199-202 7211191-1 1981 Plasma dopamine-beta-hydroxylase activity (DBH) was estimated in 50 drug-free Parkinson patients, 30 of whom had never been treated, in 26 patients treated chronically with L-Dopa, and in 44 controls. Levodopa 173-179 dopamine beta-hydroxylase Homo sapiens 7-32 6188670-5 1981 Brain 5-HT levels were reduced in proportion to the increase of dopamine (DA) level by L-DOPA alone and Ro4-4602 plus L-DOPA. Levodopa 87-93 POU class 6 homeobox 1 Rattus norvegicus 0-7 7013595-7 1981 The relation of complications to dosage is now better understood, and the ratio of dopa-decarboxylase inhibitor to levodopa inhibitor to levodopa of 1:4 is better than the previous 1:10. Levodopa 137-145 dopa decarboxylase Homo sapiens 83-101 6188670-5 1981 Brain 5-HT levels were reduced in proportion to the increase of dopamine (DA) level by L-DOPA alone and Ro4-4602 plus L-DOPA. Levodopa 118-124 POU class 6 homeobox 1 Rattus norvegicus 0-7 7009102-1 1981 The effect of metoclopramide, a procainamide derivative with dopamine antagonistic properties, and L-dopa on plasma renin activity (PRA) was studied in adult rats. Levodopa 99-105 renin Rattus norvegicus 116-121 6790202-3 1981 In this study basal GH plasma levels and their response to TRH and L-DOPA were determined in thirty-nine cirrhotic patients and fifteen controls. Levodopa 67-73 growth hormone 1 Homo sapiens 20-22 7217982-5 1981 Growth hormone (GH) release in vivo is stimulated by levodopa in normal subjects but inhibited in acromegaly. Levodopa 53-61 growth hormone 1 Homo sapiens 0-14 7217982-5 1981 Growth hormone (GH) release in vivo is stimulated by levodopa in normal subjects but inhibited in acromegaly. Levodopa 53-61 growth hormone 1 Homo sapiens 16-18 7217982-8 1981 It is suggested that the paradoxical GH response to levodopa in acromegaly can be explained by a dual action of dopamine at hypothalamic and pituitary levels. Levodopa 52-60 growth hormone 1 Homo sapiens 37-39 6787839-9 1981 It is concluded that in subjects with sellar changes and intrasellar cisternal herniation ("empty sella"), and with moderate increases in PRL, the responses to TRH and L-dopa and to bromocriptine may help to differentiate between the empty sella syndrome and a coexisting pituitary tumour. Levodopa 168-174 prolactin Homo sapiens 138-141 6799381-9 1981 The inhibition of basal hTSH secretion and th hTSH response to TRH by L-dopa, suggest that the blocking action of dopamine is exerted at the hypothalamic as well as at the pituitary level. Levodopa 70-76 thyrotropin releasing hormone Homo sapiens 63-66 6799381-0 1981 Dissociation of thyrotropin and prolactin responsiveness to thyrotropin releasing hormone stimulation in L-dopa treated parkinsonian patients. Levodopa 105-111 thyrotropin releasing hormone Homo sapiens 60-89 7288433-0 1981 Lack of an effect of melatonin on the basal and L-dopa stimulated growth hormone secretion in men. Levodopa 48-54 growth hormone 1 Homo sapiens 66-80 6799381-4 1981 In the L-dopa-carbidopa treated patients basal hTSH levels and the hTSH response to TRH were significantly suppressed. Levodopa 7-13 thyrotropin releasing hormone Homo sapiens 84-87 7217816-0 1981 L-dopa stimulation at growth hormone release in normal subjects and in patients with Sheehan"s syndrome. Levodopa 0-6 growth hormone 1 Homo sapiens 22-36 6971297-6 1980 An advantage of this method is that one can incubate the enzyme for longer time (up to 150 min), as compared with AADC assay using L-DOPA as substrate, resulting in a very high sensitivity. Levodopa 131-137 dopa decarboxylase Homo sapiens 114-118 7264625-6 1981 During chronic L-Dopa + carbidopa therapy, the basal PRL levels, evaluated in 21 PP, showed a correlation with the severity of clinical features. Levodopa 15-21 prolactin Homo sapiens 53-56 6793694-5 1981 Potentiation of L-dopa-induced GH release by L-deprenyl indicates an increased availability of dopamine at the receptor level without a direct agonistic effect by the drug. Levodopa 16-22 growth hormone 1 Homo sapiens 31-33 7226570-1 1980 It has been reported that administration of nomifensine (Nom) or of L-dopa + carbidopa (L-dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. Levodopa 68-74 syntaxin 8 Homo sapiens 97-101 7004716-4 1980 Pre-administration of L-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. Levodopa 22-28 renin Rattus norvegicus 65-70 7004716-4 1980 Pre-administration of L-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. Levodopa 22-28 renin Rattus norvegicus 169-174 7226570-1 1980 It has been reported that administration of nomifensine (Nom) or of L-dopa + carbidopa (L-dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. Levodopa 68-74 prolactin Homo sapiens 177-180 7226570-1 1980 It has been reported that administration of nomifensine (Nom) or of L-dopa + carbidopa (L-dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. Levodopa 88-94 prolactin Homo sapiens 177-180 7226570-6 1980 PRL levels decreased in the normal controls below the basal values by 61.3% +/- 6.2 (SEM) after Nom and 77.6% +/- 4.2 after L-dopa + Carb. Levodopa 124-130 prolactin Homo sapiens 0-3 7226570-7 1980 Decreases in serum PRL of at least 50% (in three consecutive determinations) were found in group A in 20% of patients after Nom and in 25% after L-dopa + Carb; in group B in 15% and 40% of cases; in most of the hyperprolactinaemic women in group C; and some in group D. In conclusion, these two treatments did not discriminate between tumorous and non-tumorous cases of PRL hypersecretion. Levodopa 145-151 prolactin Homo sapiens 19-22 7341636-0 1980 The influence of benserazide on changes in monoamine oxidase activity in some rat tissues following treatment with L-DOPA. Levodopa 115-121 monoamine oxidase A Rattus norvegicus 43-60 7341636-8 1980 The significant increases in MAO specific activity seen in heart and kidney following L-DOPA treatment could be reduced or prevented by benserazide. Levodopa 86-92 monoamine oxidase A Rattus norvegicus 29-32 7419666-1 1980 The secretion of calcitonin (CT) by thyroid C cells has been reported to be reduced by dopamine in vitro and by L-dopa in patients with medullary thyroid carcinoma (MTC). Levodopa 112-118 calcitonin related polypeptide alpha Homo sapiens 17-27 7341636-14 1980 It is concluded that L-DOPA increases the specific activity of MAO-A in rat heart and kidney as a result of its decarboxylation. Levodopa 21-27 monoamine oxidase A Rattus norvegicus 63-68 6781216-3 1980 The pituitary release mechanism for growth hormone was evaluated using the propanolol/L-dopa stimulation test. Levodopa 86-92 growth hormone 1 Homo sapiens 36-50 6777462-1 1980 Levodopa with carbidopa suppressed prolactin release induced by thyrotrophin releasing hormone less effectively in patients with idiopathic Parkinson"s disease than in normal subjects. Levodopa 0-8 prolactin Homo sapiens 35-44 7419666-0 1980 Effects of L-dopa and bromocriptine on calcitonin secretion in medullary thyroid carcinoma. Levodopa 11-17 calcitonin related polypeptide alpha Homo sapiens 39-49 7419666-1 1980 The secretion of calcitonin (CT) by thyroid C cells has been reported to be reduced by dopamine in vitro and by L-dopa in patients with medullary thyroid carcinoma (MTC). Levodopa 112-118 calcitonin related polypeptide alpha Homo sapiens 29-31 7419666-11 1980 These results show L-dopa suppression of CT secretion only in a minority of patients with MTC; the lack of response to bromocriptine suggessts that dopamine receptor stimulation by dopaminergic ergots does not inhibit CT secretion in this same group of patients. Levodopa 19-25 calcitonin related polypeptide alpha Homo sapiens 41-43 7371936-0 1980 Influence of exogenous L-3,4,-dihydroxyphenylalanine (L-dopa) on the methionine and s-adenosylmethionine concentrations in the brain and other tissues [proceedings]. Levodopa 54-60 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 23-52 7407592-1 1980 In rats with unilateral nigrostriatal lesions, L-DOPA-induced dopamine increases in ipsilateral striata were further enhanced after inhibition of DOPA decarboxylase in cerebral microvessels by carbidopa. Levodopa 47-53 dopa decarboxylase Rattus norvegicus 146-164 6769344-2 1980 A three-compartment explanatory model was used to derive fractional rate constants for the forward flux of L-dopa into the endothelium of the brain capillaries from the blood (1.54 +/- 0.37 min-1), the back flux of dopa and/or its metabolites to the blood from the endothelium (0.67 +/- 0.05 min-1), the formation of dopamine from dopa (0.20 +/- 0.04 min-1), and the destruction of dopamine (0.04 +/- 0.02 min-1). Levodopa 107-113 CD59 molecule (CD59 blood group) Homo sapiens 190-195 6769344-2 1980 A three-compartment explanatory model was used to derive fractional rate constants for the forward flux of L-dopa into the endothelium of the brain capillaries from the blood (1.54 +/- 0.37 min-1), the back flux of dopa and/or its metabolites to the blood from the endothelium (0.67 +/- 0.05 min-1), the formation of dopamine from dopa (0.20 +/- 0.04 min-1), and the destruction of dopamine (0.04 +/- 0.02 min-1). Levodopa 107-113 CD59 molecule (CD59 blood group) Homo sapiens 292-297 6769344-2 1980 A three-compartment explanatory model was used to derive fractional rate constants for the forward flux of L-dopa into the endothelium of the brain capillaries from the blood (1.54 +/- 0.37 min-1), the back flux of dopa and/or its metabolites to the blood from the endothelium (0.67 +/- 0.05 min-1), the formation of dopamine from dopa (0.20 +/- 0.04 min-1), and the destruction of dopamine (0.04 +/- 0.02 min-1). Levodopa 107-113 CD59 molecule (CD59 blood group) Homo sapiens 292-297 6769344-2 1980 A three-compartment explanatory model was used to derive fractional rate constants for the forward flux of L-dopa into the endothelium of the brain capillaries from the blood (1.54 +/- 0.37 min-1), the back flux of dopa and/or its metabolites to the blood from the endothelium (0.67 +/- 0.05 min-1), the formation of dopamine from dopa (0.20 +/- 0.04 min-1), and the destruction of dopamine (0.04 +/- 0.02 min-1). Levodopa 107-113 CD59 molecule (CD59 blood group) Homo sapiens 292-297 7398195-0 1980 Catechol-O-methyltransferase activity: a determinant of levodopa response. Levodopa 56-64 catechol-O-methyltransferase Homo sapiens 0-28 7398195-1 1980 In 14 patients with Parkinson"s disease on long-term therapy the erythrocyte catechol-O-methyltransferase activity was found to correlate with the average plasma concentration ratio of 3-O-methyldopa to levodopa and with the fasting plasma concentration ratio of 3-O methyldopa to levodopa. Levodopa 203-211 catechol-O-methyltransferase Homo sapiens 77-105 7398195-1 1980 In 14 patients with Parkinson"s disease on long-term therapy the erythrocyte catechol-O-methyltransferase activity was found to correlate with the average plasma concentration ratio of 3-O-methyldopa to levodopa and with the fasting plasma concentration ratio of 3-O methyldopa to levodopa. Levodopa 281-289 catechol-O-methyltransferase Homo sapiens 77-105 7398195-2 1980 Patients with the higher erythrocyte catechol-O-methyltransferase activities were those with less favorable clinical responses to levodopa. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 37-65 7398195-3 1980 Since erythrocyte catechol-O-methyltransferase activity may reflect the activity of that enzyme in the major metabolizing tissues, catechol-O-methyltransferase activity would seem to be a significant determinant of response to levodopa. Levodopa 227-235 catechol-O-methyltransferase Homo sapiens 131-159 7357832-4 1980 Whereas L-dopa elicited a growth hormone response of similar magnitude in both groups, clonidine infusion induced a significant increase in serum growth hormone in normotensive, but not in hypertensive, subjects. Levodopa 8-14 growth hormone 1 Homo sapiens 26-40 7357832-6 1980 Prolactin levels were equally suppressed by L-dopa and did not change after clonidine in either group. Levodopa 44-50 prolactin Homo sapiens 0-9 6933996-5 1980 However, the two drugs known to decrease prolactin secretion (DOPA, CB 154) also caused some feminization. Levodopa 62-66 prolactin Rattus norvegicus 41-50 6933973-7 1980 Daily administration of 300 micrograms L-dopa led to a slight but insignificant increase of serum prolactin. Levodopa 39-45 prolactin Rattus norvegicus 98-107 520175-1 1979 The effect of simultaneous administration of 250 mg L-dopa + 25 mg L-carbidopa (Nacom) and 1 mg propranolol/kg body weight (maximal dose 40 mg propranolol) on growth-hormone secretion was tested in 96 children with growth retardation. Levodopa 52-58 growth hormone 1 Homo sapiens 159-173 7379312-1 1980 The effect of dopamine on vasopressin release was studied by the infusion of L-Dopa, a dopamine precursor that crosses the blood-brain barrier. Levodopa 77-83 arginine vasopressin Homo sapiens 26-37 7379312-2 1980 L-Dopa suppressed resting levels of vasopressin and inhibited the rise of vasopressin produced by head-up tilt. Levodopa 0-6 arginine vasopressin Homo sapiens 36-47 7379312-2 1980 L-Dopa suppressed resting levels of vasopressin and inhibited the rise of vasopressin produced by head-up tilt. Levodopa 0-6 arginine vasopressin Homo sapiens 74-85 7216342-0 1980 Stimulatory effect of levodopa and propranolol upon plasma growth hormone release in children and adolescents. Levodopa 22-30 growth hormone 1 Homo sapiens 59-73 6767993-5 1980 L-Dopa blocked the increase produced by TRH, but this effect could be reversed by pretreatment with carbidopa, an inhibitor of the conversion of L-dopa to catecholamines outside the blood-brain barrier. Levodopa 0-6 TRH Canis lupus familiaris 40-43 6767993-5 1980 L-Dopa blocked the increase produced by TRH, but this effect could be reversed by pretreatment with carbidopa, an inhibitor of the conversion of L-dopa to catecholamines outside the blood-brain barrier. Levodopa 145-151 TRH Canis lupus familiaris 40-43 6767993-11 1980 L-Dopa appears to act at a site outside the blood-brain barrier to prevent the prolactin response to TRH. Levodopa 0-6 TRH Canis lupus familiaris 101-104 7190718-0 1980 Potentiation of L-DOPA induced motor activity by an inhibitor of phenylethanolamine-N-methyltransferase. Levodopa 16-22 phenylethanolamine N-methyltransferase Homo sapiens 65-103 520175-0 1979 [Improvement of growth-hormone stimulation with l-dopa/l-carbidopa by simultaneous administration of propranolol (author"s transl)]. Levodopa 48-54 growth hormone 1 Homo sapiens 16-30 520175-5 1979 Some of the children who previously had failed to have a satisfactory rise in growth-hormone level after L-dopa and L-carbidopa showed satisfactory stimulation when propranolol was added. Levodopa 105-111 growth hormone 1 Homo sapiens 78-92 44547-3 1979 Cerebral PLP concentrations were reduced after some of these treatments, notably injection of ethanol, or L-dopa alone or with beta-phenylisopropylhydrazine, an inhibitor of MAO, or of 5-HTP together with N-[beta-(chlorophenoxy)ethyl]cyclopropylamine hydrochloride, Lilly 51641, another MAO inhibitor. Levodopa 106-112 monoamine oxidase A Rattus norvegicus 174-177 394552-2 1979 Serum levels of prolactin (PRL) were elevated pre-operatively and decreased after administration of L-Dopa with no increase after TRH as is usually observed in PRL-secreting adenomas. Levodopa 100-106 prolactin Homo sapiens 16-25 43786-2 1979 The serum prolactin response to cimetidine was abolished by dopamine infusion and almost completely suppressed by L-dopa plus carbidopa administration. Levodopa 114-120 prolactin Homo sapiens 10-19 119594-5 1979 In five out of six cirrhotic patients oral administration of L-Dopa was followed by the usual rise in plasma GH. Levodopa 61-67 growth hormone 1 Homo sapiens 109-111 44325-7 1979 MAO inhibitor resulted in a vast accumulation of L-dopa: e.g. (1) L-5HTP was more slowly eliminated, and (2) 5-HT blockers produced a decreased content of 5-HT after injection of L-5HTP, in contrast to the finding that DA-blockers produced an incresed content of DA after injection of L-dopa. Levodopa 49-55 monoamine oxidase A Rattus norvegicus 0-3 44325-7 1979 MAO inhibitor resulted in a vast accumulation of L-dopa: e.g. (1) L-5HTP was more slowly eliminated, and (2) 5-HT blockers produced a decreased content of 5-HT after injection of L-5HTP, in contrast to the finding that DA-blockers produced an incresed content of DA after injection of L-dopa. Levodopa 285-291 monoamine oxidase A Rattus norvegicus 0-3 119396-2 1979 L-Dopa, but not atropine pre-treatment, attenuated the prolactin (PRL) response to MET. Levodopa 0-6 prolactin Homo sapiens 55-64 44547-3 1979 Cerebral PLP concentrations were reduced after some of these treatments, notably injection of ethanol, or L-dopa alone or with beta-phenylisopropylhydrazine, an inhibitor of MAO, or of 5-HTP together with N-[beta-(chlorophenoxy)ethyl]cyclopropylamine hydrochloride, Lilly 51641, another MAO inhibitor. Levodopa 106-112 monoamine oxidase A Rattus norvegicus 287-290 231242-1 1979 In vitro phosphorylation of synaptosomal membrane preparation from rat striata was stimulated by addition of 5 microM cAMP, Administration of L-DOPA to rats treated previously with an L-amino acid decarboxylase inhibitor, or administration of bromocriptine resulted in a marked decrease in the in vitro phosphorylation presumably by increasing endogenous cAMP levels and thereby stimulating endogenous protein phosphorylation. Levodopa 142-148 cathelicidin antimicrobial peptide Rattus norvegicus 118-122 489713-4 1979 When pooling the results of the PRL-secreting adenomas, the mean levels of PRL with dopamine, L-dopa, and bromocriptine were, respectively, 49%, 55%, and 60% of the control levels. Levodopa 94-100 prolactin Homo sapiens 75-78 499111-0 1979 [Effect of long-term fasting on the blood serum insulin and growth hormone levels after loading tests with glucose, levodopa and exertion in obese patients with mormal and abnormal carbohydrate tolerance]. Levodopa 116-124 growth hormone 1 Homo sapiens 60-74 93948-0 1979 Modulation of tyrosinase activity and viral information by 5-iodo-deoxyuridine and L-dopa in a human melanoma cell line [proceedings]. Levodopa 83-89 tyrosinase Homo sapiens 14-24 485891-0 1979 Administration of human somatotropin in levodopa-treated patients with Parkinsonism. Levodopa 40-48 growth hormone 1 Homo sapiens 24-36 113092-3 1979 The electrophoretic patterns of serum tyrosinase, resolved by electrophoresis of a serum tyrosinase fraction followed by incubation of the gel sample with L-dopa, and represented as sets of RF"s of melanin bands, were characteristically different in melanoma, breast carcinoma, and certain other diseases. Levodopa 155-161 tyrosinase Homo sapiens 38-48 480187-0 1979 Role of peripheral adrenoreceptors and vasopressin in the suppression of plasma renin activity by L-dopa in carbidopa-treated dogs. Levodopa 98-104 renin Canis lupus familiaris 80-85 112817-2 1979 It was found that in patients with pituitary adenoma the basal prolactin (PRL) level often exceeded 150 micrograms/l and the response to stimulation with TRH and/or metoclopramide was markedly diminished or even nonexistent, while the response to L-DOPA was usually retained. Levodopa 247-253 prolactin Homo sapiens 63-72 112817-2 1979 It was found that in patients with pituitary adenoma the basal prolactin (PRL) level often exceeded 150 micrograms/l and the response to stimulation with TRH and/or metoclopramide was markedly diminished or even nonexistent, while the response to L-DOPA was usually retained. Levodopa 247-253 prolactin Homo sapiens 74-77 112817-2 1979 It was found that in patients with pituitary adenoma the basal prolactin (PRL) level often exceeded 150 micrograms/l and the response to stimulation with TRH and/or metoclopramide was markedly diminished or even nonexistent, while the response to L-DOPA was usually retained. Levodopa 247-253 thyrotropin releasing hormone Homo sapiens 154-157 114228-2 1979 Tyrosinase activity decreases as the reaction proceeds and is inhibited by L-3,4-dihydroxyphenylalanine oxidation products. Levodopa 75-103 tyrosinase Bos taurus 0-10 520077-1 1979 A comparison between insulin-induced hypoglycaemia and levodopa as stimuli for growth hormone secretion in patients with hypothalamic-pituitary insufficiency and in normal subjects. Levodopa 55-63 growth hormone 1 Homo sapiens 79-93 480187-1 1979 When extracerebral dopa decarboxylase is inhibited by carbidopa, L-dopa lowers plasma renin activity (PRA). Levodopa 65-71 dopa decarboxylase Canis lupus familiaris 19-37 480187-1 1979 When extracerebral dopa decarboxylase is inhibited by carbidopa, L-dopa lowers plasma renin activity (PRA). Levodopa 65-71 renin Canis lupus familiaris 86-91 112817-0 1979 The effect of metoclopramide, TRH and L-dopa on prolactin secretion in pituitary adenoma and in "functional" galactorrhoea syndrome. Levodopa 38-44 prolactin Homo sapiens 48-57 498643-1 1979 Internal fixation with plate and screws was combined with administration of L-Dopa, which presumably operates by stimulating release of growth hormone. Levodopa 76-82 somatotropin Canis lupus familiaris 136-150 490401-0 1979 Effect of L-dopa on vasopressin secretion in man [proceedings]. Levodopa 10-16 arginine vasopressin Homo sapiens 20-31 480794-0 1979 [Stimulation of growth hormone (STH) in the outpatient clinic using L-Dopa plus carbidopa and physical loading]. Levodopa 68-74 growth hormone 1 Homo sapiens 16-30 480794-0 1979 [Stimulation of growth hormone (STH) in the outpatient clinic using L-Dopa plus carbidopa and physical loading]. Levodopa 68-74 saitohin Homo sapiens 32-35 86882-6 1979 Prolactin response to the acute oral administration of L-dopa and bromocriptine was of less diagnostic value. Levodopa 55-61 prolactin Homo sapiens 0-9 451694-0 1979 Combined oral L-dopa and propranolol for growth hormone provocation. Levodopa 14-20 growth hormone 1 Homo sapiens 41-55 222787-3 1979 Light and electron microscope cytochemistry with the L-dopa reaction indicated that the two cell lines differ in their ability to transfer Golgi-associated tyrosinase to developing premelanosomes. Levodopa 53-59 tyrosinase Mus musculus 156-166 110148-3 1979 Prolactin levels responded to thyrotropin releasing hormone and L-dopa administration, but not chlorpromazine. Levodopa 64-70 prolactin Homo sapiens 0-9 536826-11 1979 Both L-DOPA and apomorphine are known to stimulate GH production through hypothalamic-pituitary pathways. Levodopa 5-11 growth hormone Mus musculus 51-53 428424-2 1979 L-dopa increased brain and liver putrescine levels in a dose-dependent manner that reached its maximum effect in 4-6 h. The increase in liver putrescine was associated with a concomitant increase in ornithine decarboxylase activity. Levodopa 0-6 ornithine decarboxylase 1 Rattus norvegicus 199-222 225167-4 1979 Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. Levodopa 41-49 prolactin Homo sapiens 22-31 225167-4 1979 Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. Levodopa 51-57 prolactin Homo sapiens 22-31 528597-9 1979 of the administered L-DOPA was excreted as DM-O-sulfates. Levodopa 20-26 DMRT like family A1 Homo sapiens 43-47 467382-0 1979 [Growth hormone secretion after oral administration of L-dopa in primary hypothyroidism]. Levodopa 55-61 growth hormone 1 Homo sapiens 1-15 447211-0 1979 Cimetidine and L-dopa in the control of prolactin secretion in man. Levodopa 15-21 prolactin Homo sapiens 40-49 162179-3 1979 Data on prolactin and growth hormone response to levodopa in bipolar and unipolar illness presented. Levodopa 49-57 growth hormone 1 Homo sapiens 22-36 571063-1 1979 In 19 patients with Parkinson disease, we studied the relationship of the therapeutic effect of levodopa, or dyskinesia, to the plasma content of DOPA and growth hormone (GH). Levodopa 96-104 growth hormone 1 Homo sapiens 155-169 571063-1 1979 In 19 patients with Parkinson disease, we studied the relationship of the therapeutic effect of levodopa, or dyskinesia, to the plasma content of DOPA and growth hormone (GH). Levodopa 96-104 growth hormone 1 Homo sapiens 171-173 440533-0 1979 The effect of L-3,4-dihydroxyphenylalanine (L-dopa) on the prolactin response to sexual behavior in the male rat. Levodopa 14-42 prolactin Rattus norvegicus 59-68 581754-7 1979 We calculated the responsiveness of the plasma GH level as follows: GH responsiveness (%) = (mean plasma GH level after the administration of CB-154 or L-DOPA)/ (basal GH level) x 100. Levodopa 152-158 growth hormone 1 Homo sapiens 47-49 517160-0 1979 Secretion of growth hormone after L-dopa stimulation in patients with renal failure treated with dialyses. Levodopa 34-40 growth hormone 1 Homo sapiens 13-27 114343-4 1979 On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. Levodopa 105-111 prolactin Homo sapiens 65-68 114343-4 1979 On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. Levodopa 105-111 prolactin Homo sapiens 145-148 114343-4 1979 On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. Levodopa 105-111 prolactin Homo sapiens 145-148 114343-4 1979 On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. Levodopa 105-111 prolactin Homo sapiens 145-148 114343-5 1979 The ratio between the fall in PRL concentrations (as percent of the baseline) after L-Dopa administration (delta%L) versus the PRL decrement after bromocriptine treatment (delta%B) was calculated. Levodopa 84-90 prolactin Homo sapiens 30-33 104513-5 1979 However, administration of L-DOPA resulted in a similar suppression of serum PRL in the SHR and in the normotensive controls. Levodopa 27-33 prolactin Rattus norvegicus 77-80 104513-7 1979 Observations of elevated basal PRL, exaggerated PRL in response to L-DOPA in SHR are consistent with normal pituitary responsiveness to dopamine suppression of PRL release, but defective hypothalamic metabolism of dopamine. Levodopa 67-73 prolactin Rattus norvegicus 48-51 104513-7 1979 Observations of elevated basal PRL, exaggerated PRL in response to L-DOPA in SHR are consistent with normal pituitary responsiveness to dopamine suppression of PRL release, but defective hypothalamic metabolism of dopamine. Levodopa 67-73 prolactin Rattus norvegicus 48-51 288372-3 1979 Dopaminergic agonists (apomorphine, piribedil, d-amphetamine, L-DOPA, and the ergot derivatives bromocriptine and lisuride) all caused a decrease of serum prolactin levels. Levodopa 62-68 prolactin Homo sapiens 155-164 114872-0 1979 Reduction in the level of immunotitratable dopamine beta-hydroxylase after chronic administration of L-dopa or alpha-methyldopa. Levodopa 101-107 dopamine beta-hydroxylase Homo sapiens 43-68 155781-4 1979 Oral administration of Bro (2.5 mg po) or L-dopa (500 mg), or subcutaneous administration of Apo (1.0 mg) resulted in a significantly greater and more prompt (Bro, L-dopa) increase in plasma GH in patients than in controls. Levodopa 42-48 growth hormone 1 Homo sapiens 191-193 155781-4 1979 Oral administration of Bro (2.5 mg po) or L-dopa (500 mg), or subcutaneous administration of Apo (1.0 mg) resulted in a significantly greater and more prompt (Bro, L-dopa) increase in plasma GH in patients than in controls. Levodopa 164-170 growth hormone 1 Homo sapiens 191-193 440533-0 1979 The effect of L-3,4-dihydroxyphenylalanine (L-dopa) on the prolactin response to sexual behavior in the male rat. Levodopa 44-50 prolactin Rattus norvegicus 59-68 744948-5 1978 The large AChE-positive cells are of similar size and distribution to fluorescent cells which become apparent after treatment of the mothers with L-DOPA. Levodopa 146-152 acetylcholinesterase Rattus norvegicus 10-14 440533-4 1979 Both the prolactin (Prl) response to ether and the Prl response to mating were suppressed by L-dopa. Levodopa 93-99 prolactin Rattus norvegicus 9-18 440533-4 1979 Both the prolactin (Prl) response to ether and the Prl response to mating were suppressed by L-dopa. Levodopa 93-99 prolactin Rattus norvegicus 20-23 440533-4 1979 Both the prolactin (Prl) response to ether and the Prl response to mating were suppressed by L-dopa. Levodopa 93-99 prolactin Rattus norvegicus 51-54 731719-5 1978 The mean serum GH concentration was 2.2 ng/ml, which suppressed to 0.6 ng/ml during the GTT; increased to 24 ng/ml during hypoglycemia; and increased to 10.3 ng/ml after L-dopa ingestion. Levodopa 170-176 growth hormone 1 Homo sapiens 15-17 103087-3 1978 L-DOPA and chlostylbegit were capable of reducing prolactin level in patients with the persisting lactorrhea-amenorrhea syndrome, this being accompanied by restoration of biphasic menstrual cycle in some of the patients. Levodopa 0-6 prolactin Homo sapiens 50-59 731241-0 1978 Effects of levodopa alone and in combination with dopa-decarboxylase inhibitors on plasma renin activity in patients with Parkinson"s disease. Levodopa 11-19 renin Homo sapiens 90-95 105899-0 1978 The effect of L-DOPA administration on thyrotropin (TSH) and thyrotropin releasing hormone (TRH) levels in serum in primary or pituitary hypothyroidism. Levodopa 14-20 thyrotropin releasing hormone Homo sapiens 61-90 105899-0 1978 The effect of L-DOPA administration on thyrotropin (TSH) and thyrotropin releasing hormone (TRH) levels in serum in primary or pituitary hypothyroidism. Levodopa 14-20 thyrotropin releasing hormone Homo sapiens 92-95 105899-1 1978 The effect of acute administration of L-DOPA on TSH and TRH levels in serum was studied in primary or pituitary hypothyroidism. Levodopa 38-44 thyrotropin releasing hormone Homo sapiens 56-59 105899-2 1978 TRH levels in serum fell and then returned to initial levels after L-DOPA administration in primary or pituitary hypothyroidism. Levodopa 67-73 thyrotropin releasing hormone Homo sapiens 0-3 731241-4 1978 Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release. Levodopa 249-257 renin Homo sapiens 37-42 45469-9 1978 These results suggest a dichotomy between the PRL and GH responses to combined L-dopa-carbidopa and dopamine agonist therapy. Levodopa 79-85 prolactin Homo sapiens 46-49 45469-9 1978 These results suggest a dichotomy between the PRL and GH responses to combined L-dopa-carbidopa and dopamine agonist therapy. Levodopa 79-85 gamma-glutamyl hydrolase Homo sapiens 54-56 263317-0 1978 Carbidopa inhibits the growth hormone- and prolactin-suppressive effect of L-dopa in acromegalic patients. Levodopa 75-81 growth hormone 1 Homo sapiens 23-37 709890-6 1978 Under chronic sulpiride-induced hyperprolactinaemia, levodopa exhibited however a very slight inhibitory effect on PRL concentrations. Levodopa 53-61 prolactin Homo sapiens 115-118 731241-4 1978 Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release. Levodopa 249-257 renin Homo sapiens 314-319 744101-3 1978 Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. Levodopa 77-83 prolactin Rattus norvegicus 20-23 665840-1 1978 Prolactin levels were determined in plasma samples obtained before and after administration of apomorphine or L-dopa to otherwise unmedicated chronic schizophrenic patients or control subjects. Levodopa 110-116 prolactin Homo sapiens 0-9 744101-3 1978 Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. Levodopa 77-83 vasoactive intestinal peptide Rattus norvegicus 35-38 744101-3 1978 Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. Levodopa 77-83 prolactin Rattus norvegicus 270-273 744101-3 1978 Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. Levodopa 77-83 vasoactive intestinal peptide Rattus norvegicus 286-289 233660-4 1978 The ingestion of L-dopa 2 h before parathyroid hormone infusion suppressed the PRL response, suggesting that dopamine and parathyroid hormone interact at a common site. Levodopa 17-23 prolactin Homo sapiens 79-82 233660-4 1978 The ingestion of L-dopa 2 h before parathyroid hormone infusion suppressed the PRL response, suggesting that dopamine and parathyroid hormone interact at a common site. Levodopa 17-23 parathyroid hormone Homo sapiens 122-141 640244-6 1978 The increase of plasma GH after L-dopa in both healthy persons and diabetics and the inhibition of this response by glucose in healthy subjects was reconfirmed. Levodopa 32-38 growth hormone 1 Homo sapiens 23-25 756876-0 1978 Effect of hyperglycemia on the growth hormone response to L-dopa in diabetic subjects. Levodopa 58-64 growth hormone 1 Homo sapiens 31-45 656281-0 1978 The effect of low dose carbidopa/levodopa on prolactin and growth hormone concentrations in patients with breast cancer and in benign breast tumours. Levodopa 33-41 prolactin Homo sapiens 45-54 656281-3 1978 3 Prolactin and growth hormone showed similar responses to carbidopa/levodopa irrespective of age or diagnosis. Levodopa 69-77 prolactin Homo sapiens 2-11 675856-2 1978 The prolactin inhibition by the Levodopa was verified, and the clinical and mammographic growth, the doubling time, and the labeling index of the tumor were determined. Levodopa 32-40 prolactin Homo sapiens 4-13 649984-0 1978 Enhancement of L-dopa incorporation into melanoma by dopa decarboxylase inhibition. Levodopa 15-21 dopa decarboxylase Homo sapiens 53-71 638883-4 1978 L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. Levodopa 0-24 prolactin Homo sapiens 44-53 638883-4 1978 L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. Levodopa 26-32 prolactin Homo sapiens 44-53 640244-7 1978 Furthermore, the same effect of exogenous glucose on the L-dopa induced GH release was observed in diabetics. Levodopa 57-63 growth hormone 1 Homo sapiens 72-74 626554-3 1978 In addition we demonstrated alterations in growth hormone regulation, characterized by (1) the lack of suppression of growth hormone by orally induced hyperglycemia and paradoxical increase in serum levels of growth hormone after the administration of intravenous glucose or glucagon; (2) lack of release of growth hormone with induced hypoglycemia and an exaggerated response to levodopa administration. Levodopa 380-388 growth hormone 1 Homo sapiens 43-57 659585-1 1978 The administration of l-dopa suppresses prolactin (PRL) secretion in normal subjects and in patients with hyperprolactinemia, although it is not known whether this effect, which requires the conversion of dopa to dopamine, is mediated peripherally or through the central nervous system. Levodopa 22-28 prolactin Homo sapiens 40-49 659585-1 1978 The administration of l-dopa suppresses prolactin (PRL) secretion in normal subjects and in patients with hyperprolactinemia, although it is not known whether this effect, which requires the conversion of dopa to dopamine, is mediated peripherally or through the central nervous system. Levodopa 22-28 prolactin Homo sapiens 51-54 659585-3 1978 Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+/-2 ng/ml) after l-dopa alone (48+/-4%) and after l-dopa plus carbidopa (58+/-6%). Levodopa 106-112 prolactin Homo sapiens 19-22 659585-3 1978 Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+/-2 ng/ml) after l-dopa alone (48+/-4%) and after l-dopa plus carbidopa (58+/-6%). Levodopa 139-145 prolactin Homo sapiens 19-22 659585-4 1978 In patients with pituitary tumors and elevated plasma PRL (73+/-14 ng/ml), l-dopa alone led to PRL suppression comparable with that in normal subjects (47+/-6%). Levodopa 75-81 prolactin Homo sapiens 54-57 659585-4 1978 In patients with pituitary tumors and elevated plasma PRL (73+/-14 ng/ml), l-dopa alone led to PRL suppression comparable with that in normal subjects (47+/-6%). Levodopa 75-81 prolactin Homo sapiens 95-98 659585-5 1978 However, l-dopa plus carbidopa resulted in only minimal suppression of plasma PRL (19+/-4%) which was significantly less than after l-dopa alone (P < 0.001). Levodopa 9-15 prolactin Homo sapiens 78-81 566402-0 1978 [Changes induced with L-dopa in the serum levels of prolactin and somatotropin in the diagnosis of amenorrhea-galactorrhea]. Levodopa 22-28 prolactin Homo sapiens 52-61 566402-0 1978 [Changes induced with L-dopa in the serum levels of prolactin and somatotropin in the diagnosis of amenorrhea-galactorrhea]. Levodopa 22-28 growth hormone 1 Homo sapiens 66-78 628352-0 1978 Growth hormone response to propranolol and L--dopa in obese subjects. Levodopa 43-50 growth hormone 1 Homo sapiens 0-14 628352-1 1978 Oral administration of propranolol and L-dopa produced a marked increase in plasma growth hormone values in 12 obese subjects who had failed to respond to L-dopa alone. Levodopa 39-45 growth hormone 1 Homo sapiens 83-97 628352-1 1978 Oral administration of propranolol and L-dopa produced a marked increase in plasma growth hormone values in 12 obese subjects who had failed to respond to L-dopa alone. Levodopa 155-161 growth hormone 1 Homo sapiens 83-97 749825-0 1978 Impaired responses of growth hormone and blood eosinophils to L-dopa in atopy [proceedings]. Levodopa 62-68 growth hormone 1 Homo sapiens 22-36 23087-2 1978 Plasma prolactin increments to single doses of chlorpromazine, and prolactin decrements to single doses of levodopa, were similar in normal and schizophrenic subjects. Levodopa 107-115 prolactin Homo sapiens 67-76 745015-5 1978 Of those tried Deprenyl, an MAO-B inhibitor, given with levodopa and carbidopa has shown the most promise. Levodopa 56-64 monoamine oxidase B Homo sapiens 28-33 37848-2 1978 In 12 parkinsonian patients aged from 40--76 years the L-dopa-potentiating effect of MIF was investigated using a doubleblind crossover design. Levodopa 55-61 macrophage migration inhibitory factor Homo sapiens 85-88 614217-0 1977 Effect of L-dopa on Centchroman induced prolactin levels in female rats. Levodopa 10-16 prolactin Rattus norvegicus 40-49 339647-0 1977 Impaired responses of growth hormone and blood eosinophils to L-dopa in atopy. Levodopa 62-68 growth hormone 1 Homo sapiens 22-36 339647-4 1977 The mean rise in GH 30 and 60 min after L-dopa was significantly lower in atopic patients as compared with controls. Levodopa 40-46 growth hormone 1 Homo sapiens 17-19 104005-0 1978 Dream phenomena induced by chronic levodopa therapy. Levodopa 35-43 potassium voltage-gated channel interacting protein 3 Homo sapiens 0-5 104005-1 1978 Twenty-seven of eighty-eight (30.7%) Parkinsonian patients on chronic levodopa or levodopa/carbidopa therapy developed drug related dream phenomena. Levodopa 70-78 potassium voltage-gated channel interacting protein 3 Homo sapiens 132-137 104005-1 1978 Twenty-seven of eighty-eight (30.7%) Parkinsonian patients on chronic levodopa or levodopa/carbidopa therapy developed drug related dream phenomena. Levodopa 82-90 potassium voltage-gated channel interacting protein 3 Homo sapiens 132-137 704657-0 1978 On the mechanism of hyperglycemia and stimulation of growth hormone secretion by L-dopa. Levodopa 81-87 somatotropin Canis lupus familiaris 53-67 704657-7 1978 L-Dopa also increased plasma growth hormone levels without affecting plasma cortisol. Levodopa 0-6 somatotropin Canis lupus familiaris 29-43 704657-9 1978 The data suggest that the L-dopa-induced hyperglycemia is due to a peripheral action, whereas stimulation of growth hormone secretion may be due to a central action of a L-dopa metabolite. Levodopa 170-176 somatotropin Canis lupus familiaris 109-123 598566-0 1977 Inhibition of L-dopa induced growth hormone release in normal and diabetic subjects by glucose administration. Levodopa 14-20 growth hormone 1 Homo sapiens 29-43 598566-1 1977 Administration of L-dopa 1 g induced an increase of plasma growth hormone (GH) levels in seven of ten healthy volunteers and in six of ten hyperglycemic insulin-dependent diabetic subjects; the maximal GH response was higher in normal subjects. Levodopa 18-24 growth hormone 1 Homo sapiens 59-73 598566-1 1977 Administration of L-dopa 1 g induced an increase of plasma growth hormone (GH) levels in seven of ten healthy volunteers and in six of ten hyperglycemic insulin-dependent diabetic subjects; the maximal GH response was higher in normal subjects. Levodopa 18-24 growth hormone 1 Homo sapiens 75-77 598566-1 1977 Administration of L-dopa 1 g induced an increase of plasma growth hormone (GH) levels in seven of ten healthy volunteers and in six of ten hyperglycemic insulin-dependent diabetic subjects; the maximal GH response was higher in normal subjects. Levodopa 18-24 growth hormone 1 Homo sapiens 202-204 591612-1 1977 In 6 normal subjects, L-dopa (500 mg PO) and apomorphine (0.6 mg sc) increased circulating growth hormone and suppressed prolactin levels in a parallel and quantitatively similar fashion, but only L-dopa induced a rise in plasma glucagon, glucose, and insulin levels. Levodopa 22-28 growth hormone 1 Homo sapiens 91-105 591612-1 1977 In 6 normal subjects, L-dopa (500 mg PO) and apomorphine (0.6 mg sc) increased circulating growth hormone and suppressed prolactin levels in a parallel and quantitatively similar fashion, but only L-dopa induced a rise in plasma glucagon, glucose, and insulin levels. Levodopa 22-28 prolactin Homo sapiens 121-130 591612-1 1977 In 6 normal subjects, L-dopa (500 mg PO) and apomorphine (0.6 mg sc) increased circulating growth hormone and suppressed prolactin levels in a parallel and quantitatively similar fashion, but only L-dopa induced a rise in plasma glucagon, glucose, and insulin levels. Levodopa 22-28 insulin Homo sapiens 252-259 413140-7 1977 was probably due to stimulation of both dopamine and noradrenaline receptors since the dopamine-beta-hydroxylase inhibitor FLA-63 partly reduced the effect of L-Dopa. Levodopa 159-165 dopamine beta hydroxylase Mus musculus 87-112 598566-2 1977 Addition of 100 g glucose orally to the L-dopa completely abolished the GH response of both groups. Levodopa 40-46 growth hormone 1 Homo sapiens 72-74 598566-3 1977 The difference between the effect of endogenous hyperglycemia and the effect of a sudden increase of blood sugar after glucose administration on L-dopa induced GH release in diabetic subjects may be explain by the resetting of the hypothalamic control for pituitary GH release to higher levels of blood glucose. Levodopa 145-151 growth hormone 1 Homo sapiens 160-162 598566-3 1977 The difference between the effect of endogenous hyperglycemia and the effect of a sudden increase of blood sugar after glucose administration on L-dopa induced GH release in diabetic subjects may be explain by the resetting of the hypothalamic control for pituitary GH release to higher levels of blood glucose. Levodopa 145-151 growth hormone 1 Homo sapiens 266-268 413140-7 1977 was probably due to stimulation of both dopamine and noradrenaline receptors since the dopamine-beta-hydroxylase inhibitor FLA-63 partly reduced the effect of L-Dopa. Levodopa 159-165 4-hydroxyphenylpyruvic acid dioxygenase Mus musculus 123-126 910982-3 1977 In another group of subjects with depression, the stimulation of growth hormone secretion by L-dopa was unaffected by amitriptyline therapy. Levodopa 93-99 growth hormone 1 Homo sapiens 65-79 914981-3 1977 Melatonin appeared to depress the level of luteinizing hormone (LH) in serum and may have inhibited in some patients the release of growth hormone from the pituitary gland after stimulation by stress or L-dopa. Levodopa 203-209 growth hormone 1 Homo sapiens 132-146 562902-2 1977 Basal serum prolactin levels were raised, and were further elevated by the administration of L-dopa, chlorpromazine and TRH. Levodopa 93-99 prolactin Homo sapiens 12-21 578618-5 1977 On the contrary, metergoline, like L-dopa, inhibited PRL release induced by pimozide pre-treatment. Levodopa 35-41 prolactin Homo sapiens 53-56 409726-9 1977 There was some suppression of prolactin levels after L-dopa. Levodopa 53-59 prolactin Homo sapiens 30-39 593428-6 1977 The accumulation of methoxytyrosine from exogeneously applied L-dopa appears to be a reliable indicator of the in vivo activity of catechol-O-methyltransferase. Levodopa 62-68 catechol-O-methyltransferase Rattus norvegicus 131-159 908155-0 1977 Effect of pimozide on levodopa-induced growth hormone release in man. Levodopa 22-30 growth hormone 1 Homo sapiens 39-53 875737-2 1977 The oral administration of cyproheptadine (12 mg daily) reduced GH responses to both L-dopa and glucagon; similarly, the mean GH response to oral glucose administration was significantly reduced after cyproheptadine administration. Levodopa 85-91 growth hormone 1 Homo sapiens 64-66 560295-0 1977 L-Dopa inhibits prolactin secretion in proestrous rats. Levodopa 0-6 prolactin Rattus norvegicus 16-25 560295-2 1977 L-Dopa reduced serum prolactin concentrations within 1 h, whether administered just prior to, or during, the normal surge in serum hormone level. Levodopa 0-6 prolactin Rattus norvegicus 21-30 878846-2 1977 In patients treated with a combination of L-dopa and a peripheral decarboxylase inhibitor (PDI), those with dyskinesias have very high plasma O-methyl-dopa levels compared with those who have no dyskinesias. Levodopa 42-48 protein disulfide isomerase family A member 2 Homo sapiens 91-94 406275-6 1977 As in the case of L-Dopa, the effect of FA-Ca on serum TSH is most clearly demonstrated in patients with primary hypothyroidism. Levodopa 18-24 FA complementation group A Homo sapiens 40-45 562688-3 1977 Like levodopa, pyridoxine suppressed the increase in PRL secretion induced by treatment with pimozide, a specific dopamine receptor blocking agent. Levodopa 5-13 prolactin Homo sapiens 53-56 20170-0 1977 Dissociation of growth hormone and prolactin response to levodopa during pyridoxine administration. Levodopa 57-65 prolactin Homo sapiens 35-44 20170-1 1977 500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. Levodopa 10-18 growth hormone 1 Homo sapiens 91-105 20170-1 1977 500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. Levodopa 10-18 growth hormone 1 Homo sapiens 107-109 20170-1 1977 500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. Levodopa 10-18 prolactin Homo sapiens 129-138 20170-1 1977 500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. Levodopa 10-18 prolactin Homo sapiens 140-143 20170-2 1977 The levodopa-induced GH release was inhibited by an intravenous infusion of pyridoxine; on the contrary, the PRL response to levodopa was enhanced by pyridoxine infusion. Levodopa 4-12 growth hormone 1 Homo sapiens 21-23 20170-2 1977 The levodopa-induced GH release was inhibited by an intravenous infusion of pyridoxine; on the contrary, the PRL response to levodopa was enhanced by pyridoxine infusion. Levodopa 125-133 prolactin Homo sapiens 109-112 20170-3 1977 This dissociation of GH and PRL responses to levodopa during pyridoxine infusion appears to be mediated by peripheral acceleration of the conversion of levodopa to dopamine. Levodopa 45-53 growth hormone 1 Homo sapiens 21-23 20170-3 1977 This dissociation of GH and PRL responses to levodopa during pyridoxine infusion appears to be mediated by peripheral acceleration of the conversion of levodopa to dopamine. Levodopa 45-53 prolactin Homo sapiens 28-31 874815-0 1977 Effect of L-dopa on plasma renin activity with and without inhibition of extracerebral dopa decarboxylase in dogs. Levodopa 10-16 renin Canis lupus familiaris 27-32 874815-2 1977 Plasma renin activity (PRA) was measured after intravenous administration of L-dopa with and without prior inhibition of extracerebral dopa decarboxylase by carbidopa (MK-486) in pentobarbital-anesthetized dogs in which changes in renal perfusion pressure were minimized by means of a suprarenal aortic clamp. Levodopa 77-83 renin Canis lupus familiaris 7-12 901702-7 1977 5 Levodopa (250 mg) with (-)-alpha-methyldopa hydrazine 25 mg (Sinemet) by mouth, caused a rise in plasma growth hormone concentration in most normal subjects. Levodopa 2-10 growth hormone 1 Homo sapiens 106-120 404308-8 1977 No significant suppression of serum PRL was seen in Group 2 patients given L-Dopa (500 mg orally),, which produced a significant response (P less than 0.05) in Group 1 subjects, while all patient showed marked reduction in serum PRL values following 2-bromo-alpha-ergocryptine (CB-154, 2.5 mg orally). Levodopa 75-81 prolactin Homo sapiens 229-232 887505-2 1977 Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline. Levodopa 52-58 kininogen 1 Homo sapiens 0-10 887505-3 1977 Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline. Levodopa 99-105 kininogen 1 Homo sapiens 48-58 838854-0 1977 Transient appearance of a provocative growth hormone response to L-dopa following incomplete adenomectomy in an acromegalic patient. Levodopa 65-71 growth hormone 1 Homo sapiens 38-52 321175-0 1977 Effects of levodopa on the renin-aldosterone system. Levodopa 11-19 renin Homo sapiens 27-32 406134-6 1977 Sulpiride treatment appeared to antagonize partially the inhibitory effect of L-dopa on prolactin release. Levodopa 78-84 prolactin Homo sapiens 88-97 66455-0 1977 Growth hormone and prolactin response to levodopa in affective illness. Levodopa 41-49 prolactin Homo sapiens 19-28 900875-2 1977 The present study aimed at testing the hypothesis that l-dopa could obtain a better growth hormone (G.H.) Levodopa 55-61 growth hormone 1 Homo sapiens 84-98 831826-5 1977 Methylation of both tRNA and histone by liver enzyme was inhibited by L-dopa, dopamine and epinephrine. Levodopa 70-76 Trng Rattus norvegicus 20-24 404727-0 1977 Abnormal growth hormone responses to L-dopa and thyrotropin-releasing hormone in patients with acromegaly. Levodopa 37-43 growth hormone 1 Homo sapiens 9-23 404727-1 1977 Changes in growth hormone (gh) release in response to L-dopa, TRH, arginine and LH-RH were studied in 15 patients with acromegaly to investigate the mechanism of so-called "paradoxical decrease" of GH secretion often observed in acromegalics after the administration of L-dopa. Levodopa 54-60 growth hormone 1 Homo sapiens 11-25 404727-1 1977 Changes in growth hormone (gh) release in response to L-dopa, TRH, arginine and LH-RH were studied in 15 patients with acromegaly to investigate the mechanism of so-called "paradoxical decrease" of GH secretion often observed in acromegalics after the administration of L-dopa. Levodopa 54-60 growth hormone 1 Homo sapiens 27-29 404727-11 1977 When this correlation is considered in connection with the reported effects of L-dopa on GH and thyroid stimulating hormne (TSH) in man, the following hypothesis might be proposed: L-dopa has two opposing actions on the hypothalamo-pituitary system; 1) inhibition of TRH release or suppression of GH release from TRH sensitive GH producing cells, and 2) arginine-like facilitation of GH release presumably via stimulation of GH-RF. Levodopa 181-187 growth hormone releasing hormone Homo sapiens 425-430 64868-1 1977 The patient with Parkinson" disease on chronic levodopa therapy, like the diabetic on insulin, is dependent on the drug. Levodopa 47-55 insulin Homo sapiens 86-93 320826-0 1977 Secretion of human growth hormone and insulin in levodopa test during carbamazepine therapy. Levodopa 49-57 growth hormone 1 Homo sapiens 19-33 320826-0 1977 Secretion of human growth hormone and insulin in levodopa test during carbamazepine therapy. Levodopa 49-57 insulin Homo sapiens 38-45 831826-5 1977 Methylation of both tRNA and histone by liver enzyme was inhibited by L-dopa, dopamine and epinephrine. Levodopa 70-76 H2B clustered histone 1 Rattus norvegicus 29-36 320826-2 1977 Serum growth hormone rose significantly from 1.3 +/- 0.3 ng/ml to 16.3 +/- 3.4 ng/ml in 60 minutes after levodopa administration (1000 mg orally) before carbamazepine, and almost similarly from 2.3 +/- 0.5 ng/ml to 15.1 +/- 4.0 ng/ml after carbamazepine during the test. Levodopa 105-113 growth hormone 1 Homo sapiens 6-20 835536-0 1977 Sequential use of insulin and levodopa to provoke pituitary secretion of growth hormone. Levodopa 30-38 growth hormone 1 Homo sapiens 73-87 556882-3 1977 Serum prolactin could be lowered with oral L-dopa. Levodopa 43-49 prolactin Homo sapiens 6-15 864480-0 1977 Plasma DOPA levels and growth hormone response to levodopa in parkinsomism. Levodopa 50-58 growth hormone 1 Homo sapiens 23-37 402377-3 1977 Prolactin concentrations were increased by TRH and were suppressed by L-dopa. Levodopa 70-76 prolactin Homo sapiens 0-9 864480-1 1977 It has been suggested that the therapeutic response to levodopa in patients with Parkinson"s disease may be related to changes in plasma growth hormone concentration. Levodopa 55-63 growth hormone 1 Homo sapiens 137-151 864480-3 1977 Levodopa caused an increase in plasma growth hormone concentration in 30 subjects. Levodopa 0-8 growth hormone 1 Homo sapiens 38-52 864480-5 1977 The growth hormone response to levodopa is normal in patients with Parkinson"s disease and not altered by long-term levodopa treatment. Levodopa 31-39 growth hormone 1 Homo sapiens 4-18 580044-11 1977 The mechanism underlying the tremor appears to involve dopaminergic pathways, since the action of LON-954 was antagonised by L-dopa and apomorphine and potentiated by pimozide. Levodopa 125-131 lon peptidase 1, mitochondrial Mus musculus 98-101 831384-0 1977 The effect of L-dopa with and without decarboxylase inhibitor on growth hormone secretion in children with short stature. Levodopa 14-20 growth hormone 1 Homo sapiens 65-79 600362-0 1977 Effect of the dopa decarboxylase inhibitor MK-486 on L-dopa-induced inhibition of prolactin secretion: evidence for CNS participation in the L-dopa effects. Levodopa 53-59 dopa decarboxylase Homo sapiens 14-32 833581-1 1977 Serum dopamine-beta-hydroxylase activities of a group of 16 parkinsonian patients under L-Dopa plus decarboxylase inhibitor showed a distribution with a drift towards higher activities compared to a group of normals of the same age range. Levodopa 88-94 dopamine beta-hydroxylase Homo sapiens 6-31 204879-3 1977 It was found that chronic treatment with CPZ, TR and L-dopa inhibits the response to TRH. Levodopa 53-59 thyrotropin releasing hormone Homo sapiens 85-88 833257-0 1977 L-Dopa stimulated growth hormone release in the blind. Levodopa 0-6 growth hormone 1 Homo sapiens 18-32 833257-1 1977 Following L-Dopa administration (single oral dose of 500 mg), plasma Growth hormone (GH) levels significantly rose in 7 out of 8 normal subjects (aged between 64-83) and in 4 out of 8 blind subjects (aged between 60-88). Levodopa 10-16 growth hormone 1 Homo sapiens 69-83 833257-1 1977 Following L-Dopa administration (single oral dose of 500 mg), plasma Growth hormone (GH) levels significantly rose in 7 out of 8 normal subjects (aged between 64-83) and in 4 out of 8 blind subjects (aged between 60-88). Levodopa 10-16 growth hormone 1 Homo sapiens 85-87 847319-5 1977 The authors express the view that abnormal movements while under L-Dopa treatment are dependent on two factors: one, the hypersensitivity of dopaminergic reception, the other, the greater or lesser preponderance of the COMT isozyme giving rise to 4-O-methylates; Levodopa 65-71 catechol-O-methyltransferase Homo sapiens 219-223 918143-0 1977 MAO activity in rat brain stem and cerebral cortex following acute and chronic treatment with L-dopa and ethanol + L-dopa. Levodopa 94-100 monoamine oxidase A Rattus norvegicus 0-3 918143-0 1977 MAO activity in rat brain stem and cerebral cortex following acute and chronic treatment with L-dopa and ethanol + L-dopa. Levodopa 115-121 monoamine oxidase A Rattus norvegicus 0-3 918143-1 1977 This work reports the effects of acute and chronic administration of L-dopa and ethanol + L-dopa on MAO activity in rat brain stem and cerebral cortex using noradrenaline (NA), dopamine (DA), serotonin (5-HT) and tryptamine (Try) as substrates. Levodopa 69-75 monoamine oxidase A Rattus norvegicus 100-103 896840-0 1977 Ethanol, levodopa and inhibitors of extracerebral aromatic L-amino acid decarboxylase: a drug-drug interaction study. Levodopa 9-17 dopa decarboxylase Homo sapiens 50-85 1036999-7 1976 Levodopa 2 g had a greater therapeutic effect and caused a greater rise in plasma growth hormone concentration than bromocriptine 100 mg. Levodopa caused emesis more commonly and hallucinations less commonly than bromocriptine. Levodopa 0-8 growth hormone 1 Homo sapiens 82-96 1088127-2 1976 Increases in plasma prolactin concentrations caused by 5-HTP (1 mg/100 g body wt iv) were abolished by the concomitant administration of L-DOPA (2 mg/100 g body wt iv). Levodopa 137-143 prolactin Rattus norvegicus 20-29 918143-1 1977 This work reports the effects of acute and chronic administration of L-dopa and ethanol + L-dopa on MAO activity in rat brain stem and cerebral cortex using noradrenaline (NA), dopamine (DA), serotonin (5-HT) and tryptamine (Try) as substrates. Levodopa 90-96 monoamine oxidase A Rattus norvegicus 100-103 11370235-2 1976 Intravenous administration of L-dopa produced a prompt, statistically significant increase in plasma growth hormone concentration. Levodopa 30-36 somatotropin Canis lupus familiaris 101-115 11370235-7 1976 The increase in plasma growth hormone concentration produced by intravenous L-dopa and clonidine was prevented by administration of phentolamine or phenoxybenzamine directly into the third ventricle. Levodopa 76-82 somatotropin Canis lupus familiaris 23-37 11370235-9 1976 In dogs in which central beta-adrenergic blockade was produced by intraventricular L-propranolol, the growth hormone response to L-dopa was greater than it was in control dogs treated with intraventricular D-propranolol. Levodopa 129-135 somatotropin Canis lupus familiaris 102-116 11370235-10 1976 The data indicate that in pentobarbital anesthetized dogs, the increase in growth hormone secretion produced by L-dopa is mediated by norepinephrine, rather than dopamine, that the site of action of the norepinephrine is central, above the median eminence and inside the "blood-brain barrier", and that the norepinephrine acts via alpha-adrenergic receptors. Levodopa 112-118 somatotropin Canis lupus familiaris 75-89 827396-1 1976 Thyrotrophin releasing factor (TRF) was given intravenously in doses of 0-5 mg and 20 mg to six patients with Parkinsonism treated with L-dopa. Levodopa 136-142 thyrotropin releasing hormone Homo sapiens 0-29 827396-1 1976 Thyrotrophin releasing factor (TRF) was given intravenously in doses of 0-5 mg and 20 mg to six patients with Parkinsonism treated with L-dopa. Levodopa 136-142 thyrotropin releasing hormone Homo sapiens 31-34 824407-4 1976 It was found that after levodopa administration the plasma free fatty acids, glucose, growth hormone and cortisol were significantly higher in the Parkinsonian group than in the young control group and only slightly higher than in the aged control group. Levodopa 24-32 growth hormone 1 Homo sapiens 86-100 824407-7 1976 We suggest that weight loss in the older Parkinsonian patients treated over long periods with high doses of levodopa, is due to the enhancement of the lipolytic activity of the ageing fat cells caused by high levels of circulating insulin. Levodopa 108-116 insulin Homo sapiens 231-238 1036999-7 1976 Levodopa 2 g had a greater therapeutic effect and caused a greater rise in plasma growth hormone concentration than bromocriptine 100 mg. Levodopa caused emesis more commonly and hallucinations less commonly than bromocriptine. Levodopa 138-146 growth hormone 1 Homo sapiens 82-96 1005491-9 1976 This discrepancy may be explained by high doses of L-DOPA causing inhibiton of catechol-O-methyl transferase (COMT), which is suggested by the observation that the forebrain homovanillic acid (HVA): 3,4-dihydroxyphenylacetic acid (DOPAC) ratio was significantly lower after the high dose of L-DOPA than in untreated mice. Levodopa 51-57 catechol-O-methyltransferase Mus musculus 79-108 970425-0 1976 Levodopa-stimulated growth hormone secretion and diabetic retinopathy. Levodopa 0-8 growth hormone 1 Homo sapiens 20-34 970425-3 1976 Basal and levodopa-stimulated levels of growth hormone were determined for each group. Levodopa 10-18 growth hormone 1 Homo sapiens 40-54 1024568-0 1976 [Effects of the treatment with an antiestrogen(tamoxifen) and levodopa on the secretion of prolactin in patients affected by breast cancer]. Levodopa 62-70 prolactin Homo sapiens 91-100 971016-4 1976 The only other, but most striking abnormality, was an excessively high serum prolactin level, which was partially suppressed with levodopa. Levodopa 130-138 prolactin Homo sapiens 77-86 10378-0 1976 The irritant properties of dopamine-beta-hydroxylase inhibitors in relation to their effects on L-dopa-induced locomotor activity. Levodopa 96-102 dopamine beta-hydroxylase Homo sapiens 27-52 1005491-9 1976 This discrepancy may be explained by high doses of L-DOPA causing inhibiton of catechol-O-methyl transferase (COMT), which is suggested by the observation that the forebrain homovanillic acid (HVA): 3,4-dihydroxyphenylacetic acid (DOPAC) ratio was significantly lower after the high dose of L-DOPA than in untreated mice. Levodopa 51-57 catechol-O-methyltransferase Mus musculus 110-114 826946-3 1976 L-Dopa in the presence of dopa decarboxylase inhibition (MK-486) depressed these responses and reversed the effect of reserpine at 0.5 h after administration. Levodopa 0-6 dopa decarboxylase Felis catus 26-44 1005491-9 1976 This discrepancy may be explained by high doses of L-DOPA causing inhibiton of catechol-O-methyl transferase (COMT), which is suggested by the observation that the forebrain homovanillic acid (HVA): 3,4-dihydroxyphenylacetic acid (DOPAC) ratio was significantly lower after the high dose of L-DOPA than in untreated mice. Levodopa 291-297 catechol-O-methyltransferase Mus musculus 79-108 1005491-9 1976 This discrepancy may be explained by high doses of L-DOPA causing inhibiton of catechol-O-methyl transferase (COMT), which is suggested by the observation that the forebrain homovanillic acid (HVA): 3,4-dihydroxyphenylacetic acid (DOPAC) ratio was significantly lower after the high dose of L-DOPA than in untreated mice. Levodopa 291-297 catechol-O-methyltransferase Mus musculus 110-114 1005491-11 1976 Pretreatment with dopamine-beta-hydroxylase inhibitor FLA (63(bis-(1-methyl-4-monopiperazinyl-thiocarbonyl)disulphide) prevented the increase in NA And MOPEG-SO4 formation observed following L-DOPA induced motor activity in these groups of animals suggesting the involvement of NA in the production of such behaviour. Levodopa 191-197 dopamine beta hydroxylase Mus musculus 18-43 1005491-11 1976 Pretreatment with dopamine-beta-hydroxylase inhibitor FLA (63(bis-(1-methyl-4-monopiperazinyl-thiocarbonyl)disulphide) prevented the increase in NA And MOPEG-SO4 formation observed following L-DOPA induced motor activity in these groups of animals suggesting the involvement of NA in the production of such behaviour. Levodopa 191-197 4-hydroxyphenylpyruvic acid dioxygenase Mus musculus 54-57 829393-0 1976 Growth hormone response to L-dopa in diabetes mellitus. Levodopa 27-33 growth hormone 1 Homo sapiens 0-14 961756-1 1976 The time course of simultaneous changes in prolactin (PRL) and growth hormone secretion in response to a single dose of L-dopa and chlorpromazine was determined in normal women. Levodopa 120-126 prolactin Homo sapiens 43-52 961756-1 1976 The time course of simultaneous changes in prolactin (PRL) and growth hormone secretion in response to a single dose of L-dopa and chlorpromazine was determined in normal women. Levodopa 120-126 prolactin Homo sapiens 54-57 961756-1 1976 The time course of simultaneous changes in prolactin (PRL) and growth hormone secretion in response to a single dose of L-dopa and chlorpromazine was determined in normal women. Levodopa 120-126 growth hormone 1 Homo sapiens 63-77 822750-0 1976 A sensitive new assay for the oxidation of 3,4-dihydroxy L-phenylalanine by tyrosinase. Levodopa 43-72 tyrosinase Homo sapiens 76-86 961756-2 1976 L-Dopa induced greater, but shorter (30 minutes), growth hormone release than concomitant suppression of PRL secretion. Levodopa 0-6 growth hormone 1 Homo sapiens 50-64 961756-3 1976 The PRL peak following chlorpromazine occurred at the same time as the nadir of PRL after L-dopa (3.5 hours). Levodopa 90-96 prolactin Homo sapiens 80-83 961756-4 1976 The quantity of PRL release inhibited by L-dopa equaled the amount of PRL secretion during the period of rebound, suggesting L-dopa inhibits PRL release, but not synthesis, by the pituitary. Levodopa 41-47 prolactin Homo sapiens 16-19 961756-4 1976 The quantity of PRL release inhibited by L-dopa equaled the amount of PRL secretion during the period of rebound, suggesting L-dopa inhibits PRL release, but not synthesis, by the pituitary. Levodopa 125-131 prolactin Homo sapiens 16-19 182325-5 1976 L-DOPA, given intraperitoneally, increased cyclic AMP levels in the perfusate. Levodopa 0-6 transmembrane serine protease 5 Rattus norvegicus 50-53 821963-0 1976 Suppression of prolactin secretion by L-dopa in the stalk-sectioned rhesus monkey. Levodopa 38-44 prolactin Macaca mulatta 15-24 795689-4 1976 Parenteral administration of synthetic SRIF inhibits the release of growth hormone, basal and stimulated by muscular exercise, arginine, L-DOPA, insulin-induced hypoglycemia, and sleeping. Levodopa 137-143 growth hormone 1 Homo sapiens 68-82 821744-6 1976 After L-dopa injection, fetal and neonatal plasma PRL values declined 26-62% from baseline levels. Levodopa 6-12 prolactin Macaca mulatta 50-53 821744-8 1976 When L-dopa and TRH were administered together, fetal plasma PRL levels declined 14-40% from initial levels, but maternal plasma PRL levels did not change in a consistent manner, and amniotic fluid PRL levels remained stable. Levodopa 5-11 prolactin Macaca mulatta 61-64 821744-11 1976 The direction and magnitude of changes in both maternal plasma and amniotic fluid PRL concentrations provide indirect evidence of placental transfer of TRH and L-dopa in some experiments, and require a biophysical explanation not apparent in others. Levodopa 160-166 prolactin Macaca mulatta 82-85 991841-0 1976 [Growth hormone concentration during sleep following L-dopa administration]. Levodopa 53-59 growth hormone 1 Homo sapiens 1-15 821963-4 1976 In both normal and stalk-sectioned monkeys, iv administration of L-dopa (3-120 mg) significantly inhibited prolactin release from the pituitary (P less than .005 normal; P less than .001 stalk section). Levodopa 65-71 prolactin Macaca mulatta 107-116 821963-5 1976 L-dopa also suppressed the TRH-induced release of prolactin in both groups. Levodopa 0-6 thyrotropin releasing hormone Macaca mulatta 27-30 821963-5 1976 L-dopa also suppressed the TRH-induced release of prolactin in both groups. Levodopa 0-6 prolactin Macaca mulatta 50-59 821963-6 1976 These results indicate that L-dopa or dopamine may act directly on the anterior pituitary to inhibit prolactin secretion. Levodopa 28-34 prolactin Macaca mulatta 101-110 14035-5 1976 As already reported, L-DOPA and diethyldithiocarbamate markedly decreased plasma prolactin levels in rats. Levodopa 21-27 prolactin Rattus norvegicus 81-90 996056-2 1976 After injections of l-DOPA in cats pretreated with RO 4-4602, an inhibitor of peripheral decarboxylase, or disulfiram, a dopamine-beta-hydroxylase inhibitor, the inhibitory action on the reinforcing system was enhanced. Levodopa 20-26 dopamine beta-hydroxylase Felis catus 121-146 1000028-4 1976 This data suggests that, in thyrotoxicosis, PRl response to TRH only is impaired, but PRL can be suppressed by L-dopa or released by metaclopramide notwithstanding the elevated values of thyroid hormone levels. Levodopa 111-117 prolactin Homo sapiens 86-89 7571-5 1976 Pretreatment with 500 mg of L-dopa suppressed the prolactin response to metoclopramide in 6 men to a mean response of 16.3 +/- 4.3 ng/ml. Levodopa 28-34 prolactin Homo sapiens 50-59 994683-0 1976 [Stimulation of growth hormone by L-dopa in mental anorexia]. Levodopa 34-40 growth hormone 1 Homo sapiens 16-30 983720-0 1976 Influence of bradykinin and drugs blocking alpha and beta-adrenergic receptor on the stimulating effect of nialamide and L--DOPA. Levodopa 121-128 kininogen 1 Homo sapiens 13-23 983720-2 1976 Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin. Levodopa 75-81 kininogen 1 Homo sapiens 120-130 1000028-0 1976 Plasma prolactin response to L-dopa TRH and metaclopramide in thyrotoxicosis. Levodopa 29-35 prolactin Homo sapiens 7-16 777023-4 1976 Pre-treatment with 500 mg L-dopa inhibited the early metoclopramide-induced prolactin increase, which is consistent with the possibility that metoclopramide acts by inhibiting dopamine-mediated hypothalamic secretion of prolactin inhibitory factor. Levodopa 26-32 prolactin Homo sapiens 76-85 971548-1 1976 In ten normal subjects and in twenty acromegalic patients plasma levels of growth hormone were studied after administration of L-dopa and a dopamine infusion. Levodopa 127-133 growth hormone 1 Homo sapiens 75-89 777023-4 1976 Pre-treatment with 500 mg L-dopa inhibited the early metoclopramide-induced prolactin increase, which is consistent with the possibility that metoclopramide acts by inhibiting dopamine-mediated hypothalamic secretion of prolactin inhibitory factor. Levodopa 26-32 prolactin Homo sapiens 220-229 932184-0 1976 Growth hormone refractory interval to levodopa stimulation. Levodopa 38-46 growth hormone 1 Homo sapiens 0-14 1012176-0 1976 [Test with levodopa in the evaluation of somatotropin secretion]. Levodopa 11-19 growth hormone 1 Homo sapiens 41-53 11370227-3 1976 Intravenous L-dopa inhibited ACTH secretion, and this inhibition was not modified by blockade of peripheral decarboxylation of L-dopa with carbidopa. Levodopa 12-18 proopiomelanocortin Canis lupus familiaris 29-33 1020916-5 1976 Administration of L-Dopa (500 mg orally) significantly suppressed the prolactin values in the 11 cases studied. Levodopa 18-24 prolactin Homo sapiens 70-79 183794-2 1976 When dopamine-beta-hydroxylase was inhibited by bis-(4-methyl-1-homopiperazinyl-thiocarbonyl)-disulfide (Fla 63) the levodopa induced increase of cAMP levels was less marked, it was suppressed by propranolol (10 mg/kg), a beta-adrenergic blocking agent. Levodopa 117-125 dopamine beta-hydroxylase Rattus norvegicus 5-30 1269163-0 1976 A comparison of the effect of levodopa and somatostatin on the plasma levels of growth hormone, insulin, glucagon and prolactin in acromegaly. Levodopa 30-38 growth hormone 1 Homo sapiens 80-94 1255091-0 1976 Prolactin inhibition test with L-dopa: decrease and restoration of plasma prolactin levels in the rat by a peripheral process. Levodopa 31-37 prolactin Rattus norvegicus 0-9 1255091-0 1976 Prolactin inhibition test with L-dopa: decrease and restoration of plasma prolactin levels in the rat by a peripheral process. Levodopa 31-37 prolactin Rattus norvegicus 74-83 1255091-1 1976 L-DOPA, within 30 min after administration, induced a highly significant decrease of plasma prolactin levels (phase 1) in a number of groups of rats, differing in age and/or endocrine status, apparently by direct inhibition of prolactin release from the pituitary. Levodopa 0-6 prolactin Rattus norvegicus 92-101 1255091-1 1976 L-DOPA, within 30 min after administration, induced a highly significant decrease of plasma prolactin levels (phase 1) in a number of groups of rats, differing in age and/or endocrine status, apparently by direct inhibition of prolactin release from the pituitary. Levodopa 0-6 prolactin Rattus norvegicus 227-236 1255091-2 1976 Three hours after administration of L-DOPA these low plasma prolactin concentrations in treated animals had increased (phase 2) and did not differ significantly from levels in control animals, indicating that the effect of L-DOPA on plasma prolactin levels is only of short duration. Levodopa 36-42 prolactin Rattus norvegicus 60-69 1255091-2 1976 Three hours after administration of L-DOPA these low plasma prolactin concentrations in treated animals had increased (phase 2) and did not differ significantly from levels in control animals, indicating that the effect of L-DOPA on plasma prolactin levels is only of short duration. Levodopa 223-229 prolactin Rattus norvegicus 240-249 1255091-8 1976 The results suggested another working mechanism of L-DOPA in decreasing plasma prolactin levels, namely by stimulating the uptake of this hormone in the periphery. Levodopa 51-57 prolactin Rattus norvegicus 79-88 1255091-9 1976 After the effect of L-DOPA had ceased, most of the prolactin from the periphery returned into the bloodstream, causing a rapid restoration of plasma prolactin levels without substantial release from the pituitary. Levodopa 20-26 prolactin Rattus norvegicus 51-60 1255091-9 1976 After the effect of L-DOPA had ceased, most of the prolactin from the periphery returned into the bloodstream, causing a rapid restoration of plasma prolactin levels without substantial release from the pituitary. Levodopa 20-26 prolactin Rattus norvegicus 149-158 1252146-1 1976 The flat serum growth hormone (GH) patterns of untreated parkinsonian patients develop diurnal rises during treatment with levodopa. Levodopa 123-131 growth hormone 1 Homo sapiens 15-29 1252146-1 1976 The flat serum growth hormone (GH) patterns of untreated parkinsonian patients develop diurnal rises during treatment with levodopa. Levodopa 123-131 growth hormone 1 Homo sapiens 31-33 1252146-3 1976 Pretreatment of mice with GH increased (1) cerebral dopa and dopamine concentrations in levodopa-treated mice, (2) cerebral accumulation of injected tritiated apomorphine and tritiated thymidine, and (3) behavioral responses to levodopa, L-m-tyrosine, apomorphine hydrochloride, and oxotremorine. Levodopa 88-96 growth hormone Mus musculus 26-28 1252146-3 1976 Pretreatment of mice with GH increased (1) cerebral dopa and dopamine concentrations in levodopa-treated mice, (2) cerebral accumulation of injected tritiated apomorphine and tritiated thymidine, and (3) behavioral responses to levodopa, L-m-tyrosine, apomorphine hydrochloride, and oxotremorine. Levodopa 228-236 growth hormone Mus musculus 26-28 1255483-7 1976 Inhibition of both peripheral and central dopa decarboxylase with Ro 4-4602 prevented all the effects of L-dopa. Levodopa 105-111 dopa decarboxylase Canis lupus familiaris 42-60 174362-0 1976 Suppressive effect of L-dopa on human prolactin release during sleep. Levodopa 22-28 prolactin Homo sapiens 38-47 985031-0 1976 [Attempt at potentiation of the action of L-dopa on the secretion of growth hormone by benserazide, disulfiram and propranolol]. Levodopa 42-48 growth hormone 1 Homo sapiens 69-83 773522-2 1976 It also focuses on recent and new therapeutic approaches: Levodopa in combindation with a Dopa-decarboxylase inhibitor or MAO-B inhibitor, dopamine agonists and an active tripeptide: L-prolyl-L-leucylglycine amide (MIF-I). Levodopa 58-66 macrophage migration inhibitory factor Homo sapiens 215-218 1261961-0 1976 Effect of metergoline, a specific serotonin antagonist, on human growth hormone response to arginine and L-dopa. Levodopa 105-111 growth hormone 1 Homo sapiens 65-79 181689-1 1976 Dopaminergic stimulants (amantadine, amphetamine, apomorphine, nomifensine and L-dopa plus benserazide) increased cyclic GMP levels in the medial forebrain and cerebellum of mice. Levodopa 79-85 5'-nucleotidase, cytosolic II Mus musculus 121-124 797502-3 1976 A large number of factors, including protein intake, gastric emptying time, pyridoxine ingestion, and dopa decarboxylase activity, affect plasma levels of levodopa attained following oral administration of this drug. Levodopa 155-163 dopa decarboxylase Homo sapiens 102-120 1253815-0 1976 Modification of the L-DOPA reversal of reserpine akinesia by inhibitors of dopamine-beta-hydroxylase. Levodopa 20-26 dopamine beta hydroxylase Mus musculus 75-100 1253815-1 1976 The effect of the dopamine-beta-hydroxylase inhibitors (DBHI) FLA-63 and U10,157 on the reversal of reserpine akinesia by L-DOPA in mice was investigated both behaviourally and by measurement of the cerebral amines dopamine and noradrenaline. Levodopa 122-128 dopamine beta hydroxylase Mus musculus 18-43 1278195-6 1976 This temporary effect may be related to the peripheral conversion of L-dopa to dopamine since insulin secretion during combined therapy was normal. Levodopa 69-75 insulin Homo sapiens 94-101 1278195-7 1976 The mechanism by which L-dopa transiently inhibits insulin release is not clear. Levodopa 23-29 insulin Homo sapiens 51-58 956809-1 1976 In the L-Dopa treated rat, a decreased urinary output of free and conjugated dopamine and an increase in free and conjugated L-Dopa excretion after administration of decarboxylase-inhibiting drugs provide a good in vivo index of Dopa decarboxylase inhibition. Levodopa 7-13 dopa decarboxylase Rattus norvegicus 229-247 181689-8 1976 However, in animals pretreated with benserazide (15 min prior to L-odopa) L-dopa produced a significant elevation of cyclic GMP and stereotyped behaviour. Levodopa 74-80 5'-nucleotidase, cytosolic II Mus musculus 124-127 1271349-0 1976 Prolactin release induced by suckling in lactating rats after L-DOPA treatment. Levodopa 62-68 prolactin Rattus norvegicus 0-9 176961-4 1975 When peripheral Dopa-decarboxylase was inhibited, smaller doses of L-Dopa were effective. Levodopa 67-73 dopa decarboxylase Rattus norvegicus 16-34 12635-3 1976 The clinical relevance of HPRL inhibiting substances as L-DOPA and 2-Br-alpha-ergocryptine is mentioned. Levodopa 56-62 prolactin receptor Homo sapiens 26-30 1028957-2 1976 In contrast, the dopaminergic agonists apomorphine (APO), lisuride hydrogen meleate (LHM), D-amphetamine (AMPH), piribedil and L-dopa greatly lowered the high serum Prl concentrations in female rats induced by i.p. Levodopa 127-133 prolactin Rattus norvegicus 165-168 176961-5 1975 Fla-63, an inhibitor of dopamine-beta-hydroxylase lowered the increase induced by L-Dopa which was completely suppressed by propranolol, not by phentolamine, suggesting that the cAMP increase is mediated through a central beta-adrenoceptor stimulation. Levodopa 82-88 dopamine beta-hydroxylase Rattus norvegicus 24-49 177112-0 1975 Effect of cyproheptadine on the spontaneous diurnal variations of plasma ACTH-cortisol and ACTH-GH secretion induced by l-dopa. Levodopa 120-126 proopiomelanocortin Homo sapiens 73-77 177112-0 1975 Effect of cyproheptadine on the spontaneous diurnal variations of plasma ACTH-cortisol and ACTH-GH secretion induced by l-dopa. Levodopa 120-126 proopiomelanocortin Homo sapiens 91-95 177112-1 1975 Cyproheptadine administration resulted in marked reduction and complete inhibition of the GH and ACTH-cortisol responses to L-dopa in a group of healthy subjects. Levodopa 124-130 proopiomelanocortin Homo sapiens 97-101 177112-2 1975 If this drug acts by antagonizing serotonin, as assumed, this study suggests that serotonin is also involved in L-dopa induced GH and ACTH release. Levodopa 112-118 proopiomelanocortin Homo sapiens 134-138 821792-1 1975 Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. Levodopa 33-39 growth hormone 1 Homo sapiens 0-14 1185416-5 1975 Growth hormone responses to arginine, insulin, sleep, L-dopa, and glucagon were uniformly less than 2.5 ng/ml. Levodopa 54-60 growth hormone 1 Homo sapiens 0-14 1206543-0 1975 Proceedings: The importance of intracerebral decarboxylation of L-DOPA in the suppression of prolactin secretion. Levodopa 64-70 prolactin Homo sapiens 93-102 1206326-10 1975 L-DOPA (5 and 10 mg) prevented the release of prolactin induced by suckling, but 1-25 and 2-5 mg L-DOPA had no effect. Levodopa 0-6 prolactin Rattus norvegicus 46-55 1221388-2 1975 Basic STH level after L-DOPA oral loading was studied in 60 and 90 minutes in all of these patients, and ti proved to be elevated in both groups. Levodopa 22-28 saitohin Homo sapiens 6-9 1158029-0 1975 Effect of glucose on the growth hormone response to L-dopa in normal and diabetic subjects. Levodopa 52-58 growth hormone 1 Homo sapiens 25-39 808553-4 1975 L-3,4-dihydroxyphenylalanine reaction on the melanocytes during mitosis demonstrated activity of the melanin-forming enzyme, tyrosinase, and ultrastructural studies demonstrated the characteristic melanosomes in variour stages of maturation. Levodopa 0-28 tyrosinase Mus musculus 125-135 1201741-0 1975 Suppressive effect of cyproheptadine on L-DOPA-induced growth hormone release in man. Levodopa 40-46 growth hormone 1 Homo sapiens 55-69 1159580-0 1975 Evaluation of growth hormone release in children using arginine and L-dopa in combination. Levodopa 68-74 growth hormone 1 Homo sapiens 14-28 1227747-0 1975 [Effect of carbidopa and L-dopa combination on the secretion of growth hormone in normal subjects and in patients with Parkinsonism]. Levodopa 25-31 growth hormone 1 Homo sapiens 64-78 239963-0 1975 Suppression by thyrotropin-releasing hormone (TRH) of human growth hormone release induced by L-dopa. Levodopa 94-100 thyrotropin releasing hormone Homo sapiens 15-44 239963-0 1975 Suppression by thyrotropin-releasing hormone (TRH) of human growth hormone release induced by L-dopa. Levodopa 94-100 thyrotropin releasing hormone Homo sapiens 46-49 239963-0 1975 Suppression by thyrotropin-releasing hormone (TRH) of human growth hormone release induced by L-dopa. Levodopa 94-100 growth hormone 1 Homo sapiens 60-74 239963-1 1975 Oral administration of L-dopa (600 mg) significantly raised plasma human growth hormone (hGH) in 6 of 7 normal subjects examined. Levodopa 23-29 growth hormone 1 Homo sapiens 73-87 239963-2 1975 This L-dopa induced hGH release was significantly suppressed by the intravenous infusion of 1 mg of thyrotropin-releasing hormone (TRH). Levodopa 5-11 thyrotropin releasing hormone Homo sapiens 100-129 239963-2 1975 This L-dopa induced hGH release was significantly suppressed by the intravenous infusion of 1 mg of thyrotropin-releasing hormone (TRH). Levodopa 5-11 thyrotropin releasing hormone Homo sapiens 131-134 239963-5 1975 L-dopa significantly lowered basal plasma hPRL levels and also significantly blunted TRH-induced hPRL release. Levodopa 0-6 prolactin Homo sapiens 42-46 239963-5 1975 L-dopa significantly lowered basal plasma hPRL levels and also significantly blunted TRH-induced hPRL release. Levodopa 0-6 thyrotropin releasing hormone Homo sapiens 85-88 239963-5 1975 L-dopa significantly lowered basal plasma hPRL levels and also significantly blunted TRH-induced hPRL release. Levodopa 0-6 prolactin Homo sapiens 97-101 1158029-1 1975 The effect of hyperglycemia on the growth hormone response to oral L-dopa (500 mg.) was assessed in eight normal and eight insulin-dependent diabetic subjects. Levodopa 67-73 growth hormone 1 Homo sapiens 35-49 1158029-8 1975 oral glucose with the L-dopa, or thirty minutes thereafter, totally suppressed the growth hormone response in all eight and six of the subjects, respectively. Levodopa 22-28 growth hormone 1 Homo sapiens 83-97 806638-1 1975 Melanosomal "tyrosinase" (L-dopa) was isolated from trypsin digest of B-16 mouse melanoma melanosomes, using polyacrylamide gel disc electrophoresis. Levodopa 26-32 tyrosinase Mus musculus 12-23 1095122-2 1975 L-Dopa lowers plasma prolactin levels, and there have been reports that patients with advanced breast cancer have been successfully treated with L-dopa. Levodopa 0-6 prolactin Homo sapiens 21-30 1148534-0 1975 Proceedings: The mechanism of the effect of dopamine-beta-hydroxylase inhibitor FLA-63 on the L-DOPA reversal of reserpine akinesia. Levodopa 94-100 dopamine beta-hydroxylase Homo sapiens 44-69 1149303-0 1975 Comparison of the effect of apomorphine and L-DOPA on serum growth hormone levels in normal men. Levodopa 44-50 growth hormone 1 Homo sapiens 60-74 808981-0 1975 Facile synthesis of L-3-(3,4-dihydroxyphenyl)alanine (L-DOPA) and related compounds. Levodopa 54-60 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 20-23 1158662-0 1975 Under-responsiveness of growth hormone secretion after L-dopa and deep sleep stimulation in obese subjects. Levodopa 55-61 growth hormone 1 Homo sapiens 24-38 806638-4 1975 These data further support previous studies in our laboratory demonstrating an inability of so-called mamalian "tyrosinase" to convert tyrosine to melanin; since this enzyme readily converts L-dopa to melanin, it seems more reasonable to term this enzyme an L-dopa oxidase. Levodopa 191-197 tyrosinase Mus musculus 111-122 1134455-0 1975 [Effects of oral administration of L-dopa on the secretion of plasma growth hormone in subjects of pediatric age]. Levodopa 35-41 growth hormone 1 Homo sapiens 69-83 1153917-0 1975 The effect of somatostatin on the rise of growth hormone and glucagon secretion induced by arginine and L-dopa in diabetic patients. Levodopa 104-110 growth hormone 1 Homo sapiens 42-56 1153917-2 1975 The plasma growth hormone response to arginine and L-dopa was completely inhibited by somatostatin. Levodopa 51-57 growth hormone 1 Homo sapiens 11-25 1168655-5 1975 L-Dopa suppression of serum PRL was not significantly influenced by T4 in these patients. Levodopa 0-6 prolactin Homo sapiens 28-31 1172495-0 1975 Spontaneous diurnal variations of serum prolactin and prolactin response to L-dopa in man. Levodopa 76-82 prolactin Homo sapiens 54-63 1119901-0 1975 Human growth hormone response to levodopa. Levodopa 33-41 growth hormone 1 Homo sapiens 6-20 1119901-2 1975 After ingestion of 500 mg of levodopa, postmenopausal women had significantly diminished human growth hormone (HGH) responses (mean, 4.6 ng/ml), as compared with those of age-matched men (mean, 9.1 ng/ml; P smaller than .05). Levodopa 29-37 growth hormone 1 Homo sapiens 95-109 165915-8 1975 L-Dopa produced a consistent rise in both ACTH and cortisol that was significantly different from control subjects. Levodopa 0-6 proopiomelanocortin Homo sapiens 42-46 238221-1 1975 The present work deals with the action of MIF (melanocyte stimulating hormone release-inhibiting factor), TRF (thyrotropin releasing factor), and angiotensin II on the behavioral effects of L-DOPA and of D, L-5-hydroxytrytophan (5-HTP) in mice. Levodopa 192-198 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 43-46 165476-3 1975 There was an increase in the plasma content of STH, TTH and ACTH with a maximum 60 min after the administration of L-DOPA. Levodopa 115-121 saitohin Homo sapiens 47-50 238221-3 1975 MIF and TRF, injected i.p., intensify the effects of L-DOPA in mice. Levodopa 53-59 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 0-3 165476-3 1975 There was an increase in the plasma content of STH, TTH and ACTH with a maximum 60 min after the administration of L-DOPA. Levodopa 115-121 proopiomelanocortin Homo sapiens 60-64 238221-3 1975 MIF and TRF, injected i.p., intensify the effects of L-DOPA in mice. Levodopa 53-59 thyrotropin releasing hormone Mus musculus 8-11 238221-5 1975 When MIF or TRF are injected into the brain, potentiation of L-DOPA is obtained with exceedingly small quantities of MIF (0.1 pg); the effective dose of TRF is 1 microgram. Levodopa 61-67 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 5-8 238221-5 1975 When MIF or TRF are injected into the brain, potentiation of L-DOPA is obtained with exceedingly small quantities of MIF (0.1 pg); the effective dose of TRF is 1 microgram. Levodopa 61-67 thyrotropin releasing hormone Mus musculus 12-15 238221-5 1975 When MIF or TRF are injected into the brain, potentiation of L-DOPA is obtained with exceedingly small quantities of MIF (0.1 pg); the effective dose of TRF is 1 microgram. Levodopa 61-67 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 117-120 238221-5 1975 When MIF or TRF are injected into the brain, potentiation of L-DOPA is obtained with exceedingly small quantities of MIF (0.1 pg); the effective dose of TRF is 1 microgram. Levodopa 61-67 thyrotropin releasing hormone Mus musculus 153-156 1115151-2 1975 In this laboratory, HPRL suppression with L-dopa was variable and short lived. Levodopa 42-48 prolactin receptor Homo sapiens 20-24 1132216-0 1975 [Progress in the therapy of parkinsonism with L-dopa: inhibition of dopa decarboxylase]. Levodopa 46-52 dopa decarboxylase Homo sapiens 68-86 1171032-0 1975 [A low response of pituitary growth hormone secretion in the patient with diabetes mellitus after intravenous administration of L-dopa (author"s transl)]. Levodopa 128-134 growth hormone 1 Homo sapiens 29-43 1168856-7 1975 L-Dopa produced appropriate suppression of serum PRL concentrations in the normals and both patient groups. Levodopa 0-6 prolactin Homo sapiens 49-52 1117978-0 1975 Inhibition of L-dopa-induced growth hormone stimulation by pyridoxine and chlorpromazine. Levodopa 14-20 growth hormone 1 Homo sapiens 29-43 1117978-1 1975 One gram of L-dopa was administered orally to 12 male control subjects and induced an increase of growth hormone (GH) secretion. Levodopa 12-18 growth hormone 1 Homo sapiens 98-112 1117978-1 1975 One gram of L-dopa was administered orally to 12 male control subjects and induced an increase of growth hormone (GH) secretion. Levodopa 12-18 growth hormone 1 Homo sapiens 114-116 1117978-2 1975 The L-dopa-induced GH response was inhibited by an intravenous infusion of pyridoxine, but pyridoxine did not inhibit the GH response to hypoglycemia. Levodopa 4-10 growth hormone 1 Homo sapiens 19-21 1117978-3 1975 Chlorpromazine also inhibited L-dopa-induced GH stimulation. Levodopa 30-36 growth hormone 1 Homo sapiens 45-47 1117978-5 1975 The mechanism of the suppressed L-dopa-induced GH response by pyridoxine appears to be mediated by peripheral accleration of the conversion of L-dopa to dopamine, while that of chlorpromazine appears to be mediated through hypothalamic centers. Levodopa 32-38 growth hormone 1 Homo sapiens 47-49 1117978-5 1975 The mechanism of the suppressed L-dopa-induced GH response by pyridoxine appears to be mediated by peripheral accleration of the conversion of L-dopa to dopamine, while that of chlorpromazine appears to be mediated through hypothalamic centers. Levodopa 143-149 growth hormone 1 Homo sapiens 47-49 1117978-6 1975 Pyridoxine and chlorpromazine should be added to the list of other factors affecting the response to L-dopa-induced GH stimulation Levodopa 101-107 growth hormone 1 Homo sapiens 116-118 1171032-1 1975 Recently, L-dopa has been known as one of drugs to stimulate the secretion of growth hormone from the pituitary gland through dopamine, which is a metabolic of L-dopa, without any changes of serum insulin levels, blood sugar values, fatty acids and amino acids concentrations in the serum of human being. Levodopa 10-16 growth hormone 1 Homo sapiens 78-92 1171032-1 1975 Recently, L-dopa has been known as one of drugs to stimulate the secretion of growth hormone from the pituitary gland through dopamine, which is a metabolic of L-dopa, without any changes of serum insulin levels, blood sugar values, fatty acids and amino acids concentrations in the serum of human being. Levodopa 160-166 growth hormone 1 Homo sapiens 78-92 1171032-2 1975 The present study was thus designed to assess the effect of L-dopa on the pituitary gland to secrete the growth hormone in the normal subject and the study was further extended to compare the response of the pituitary secretion of the growth hormone following the administration of L-dopa between in the patient with diabetes mellitus and in the normal subject. Levodopa 60-66 growth hormone 1 Homo sapiens 105-119 1171032-2 1975 The present study was thus designed to assess the effect of L-dopa on the pituitary gland to secrete the growth hormone in the normal subject and the study was further extended to compare the response of the pituitary secretion of the growth hormone following the administration of L-dopa between in the patient with diabetes mellitus and in the normal subject. Levodopa 282-288 growth hormone 1 Homo sapiens 235-249 1171032-6 1975 In the patients with diabetes mellitus, on the other hand, maximum value of serum concentration of the growth hormone was only approximately 5 ng/ml of serum obtained between 45 and 75 min after the administration of L-dopa. Levodopa 217-223 growth hormone 1 Homo sapiens 103-117 1109897-3 1975 Posterolateral deafferentation was as effective as complete deafferentation in preventing the stress-induced prolactin release, whereas anterior frontal deafferentation had only a small effect, L-Dopa (100 mg/kg body wt, ip) decreased prolactin titers in both control and deafferented animals, whereas reserpine (1 mg/kg body wt, ip) had the opposite effect. Levodopa 194-200 prolactin Rattus norvegicus 235-244 803259-7 1975 L-dopa administration significantly reduced serum prolactin values but had no significant effect on serum TSH. Levodopa 0-6 prolactin Rattus norvegicus 50-59 803259-9 1975 This suggest that L-dopa acts directly or indirectly on the pituitary prolactin cells to inhibit TRH stimulation of prolactin release, but does not influence the action of TRH on pituitary TSH cells. Levodopa 18-24 prolactin Rattus norvegicus 70-79 803259-9 1975 This suggest that L-dopa acts directly or indirectly on the pituitary prolactin cells to inhibit TRH stimulation of prolactin release, but does not influence the action of TRH on pituitary TSH cells. Levodopa 18-24 prolactin Rattus norvegicus 116-125 1109897-4 1975 Since both drugs inhibited prolactin release from pituitaries in vitro, the decrease of prolactin levels following L-dopa in vivo might have been caused not only by stimulation of PIF release but also at least partly by the direct effect of the drug on the pituitary. Levodopa 115-121 prolactin Rattus norvegicus 88-97 5613-4 1975 Principally the effect of a) the administration of drugs and precursors such as L-dopa, 3H-dopa, 6-OH dopa; b) the prenatal administration of reserpine; c) the blockade of cholinergic receptors; d) the nerve growth factor (NGF) is analyzed. Levodopa 80-86 nerve growth factor Gallus gallus 202-221 54462-0 1975 [Method of determination of somatotropin level in blood plasma with L-dopa loading in patients with diabetes mellitus complicated by microangiopathies]. Levodopa 68-74 growth hormone 1 Homo sapiens 28-40 1172524-0 1975 The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil. Levodopa 51-57 monoamine oxidase B Homo sapiens 87-92 1120949-2 1975 The administration of L-DOPA, 100 mg/kg i.p., after inhibition of peripheral dopa decarboxylase, disrupts the discrimination but not the acoidance behaviour, whereas the administration of the antipsychotic agent haloperidol (HPD), 0.125 mg/kg i.p., disrupts the avoidance behaviour but not the discrimination. Levodopa 22-28 dopa decarboxylase Rattus norvegicus 77-95 1241606-0 1975 L-Dopa effects on serum LH and prolactin in old and young female rats. Levodopa 0-6 prolactin Rattus norvegicus 31-40 1241606-1 1975 Serum LH and prolactin changes in response to an acute systemic L-dopa injection were measured in young (4-6 months) proestrous, estrous and 2nd day diestrous rats, and in aged (23-30 months) constant estrous and pseudopregnant (long diestrous) Long-Evans rats. Levodopa 64-70 prolactin Rattus norvegicus 13-22 1129359-4 1975 The anorectic effect of both amphetamine and l-dopa was antagonized by propranolol, a beta adrenergic antagonist. Levodopa 45-51 amyloid beta precursor protein Rattus norvegicus 84-90 1241606-6 1975 The reduction in serum prolactin following 3 mg of L-dopa was less in both the aged groups than in the young rats. Levodopa 51-57 prolactin Rattus norvegicus 23-32 4426291-0 1974 Effect of 1-dihydroxyphenylalanine (l-dopa), anesthesia and surgical stress on the secretion of growth hormone in the dog. Levodopa 36-42 somatotropin Canis lupus familiaris 96-110 4139577-0 1974 Letter: Enhancement of levodopa-induced growth-hormone stimulation by practolol. Levodopa 23-31 growth hormone 1 Homo sapiens 40-54 4428963-0 1974 The effect of L-dopa on the blood concentrations of growth hormone, thyrotrophin, gonadotrophins, cortisol and glucose in children with short stature. Levodopa 14-20 growth hormone 1 Homo sapiens 52-66 4439528-0 1974 [Stimulation of growth hormone (HGH) with L-dopa]. Levodopa 42-48 growth hormone 1 Homo sapiens 16-30 4606498-0 1974 Effect of synthetic somatotropin release inhibiting factor on the increase in plasma growth hormone elicited by L-dopa in the dog. Levodopa 112-118 somatotropin Canis lupus familiaris 85-99 4447697-0 1974 [Action of a peripheral inhibitor of dopa-decarboxylase on the inhibition by L-DOPA of the hypothalamo-hypophyseo-adrenocortical system in man]. Levodopa 77-83 dopa decarboxylase Homo sapiens 37-55 4153252-0 1974 [Trial use of L-dopa associated with a dopa-decarboxylase inhibitor in Parkinson"s syndrome]. Levodopa 14-20 dopa decarboxylase Homo sapiens 39-57 4356808-0 1973 Growth hormone and prolactin in unipolar and bipolar depressed patients: responses to hypoglycemia and L-dopa. Levodopa 103-109 growth hormone 1 Homo sapiens 0-14 4454413-0 1974 [Stimulation of growth hormone secretion by the anterior pituitary gland using L-DOPA compared to growth hormone secretion following argine, insulin and sleep]. Levodopa 79-85 growth hormone 1 Homo sapiens 16-30 4133478-0 1974 Letter: Enhancement of levodopa-induced growth-hormone stimulation by propranolol. Levodopa 23-31 growth hormone 1 Homo sapiens 40-54 4813957-0 1974 Plasma growth hormone response to L-dopa in obese subjects. Levodopa 34-40 growth hormone 1 Homo sapiens 7-21 4356808-0 1973 Growth hormone and prolactin in unipolar and bipolar depressed patients: responses to hypoglycemia and L-dopa. Levodopa 103-109 prolactin Homo sapiens 19-28 4709329-0 1973 Glucose-suppressible growth hormone release after L-dopa administration to normal subjects. Levodopa 50-56 growth hormone 1 Homo sapiens 21-35 4767002-0 1973 Amantadine enhancement of L-DOPA induced growth hormone stimulation. Levodopa 26-32 growth hormone 1 Homo sapiens 41-55 4732567-0 1973 Enhancement of the pharmacological action of 3,4-dihydroxy-L-phenylalanine(L-dopa) and reduction of dopa decarboxylase activity in rat liver after chronic treatment with L-dopa. Levodopa 170-176 dopa decarboxylase Rattus norvegicus 100-118 4200807-0 1973 The levodopa test of growth hormone reserve in children. Levodopa 4-12 growth hormone 1 Homo sapiens 21-35 4632690-1 1973 Prolactin secretion was assessed in 23 patients with hypothalamic-pituitary disorders using L-Dopa suppression, chlorpromazine (CPZ), and thyrotropin-releasing hormone (TRH) stimulation tests. Levodopa 92-98 prolactin Homo sapiens 0-9 4698567-0 1973 Potentiation of levodopa stimulation of human growth hormone by systemic decarboxylase inhibition. Levodopa 16-24 growth hormone 1 Homo sapiens 46-60 4196300-0 1973 [Effect of L-Dopa on the secretion of prolactin in eels]. Levodopa 11-17 prolactin Homo sapiens 38-47 4682676-0 1973 Defective release of growth hormone in parkinsonism improved by levodopa. Levodopa 64-72 growth hormone 1 Homo sapiens 21-35 4350369-0 1973 [Effect of oral administration of L-dopa on plasma levels of TSH, ACTH and GH in normal subjects]. Levodopa 34-40 proopiomelanocortin Homo sapiens 66-70 4717022-3 1973 The increased secretion induced by the infusion of L-DOPA (100 mug/min) was completely antagonized by Ro 4-4602 (300 mug), a DOPA decarboxylase inhibitor.3. Levodopa 51-57 dopa decarboxylase Canis lupus familiaris 125-143 4570903-2 1973 Brocresine, an aromatic L-amino acid decarboxylase inhibitor with both a peripheral and central action was shown to potentiate the therapeutic effect of levodopa in Parkinson"s disease. Levodopa 153-161 dopa decarboxylase Homo sapiens 15-50 4630270-0 1973 Suppression of serum thyrotropin (TSH) by L-dopa in chronic hypothyroidism: interrelationships in the regulation of TSH and prolactin secretion. Levodopa 42-48 prolactin Homo sapiens 124-133 4770263-0 1973 Effect of L-dopa on the secretion of plasma growth hormone in children and adolescents. Levodopa 10-16 growth hormone 1 Homo sapiens 44-58 4722572-0 1973 Plasma growth hormone and insulin response to levodopa and amantadine. Levodopa 46-54 growth hormone 1 Homo sapiens 7-21 4706921-0 1973 Effect of intravenous infusion of L-DOPA on plasma growth hormone levels in man. Levodopa 34-40 growth hormone 1 Homo sapiens 51-65 4722572-0 1973 Plasma growth hormone and insulin response to levodopa and amantadine. Levodopa 46-54 insulin Homo sapiens 26-33 4637935-0 1972 The effect of inhibition of catechol O-methyltransferase on some cardiovascular responses to l-dopa in the dog. Levodopa 93-99 catechol-O-methyltransferase Canis lupus familiaris 28-56 4640070-0 1972 Growth hormone responses to L-dopa in depressed patients. Levodopa 28-34 growth hormone 1 Homo sapiens 0-14 4640070-1 1972 Plasma human growth hormone responses to oral administration of 500 milligrams of L-dopa were analyzed in three groups of subjects: normals, age 20 to 32; normals, age 48 to 68; and unipolar depressed patients, age 45 to 68. Levodopa 82-88 growth hormone 1 Homo sapiens 13-27 4275115-0 1973 Biogenic amines in the hypothalamus: effect of L-DOPA on human growth hormone levels in patients with Huntington"s chorea. Levodopa 47-53 growth hormone 1 Homo sapiens 63-77 4668972-0 1972 Release of human growth hormone, follicle stimulating hormone, and luteinizing hormone in response to L-dihydroxy-phenylalanine (L-dopa) in normal man. Levodopa 129-135 growth hormone 1 Homo sapiens 17-31 5074361-0 1972 Effect of L-dihydroxyphenylalanine upon serum growth hormone concentrations in children and adolescents. Levodopa 10-34 growth hormone 1 Homo sapiens 46-60 5066290-0 1972 [Effect of L-dopa on pituitary TSH and GH secretion in Parkinson"s disease]. Levodopa 11-17 gamma-glutamyl hydrolase Homo sapiens 39-41 5071365-0 1972 Effect of L-dopa administration on growth hormone secretion in normal subjects and Parkinsonian patients. Levodopa 10-16 growth hormone 1 Homo sapiens 35-49 5070092-0 1972 [In-vitro action of L-dopa (3-4 dihydroxyphenylalanine) on cerebral glutamate decarboxylase (GAD) and on -aminobutyric transaminase (GABA-T) in rats]. Levodopa 20-26 4-aminobutyrate aminotransferase Rattus norvegicus 134-140 4624348-0 1972 L-DOPA suppression of thyrotropin-releasing hormone response in man. Levodopa 0-6 thyrotropin releasing hormone Homo sapiens 22-51 4403307-1 1972 Activity of serotonin N-acetyltransferase (EC 2.3.1.5) in rat pineal organ is rapidly and markedly elevated in vivo after administration of beta-(3,4-dihydroxyphenyl)-L-alanine (L-DOPA), norepinephrine, epinephrine, isoproterenol, monoamine oxidase inhibitors, or theophylline. Levodopa 140-176 aralkylamine N-acetyltransferase Rattus norvegicus 12-41 4403307-1 1972 Activity of serotonin N-acetyltransferase (EC 2.3.1.5) in rat pineal organ is rapidly and markedly elevated in vivo after administration of beta-(3,4-dihydroxyphenyl)-L-alanine (L-DOPA), norepinephrine, epinephrine, isoproterenol, monoamine oxidase inhibitors, or theophylline. Levodopa 178-184 aralkylamine N-acetyltransferase Rattus norvegicus 12-41 4403307-4 1972 When rat pineal organ is denervated by ganglionectomy, beta-(3,4-dihydroxyphenyl)-L-alanine induces much more serotonin N-acetyltransferase than in the innervated gland. Levodopa 55-91 aralkylamine N-acetyltransferase Rattus norvegicus 110-139 4673195-0 1972 [Fluctuations of plasma concentration of growth hormone (GH) and cortisol in man during administration of L-DOPA. Levodopa 106-112 growth hormone 1 Homo sapiens 41-55 4673195-0 1972 [Fluctuations of plasma concentration of growth hormone (GH) and cortisol in man during administration of L-DOPA. Levodopa 106-112 growth hormone 1 Homo sapiens 57-59 4346623-0 1972 [Effect of oral administration of L-Dopa on plasma TSH, ACTH and GH levels in normal subjects]. Levodopa 34-40 proopiomelanocortin Homo sapiens 56-60 16746558-0 1937 A comparative study of the production of l-3:4-dihydroxyphenylalanine from tyrosine by tyrosinase from various sources. Levodopa 41-69 tyrosinase Homo sapiens 87-97 4622109-4 1972 L-Dopa (D,L-alpha-hydrazino-alpha-methyl-beta-[3,4-di-hydroxyphenyl]) has the opposite effect; it inhibits prolactin secretion and may be effective in suppressing galactorrhea. Levodopa 0-6 prolactin Homo sapiens 107-116 5016575-0 1972 Metabolism of L-dopa after inhibition of catechol-O-methyl transferase. Levodopa 14-20 catechol-O-methyltransferase Homo sapiens 41-70 5112212-0 1971 Potentiation of the L-Dopa effect in man by the use of catechol-O-methyltransferase inhibitors. Levodopa 20-26 catechol-O-methyltransferase Homo sapiens 55-83 5289371-0 1971 Decrease in liver aromatic L-amino-acid decarboxylase produced by chronic administration of L-dopa. Levodopa 92-98 dopa decarboxylase Rattus norvegicus 18-53 5289371-3 1971 In the present study, it was found that when L-dopa was administered to rats, the activity of liver aromatic L-amino-acid decarboxylase, the enzyme which catalyzes the conversion of dopa to dopamine, was reduced by as much as 50%. Levodopa 45-51 dopa decarboxylase Rattus norvegicus 100-135 5148757-0 1971 Potentiation of effects of L-dopa on conditioned avoidance behavior by inhibition of extracerebral dopa decarboxylase. Levodopa 27-33 dopa decarboxylase Homo sapiens 99-117 5481776-0 1970 Stimulation of human-growth-hormone secretion by L-dopa. Levodopa 49-55 growth hormone 1 Homo sapiens 21-35 4324569-0 1970 Corticosteroid and growth hormone secretion in patients treated with L-dopa. Levodopa 69-75 growth hormone 1 Homo sapiens 19-33 4554974-0 1972 Phentolamine inhibition of human growth hormone secretion induced by L-DOPA. Levodopa 69-75 growth hormone 1 Homo sapiens 33-47 5107027-0 1971 Levodopa suppression of prolactin in nonpuerperal galactorrhea. Levodopa 0-8 prolactin Homo sapiens 24-33 4935302-11 1971 * Levodopa as a possible specific stimulus to growth hormone release has just been reported and the implications of this finding for the child of short stature cannot yet be assessed. Levodopa 2-10 growth hormone 1 Homo sapiens 46-60 5578236-3 1971 Pretreatment of dogs with an extracerebral inhibitor of dopa decarboxylase [D,L-alpha-hydrazino-alpha-methyl-beta-(3.4-dihydroxyphenyl) propionic acid] prevented the development of hypertension and arrhythmias with infusion of L-dopa. Levodopa 227-233 dopa decarboxylase Canis lupus familiaris 56-74 5578236-10 1971 Pretreatment with a drug which inhibits brain as well as extracerebral dopa decarboxylase [D,L-seryl-2,3,4-trihydroxybenzylhydrazine hydrochloride] abolished all effects of L-dopa on blood pressure. Levodopa 173-179 dopa decarboxylase Canis lupus familiaris 71-89 5089105-0 1971 L-DOPA induced effects on motor activity in mice after inhibition of dopamine-beta-hydroxylase. Levodopa 0-6 dopamine beta hydroxylase Mus musculus 69-94 33275784-9 2021 The MPTP-induced increase in alpha-synuclein levels was abolished in animals having received L-DOPA in all the brain regions, except in the substantia nigra. Levodopa 93-99 synuclein alpha Homo sapiens 29-44 33686657-1 2021 L-DOPA prolonged treatment leads to disabling motor complications as dyskinesia that could be decreased by drugs acting on 5-HT1A receptors. Levodopa 0-6 5-hydroxytryptamine receptor 1A Rattus norvegicus 123-129 33275784-0 2021 L-DOPA regulates alpha-synuclein accumulation in experimental parkinsonism. Levodopa 0-6 synuclein alpha Homo sapiens 17-32 33873118-0 2021 Levodopa facilitates improvements in gait kinetics at the hip, not the ankle, in individuals with Parkinson"s disease. Levodopa 0-8 hedgehog interacting protein Homo sapiens 58-61 33687725-0 2021 Interferon-gamma Involvement in the Neuroinflammation Associated with Parkinson"s Disease and L-DOPA-Induced Dyskinesia. Levodopa 94-100 interferon gamma Mus musculus 0-16 33687725-3 2021 We investigated whether the IFN-gamma deficiency could interfere with nigrostriatal degeneration induced by the neurotoxin 6-hydroxydopamine, L-DOPA-induced dyskinesia, and the neuroinflammatory features as astrogliosis, microgliosis, and induced nitric oxide synthase (iNOS) immunoreactivity induced by L-DOPA treatment. Levodopa 142-148 interferon gamma Homo sapiens 28-37 33687725-3 2021 We investigated whether the IFN-gamma deficiency could interfere with nigrostriatal degeneration induced by the neurotoxin 6-hydroxydopamine, L-DOPA-induced dyskinesia, and the neuroinflammatory features as astrogliosis, microgliosis, and induced nitric oxide synthase (iNOS) immunoreactivity induced by L-DOPA treatment. Levodopa 304-310 interferon gamma Homo sapiens 28-37 33989370-9 2021 We hypothesized that the l-Dopa released from MSN materials is mediated by the size and solubility of the DSDAs, and the surface chemical interactions between the DSDAs and MSN hosts. Levodopa 25-31 moesin Homo sapiens 46-49 33989370-9 2021 We hypothesized that the l-Dopa released from MSN materials is mediated by the size and solubility of the DSDAs, and the surface chemical interactions between the DSDAs and MSN hosts. Levodopa 25-31 moesin Homo sapiens 173-176 33875558-0 2021 Pearls and Oy-sters: Levodopa Responsive Adult NCL (Type B Kufs Disease) Due to CLN6 Mutation. Levodopa 21-29 nucleolin Homo sapiens 47-50 33875558-0 2021 Pearls and Oy-sters: Levodopa Responsive Adult NCL (Type B Kufs Disease) Due to CLN6 Mutation. Levodopa 21-29 CLN6 transmembrane ER protein Homo sapiens 80-84 33687725-9 2021 Remarkably, IFN-gamma/KO mice treated with L-DOPA presented in the lesioned striatum an increase of iNOS and glial fibrilary acid protein (GFAP) density, compared with the WT group. Levodopa 43-49 interferon gamma Mus musculus 12-21 33687725-9 2021 Remarkably, IFN-gamma/KO mice treated with L-DOPA presented in the lesioned striatum an increase of iNOS and glial fibrilary acid protein (GFAP) density, compared with the WT group. Levodopa 43-49 nitric oxide synthase 2, inducible Mus musculus 100-104 33687725-11 2021 In conclusion, IFN-gamma/KO mice presented an intensification of the inflammatory reaction accompanying L-DOPA treatment and suggest that iNOS and GFAP increase, and the activation of astrocytes and microglia induced afterward L-DOPA treatment was IFN-gamma independent events. Levodopa 104-110 interferon gamma Mus musculus 15-27 33687725-11 2021 In conclusion, IFN-gamma/KO mice presented an intensification of the inflammatory reaction accompanying L-DOPA treatment and suggest that iNOS and GFAP increase, and the activation of astrocytes and microglia induced afterward L-DOPA treatment was IFN-gamma independent events. Levodopa 104-110 interferon gamma Mus musculus 15-24 33687725-11 2021 In conclusion, IFN-gamma/KO mice presented an intensification of the inflammatory reaction accompanying L-DOPA treatment and suggest that iNOS and GFAP increase, and the activation of astrocytes and microglia induced afterward L-DOPA treatment was IFN-gamma independent events. Levodopa 227-233 interferon gamma Mus musculus 15-27 33687725-11 2021 In conclusion, IFN-gamma/KO mice presented an intensification of the inflammatory reaction accompanying L-DOPA treatment and suggest that iNOS and GFAP increase, and the activation of astrocytes and microglia induced afterward L-DOPA treatment was IFN-gamma independent events. Levodopa 227-233 interferon gamma Mus musculus 15-24 34004240-4 2021 Adenosine A2A receptor (A2A R) antagonist (Istradephylline) combined with levodopa shows a promising therapy for PD. Levodopa 74-82 adenosine A2a receptor Homo sapiens 0-22 34011807-6 2021 After reducing the levodopa equivalent dose to control the dyskinesia to an almost negligible level, his FOG also improved and his activities of daily living improved markedly. Levodopa 19-27 zinc finger protein, FOG family member 1 Homo sapiens 105-108 34054505-11 2021 Preprodynorphin mRNA expression was higher in L-dopa-treated young-lesioned rats than in in L-dopa-treated old-lesioned rats. Levodopa 46-52 prodynorphin Rattus norvegicus 0-15 34054505-11 2021 Preprodynorphin mRNA expression was higher in L-dopa-treated young-lesioned rats than in in L-dopa-treated old-lesioned rats. Levodopa 92-98 prodynorphin Rattus norvegicus 0-15 34007239-3 2021 Catechol-O-methyl transferase (COMT) inhibitors (COMT-i) are used as first-line adjuvant therapy to L-dopa for end-of-dose (EoD) motor fluctuations, since they increase L-dopa availability in the brain by inhibiting its peripheral metabolism. Levodopa 100-106 catechol-O-methyltransferase Homo sapiens 0-29 34007239-3 2021 Catechol-O-methyl transferase (COMT) inhibitors (COMT-i) are used as first-line adjuvant therapy to L-dopa for end-of-dose (EoD) motor fluctuations, since they increase L-dopa availability in the brain by inhibiting its peripheral metabolism. Levodopa 100-106 catechol-O-methyltransferase Homo sapiens 31-35 34007239-3 2021 Catechol-O-methyl transferase (COMT) inhibitors (COMT-i) are used as first-line adjuvant therapy to L-dopa for end-of-dose (EoD) motor fluctuations, since they increase L-dopa availability in the brain by inhibiting its peripheral metabolism. Levodopa 169-175 catechol-O-methyltransferase Homo sapiens 0-29 34007239-3 2021 Catechol-O-methyl transferase (COMT) inhibitors (COMT-i) are used as first-line adjuvant therapy to L-dopa for end-of-dose (EoD) motor fluctuations, since they increase L-dopa availability in the brain by inhibiting its peripheral metabolism. Levodopa 169-175 catechol-O-methyltransferase Homo sapiens 31-35 33962918-2 2021 GTP cyclohydrolase 1 (GCH-1) deficiency, which triggers pteridine hypometabolism and normally develops in childhood, can mediate an adult-onset decrease in levodopa production and dopa-responsive dystonia (DRD), with normal dopamine transporter single-photon emission computed tomography (DAT-SPECT). Levodopa 156-164 GTP cyclohydrolase 1 Homo sapiens 0-20 33895825-7 2021 A linear mixed model revealed that the diabetic group with Parkinson"s disease being treated with DPP4 inhibitors had a slower longitudinal increase in levodopa-equivalent dose than the other groups (P = 0.003). Levodopa 152-160 dipeptidyl peptidase 4 Homo sapiens 98-102 33962918-2 2021 GTP cyclohydrolase 1 (GCH-1) deficiency, which triggers pteridine hypometabolism and normally develops in childhood, can mediate an adult-onset decrease in levodopa production and dopa-responsive dystonia (DRD), with normal dopamine transporter single-photon emission computed tomography (DAT-SPECT). Levodopa 156-164 solute carrier family 6 member 3 Homo sapiens 224-244 33895825-8 2021 Survival analyses showed that the rate of levodopa-induced dyskinesia was significantly lower in the diabetic group with a prior treatment with DPP4 inhibitors than the diabetic group without DPP4 inhibitors (hazard ratio = 0.194, P = 0.037). Levodopa 42-50 dipeptidyl peptidase 4 Homo sapiens 144-148 33895825-8 2021 Survival analyses showed that the rate of levodopa-induced dyskinesia was significantly lower in the diabetic group with a prior treatment with DPP4 inhibitors than the diabetic group without DPP4 inhibitors (hazard ratio = 0.194, P = 0.037). Levodopa 42-50 dipeptidyl peptidase 4 Homo sapiens 192-196 33960511-11 2021 Monoamine oxidase type B inhibitors, as initial levodopa-sparing therapy was more cost-effective, with similar quality-adjusted life-years but lower costs than dopamine agonists. Levodopa 48-56 monoamine oxidase B Homo sapiens 0-24 33517217-1 2021 Tyrosinase is the key enzyme for melanogenesis with both monophenolase activity and diphenolase activity, which catalyzes the hydroxylation of tyrosine to L-DOPA and the further oxidation of DOPA, respectively. Levodopa 155-161 tyrosinase Homo sapiens 0-10 33960511-2 2021 OBJECTIVES: The objective was to estimate the cost-effectiveness of levodopa-sparing therapy (dopamine agonists or monoamine oxidase type B inhibitors compared with levodopa alone. Levodopa 68-76 monoamine oxidase B Homo sapiens 115-139 33850083-6 2021 The l-dopa-induced enhancement of AIMs in D2L KO mice was significantly reduced by the D2R antagonist eticlopride. Levodopa 4-10 dopamine receptor D2 Mus musculus 87-90 32108308-2 2021 However, due to extensive peripheral metabolism by aromatic L-amino acid decarboxylase and catechol-O-methyltransferase (COMT), only a fraction of the levodopa dose reaches the brain unchanged. Levodopa 151-159 catechol-O-methyltransferase Homo sapiens 91-119 33460487-4 2021 RESULTS: We found that l-dopa-induced dyskinesia is associated with accumulation of the autophagy-specific substrate p62, a marker of autophagy deficiency. Levodopa 23-29 nucleoporin 62 Homo sapiens 117-120 33460487-5 2021 Increased p62 was observed in a subset of projection neurons located in the striatum and depended on l-dopa-mediated activation of dopamine D1 receptors, and mammalian target of rapamycin. Levodopa 101-107 nucleoporin 62 Homo sapiens 10-13 33861617-1 2021 Previously, we found that ONO-2160, an ester-type prodrug of levodopa (3-hydroxy-l-tyrosine), was mainly hydrolyzed in human plasma by alpha1-acid glycoprotein (AGP) with a partial contribution of albumin. Levodopa 61-69 albumin Canis lupus familiaris 197-204 33861617-1 2021 Previously, we found that ONO-2160, an ester-type prodrug of levodopa (3-hydroxy-l-tyrosine), was mainly hydrolyzed in human plasma by alpha1-acid glycoprotein (AGP) with a partial contribution of albumin. Levodopa 71-91 albumin Canis lupus familiaris 197-204 33242649-7 2021 Furthermore, we were able to increase the L-DOPA levels further by elevating the expression of the metabolic master regulator, MYB12, specifically in tomato fruit, together with BvCYP76AD6. Levodopa 42-48 Myb12 transcription factor Solanum lycopersicum 127-132 32108308-2 2021 However, due to extensive peripheral metabolism by aromatic L-amino acid decarboxylase and catechol-O-methyltransferase (COMT), only a fraction of the levodopa dose reaches the brain unchanged. Levodopa 151-159 catechol-O-methyltransferase Homo sapiens 121-125 32108308-3 2021 Thus, by preventing levodopa metabolism and increasing the availability of levodopa for uptake into the brain, the inhibition of COMT would be beneficial in Parkinson"s disease. Levodopa 20-28 catechol-O-methyltransferase Homo sapiens 129-133 32108308-3 2021 Thus, by preventing levodopa metabolism and increasing the availability of levodopa for uptake into the brain, the inhibition of COMT would be beneficial in Parkinson"s disease. Levodopa 75-83 catechol-O-methyltransferase Homo sapiens 129-133 33933805-3 2021 The recognition and binding processes of LAT1-ligands, such as amino acids and clinically used small molecules, including l-dopa, gabapentin, and melphalan, are today well-known. Levodopa 122-128 solute carrier family 7 member 5 Homo sapiens 41-45 33832800-0 2021 Monozygotic twins with DYT-TOR1A showing jerking movements and levodopa responsiveness. Levodopa 63-71 torsin family 1 member A Homo sapiens 27-32 33571594-6 2021 Kinetic parameters indicated that rTYR displayed a relatively good affinity for both l-tyrosine and l-DOPA. Levodopa 100-106 tyrosinase Rattus norvegicus 34-38 33832800-10 2021 This finding may expand the spectrum of phenotypes associated with DYT-TOR1A, and suggests that levodopa has potential as a treatment for DYT-TOR1A with DYT/PARK-GCH1-associated features. Levodopa 96-104 torsin family 1 member A Homo sapiens 71-76 33832800-10 2021 This finding may expand the spectrum of phenotypes associated with DYT-TOR1A, and suggests that levodopa has potential as a treatment for DYT-TOR1A with DYT/PARK-GCH1-associated features. Levodopa 96-104 torsin family 1 member A Homo sapiens 142-147 33832800-10 2021 This finding may expand the spectrum of phenotypes associated with DYT-TOR1A, and suggests that levodopa has potential as a treatment for DYT-TOR1A with DYT/PARK-GCH1-associated features. Levodopa 96-104 GTP cyclohydrolase 1 Homo sapiens 157-166 33309753-1 2021 Tyrosine hydroxylase (TH) catalyses the (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4)-dependent conversion of l-tyrosine to L-3,4-dihydroxyphenylalanine (l-Dopa), which is the rate-limiting step in the synthesis of dopamine and other catecholamine neurotransmitters and hormones. Levodopa 127-155 tyrosine hydroxylase Homo sapiens 0-20 33309753-1 2021 Tyrosine hydroxylase (TH) catalyses the (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4)-dependent conversion of l-tyrosine to L-3,4-dihydroxyphenylalanine (l-Dopa), which is the rate-limiting step in the synthesis of dopamine and other catecholamine neurotransmitters and hormones. Levodopa 127-155 tyrosine hydroxylase Homo sapiens 22-24 33309753-1 2021 Tyrosine hydroxylase (TH) catalyses the (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4)-dependent conversion of l-tyrosine to L-3,4-dihydroxyphenylalanine (l-Dopa), which is the rate-limiting step in the synthesis of dopamine and other catecholamine neurotransmitters and hormones. Levodopa 157-163 tyrosine hydroxylase Homo sapiens 0-20 33309753-1 2021 Tyrosine hydroxylase (TH) catalyses the (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4)-dependent conversion of l-tyrosine to L-3,4-dihydroxyphenylalanine (l-Dopa), which is the rate-limiting step in the synthesis of dopamine and other catecholamine neurotransmitters and hormones. Levodopa 157-163 tyrosine hydroxylase Homo sapiens 22-24 33309753-2 2021 Dysfunctional mutant TH causes tyrosine hydroxylase deficiency (THD), characterized by symptoms ranging from mild l-Dopa responsive dystonia to severe neuropathy. Levodopa 114-120 tyrosine hydroxylase Homo sapiens 21-23 33823126-0 2021 Effects of L-dopa on expression of prolactin and synaptotagmin IV in 17-beta-estradiol-induced prolactinomas of ovariectomized hemiparkinsonian rats. Levodopa 11-17 prolactin Rattus norvegicus 35-44 33600923-12 2021 Our findings confirm that chronic treatment with hWJ-MSC, alone and in combination with L-Dopa, improved nociception and cognitive deficit in PD rats which may be the result of increasing IGF-1 and protect the viability of dopaminergic neurons. Levodopa 88-94 insulin-like growth factor 1 Rattus norvegicus 188-193 33639572-4 2021 In longitudinal mixed effects models that controlled for age, gender, disease duration, and levodopa equivalent drug dose, higher levels of serum NFL at baseline were associated with greater increases of UPDRS-III and total UPDRS scores, with greater worsening of postural instability and gait disorder (PIGD) scores but not tremor scores over time. Levodopa 92-100 neurofilament light chain Homo sapiens 146-149 33831661-4 2021 A2AR availability was measured using PET imaging with a [7-methyl-11C]-(E)-8-(3,4,5-trimethoxystyryl)-1,3,7-trimethylxanthine ([11C]TMSX) radioligand after a short term cessation of dopaminergic medication (12hrs for levodopa, 24hrs for dopamine agonists and MAO-B inhibitors). Levodopa 217-225 adenosine A2a receptor Homo sapiens 0-4 33823126-0 2021 Effects of L-dopa on expression of prolactin and synaptotagmin IV in 17-beta-estradiol-induced prolactinomas of ovariectomized hemiparkinsonian rats. Levodopa 11-17 synaptotagmin 4 Rattus norvegicus 49-65 33823126-4 2021 Since both estradiol (E2) and L-dopa act as regulators of prolactin (PRL) secretion from the pituitary gland, we investigated their effect on the expression of PRL in prolactinomas that developed in ovariectomized hemiparkinsonian rats treated with 17b-E2. Levodopa 30-36 prolactin Rattus norvegicus 58-67 33823126-5 2021 We also investigated the effect of E2 and L-dopa on the expression of synaptotagmin IV (Syt IV), an immediate early gene whose product is abundant in the pituitary gland and was found to be highly co-expressed with PRL in lactotrophs (>90%). Levodopa 42-48 synaptotagmin 4 Rattus norvegicus 70-86 33823126-5 2021 We also investigated the effect of E2 and L-dopa on the expression of synaptotagmin IV (Syt IV), an immediate early gene whose product is abundant in the pituitary gland and was found to be highly co-expressed with PRL in lactotrophs (>90%). Levodopa 42-48 synaptotagmin 4 Rattus norvegicus 88-94 33823126-9 2021 We found that high levels of serum 17b-E2 were associated with the upregulation of Syt IV and PRL in PRL-ir cells, while treatment with L-dopa decreased the size of prolactinomas and downregulated Syt IV but had no effect on PRL expression or serum concentrations. Levodopa 136-142 synaptotagmin 4 Rattus norvegicus 197-203 33841314-2 2021 Mutations of three genes, PRKN, PINK1, and DJ-1 cause pure phenotypes usually characterized by levodopa-responsive Parkinson"s disease. Levodopa 95-103 parkin RBR E3 ubiquitin protein ligase Homo sapiens 26-30 33841314-2 2021 Mutations of three genes, PRKN, PINK1, and DJ-1 cause pure phenotypes usually characterized by levodopa-responsive Parkinson"s disease. Levodopa 95-103 Parkinsonism associated deglycase Homo sapiens 43-47 33841314-2 2021 Mutations of three genes, PRKN, PINK1, and DJ-1 cause pure phenotypes usually characterized by levodopa-responsive Parkinson"s disease. Levodopa 95-103 PTEN induced kinase 1 Homo sapiens 32-37 33841314-3 2021 By contrast, mutations of other genes, including ATP13A2, PLA2G6, FBXO7, DNAJC6, SYNJ1, VPS13C, and PTRHD1, cause rarer, more severe diseases with a poor response to levodopa, generally with additional atypical features. Levodopa 166-174 ATPase cation transporting 13A2 Homo sapiens 49-56 33841314-3 2021 By contrast, mutations of other genes, including ATP13A2, PLA2G6, FBXO7, DNAJC6, SYNJ1, VPS13C, and PTRHD1, cause rarer, more severe diseases with a poor response to levodopa, generally with additional atypical features. Levodopa 166-174 phospholipase A2 group VI Homo sapiens 58-64 33841314-3 2021 By contrast, mutations of other genes, including ATP13A2, PLA2G6, FBXO7, DNAJC6, SYNJ1, VPS13C, and PTRHD1, cause rarer, more severe diseases with a poor response to levodopa, generally with additional atypical features. Levodopa 166-174 F-box protein 7 Homo sapiens 66-71 33536274-7 2021 PC2 was significantly correlated with the presence of parkinsonism (p = 5.34 x 10-5) and a positive levodopa response (p = 0.044), with age as a cofactor. Levodopa 100-108 polycystin 2, transient receptor potential cation channel Homo sapiens 0-3 33841314-3 2021 By contrast, mutations of other genes, including ATP13A2, PLA2G6, FBXO7, DNAJC6, SYNJ1, VPS13C, and PTRHD1, cause rarer, more severe diseases with a poor response to levodopa, generally with additional atypical features. Levodopa 166-174 DnaJ heat shock protein family (Hsp40) member C6 Homo sapiens 73-79 33841314-3 2021 By contrast, mutations of other genes, including ATP13A2, PLA2G6, FBXO7, DNAJC6, SYNJ1, VPS13C, and PTRHD1, cause rarer, more severe diseases with a poor response to levodopa, generally with additional atypical features. Levodopa 166-174 synaptojanin 1 Homo sapiens 81-86 33734312-8 2021 Bioinformatic and biochemical analyses on recombinant AADC predicted that the activity of one variant could be improved by L-3,4-dihydroxyphenylalanine (L-DOPA) administration; this hypothesis was corroborated in the patient-derived neuronal model, where L-DOPA treatment leads to amelioration of dopamine metabolites. Levodopa 123-151 dopa decarboxylase Homo sapiens 54-58 33741988-1 2021 Peripheral decarboxylase inhibitors (PDIs) prevent conversion of levodopa to dopamine in the blood by the enzyme aromatic L-amino acid decarboxylase (AADC). Levodopa 65-73 dopa decarboxylase Homo sapiens 122-148 33741988-1 2021 Peripheral decarboxylase inhibitors (PDIs) prevent conversion of levodopa to dopamine in the blood by the enzyme aromatic L-amino acid decarboxylase (AADC). Levodopa 65-73 dopa decarboxylase Homo sapiens 150-154 33741988-3 2021 We evaluated the effect of levodopa/PDI use on serum AADC enzyme activity. Levodopa 27-35 dopa decarboxylase Homo sapiens 53-57 33741988-5 2021 AADC enzyme activity was elevated in 62% of patients on levodopa/PDI treatment, compared to 19% of patients not on levodopa/PDI (median 90 mU/L vs. 50 mU/L, p < 0.001). Levodopa 56-64 dopa decarboxylase Homo sapiens 0-4 33741988-6 2021 Patients with elevated AADC activity had longer disease duration and higher doses of levodopa/PDI. Levodopa 85-93 dopa decarboxylase Homo sapiens 23-27 33741988-7 2021 These findings may implicate that peripheral AADC induction could underlie a waning effect of levodopa, necessitating dose increases to maintain a sustained therapeutic effect. Levodopa 94-102 dopa decarboxylase Homo sapiens 45-49 33734312-8 2021 Bioinformatic and biochemical analyses on recombinant AADC predicted that the activity of one variant could be improved by L-3,4-dihydroxyphenylalanine (L-DOPA) administration; this hypothesis was corroborated in the patient-derived neuronal model, where L-DOPA treatment leads to amelioration of dopamine metabolites. Levodopa 153-159 dopa decarboxylase Homo sapiens 54-58 33734312-8 2021 Bioinformatic and biochemical analyses on recombinant AADC predicted that the activity of one variant could be improved by L-3,4-dihydroxyphenylalanine (L-DOPA) administration; this hypothesis was corroborated in the patient-derived neuronal model, where L-DOPA treatment leads to amelioration of dopamine metabolites. Levodopa 255-261 dopa decarboxylase Homo sapiens 54-58 33676939-8 2021 CSF LPO level inversely correlated with the dose intensity of the dopaminergic medication regimen, as evaluated with levodopa equivalent dose or LED (mg/day; p<.0001). Levodopa 117-125 lactoperoxidase Homo sapiens 4-7 33713342-10 2021 In conclusion, GCH1 mutations may cause HSP; therefore, we suggest a levodopa trial in HSP patients and including GCH1 in the screening panels of HSP genes. Levodopa 69-77 GTP cyclohydrolase 1 Homo sapiens 15-19 33707771-1 2021 L-Dopa-induced dyskinesia (LID) is associated with the upregulation of striatal FosB in animal models and patients with Parkinson"s disease (PD). Levodopa 0-6 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85 33707771-6 2021 The development of AIMs during the entire L-Dopa treatment period was markedly inhibited by FosB gene knockdown and its associated molecular changes. Levodopa 42-48 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 93-97 33707771-7 2021 The antiparkinsonian action of L-Dopa was unchanged by FosB gene knockdown. Levodopa 31-37 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 56-60 33422541-6 2021 The administration of levodopa increased c-Fos expression in a subpopulation of sensorimotor striatum neurons of dyskinetic rats, but not in non-dyskinetic rats. Levodopa 22-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 41-46 33230949-1 2021 The L-type amino acid transporter 1 (LAT1, SLC7A5) imports dietary amino acids and amino acid drugs (e.g. L-DOPA) into the brain, and it plays a role in cancer metabolism. Levodopa 106-112 solute carrier family 7 member 5 Homo sapiens 4-35 33230949-1 2021 The L-type amino acid transporter 1 (LAT1, SLC7A5) imports dietary amino acids and amino acid drugs (e.g. L-DOPA) into the brain, and it plays a role in cancer metabolism. Levodopa 106-112 solute carrier family 7 member 5 Homo sapiens 37-41 33230949-1 2021 The L-type amino acid transporter 1 (LAT1, SLC7A5) imports dietary amino acids and amino acid drugs (e.g. L-DOPA) into the brain, and it plays a role in cancer metabolism. Levodopa 106-112 solute carrier family 7 member 5 Homo sapiens 43-49 33676939-0 2021 Cerebrospinal fluid lactoperoxidase level is enhanced in idiopathic Parkinson"s disease, and correlates with levodopa equivalent daily dose. Levodopa 109-117 lactoperoxidase Homo sapiens 20-35 33422541-0 2021 Inhibition of striatal dopamine D5 receptor attenuates levodopa-induced dyskinesia in a rat model of Parkinson"s disease. Levodopa 55-63 dopamine receptor D5 Rattus norvegicus 23-43 33422541-7 2021 The majority of the c-Fos+ neurons activated by levodopa in the striatum are positive for D5 receptor staining. Levodopa 48-56 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-25 33131114-8 2021 Using a 14-3-3 antagonist (R18) we were able to reduce the synthesis of L-DOPA and dopamine in ex vivo cerebro-buccal complexes. Levodopa 72-78 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein theta Homo sapiens 8-14 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. Levodopa 41-47 glycogen synthase kinase 3 beta Mus musculus 94-124 33840171-0 2021 In silico discovery and evaluation of phytochemicals binding mechanism against human catechol-O-methyltransferase as a putative bioenhancer of L-DOPA therapy in Parkinson disease. Levodopa 143-149 catechol-O-methyltransferase Homo sapiens 85-113 33840171-2 2021 Additionally, several inhibitory drugs such as Entacapone and Opicapone are also cosupplemented to protect peripheral inactivation of exogenous L-DOPA (~80%) that occurs due to metabolic activity of the enzyme catechol-O-methyltransferase (COMT). Levodopa 144-150 catechol-O-methyltransferase Homo sapiens 210-238 33840171-2 2021 Additionally, several inhibitory drugs such as Entacapone and Opicapone are also cosupplemented to protect peripheral inactivation of exogenous L-DOPA (~80%) that occurs due to metabolic activity of the enzyme catechol-O-methyltransferase (COMT). Levodopa 144-150 catechol-O-methyltransferase Homo sapiens 240-244 33011852-9 2021 Participant #2, walking FOG frequency and turning duration was reduced by 39.0% (OFF-L-dopa), and ON-L-dopa UPDRS-III score worsened (+ 5 points) at 12 months. Levodopa 85-91 zinc finger protein, FOG family member 1 Homo sapiens 24-27 33155746-10 2021 Those with Pick"s disease showed milder substantia nigra degeneration and better response to levodopa. Levodopa 93-101 protein interacting with PRKCA 1 Homo sapiens 11-15 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. Levodopa 41-47 glycogen synthase kinase 3 alpha Mus musculus 126-135 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. Levodopa 41-47 glycogen synthase kinase 3 alpha Mus musculus 164-173 33220276-9 2021 Opicapone potentiated the improvements in Parkinson s-like symptoms produced by levodopa/benserazide combinations with concomitant increase in plasma levodopa exposure, reduction of plasma 3-O-methyldopa levels and erythrocyte catechol-O-methyltransferase activity, results that were later demonstrated in 2 large Phase 3 studies in Parkinson s disease patients. Levodopa 80-88 catechol-O-methyltransferase Homo sapiens 227-255 33615192-0 2021 Docking Prediction of Levodopa in the Receptor Binding Domain of Spike Protein of SARS-CoV-2. Levodopa 22-30 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 65-70 33544218-6 2021 Higher Levodopa intake and MDS-UPDRS part IV scores (indicating motor fluctuations) predicted worse PDSS-2 and higher subjective nocturnal immobility scores, while disease duration and severity were not predictive. Levodopa 7-15 decaprenyl diphosphate synthase subunit 2 Homo sapiens 100-106 33119328-1 2021 Dopamine D2/3 receptor agonists are less likely to trigger dyskinesias than L-dopa while still offering relief from the motor symptoms of Parkinson"s disease (PD). Levodopa 76-82 dopamine receptor D3 Rattus norvegicus 0-22 33249031-0 2021 Genetic suppression of the dopamine D3 receptor in striatal D1 cells reduces the development of L-DOPA-induced dyskinesia. Levodopa 96-102 dopamine receptor D3 Rattus norvegicus 27-47 33597857-0 2020 Systemic Inflammation Increases the Susceptibility to Levodopa-Induced Dyskinesia in 6-OHDA Lesioned Rats by Targeting the NR2B-Medicated PKC/MEK/ERK Pathway. Levodopa 54-62 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 123-127 33597857-0 2020 Systemic Inflammation Increases the Susceptibility to Levodopa-Induced Dyskinesia in 6-OHDA Lesioned Rats by Targeting the NR2B-Medicated PKC/MEK/ERK Pathway. Levodopa 54-62 Eph receptor B1 Rattus norvegicus 146-149 33597857-11 2020 The PD rats that received the LPS injection showed the overexpression of p-NR2B and NR2B, as well as activated PKC/MEK/ERK and NF-kappaB signal pathways in response to the L-dopa administration. Levodopa 172-178 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 75-79 33597857-11 2020 The PD rats that received the LPS injection showed the overexpression of p-NR2B and NR2B, as well as activated PKC/MEK/ERK and NF-kappaB signal pathways in response to the L-dopa administration. Levodopa 172-178 Eph receptor B1 Rattus norvegicus 119-122 33510643-0 2020 Contributive Role of TNF-alpha to L-DOPA-Induced Dyskinesia in a Unilateral 6-OHDA Lesion Model of Parkinson"s Disease. Levodopa 34-40 tumor necrosis factor Mus musculus 21-30 33491134-10 2021 CONCLUSION: Our findings further demonstrated the safety of levodopa with dopa-decarboxylase treatment in PINK1-associated juvenile PD during pregnancy. Levodopa 60-68 PTEN induced kinase 1 Homo sapiens 106-111 33212219-7 2021 TMEM230-linked PD cases exhibit late-onset, good-response to levodopa, and typical clinical features of sporadic PD with DA neuronal loss in substantial nigra and Lewy body pathology. Levodopa 61-69 transmembrane protein 230 Homo sapiens 0-7 33450959-2 2021 Tyr catalyzes the oxidation of the substrate L-DOPA into dopachrome and melanin. Levodopa 45-51 tyrosinase Homo sapiens 0-3 33398040-3 2021 Here, we studied the effects on Abeta aggregation of DOPAL, a reactive catecholaldehyde intermediate of dopamine metabolism. Levodopa 53-58 amyloid beta precursor protein Homo sapiens 32-37 32628915-4 2021 Retinal pigment epithelial cells express a G protein-coupled receptor, GPR143, which down-regulates VEGF in response to levodopa. Levodopa 120-128 G protein-coupled receptor 143 Homo sapiens 71-77 32628915-4 2021 Retinal pigment epithelial cells express a G protein-coupled receptor, GPR143, which down-regulates VEGF in response to levodopa. Levodopa 120-128 vascular endothelial growth factor A Homo sapiens 100-104 32628915-9 2021 RESULTS: Levodopa was safe, well-tolerated and delayed anti-VEGF injection therapy while improving visual outcomes. Levodopa 9-17 vascular endothelial growth factor A Homo sapiens 60-64 33136226-0 2021 Impact of the catechol-O-methyltransferase Val158Met polymorphism on the pharmacokinetics of L-dopa and its metabolite 3-O-methyldopa in combination with entacapone. Levodopa 93-99 catechol-O-methyltransferase Homo sapiens 14-42 33338668-4 2021 By trio exome sequencing we now identified the variant p.(Glu198Lys) in a 29 year old woman presenting with typical clinical manifestations of PPP2R5D-related neurodevelopmental disorder and additionally with motor decline and levodopa responsive, early-onset parkinsonism from her mid-twenties on. Levodopa 227-235 protein phosphatase 2 regulatory subunit B'delta Homo sapiens 143-150 33459660-10 2021 Based on available data, levodopa showed an overall good outcome, especially in LRRK2, VPS35, Parkin, and PINK1 mutation carriers ("good" response in 94.6-100%). Levodopa 25-33 leucine rich repeat kinase 2 Homo sapiens 80-85 33459660-10 2021 Based on available data, levodopa showed an overall good outcome, especially in LRRK2, VPS35, Parkin, and PINK1 mutation carriers ("good" response in 94.6-100%). Levodopa 25-33 VPS35 retromer complex component Homo sapiens 87-92 33459660-10 2021 Based on available data, levodopa showed an overall good outcome, especially in LRRK2, VPS35, Parkin, and PINK1 mutation carriers ("good" response in 94.6-100%). Levodopa 25-33 PTEN induced kinase 1 Homo sapiens 106-111 33171229-0 2021 Irreversible incorporation of L-dopa into the C-terminus of alpha-tubulin inhibits binding of molecular motor KIF5B to microtubules and alters mitochondrial traffic along the axon. Levodopa 30-36 tubulin alpha 1b Homo sapiens 60-73 33171229-0 2021 Irreversible incorporation of L-dopa into the C-terminus of alpha-tubulin inhibits binding of molecular motor KIF5B to microtubules and alters mitochondrial traffic along the axon. Levodopa 30-36 kinesin family member 5B Homo sapiens 110-115 33171229-4 2021 We demonstrated previously that L-dopa can be post-translationally incorporated into the C-terminus of alpha-tubulin in living cells. Levodopa 32-38 tubulin alpha 1b Homo sapiens 103-116 33171229-5 2021 In the present study, we investigated the effect of the presence of L-dopa-tubulin-enriched microtubules on mitochondrial traffic mediated by molecular motor KIF5B. Levodopa 68-74 kinesin family member 5B Homo sapiens 158-163 33136226-2 2021 The effect of entacapone on the pharmacokinetics of L-dopa differs between patients with high-activity (H/H) and low-activity (L/L) catechol-O-methyltransferase (COMT) Val158Met polymorphisms, but the effects are unclear in heterozygous (H/L) patients. Levodopa 52-58 catechol-O-methyltransferase Homo sapiens 132-160 33136226-2 2021 The effect of entacapone on the pharmacokinetics of L-dopa differs between patients with high-activity (H/H) and low-activity (L/L) catechol-O-methyltransferase (COMT) Val158Met polymorphisms, but the effects are unclear in heterozygous (H/L) patients. Levodopa 52-58 catechol-O-methyltransferase Homo sapiens 162-166 33136226-4 2021 Therefore, the present study aimed to clarify the effect of the COMT Val158Met polymorphism on the concentrations of L-dopa and 3-OMD in the presence of entacapone. Levodopa 117-123 catechol-O-methyltransferase Homo sapiens 64-68 33216337-1 2021 AIM: In this study, we planned to investigate the effect of preoperative levodopa responsiveness to clinical outcomes in the first postoperative year and to evaluate the changes in the postoperative levodopa responsiveness in patients undergoing STN DBS. Levodopa 199-207 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 246-249 33216337-10 2021 CONCLUSION: In this study, we confirm that the response of L-dopa decreases after DBS of the STN. Levodopa 59-65 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 93-96 33308130-3 2021 Melanin synthesis starts via the hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine (DOPA) catalyzed by the enzyme known as tyrosinase (TYR), which triggers further conversion reaction to DOPAquinone and then to DOPAchrome. Levodopa 64-92 tyrosinase Homo sapiens 133-143 33352833-1 2020 Entacapone, a reversible inhibitor of catechol-O-methyl transferase, is used for patients in Parkinson"s disease because it increases the bioavailability and effectiveness of levodopa. Levodopa 175-183 catechol-O-methyltransferase Homo sapiens 38-67 33367937-8 2020 While the concept works to some extent, a lot of challenges have been encountered in terms of obtaining efficient inhibition while avoiding adverse effects.Some CNS drug compounds enter the brain via nutrient transport proteins, an example is the levodopa, a prodrug of Dopamine, which crosses the BBB via the large neutral amino acid transporter LAT1. Levodopa 247-255 solute carrier family 7 member 5 Homo sapiens 347-351 33409346-5 2021 Co-expression of the Arabidopsis transcription factor, AtMYB12, in fruit, increased L-DOPA levels further. Levodopa 84-90 myb domain protein 12 Arabidopsis thaliana 55-62 25577942-0 1993 C9orf72-Related Amyotrophic Lateral Sclerosis and Frontotemporal Dementia CLINICAL CHARACTERISTICS: C9orf72-related amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is characterized by: Motor neuron disease, including upper or lower motor neuron dysfunction (or both) that may or may not fulfill criteria for the ALS phenotype; Frontotemporal lobar degeneration (FTLD), including progressive changes in behavior, executive dysfunction, and/or language impairment; and Some degree of parkinsonism (typically of the akinetic-rigid type without tremor that is levodopa unresponsive). Levodopa 578-586 C9orf72-SMCR8 complex subunit Homo sapiens 0-7 25577942-0 1993 C9orf72-Related Amyotrophic Lateral Sclerosis and Frontotemporal Dementia CLINICAL CHARACTERISTICS: C9orf72-related amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is characterized by: Motor neuron disease, including upper or lower motor neuron dysfunction (or both) that may or may not fulfill criteria for the ALS phenotype; Frontotemporal lobar degeneration (FTLD), including progressive changes in behavior, executive dysfunction, and/or language impairment; and Some degree of parkinsonism (typically of the akinetic-rigid type without tremor that is levodopa unresponsive). Levodopa 578-586 C9orf72-SMCR8 complex subunit Homo sapiens 100-107 33038358-0 2020 Improved functional and histochemical outcomes in l-DOPA plus tolcapone treated VMAT2-deficient mice. Levodopa 50-56 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 80-85 33308130-3 2021 Melanin synthesis starts via the hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine (DOPA) catalyzed by the enzyme known as tyrosinase (TYR), which triggers further conversion reaction to DOPAquinone and then to DOPAchrome. Levodopa 64-92 tyrosinase Homo sapiens 145-148 33308130-3 2021 Melanin synthesis starts via the hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine (DOPA) catalyzed by the enzyme known as tyrosinase (TYR), which triggers further conversion reaction to DOPAquinone and then to DOPAchrome. Levodopa 94-98 tyrosinase Homo sapiens 133-143 33308130-3 2021 Melanin synthesis starts via the hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine (DOPA) catalyzed by the enzyme known as tyrosinase (TYR), which triggers further conversion reaction to DOPAquinone and then to DOPAchrome. Levodopa 94-98 tyrosinase Homo sapiens 145-148 32852534-12 2020 The other 3 patients carried GGC repeats of 79 or more units, 2 with 122 and 79 repeats, respectively, exhibited typical parkinsonism and were responsive to small dosages of levodopa over many years, with no clinical or imaging features of NIID. Levodopa 174-182 gamma-glutamylcyclotransferase Homo sapiens 29-32 33141179-11 2020 Furthermore, intraperitoneal injection of levodopa could significantly improve the motor dysfunction in UQCRC1 p.Tyr314Ser mutant knock-in mice. Levodopa 42-50 ubiquinol-cytochrome c reductase core protein 1 Mus musculus 104-110 32015009-8 2020 Following DA depletion, RGS9, through its inhibition of MSN D2R signaling, suppresses motor dysfunction induced by L-DOPA or D2R-selective agonists. Levodopa 115-121 regulator of G-protein signaling 9 Mus musculus 24-28 32015009-8 2020 Following DA depletion, RGS9, through its inhibition of MSN D2R signaling, suppresses motor dysfunction induced by L-DOPA or D2R-selective agonists. Levodopa 115-121 moesin Mus musculus 56-59 33181391-0 2020 Levodopa responsive-generalized dystonic spells and moaning in DNAJC6 related Juvenile Parkinson"s disease. Levodopa 0-8 DnaJ heat shock protein family (Hsp40) member C6 Homo sapiens 63-69 33279909-10 2021 CONCLUSIONS: PPN-DBS remains an investigational treatment for levodopa-refractory FOG. Levodopa 62-70 zinc finger protein, FOG family member 1 Homo sapiens 82-85 32852534-15 2020 Conclusions and Relevance: This study demonstrated that individuals with sporadic PD who carried pathogenic NOTCH2NLC GGC repeat expansions can present with typical parkinsonism, requiring only low dosages of levodopa, without displaying other clinical or imaging features of NIID even after several years of follow-up. Levodopa 209-217 notch receptor 2 Homo sapiens 108-114 32852534-15 2020 Conclusions and Relevance: This study demonstrated that individuals with sporadic PD who carried pathogenic NOTCH2NLC GGC repeat expansions can present with typical parkinsonism, requiring only low dosages of levodopa, without displaying other clinical or imaging features of NIID even after several years of follow-up. Levodopa 209-217 gamma-glutamylcyclotransferase Homo sapiens 118-121 33230756-6 2021 PD patients with FOG were older and had longer disease duration, higher levodopa equivalent dose, higher modified Hoehn and Yahr stage, higher Unified PD Rating Scale motor score, higher FOG-Q score, higher total Non-Motor Symptom Scale score, and lower BMD scores in the femoral neck area than those without FOG. Levodopa 72-80 zinc finger protein, FOG family member 1 Homo sapiens 17-20 33328857-7 2020 The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. Levodopa 24-32 brain-derived neurotrophic factor Rattus norvegicus 378-382 33328857-7 2020 The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. Levodopa 24-32 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 384-388 33328857-7 2020 The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. Levodopa 24-32 discs large MAGUK scaffold protein 4 Rattus norvegicus 390-395 33328857-7 2020 The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. Levodopa 24-32 drebrin 1 Rattus norvegicus 401-408 32621059-8 2020 Reversible MAO-A inhibition with moclobemide appears as an effective way to increase the anti-parkinsonian action of L-DOPA, without negatively affecting dyskinesia or dopaminergic psychosis. Levodopa 117-123 monoamine oxidase A Homo sapiens 11-16 33170152-0 2020 S-adenosylmethionine administration inhibits levodopa-induced vascular endothelial growth factor-A expression. Levodopa 45-53 vascular endothelial growth factor A Homo sapiens 62-98 33170152-2 2020 RESULTS: S-adenosylmethionine and levodopa had opposite effects on the protein stability of vascular endothelial growth factor-A. Levodopa 34-42 vascular endothelial growth factor A Homo sapiens 92-128 33170152-8 2020 CONCLUSIONS: These observations suggested that methyl donor S-adenosylmethionine could act as a potential agent against vascular endothelial growth factor-A-related diseases induced by levodopa treatment. Levodopa 185-193 vascular endothelial growth factor A Homo sapiens 120-156 33170152-9 2020 METHODS: We performed in vitro cytological analyses to assess whether S-adenosylmethionine intake could influence levodopa-induced vascular endothelial growth factor-A expression in human umbilical vein endothelial cells. Levodopa 114-122 vascular endothelial growth factor A Homo sapiens 131-167 32755645-12 2020 Moreover, a decrease microglial immunoreactivity for CD68, considered a marker of phagocytosis and lysosomal activity, was measured in the MPTP monkeys treated with L-Dopa, compared with non-treated MPTP animals. Levodopa 165-171 CD68 molecule Homo sapiens 53-57 32823188-0 2020 Mania triggered by levodopa treatment in a patient with frontotemporal dementia caused by A C9orf72 repeat expansion: A case report. Levodopa 19-27 C9orf72-SMCR8 complex subunit Homo sapiens 92-99 33151475-7 2020 Multivariate Cox regression analysis showed increased risk to LID development for both Levodopa Dose Equivalency (LED) (Hazard ratios (HR) = 1.001; 95% CI 1.00-1.01; p = 0.009) and individuals carrying the COMT L/L genotype (HR = 2.974; 95% CI 1.12-7.83; p = 0.010). Levodopa 87-95 catechol-O-methyltransferase Homo sapiens 206-210 32601846-1 2020 Monoamine oxidase (MAO) type B (MAO-B) inhibition was shown to confer anti-parkinsonian benefit as monotherapy and adjunct to L-3,4-dihydroxyphenylalanine (L-DOPA) in clinical trials. Levodopa 126-154 amine oxidase [flavin-containing] B Callithrix jacchus 32-37 33027712-2 2020 The sensitivity of these situations to detect FOG and the relative FOG response to l-dopa and subthalamic nucleus deep brain stimulation (STN-DBS) is unknown. Levodopa 83-89 zinc finger protein, FOG family member 1 Homo sapiens 67-70 32601846-6 2020 MAO-A inhibition with moclobemide may provide anti-parkinsonian benefit when administered without L-DOPA and might perhaps be considered as monotherapy for the treatment of Parkinson"s disease in the early stages of the condition. Levodopa 98-104 monoamine oxidase A Homo sapiens 0-5 32621059-0 2020 Monoamine oxidase A inhibition with moclobemide enhances the anti-parkinsonian effect of L-DOPA in the MPTP-lesioned marmoset. Levodopa 89-95 amine oxidase [flavin-containing] A Callithrix jacchus 0-19 33027712-14 2020 STN-DBS and l-dopa improve all FOG subtypes similarly, their effect is stronger in combination. Levodopa 12-18 zinc finger protein, FOG family member 1 Homo sapiens 31-34 33349576-6 2020 There is consensus that adenosine A2A receptor antagonists - administered either as a monotherapy or in combination with l-DOPA or dopamine agonists - improve motor function in both rodent and primate models of PD, and should be effective for treating the motor symptoms of PD in humans. Levodopa 121-127 adenosine A2a receptor Homo sapiens 24-46 33011475-9 2020 Patients with arousal-related disorders captured at V-PSG have a longer disease duration (p = 0.003), higher UPDRS score (p = 0.039), longer duration of treatment with levodopa (p = 0.017) and dopamine agonists (p = 0.018), worse H&Y staging (p = 0.001), lower MMSE score (p = 0.019) and more frequently hallucinations (p = 0.004). Levodopa 168-176 pregnancy specific beta-1-glycoprotein 5 Homo sapiens 54-57 33250838-0 2020 Polymorphism of the Dopa-Decarboxylase Gene Modifies the Motor Response to Levodopa in Chinese Patients With Parkinson"s Disease. Levodopa 75-83 dopa decarboxylase Homo sapiens 20-38 33192978-12 2020 Low vitamin B12 levels were also associated with deficits of peripheral nerve function, cumulative levodopa dose, and poor balance in PD (P < 0.05). Levodopa 99-107 NADH:ubiquinone oxidoreductase subunit B3 Homo sapiens 12-15 33250838-8 2020 We found that patients carrying the DDC CT or TT genotype exhibited a better motor response to L-DOPA than patients with the DDC CC genotype, and there was still a significant difference after adjustment for the L-DOPA dose in the acute challenge. Levodopa 95-101 dopa decarboxylase Homo sapiens 36-39 33250838-8 2020 We found that patients carrying the DDC CT or TT genotype exhibited a better motor response to L-DOPA than patients with the DDC CC genotype, and there was still a significant difference after adjustment for the L-DOPA dose in the acute challenge. Levodopa 212-218 dopa decarboxylase Homo sapiens 36-39 33250838-8 2020 We found that patients carrying the DDC CT or TT genotype exhibited a better motor response to L-DOPA than patients with the DDC CC genotype, and there was still a significant difference after adjustment for the L-DOPA dose in the acute challenge. Levodopa 212-218 dopa decarboxylase Homo sapiens 125-128 33250838-8 2020 We found that patients carrying the DDC CT or TT genotype exhibited a better motor response to L-DOPA than patients with the DDC CC genotype, and there was still a significant difference after adjustment for the L-DOPA dose in the acute challenge. Levodopa 95-101 dopa decarboxylase Homo sapiens 125-128 33250838-11 2020 The DDC single nucleotide polymorphism rs921451 modulated the motor response to L-DOPA in Chinese PD patients. Levodopa 80-86 dopa decarboxylase Homo sapiens 4-7 33045815-5 2020 Patients with PRKN mutations had an earlier age at onset, and less asymmetry, levodopa-induced motor complications, dysautonomia, and dementia than those without mutations. Levodopa 78-86 parkin RBR E3 ubiquitin protein ligase Homo sapiens 14-18 33250838-12 2020 Our results suggested that DDC may be a modifier gene for the L-DOPA treatment response in PD. Levodopa 62-68 dopa decarboxylase Homo sapiens 27-30 33093598-2 2020 The aim of this study was to characterize the population pharmacokinetics of levodopa following LECIG and levodopa-carbidopa intestinal gel (LCIG) infusion to investigate suitable translation of dose from LCIG to LECIG treatment, and the impact of common variations in the dopa-decarboxylase (DDC) and catechol-O-methyltransferase (COMT) genes on levodopa pharmacokinetics. Levodopa 77-85 dopa decarboxylase Homo sapiens 273-291 33093598-2 2020 The aim of this study was to characterize the population pharmacokinetics of levodopa following LECIG and levodopa-carbidopa intestinal gel (LCIG) infusion to investigate suitable translation of dose from LCIG to LECIG treatment, and the impact of common variations in the dopa-decarboxylase (DDC) and catechol-O-methyltransferase (COMT) genes on levodopa pharmacokinetics. Levodopa 77-85 dopa decarboxylase Homo sapiens 293-296 33093598-2 2020 The aim of this study was to characterize the population pharmacokinetics of levodopa following LECIG and levodopa-carbidopa intestinal gel (LCIG) infusion to investigate suitable translation of dose from LCIG to LECIG treatment, and the impact of common variations in the dopa-decarboxylase (DDC) and catechol-O-methyltransferase (COMT) genes on levodopa pharmacokinetics. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 302-330 33093598-2 2020 The aim of this study was to characterize the population pharmacokinetics of levodopa following LECIG and levodopa-carbidopa intestinal gel (LCIG) infusion to investigate suitable translation of dose from LCIG to LECIG treatment, and the impact of common variations in the dopa-decarboxylase (DDC) and catechol-O-methyltransferase (COMT) genes on levodopa pharmacokinetics. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 332-336 33093598-8 2020 The individuals with higher DDC and COMT enzyme activity showed tendencies towards higher levodopa CL/F. Levodopa 90-98 dopa decarboxylase Homo sapiens 28-31 33093598-8 2020 The individuals with higher DDC and COMT enzyme activity showed tendencies towards higher levodopa CL/F. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 36-40 32721557-6 2020 Notably, when administered alone, levodopa decreased the levels of functional Bregs and SLAMF1+ tolerogenic DCs and increased the levels of total and HLA-DR+ classical monocytes, while the pramipexole/levodopa combo may promote Treg- and tolerogenic DC-mediated regulatory responses. Levodopa 34-42 signaling lymphocytic activation molecule family member 1 Homo sapiens 88-94 32781320-4 2020 The difference between the two strip signals with or without the tyrosinase extracted the levodopa signal from the samples. Levodopa 90-98 tyrosinase Homo sapiens 65-75 33050305-8 2020 L-DOPA treatment drastically increased the expression of dynorphin (direct pathway), 5-HT1B, and zif268 mRNA in the striatum ipsilateral to the lesion. Levodopa 0-6 5-hydroxytryptamine receptor 1B Rattus norvegicus 85-91 33050305-8 2020 L-DOPA treatment drastically increased the expression of dynorphin (direct pathway), 5-HT1B, and zif268 mRNA in the striatum ipsilateral to the lesion. Levodopa 0-6 early growth response 1 Rattus norvegicus 97-103 32615138-5 2020 NLX-112 is a very potent, highly-selective, and fully efficacious 5-HT1A receptor agonist, which has been developed for the treatment of L-DOPA-induced dyskinesia in Parkinson"s disease patients. Levodopa 137-143 5-hydroxytryptamine receptor 1A Homo sapiens 66-81 32707436-10 2020 The histological and immunohistochemical studies showed that l-dopa caused a remarkable neurodegeneration and increased glial fibrillary acidic protein (GFAP) immunoexpression in the striatal area. Levodopa 61-67 glial fibrillary acidic protein Rattus norvegicus 120-151 32707436-10 2020 The histological and immunohistochemical studies showed that l-dopa caused a remarkable neurodegeneration and increased glial fibrillary acidic protein (GFAP) immunoexpression in the striatal area. Levodopa 61-67 glial fibrillary acidic protein Rattus norvegicus 153-157 32835737-0 2020 Human L-Dopa decarboxylase interaction with annexin V and expression during apoptosis. Levodopa 6-12 annexin A5 Homo sapiens 44-53 32835737-3 2020 We have shown that Annexin V, a fundamental apoptosis marker, is an inhibitor of l-Dopa decarboxylase activity. Levodopa 81-87 annexin A5 Homo sapiens 19-28 32464200-5 2020 Circular dichroism and molecular docking suggested that anthraquinones could not chelate directly the copper ions but they could bind to amino acid residues in the active site of tyrosinase via electrostatic forces and hydrophobic interactions, as well as hydrogen bonds, and the binding processes resulted in the conformational changes of tyrosinase and prevented the substrate (L-DOPA) from entering the active site, which led to the decrease of tyrosinase activity. Levodopa 380-386 tyrosinase Homo sapiens 179-189 33215284-0 2020 BDNF rs6265 Variant Alters Outcomes with Levodopa in Early-Stage Parkinson"s Disease. Levodopa 41-49 brain derived neurotrophic factor Homo sapiens 0-4 32763057-3 2020 Recently, G-protein coupled receptor GPR143, was identified as a receptor for l-DOPA. Levodopa 78-84 G protein-coupled receptor 143 Mus musculus 37-43 32643147-8 2020 In parkinsonian D1R-/- mice, the spine density decreases in i-SPNs, and this spine loss recovers after chronic levodopa. Levodopa 111-119 dopamine receptor D1 Mus musculus 16-19 32333181-9 2020 FOG was related to functional dependency (OR = 3.470; 95%CI 1.411-8.530; p = 0.007) after adjustment to age, gender, disease duration, daily equivalent levodopa dose, comorbidity (number of non-antiparkinsonian drugs/day), motor status (UPDRS-III), PIGD phenotype, motor complications (UPDRS-IV), NMS burden (NMSS total score), cognition (PD-CRS), and mood (BDI-II). Levodopa 152-160 zinc finger protein, FOG family member 1 Homo sapiens 0-3 33215284-7 2020 Similar effects of worse outcomes associated with levodopa monotherapy were observed in the BDNF rs11030094, rs10501087, and rs1491850 SNPs. Levodopa 50-58 brain derived neurotrophic factor Homo sapiens 92-96 33215284-8 2020 This study suggests the levodopa monotherapy strategy is associated with worse disease outcomes in BDNF rs6265 T carriers. Levodopa 24-32 brain derived neurotrophic factor Homo sapiens 99-103 32750392-0 2020 Lack of correlation between dyskinesia and pallidal serotonin transporter expression-induced by L-Dopa and Pramipexole in hemiparkinsonian rats. Levodopa 96-102 solute carrier family 6 member 4 Rattus norvegicus 52-73 32750392-1 2020 The role of pallidal serotonergic terminals in the development of L-Dopa-induced dyskinesias (LIDs) in Parkinson"s disease (PD) has been recently highlighted correlating pallidal serotonin transporter (SERT) expression levels with dyskinesias severity. Levodopa 66-72 solute carrier family 6 member 4 Rattus norvegicus 179-200 32750392-1 2020 The role of pallidal serotonergic terminals in the development of L-Dopa-induced dyskinesias (LIDs) in Parkinson"s disease (PD) has been recently highlighted correlating pallidal serotonin transporter (SERT) expression levels with dyskinesias severity. Levodopa 66-72 solute carrier family 6 member 4 Rattus norvegicus 202-206 32750392-8 2020 The number of GP SERT-positive axon varicosities was increased in L-Dopa (p < 0.05) and Pramipexole (p < 0.01) treated rats. Levodopa 66-72 solute carrier family 6 member 4 Rattus norvegicus 17-21 32464686-9 2020 In the 6-OHDA L-DOPA group, increased 5-HT transporter and decreased 5-HT1A receptor expression was found. Levodopa 14-20 solute carrier family 6 member 4 Rattus norvegicus 38-54 32771675-5 2020 For instance, the catecholamine biosynthetic pathway, which leads to L-DOPA production, could occur by hydroxylation of tyrosine to L-DOPA either by polyphenol oxidase (PPO) or tyrosine hydroxylase (TH). Levodopa 69-75 protoporphyrinogen oxidase Bos taurus 169-172 32771675-5 2020 For instance, the catecholamine biosynthetic pathway, which leads to L-DOPA production, could occur by hydroxylation of tyrosine to L-DOPA either by polyphenol oxidase (PPO) or tyrosine hydroxylase (TH). Levodopa 132-138 protoporphyrinogen oxidase Bos taurus 169-172 32771675-8 2020 Enzyme inhibitor studies showed significant inhibition of PPO enzyme with corresponding decrease in L-DOPA synthesis while TH and CYP inhibition had no effect on L-DOPA synthesis. Levodopa 100-106 protoporphyrinogen oxidase Bos taurus 58-61 33041762-9 2020 Conversely, Iba1+ microglia soma size was significantly increased (p < 0.01) in the lesioned striatum of levodopa-treated but not saline-treated rats. Levodopa 105-113 allograft inflammatory factor 1 Rattus norvegicus 12-16 32896531-7 2021 These findings suggest that DOPA-GPR143 signaling may be involved in the nicotine action in the nigrostriatal and mesolimbic dopaminergic systems. Levodopa 28-32 G protein-coupled receptor 143 Homo sapiens 33-39 32879346-3 2020 However, in Parkinson"s disease (PD), alterations in this pathway lead to functional upregulation of extracellular regulated kinases 1/2 (ERK1/2), contributing to L-DOPA-induced dyskinesia (LID). Levodopa 163-169 mitogen activated protein kinase 3 Rattus norvegicus 138-144 32588409-2 2020 MAO-B inhibitors are used as monotherapy as well as in combination with levodopa, whereas COMT inhibitors exert their effects only in conjungtion with levodopa. Levodopa 72-80 monoamine oxidase B Homo sapiens 0-5 32450711-1 2020 INTRODUCTION: Opicapone (OPC) is a well-established catechol-O-methyltransferase (COMT) inhibitor that is approved for the treatment of Parkinson"s disease (PD) associated with L-DOPA/L-amino acid decarboxylase inhibitor (DDI) therapy allowing for prolonged activity due to a more continuous supply of L-DOPA in the brain. Levodopa 177-183 catechol-O-methyltransferase Homo sapiens 52-80 32450711-1 2020 INTRODUCTION: Opicapone (OPC) is a well-established catechol-O-methyltransferase (COMT) inhibitor that is approved for the treatment of Parkinson"s disease (PD) associated with L-DOPA/L-amino acid decarboxylase inhibitor (DDI) therapy allowing for prolonged activity due to a more continuous supply of L-DOPA in the brain. Levodopa 177-183 catechol-O-methyltransferase Homo sapiens 82-86 32450711-1 2020 INTRODUCTION: Opicapone (OPC) is a well-established catechol-O-methyltransferase (COMT) inhibitor that is approved for the treatment of Parkinson"s disease (PD) associated with L-DOPA/L-amino acid decarboxylase inhibitor (DDI) therapy allowing for prolonged activity due to a more continuous supply of L-DOPA in the brain. Levodopa 302-308 catechol-O-methyltransferase Homo sapiens 82-86 32588409-2 2020 MAO-B inhibitors are used as monotherapy as well as in combination with levodopa, whereas COMT inhibitors exert their effects only in conjungtion with levodopa. Levodopa 151-159 catechol-O-methyltransferase Homo sapiens 90-94 33006509-2 2020 There is increasing evidence of a-synuclein deposition and pointing to a form of small fiber neuropathy intrinsic to PD, medium-large fiber PN is also a relatively frequent and potentially severe complication in advanced levodopa-treated PD, but degenerative factors and vitamin deficiency were related. Levodopa 221-229 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 140-142 33109837-5 2020 Gold fish brain has the "nucleus pars medialis," similar to the substanitia nigra of the human brain can be destructed by chemicals like MPTP, 6-hydroxydopamine and has selective protection by L-Dopa (Levodopa) and MAO-B (Monoamine oxidase B) inhibitors. Levodopa 201-209 monoamine oxidase B Homo sapiens 222-241 33109837-5 2020 Gold fish brain has the "nucleus pars medialis," similar to the substanitia nigra of the human brain can be destructed by chemicals like MPTP, 6-hydroxydopamine and has selective protection by L-Dopa (Levodopa) and MAO-B (Monoamine oxidase B) inhibitors. Levodopa 201-209 monoamine oxidase B Homo sapiens 215-220 32921640-7 2020 In this study, we first showed that a low concentration of L-DOPA (100 muM) rescues locomotion defects (i.e., speed, angular velocity, pause time) in Drosophila larvae expressing human mutant alpha-synuclein (A53T). Levodopa 59-65 synuclein alpha Homo sapiens 192-207 32434902-1 2020 Dynactin-1 (DCTN1)-related Parkinson-plus disorder (Perry syndrome) is an autosomal dominant neurodegenerative disorder characterised by levodopa-resistant parkinsonism, weight loss, mood change and central hypoventilation. Levodopa 137-145 dynactin subunit 1 Homo sapiens 0-10 32767480-2 2020 FBXO7defects cause a levodopa-responsive parkinsonian-pyramidal syndrome(PPS). Levodopa 21-29 F-box protein 7 Homo sapiens 0-5 32767480-4 2020 RESULTS: A novel homozygous c.368C>G (p.S123*) FBXO7 mutation was identified in a child with spastic paraplegia, epilepsy, cerebellar degeneration, levodopa nonresponsive parkinsonism, and brain iron deposition. Levodopa 148-156 F-box protein 7 Homo sapiens 47-52 32125460-0 2020 5-HT2A receptors but not cannabinoid receptors in the central nervous system mediate levodopa-induced visceral antinociception in conscious rats. Levodopa 85-93 5-hydroxytryptamine receptor 2A Rattus norvegicus 0-6 32125460-5 2020 Subsequently, we examined the roles of three 5-HT receptor subtypes: 5-HT1A, 5-HT1B, and 5-HT2A, in levodopa-induced visceral antinociception. Levodopa 100-108 5-hydroxytryptamine receptor 1B Rattus norvegicus 77-83 32125460-5 2020 Subsequently, we examined the roles of three 5-HT receptor subtypes: 5-HT1A, 5-HT1B, and 5-HT2A, in levodopa-induced visceral antinociception. Levodopa 100-108 5-hydroxytryptamine receptor 2A Rattus norvegicus 89-95 32125460-10 2020 These results suggest that 5-HT2A receptors in the central nervous system may play specific roles in levodopa-dopamine D2 receptor-induced antinociceptive action against colonic distension. Levodopa 101-109 5-hydroxytryptamine receptor 2A Rattus norvegicus 27-33 32848709-5 2020 In addition, within striatum, ERK1/2 is also able to modulate in a D1 receptor-dependent manner the activity of the mammalian target of rapamycin complex 1 (mTORC1) pathway under DA depletion and L-DOPA therapy. Levodopa 196-202 mitogen-activated protein kinase 3 Homo sapiens 30-36 32848709-5 2020 In addition, within striatum, ERK1/2 is also able to modulate in a D1 receptor-dependent manner the activity of the mammalian target of rapamycin complex 1 (mTORC1) pathway under DA depletion and L-DOPA therapy. Levodopa 196-202 CREB regulated transcription coactivator 1 Mus musculus 157-163 32848709-6 2020 Consistently, increased mTORC1 signaling appears during chronic administration of L-DOPA and shows a high correlation with the severity of dyskinesia. Levodopa 82-88 CREB regulated transcription coactivator 1 Mus musculus 24-30 32848709-9 2020 In our study, we investigated the role of mTORC1 pathway activation in modulating bidirectional striatal synaptic plasticity in L-DOPA-treated parkinsonian rats. Levodopa 128-134 CREB regulated transcription coactivator 1 Mus musculus 42-48 32848709-10 2020 Inhibition of mTORC1 by coadministration of rapamycin to L-DOPA was able to limit the magnitude of LID expression, accounting for a therapeutic effect of this drug. Levodopa 57-63 CREB regulated transcription coactivator 1 Mus musculus 14-20 32848709-12 2020 Furthermore, ex vivo patch clamp and intracellular recordings of SPNs revealed that pharmacological inhibition of mTORC1 also resulted associated with a physiological bidirectional plasticity, when compared to dyskinetic rats treated with L-DOPA alone. Levodopa 239-245 CREB regulated transcription coactivator 1 Mus musculus 114-120 32848709-13 2020 This study uncovers the important role of mTORC1 inhibition to prevent the loss of striatal bidirectional plasticity under chronic L-DOPA treatment in rodent models of PD. Levodopa 131-137 CREB regulated transcription coactivator 1 Mus musculus 42-48 32776353-4 2021 The action of tyrosinase on the enantiomers of tyrosine (L-tyrosine and D-tyrosine) and dopa (L-dopa and D-dopa) were studied for the first time focusing on quantitative transient phase kinetics. Levodopa 94-100 tyrosinase Homo sapiens 14-24 30809759-12 2020 Moreover, SMA activity was reduced during STN-DBS, while dopamine-induced hyperactivation of SMA which might underpin hyperdynamic L-dopa related overcompensation. Levodopa 131-137 survival of motor neuron 1, telomeric Homo sapiens 93-96 32520511-2 2020 The neurologist decided to perform dopamine transporter imaging (F-FP-CIT PET/CT) for accurate diagnosis, taking into account the potential adverse effects of L-dopa that the patient had been taking for a long time. Levodopa 159-165 solute carrier family 6 member 3 Homo sapiens 35-55 32387398-0 2020 Striatal Nurr1, but not FosB expression links a levodopa-induced dyskinesia phenotype to genotype in fisher 344 vs. Lewis hemiparkinsonian rats. Levodopa 48-56 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 9-14 32387398-5 2020 Following chronic levodopa, LID+ SD rats showed significant increases in candidate gene expression: Nr4a2/(Nurr1) > > Trh > Inhba = Fosb. Levodopa 18-26 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 100-105 32387398-5 2020 Following chronic levodopa, LID+ SD rats showed significant increases in candidate gene expression: Nr4a2/(Nurr1) > > Trh > Inhba = Fosb. Levodopa 18-26 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 107-112 32387398-5 2020 Following chronic levodopa, LID+ SD rats showed significant increases in candidate gene expression: Nr4a2/(Nurr1) > > Trh > Inhba = Fosb. Levodopa 18-26 thyrotropin releasing hormone Rattus norvegicus 118-121 32387398-5 2020 Following chronic levodopa, LID+ SD rats showed significant increases in candidate gene expression: Nr4a2/(Nurr1) > > Trh > Inhba = Fosb. Levodopa 18-26 inhibin subunit beta A Rattus norvegicus 124-129 32387398-5 2020 Following chronic levodopa, LID+ SD rats showed significant increases in candidate gene expression: Nr4a2/(Nurr1) > > Trh > Inhba = Fosb. Levodopa 18-26 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 132-136 32387398-6 2020 However, SD rats with long-standing striatal dopamine (DA) depletion treated with first-ever versus chronic high-dose levodopa revealed that despite identical levels of LID severity: 1) Fosb and Nurr1 transcripts but not protein were elevated with acute LID expression; 2) FOSB/DeltaFOSB and NURR1 proteins were elevated only with chronic LID; and 3) Trh transcript and protein were elevated only with chronic LID. Levodopa 118-126 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 186-190 32590294-12 2020 To the best of our knowledge, this case is the first PSEN1 mutation with a l-dopa responsive Parkinsonism lacking distinctive classical AD biomarkers. Levodopa 75-81 presenilin 1 Homo sapiens 53-58 32434902-1 2020 Dynactin-1 (DCTN1)-related Parkinson-plus disorder (Perry syndrome) is an autosomal dominant neurodegenerative disorder characterised by levodopa-resistant parkinsonism, weight loss, mood change and central hypoventilation. Levodopa 137-145 dynactin subunit 1 Homo sapiens 12-17 32802307-9 2020 The PD patients" L-dopa equivalent dose seems to be a strong predictor of the ADL-level in the morning. Levodopa 17-23 sarcoglycan alpha Homo sapiens 78-81 32671919-6 2020 Then, we explored the effects of l-dopa with respect to the secretion of PRL from anterior pituitary fragments. Levodopa 33-39 prolactin Mus musculus 73-76 32464747-8 2020 The expression level of pathogenesis-related protein 1 and inspection of plant morphology clearly revealed that both the l-DOPA and CAVA products stimulate plants to respond to biotic stresses. Levodopa 121-127 pathogenesis-related protein 1 Arabidopsis thaliana 24-54 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 219-247 tyrosinase Homo sapiens 0-10 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 219-247 tyrosinase Homo sapiens 12-15 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 219-247 tyrosinase Homo sapiens 0-3 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 249-255 tyrosinase Homo sapiens 0-10 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 249-255 tyrosinase Homo sapiens 12-15 32640730-1 2020 Tyrosinase (TYR) is a metalloenzyme classified as a type-3 copper protein, which is involved in the synthesis of melanin through a catalytic process beginning with the conversion of the amino acid l-Tyrosine (l-Tyr) to l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 249-255 tyrosinase Homo sapiens 0-3 32648885-7 2020 Additionally, OXY and the tyrosinase substrate L-dopa did not have a competitive relationship; OXY is a non-competitive inhibitor. Levodopa 47-53 tyrosinase Mus musculus 26-36 32735501-8 2020 CONCLUSION: Pramipexole combined with levodopa relieved PD symptoms and improved the quality of life of PD patients, potentially by suppressing serum TNF-alpha levels. Levodopa 38-46 tumor necrosis factor Homo sapiens 150-159 32671919-9 2020 Also, the presence of l-dopa increased DA levels in incubation media and reduced PRL secretion. Levodopa 22-28 prolactin Mus musculus 81-84 32671919-11 2020 In addition, l-dopa reduced corticotrophin-releasing hormone-stimulated adrenocorticotrophic hormone release from these cells after AADC activity was inhibited by NSD-1015. Levodopa 13-19 dopa decarboxylase Mus musculus 132-136 32671919-14 2020 These results suggest that the anterior pituitary synthesises DA from l-dopa by AADC and this catecholamine can be released from this gland contributing to the control of PRL secretion. Levodopa 70-76 dopa decarboxylase Mus musculus 80-84 32367255-1 2020 Tyrosinase (TYR) converts L-tyrosine into 3,4-dihydroxyphenylalanine (L-DOPA) and L-DOPA into L-dopaquinone, which can produce melanin pigment. Levodopa 70-76 tyrosinase Danio rerio 0-10 32367255-1 2020 Tyrosinase (TYR) converts L-tyrosine into 3,4-dihydroxyphenylalanine (L-DOPA) and L-DOPA into L-dopaquinone, which can produce melanin pigment. Levodopa 70-76 tyrosinase Danio rerio 12-15 32367255-1 2020 Tyrosinase (TYR) converts L-tyrosine into 3,4-dihydroxyphenylalanine (L-DOPA) and L-DOPA into L-dopaquinone, which can produce melanin pigment. Levodopa 82-88 tyrosinase Danio rerio 0-10 32367255-1 2020 Tyrosinase (TYR) converts L-tyrosine into 3,4-dihydroxyphenylalanine (L-DOPA) and L-DOPA into L-dopaquinone, which can produce melanin pigment. Levodopa 82-88 tyrosinase Danio rerio 12-15 32354665-3 2020 METHODS: Twelve Parkinson"s disease (PD) patients suffering from levodopa-responsive-FoG (off-FoG) were compared with 12 PD patients without FoG and 12 healthy subjects of similar age/sex. Levodopa 65-73 zinc finger protein, FOG family member 1 Homo sapiens 85-88 32541823-6 2020 alpha-synuclein overexpression led to an early loss of DACs associated with a decrease of light-adapted ERG responses and visual acuity that could be rescued by systemic injections of L-DOPA. Levodopa 184-190 synuclein alpha Homo sapiens 0-15 32555131-10 2020 CONCLUSIONS Our results indicate that levodopa combined with Bushen Zhichan recipe significantly improves behavior and protects dopaminergic neurons in a rodent Parkinson disease model, and suggest that the mechanism involves the decrease of excitatory amino acid toxicity and the increase in the expression of EAAT1. Levodopa 38-46 solute carrier family 1 member 3 Rattus norvegicus 311-316 32490491-5 2020 Molecular docking results showed that hydrophobic and hydrogen bonding forces played a dominant role in the binding of ECG to tyrosinase, affecting the binding affinity of l-dopa to tyrosinase, leading to a decrease in tyrosinase activity. Levodopa 172-178 tyrosinase Homo sapiens 126-136 32490491-5 2020 Molecular docking results showed that hydrophobic and hydrogen bonding forces played a dominant role in the binding of ECG to tyrosinase, affecting the binding affinity of l-dopa to tyrosinase, leading to a decrease in tyrosinase activity. Levodopa 172-178 tyrosinase Homo sapiens 182-192 32490491-5 2020 Molecular docking results showed that hydrophobic and hydrogen bonding forces played a dominant role in the binding of ECG to tyrosinase, affecting the binding affinity of l-dopa to tyrosinase, leading to a decrease in tyrosinase activity. Levodopa 172-178 tyrosinase Homo sapiens 182-192 32236790-1 2020 After more than two decades of preclinical and clinical studies, on August 27, 2019, the US Food and Drug Administration (FDA) approved the adenosine A2A receptor antagonist Nourianz (istradefylline) developed by Kyowa Hakko Kirin Inc., Japan, as an add-on treatment to levodopa in Parkinson"s disease (PD) with "OFF" episodes. Levodopa 271-279 adenosine A2a receptor Homo sapiens 140-162 32515486-4 2020 Opicapone is a recent and selective third-generation COMT inhibitor which achieves marked increase in the bioavailability of levodopa. Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 53-57 31392531-0 2020 Imaging SERT Availability in a Rat Model of L-DOPA-Induced Dyskinesia. Levodopa 44-50 solute carrier family 6 member 4 Rattus norvegicus 8-12 31392531-3 2020 To evaluate the effect of chronic L-DOPA treatment on SERT availability in an animal model of LID, we performed a longitudinal PET study. Levodopa 34-40 solute carrier family 6 member 4 Rattus norvegicus 54-58 31392531-7 2020 Chronic L-DOPA priming resulted in a relative preservation of SERT availability in the lesioned and healthy hemisphere compared to baseline measurements. Levodopa 8-14 solute carrier family 6 member 4 Rattus norvegicus 62-66 31392531-8 2020 CONCLUSIONS: Our longitudinal PET data support a preservation of SERT availability after the induction of L-DOPA-induced dyskinesia, which is in line with previous reports in dyskinetic PD patients. Levodopa 106-112 solute carrier family 6 member 4 Homo sapiens 65-69 32533012-0 2020 Genetic variations in catechol-O-methyltransferase gene are associated with levodopa response variability in Chinese patients with Parkinson"s disease. Levodopa 76-84 catechol-O-methyltransferase Homo sapiens 22-50 32533012-9 2020 Our primary results showed the possible association of SNPs other than the most common functional rs4680 in COMT with interindividual variance in the L-dopa daily dose and susceptibility to dyskinesia in Chinese patients, although this was an exploratory study based on a small sample size. Levodopa 150-156 catechol-O-methyltransferase Homo sapiens 108-112 32509261-4 2020 Objective: To study the effects of intestinal levodopa/carbidopa infusion in unresponsive-FOG that appears in PD patients treated with subthalamic nucleus deep brain stimulation. Levodopa 46-54 zinc finger protein, FOG family member 1 Homo sapiens 90-93 32472966-5 2020 Patients with PRKN mutations had an earlier age at onset, and less asymmetry, levodopa-induced motor complications, dysautonomia, and dementia than those without mutations. Levodopa 78-86 parkin RBR E3 ubiquitin protein ligase Homo sapiens 14-18 32441567-4 2022 In addition, we analyzed the association with clinical factors and evaluated whether clinical factors affected the COMT inhibitory activity of bLF in vitro.Results: Although not statistically significant, the peak plasma concentration (Cmax) of levodopa increased by 18.5%. Levodopa 245-253 catechol-O-methyltransferase Mus musculus 115-119 32509261-7 2020 Results: Administration of intestinal levodopa caused improvement of FOG in the "ON" state in four patients (80%) by 2 or more points in item 14 of the Unified Parkinson"s Disease Rating Scale. Levodopa 38-46 zinc finger protein, FOG family member 1 Homo sapiens 69-72 32509261-9 2020 Conclusions: Intestinal levodopa infusion may be a valuable therapeutic option for unresponsive-FOG developed after subthalamic nucleus deep brain stimulation. Levodopa 24-32 zinc finger protein, FOG family member 1 Homo sapiens 96-99 32238065-7 2020 Constraint of catechol-O-methyltransferase reduces homocysteine synthesis due to diminished consumption of methyl groups for levodopa turnover at least in the periphery. Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 14-42 32377929-6 2020 Thus, the anti-parkinsonian drug, L-Dopa, the anti-cancer drug, melphalan and the anti-epileptic drug gabapentin, all used in clinical practice, utilize LAT1 to reach their target site. Levodopa 34-40 solute carrier family 7 member 5 Homo sapiens 153-157 32204589-0 2020 Continuous Fluorometric Method for Determining the Monophenolase Activity of Tyrosinase on L-Tyrosine, through Quenching L-DOPA Fluorescence by Borate. Levodopa 121-127 tyrosinase Homo sapiens 77-87 31562557-1 2020 Monoamine oxidase B (MAO-B) inhibitors have an established role in the treatment of Parkinson"s disease as monotherapy or adjuvant to levodopa. Levodopa 134-142 monoamine oxidase B Homo sapiens 0-19 31562557-1 2020 Monoamine oxidase B (MAO-B) inhibitors have an established role in the treatment of Parkinson"s disease as monotherapy or adjuvant to levodopa. Levodopa 134-142 monoamine oxidase B Homo sapiens 21-26 32149427-0 2020 Aromatic L-Amino Acid Decarboxylase Gene Therapy Enhances Levodopa Response in Parkinson"s Disease. Levodopa 58-66 dopa decarboxylase Homo sapiens 0-35 32149427-1 2020 BACKGROUND: As Parkinson"s disease progresses, levodopa treatment loses efficacy, partly through the loss of the endogenous dopamine-synthesizing enzyme L-amino acid decarboxylase (AADC). Levodopa 47-55 dopa decarboxylase Homo sapiens 153-179 32149427-1 2020 BACKGROUND: As Parkinson"s disease progresses, levodopa treatment loses efficacy, partly through the loss of the endogenous dopamine-synthesizing enzyme L-amino acid decarboxylase (AADC). Levodopa 47-55 dopa decarboxylase Homo sapiens 181-185 32426479-0 2020 RasGRP1 is a causal factor in the development of l-DOPA-induced dyskinesia in Parkinson"s disease. Levodopa 49-55 RAS guanyl releasing protein 1 Homo sapiens 0-7 32426479-4 2020 l-DOPA treatment rapidly up-regulated RasGRP1 in the striatum of mouse and macaque model of PD. Levodopa 0-6 RAS guanyl releasing protein 1 Mus musculus 38-45 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 Rho/Rac guanine nucleotide exchange factor 2 Homo sapiens 20-23 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 Ras homolog, mTORC1 binding Homo sapiens 63-67 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 mechanistic target of rapamycin kinase Homo sapiens 91-127 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 mechanistic target of rapamycin kinase Homo sapiens 129-133 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 RAS guanyl releasing protein 1 Homo sapiens 136-143 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 mitogen-activated protein kinase 1 Homo sapiens 168-205 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 mitogen-activated protein kinase 1 Homo sapiens 207-210 32426479-6 2020 Besides acting as a GEF for Ras homolog enriched in the brain (Rheb), the activator of the mammalian target of rapamycin kinase (mTOR), RasGRP1 promotes l-DOPA-induced extracellular signal-regulated kinase (ERK) and the mTOR signaling in the striatum. Levodopa 153-159 mechanistic target of rapamycin kinase Homo sapiens 220-224 32344082-4 2020 It happened because vitamin-B12 is highly hydrophilic, interacting more with the medium than with the CAS/CS matrix, while l-dopa is less polar than vitamin-B12, interacting more with the CAS/CS matrix. Levodopa 123-129 BCAR1 scaffold protein, Cas family member Homo sapiens 188-194 32278297-3 2020 METHODS: Clinical trajectories of four patients from three families with pathogenic variants in GCH1 are described, illustrated by videos of the motor phenotype before and during treatment with levodopa. Levodopa 194-202 GTP cyclohydrolase 1 Homo sapiens 96-100 32238479-0 2020 Striatal Nurr1 Facilitates the Dyskinetic State and Exacerbates Levodopa-Induced Dyskinesia in a Rat Model of Parkinson"s Disease. Levodopa 64-72 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 9-14 32238479-1 2020 The transcription factor Nurr1 has been identified to be ectopically induced in the striatum of rodents expressing L-DOPA-induced dyskinesia (LID). Levodopa 115-121 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 25-30 32238479-8 2020 We additionally determined that in L-DOPA-naive rats striatal rAAV-Nurr1 overexpression 1) increased cortically-evoked firing in a sub-population of identified striatonigral MSNs, and 2) altering spine density and thin-spine morphology on striatal MSN; both phenomena mimicking changes seen in dyskinetic rats. Levodopa 35-41 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 67-72 32238479-9 2020 Finally, we provide post-mortem evidence of Nurr1 expression in striatal neurons of L-DOPA treated PD patients.Our data demonstrate that ectopic induction of striatal Nurr1 is capable of inducing LID behavior and associated neuropathology, even in resistant subjects. Levodopa 84-90 nuclear receptor subfamily 4 group A member 2 Homo sapiens 44-49 32238479-9 2020 Finally, we provide post-mortem evidence of Nurr1 expression in striatal neurons of L-DOPA treated PD patients.Our data demonstrate that ectopic induction of striatal Nurr1 is capable of inducing LID behavior and associated neuropathology, even in resistant subjects. Levodopa 84-90 nuclear receptor subfamily 4 group A member 2 Homo sapiens 167-172 32238479-10 2020 These data support a direct role of Nurr1 in aberrant neuronal plasticity and LID induction, providing a potential novel target for therapeutic development.Significance Statement The transcription factor Nurr1 is ectopically induced in striatal neurons of rats exhibiting levodopa-induced dyskinesia (LID; a side-effect to dopamine replacement strategies in Parkinson"s disease (PD)). Levodopa 272-280 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 36-41 32238479-10 2020 These data support a direct role of Nurr1 in aberrant neuronal plasticity and LID induction, providing a potential novel target for therapeutic development.Significance Statement The transcription factor Nurr1 is ectopically induced in striatal neurons of rats exhibiting levodopa-induced dyskinesia (LID; a side-effect to dopamine replacement strategies in Parkinson"s disease (PD)). Levodopa 272-280 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 204-209 32238479-13 2020 Moreover, we found that expression of Nurr1 in L-DOPA naive hemiparkinsonian rats resulted in the formation of morphological and electrophysiological signatures of maladaptive neuronal plasticity-a phenomenon associated with LID. Levodopa 47-53 nuclear receptor subfamily 4, group A, member 2 Rattus norvegicus 38-43 32238479-14 2020 Finally, we determined that ectopic Nurr1 expression can be found in the putamen of L-DOPA treated Parkinson"s disease patients. Levodopa 84-90 nuclear receptor subfamily 4 group A member 2 Homo sapiens 36-41 32431656-6 2020 We correlated the FoG outcome, calculated as improvement of Freezing of Gait Assessment Course (FoG-AC) from baseline MedOff to 6-month follow-up MedOn/StimOn, with the levodopa response of preoperative clinical and kinematic gait measures. Levodopa 169-177 zinc finger protein, FOG family member 1 Homo sapiens 18-21 32431656-6 2020 We correlated the FoG outcome, calculated as improvement of Freezing of Gait Assessment Course (FoG-AC) from baseline MedOff to 6-month follow-up MedOn/StimOn, with the levodopa response of preoperative clinical and kinematic gait measures. Levodopa 169-177 zinc finger protein, FOG family member 1 Homo sapiens 96-99 32431656-8 2020 Results: We found that the postoperative gait and FoG outcomes were associated with the preoperative levodopa response of clinical and kinematic gait measures. Levodopa 101-109 zinc finger protein, FOG family member 1 Homo sapiens 50-53 32431656-9 2020 In particular, preoperative levodopa sensitivity of FoG showed high correlation with a favorable quantitative FoG outcome. Levodopa 28-36 zinc finger protein, FOG family member 1 Homo sapiens 52-55 32431656-9 2020 In particular, preoperative levodopa sensitivity of FoG showed high correlation with a favorable quantitative FoG outcome. Levodopa 28-36 zinc finger protein, FOG family member 1 Homo sapiens 110-113 32431656-10 2020 Among kinematic measures, preoperative levodopa response of stride length and range of motion showed high correlation with favorable FoG outcome. Levodopa 39-47 zinc finger protein, FOG family member 1 Homo sapiens 133-136 32431656-11 2020 In addition, the preoperative levodopa sensitivity of FoG predicted postoperative FoG outcome with high accuracy (R 2 = 0.952; 95% CI: 0.95-1.29; P < 0.001). Levodopa 30-38 zinc finger protein, FOG family member 1 Homo sapiens 54-57 32431656-11 2020 In addition, the preoperative levodopa sensitivity of FoG predicted postoperative FoG outcome with high accuracy (R 2 = 0.952; 95% CI: 0.95-1.29; P < 0.001). Levodopa 30-38 zinc finger protein, FOG family member 1 Homo sapiens 82-85 32265703-9 2020 However, following chronic treatment with L-DOPA, FRL rats developed sensitization of turning and abnormal involuntary movements (AIMs); these effects were counteracted by the anti-dyskinetic 5-HT1 A agonist/D2 partial agonist sarizotan. Levodopa 42-48 5-hydroxytryptamine receptor 1A Rattus norvegicus 192-199 32313102-5 2020 Additional analysis revealed significant association of alpha-syn-specific T cell responses with age and lower levodopa equivalent dose. Levodopa 111-119 synuclein alpha Homo sapiens 56-65 32004527-0 2020 Selective metabotropic glutamate receptor 2 positive allosteric modulation alleviates L-DOPA-induced psychosis-like behaviours and dyskinesia in the MPTP-lesioned marmoset. Levodopa 86-92 metabotropic glutamate receptor 2 Callithrix jacchus 10-43 32004527-3 2020 We have recently shown that activation of metabotropic glutamate 2 and 3 (mGlu2/3) receptors produced significant relief of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced psychosis-like behaviours (PLBs) and dyskinesia in experimental models of PD. Levodopa 124-152 glutamate receptor, metabotropic 3 Mus musculus 74-81 32004527-3 2020 We have recently shown that activation of metabotropic glutamate 2 and 3 (mGlu2/3) receptors produced significant relief of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced psychosis-like behaviours (PLBs) and dyskinesia in experimental models of PD. Levodopa 154-160 glutamate receptor, metabotropic 3 Mus musculus 74-81 32044685-0 2020 Neuroimaging evaluation and successful treatment by using directional deep brain stimulation and levodopa in a patient with GNAO1-associated movement disorder: A case report. Levodopa 97-105 G protein subunit alpha o1 Homo sapiens 124-129 32144743-0 2020 Ameliorative effects of a phosphodiesterase 10A inhibitor, MR1916 on L-DOPA-induced dyskinesia in parkinsonian rats. Levodopa 69-75 phosphodiesterase 10A Rattus norvegicus 26-47 32322387-7 2020 Despite the limited effectiveness of current medications for FOG, especially levodopa resistant FOG, there were some drugs that showed promise such as istradefylline and rasagiline. Levodopa 77-85 zinc finger protein, FOG family member 1 Homo sapiens 96-99 32276449-6 2020 Lastly, we summarize the past findings of a large retrospective study that investigated the relationship between the stimulation of GPR143 with L-DOPA, the pigmentation pathway, and AMD, to potentially help develop new ways to prevent or treat AMD. Levodopa 144-150 G protein-coupled receptor 143 Homo sapiens 132-138 32346620-0 2020 Monoamine oxidase B rs1799836 G allele polymorphism is a risk factor for early development of levodopa-induced dyskinesia in Parkinson"s disease. Levodopa 94-102 monoamine oxidase B Homo sapiens 0-19 31931066-3 2020 The incorporation of 5% of silica nanospheres, in mass, for all CAS/CS matrices promoted a better-controlled and sustained release of l-dopa, focusing on the matrix based on 70% of CAS, 30% of CS and 5% of silica, whose l-dopa release lasted for 87 h. Besides, hydrogels are cytocompatible. Levodopa 134-140 BCAR1 scaffold protein, Cas family member Homo sapiens 64-70 31613174-2 2020 The mutation of POLG can result in mitochondrial dysfunction leading to a broad spectrum of disease.Methods: We report a 29-year-old Chinese female presented with levodopa-responsive parkinsonism, external ophthalmoplegia and optic atrophy. Levodopa 163-171 DNA polymerase gamma, catalytic subunit Homo sapiens 16-20 31872915-8 2020 CONCLUSIONS: Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. Levodopa 13-21 heat shock protein family B (small) member 1 Homo sapiens 94-99 31926127-0 2020 Ondansetron, a highly selective 5-HT3 receptor antagonist, reduces L-DOPA-induced dyskinesia in the 6-OHDA-lesioned rat model of Parkinson"s disease. Levodopa 67-73 5-hydroxytryptamine receptor 3A Rattus norvegicus 32-46 31926127-12 2020 Our results suggest that selective 5-HT3 blockade is a promising strategy to reduce the severity of L-DOPA-induced dyskinesia and may also attenuate its development. Levodopa 100-106 5-hydroxytryptamine receptor 3A Rattus norvegicus 35-40 31877419-4 2020 Previous studies demonstrated beneficial effect of D1/D2 dopamine-receptors chronic-stimulation on detrusor overactivity of PD-patients.The present study was aimed to evaluate possible effect of extended-release (ER) Levodopa administered at bed-time on both nocturia and nocturia-related quality-of-life (NQoL) in PD-patients. Levodopa 217-225 leiomodin 1 Homo sapiens 51-56 32292555-2 2020 New insights implicating c-Abl activation as a driving force in PD have opened a new drug development avenue for PD treatment beyond the symptomatic relief by L-DOPA. Levodopa 159-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 25-30 32165689-0 2020 Publisher Correction: The Dopamine D5 receptor contributes to activation of cholinergic interneurons during L-DOPA induced dyskinesia. Levodopa 108-114 dopamine receptor D5 Homo sapiens 26-46 32039920-1 2020 Dopamine receptor D1 modulates glutamatergic transmission in cortico-basal ganglia circuits and represents a major target of L-DOPA therapy in Parkinson"s disease. Levodopa 125-131 dopamine receptor D1 Homo sapiens 0-20 32258233-1 2020 Background: The relationship between freezing of gait (FOG) and levodopa response is complex. Levodopa 64-72 zinc finger protein, FOG family member 1 Homo sapiens 55-58 32258233-2 2020 Some patients respond, some have no response and in some patients levodopa causes FOG. Levodopa 66-74 zinc finger protein, FOG family member 1 Homo sapiens 82-85 32258233-3 2020 We present 2 cases demonstrating a diphasic worsening of FOG after levodopa dosing. Levodopa 67-75 zinc finger protein, FOG family member 1 Homo sapiens 57-60 32039920-5 2020 In turn, D1-mGlu5-dependent PLC signaling was causally linked with excessive activation of extracellular signal-regulated kinases in striatal neurons, leading to dyskinesia in animals treated with L-DOPA or D1 receptor agonists. Levodopa 197-203 heparan sulfate proteoglycan 2 Homo sapiens 28-31 31805305-4 2020 Therefore, we investigated if levodopa has an effect on the expression of synaptogyrin 1. Levodopa 30-38 synaptogyrin 1 Mus musculus 74-88 32189864-11 2020 BTL syndrome due to NKX2-1 mutation responded to levodopa while we did not find any case of chorea due to ADCY-5 mutation responding to levodopa. Levodopa 49-57 NK2 homeobox 1 Homo sapiens 20-26 32120303-4 2020 RESULTS: WES analysis identified biallelic variants in WARS2, encoding the mitochondrial tryptophanyl tRNA synthetase (mtTrpRS), a gene whose mutations have recently been associated with multiple neurological phenotypes, including childhood-onset, levodopa-responsive or unresponsive parkinsonism in a few patients. Levodopa 248-256 tryptophanyl tRNA synthetase 2, mitochondrial Homo sapiens 55-60 32120303-4 2020 RESULTS: WES analysis identified biallelic variants in WARS2, encoding the mitochondrial tryptophanyl tRNA synthetase (mtTrpRS), a gene whose mutations have recently been associated with multiple neurological phenotypes, including childhood-onset, levodopa-responsive or unresponsive parkinsonism in a few patients. Levodopa 248-256 tryptophanyl tRNA synthetase 2, mitochondrial Homo sapiens 75-117 32120303-4 2020 RESULTS: WES analysis identified biallelic variants in WARS2, encoding the mitochondrial tryptophanyl tRNA synthetase (mtTrpRS), a gene whose mutations have recently been associated with multiple neurological phenotypes, including childhood-onset, levodopa-responsive or unresponsive parkinsonism in a few patients. Levodopa 248-256 tryptophanyl tRNA synthetase 2, mitochondrial Homo sapiens 119-126 31872821-1 2020 Tyrosinase is a key enzyme that has long been considered as a biomarker for melanoma as it catalyzes the oxidation of tyrosine and l-DOPA in melanogenesis. Levodopa 131-137 tyrosinase Homo sapiens 0-10 32054879-0 2020 The Dopamine D5 receptor contributes to activation of cholinergic interneurons during L-DOPA induced dyskinesia. Levodopa 86-92 dopamine receptor D5 Mus musculus 4-24 32054879-2 2020 Together with the dopamine D2 receptor it is highly expressed in striatal cholinergic interneurons and therefore is poised to be a positive regulator of cholinergic activity in response to L-DOPA in the dopamine-depleted parkinsonian brain. Levodopa 189-195 dopamine receptor D2 Mus musculus 18-38 32054879-8 2020 However, mice lacking D5R exhibited slightly worsened locomotor performance in response to L-DOPA and enhanced LID scores. Levodopa 91-97 dopamine receptor D5 Mus musculus 22-25 32054879-9 2020 Our findings suggest that D5R can modulate L-DOPA induced dyskinesia and is a critical activator of CINs via pERK and pS6. Levodopa 43-49 dopamine receptor D5 Mus musculus 26-29 31669673-0 2020 Targeting the cannabinoid receptor CB2 in a mouse model of l-dopa induced dyskinesia. Levodopa 59-65 cannabinoid receptor 2 (macrophage) Mus musculus 35-38 31713727-11 2020 A linear correlation was demonstrated between VGF immunoreactivity and disease duration, levodopa equivalent dose and olfactory dysfunction. Levodopa 89-97 VGF nerve growth factor inducible Homo sapiens 46-49 31874188-12 2020 Moreover, we concluded glutamine transaminase-K represents a predominant cytosolic enzyme in rat brain that"s capable of catalyzing in vitro transamination of p-tyrosine and other aromatic amino acids, including the neurotransmitter precursors L-dopa and 5-hydroxytryptophan. Levodopa 244-250 kynurenine aminotransferase 1 Rattus norvegicus 23-47 31952126-5 2020 Using l-tyrosine and l-dopa as substrates, the effects of puerarin on the monophenolase and diphenolase activity of tyrosinase activity were investigated by the enzyme kinetics method. Levodopa 21-27 tyrosinase Homo sapiens 116-126 31990459-4 2020 OBJECTIVES: The study assessed the practical value of determining tau protein and amyloid beta (Abeta42) in the blood serum of patients with PD and their relationship with cognitive impairments, radiographic image and the used dose of L-DOPA. Levodopa 235-241 microtubule associated protein tau Homo sapiens 66-69 31990459-4 2020 OBJECTIVES: The study assessed the practical value of determining tau protein and amyloid beta (Abeta42) in the blood serum of patients with PD and their relationship with cognitive impairments, radiographic image and the used dose of L-DOPA. Levodopa 235-241 amyloid beta precursor protein Homo sapiens 82-94 32019134-5 2020 Michaelis-Menten constants were measured spectrophotometrically from diphenol oxidase reactions of Tyr, using L-3,4-dihydroxyphenylalanine (L-DOPA) as a substrate, at temperatures: 25, 31, 37, and 43 C. Under the same conditions, the Tyr structure and the L-DOPA binding activity were simulated using 3 ns molecular dynamics and docking. Levodopa 110-138 tyrosinase Homo sapiens 99-102 32019134-5 2020 Michaelis-Menten constants were measured spectrophotometrically from diphenol oxidase reactions of Tyr, using L-3,4-dihydroxyphenylalanine (L-DOPA) as a substrate, at temperatures: 25, 31, 37, and 43 C. Under the same conditions, the Tyr structure and the L-DOPA binding activity were simulated using 3 ns molecular dynamics and docking. Levodopa 140-146 tyrosinase Homo sapiens 99-102 32019134-5 2020 Michaelis-Menten constants were measured spectrophotometrically from diphenol oxidase reactions of Tyr, using L-3,4-dihydroxyphenylalanine (L-DOPA) as a substrate, at temperatures: 25, 31, 37, and 43 C. Under the same conditions, the Tyr structure and the L-DOPA binding activity were simulated using 3 ns molecular dynamics and docking. Levodopa 257-263 tyrosinase Homo sapiens 99-102 32019134-7 2020 The temperature-dependent analysis suggests that the association of L-DOPA with Tyr is a spontaneous enthalpy-driven reaction, which becomes unfavorable at the final step of dopachrome formation. Levodopa 68-74 tyrosinase Homo sapiens 80-83 32002361-8 2020 The Au/CILCE can detect L-dopa in human serum in the linear concentration range of 0.1 muM to 90 muM with detection and quantification limits of 4.5 nM and 15.0 nM, respectively. Levodopa 24-30 latexin Homo sapiens 87-90 32002361-8 2020 The Au/CILCE can detect L-dopa in human serum in the linear concentration range of 0.1 muM to 90 muM with detection and quantification limits of 4.5 nM and 15.0 nM, respectively. Levodopa 24-30 latexin Homo sapiens 97-100 32342808-6 2020 MATERIALS AND METHODS: In this study, the metabolomic profile changes related to GSTs polymorphism were searched in 54 Tunisian PD patients treated with L-dopa, using a gas chromatography-mass spectrometry (GCMS) technique. Levodopa 153-159 glutathione S-transferase kappa 1 Homo sapiens 81-85 32238135-10 2020 Clinical evidence illustrated that MAO-B inhibitors are recommended as monotherapy and added on therapy to levodopa. Levodopa 107-115 monoamine oxidase B Homo sapiens 35-40 32703142-7 2020 We furthermore review current evidence of the L-dopa-induced side effects and perspectives of L-dopa treatment in PD compared to other established treatments such as DA-agonists and the inhibitors of catechol-o-methyltransferase and monoamine oxidase B. Levodopa 46-52 monoamine oxidase B Homo sapiens 233-252 32703142-7 2020 We furthermore review current evidence of the L-dopa-induced side effects and perspectives of L-dopa treatment in PD compared to other established treatments such as DA-agonists and the inhibitors of catechol-o-methyltransferase and monoamine oxidase B. Levodopa 94-100 monoamine oxidase B Homo sapiens 233-252 31704349-6 2020 Furthermore, c-Fos expression increased more in the habenula nucleus (LHb) after SVS than it did after levodopa in 6-OHDA hemilesioned animals and after saline in the sham-lesioned animals. Levodopa 103-111 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-18 31868682-7 2020 RESULTS: Independent and model-free evaluation of a wide range of possible sets of conversion factors to LED suggested a set of normalized conversion factors for immediate release levodopa (1.00), controlled release levodopa (0.88), and amantadine (1.23). Levodopa 180-188 small integral membrane protein 10 like 2A Homo sapiens 105-108 31868682-7 2020 RESULTS: Independent and model-free evaluation of a wide range of possible sets of conversion factors to LED suggested a set of normalized conversion factors for immediate release levodopa (1.00), controlled release levodopa (0.88), and amantadine (1.23). Levodopa 216-224 small integral membrane protein 10 like 2A Homo sapiens 105-108 31868682-10 2020 CONCLUSIONS: Independent from previous studies and prior assumptions we show that the currently-used LED conversion factors for immediate release levodopa, controlled release levodopa and amantadine are largely correct and that dopamine agonists, MAO-B inhibitors and entacapone, given in addition to levodopa, have little additional clinical value for PD patients with motor fluctuations. Levodopa 146-154 small integral membrane protein 10 like 2A Homo sapiens 101-104 31868682-10 2020 CONCLUSIONS: Independent from previous studies and prior assumptions we show that the currently-used LED conversion factors for immediate release levodopa, controlled release levodopa and amantadine are largely correct and that dopamine agonists, MAO-B inhibitors and entacapone, given in addition to levodopa, have little additional clinical value for PD patients with motor fluctuations. Levodopa 175-183 small integral membrane protein 10 like 2A Homo sapiens 101-104 31868682-10 2020 CONCLUSIONS: Independent from previous studies and prior assumptions we show that the currently-used LED conversion factors for immediate release levodopa, controlled release levodopa and amantadine are largely correct and that dopamine agonists, MAO-B inhibitors and entacapone, given in addition to levodopa, have little additional clinical value for PD patients with motor fluctuations. Levodopa 175-183 small integral membrane protein 10 like 2A Homo sapiens 101-104 31868685-6 2020 RESULTS: Part B of the Fahn-Tolosa-Marin Tremor Rating Scale was the most sensitive to acute levodopa challenge (Cohen"s d = -1.04, eta2 = 0.12). Levodopa 93-101 DNA polymerase iota Homo sapiens 132-136 31704349-7 2020 SVS and levodopa induced similar c-Fos expression in several regions, e.g. the caudate putamen (CPu), where saline had no effect. Levodopa 8-16 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 33-38 32651332-1 2020 BACKGROUND: We recently showed that striatal overexpression of brain derived neurotrophic factor (BDNF) by adeno-associated viral (AAV) vector exacerbated L-DOPA-induced dyskinesia (LID) in 6-OHDA-lesioned rats. Levodopa 155-161 brain-derived neurotrophic factor Rattus norvegicus 63-96 32651332-1 2020 BACKGROUND: We recently showed that striatal overexpression of brain derived neurotrophic factor (BDNF) by adeno-associated viral (AAV) vector exacerbated L-DOPA-induced dyskinesia (LID) in 6-OHDA-lesioned rats. Levodopa 155-161 brain-derived neurotrophic factor Rattus norvegicus 98-102 31666199-0 2020 Genetic deletion of GPR88 enhances the locomotor response to L-DOPA in experimental parkinsonism while counteracting the induction of dyskinesia. Levodopa 61-67 G-protein coupled receptor 88 Mus musculus 20-25 31666199-5 2020 Chronic L-DOPA administration to male GPR88 KO mice, subjected to unilateral 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle, resulted in more rotations than in their WT counterparts. Levodopa 8-14 G-protein coupled receptor 88 Mus musculus 38-43 31666199-7 2020 These behavioral responses were accompanied by altered transcription of L-DOPA upregulated genes in lesioned GPR88 KO compared to WT striata. Levodopa 72-78 G-protein coupled receptor 88 Mus musculus 109-114 31666199-11 2020 In conclusion, genetic deletion of GPR88 promotes L-DOPA-induced rotation and spontaneous locomotion yet suppresses the induction of LIDs and also reduces tremor. Levodopa 50-56 G-protein coupled receptor 88 Mus musculus 35-40 31819070-1 2019 Tyrosine hydroxylase (TH) catalyzes the hydroxylation of L-tyrosine to L-DOPA. Levodopa 71-77 tyrosine hydroxylase Rattus norvegicus 0-20 31891566-0 2019 beta-arrestin2 alleviates L-dopa-induced dyskinesia via lower D1R activity in Parkinson"s rats. Levodopa 26-32 arrestin, beta 2, pseudogene Rattus norvegicus 0-14 31891566-1 2019 The cause of the L-dopa-induced dyskinesia (LID) has been ascribed to G-protein coupled receptor (GPCR) supersensitivity and uncontrolled downstream signaling. Levodopa 17-23 G protein-coupled bile acid receptor 1 Rattus norvegicus 70-96 31891566-1 2019 The cause of the L-dopa-induced dyskinesia (LID) has been ascribed to G-protein coupled receptor (GPCR) supersensitivity and uncontrolled downstream signaling. Levodopa 17-23 G protein-coupled bile acid receptor 1 Rattus norvegicus 98-102 31891566-9 2019 These data not only demonstrate a central role for beta-arrestin2/GPCR signaling in LID, but also show the D1R signal pathway changes occurring in response to dopaminergic denervation and pulsatile administration of L-dopa. Levodopa 216-222 arrestin, beta 2, pseudogene Rattus norvegicus 51-65 31891566-9 2019 These data not only demonstrate a central role for beta-arrestin2/GPCR signaling in LID, but also show the D1R signal pathway changes occurring in response to dopaminergic denervation and pulsatile administration of L-dopa. Levodopa 216-222 G protein-coupled bile acid receptor 1 Rattus norvegicus 66-70 31819070-1 2019 Tyrosine hydroxylase (TH) catalyzes the hydroxylation of L-tyrosine to L-DOPA. Levodopa 71-77 tyrosine hydroxylase Rattus norvegicus 22-24 31216095-8 2019 Increased striatal dopamine turnover was observed in Hdc KO mice after treatment with dopamine precursor l-Dopa. Levodopa 105-111 histidine decarboxylase Mus musculus 53-56 31491493-0 2019 Striatal overexpression of beta-arrestin2 counteracts L-dopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson"s disease rats. Levodopa 54-60 arrestin, beta 2, pseudogene Rattus norvegicus 27-41 31491493-6 2019 We found that striatal overexpression of AAV-mediated beta-arrestin2 produced less severe AIMs (abnormal involuntary movements) in response to L-dopa, whereas selective deletion of beta-arrestin2 in the striatal neurons dramatically enhanced the severity of dyskinesia induced by L-dopa. Levodopa 143-149 arrestin, beta 2, pseudogene Rattus norvegicus 54-68 31491493-6 2019 We found that striatal overexpression of AAV-mediated beta-arrestin2 produced less severe AIMs (abnormal involuntary movements) in response to L-dopa, whereas selective deletion of beta-arrestin2 in the striatal neurons dramatically enhanced the severity of dyskinesia induced by L-dopa. Levodopa 280-286 arrestin, beta 2, pseudogene Rattus norvegicus 54-68 31491493-8 2019 Finally, overexpression of beta-arrestin2 diminished L-dopa-induced D1R and phosphor-DARPP32/ERK levels. Levodopa 53-59 arrestin, beta 2, pseudogene Rattus norvegicus 27-41 31491493-8 2019 Finally, overexpression of beta-arrestin2 diminished L-dopa-induced D1R and phosphor-DARPP32/ERK levels. Levodopa 53-59 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 85-92 31491493-8 2019 Finally, overexpression of beta-arrestin2 diminished L-dopa-induced D1R and phosphor-DARPP32/ERK levels. Levodopa 53-59 Eph receptor B1 Rattus norvegicus 93-96 31781365-10 2019 In conclusion, L-dopa is now the most commonly prescribed medication for cases of PD but there is large variation in the prescribing rates of catechol-O-methyltransferase (COMT) inhibitors, monoamine oxidase B (MAO-B) inhibitors, amantadine, and anticholinergics between countries. Levodopa 15-21 monoamine oxidase B Homo sapiens 211-216 31866812-9 2019 Levodopa equivalent dose, age (direct), age at disease onset (inverse), and WCST were significant predictors of FoG (p = 0.01, p = 0.0025, p = 0.0016, and p = 0.029, respectively). Levodopa 0-8 zinc finger protein, FOG family member 1 Homo sapiens 112-115 31866812-11 2019 The main explanatory variables of FoG occurrence are levodopa equivalent dose, age, age at disease onset, and WCST. Levodopa 53-61 zinc finger protein, FOG family member 1 Homo sapiens 34-37 31335998-6 2019 Striatal levels of GLUR1 were measured as a l-dopa-induced postsynaptic change that is under tumor necrosis factor-alpha control. Levodopa 44-50 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 19-24 31335998-6 2019 Striatal levels of GLUR1 were measured as a l-dopa-induced postsynaptic change that is under tumor necrosis factor-alpha control. Levodopa 44-50 tumor necrosis factor Rattus norvegicus 93-120 31335998-8 2019 Moreover, both compounds inhibited the l-dopa-induced microgliosis and excessive tumor necrosis factor-alpha in the striatum and substantia nigra reticulata, while restoring physiological levels of the anti-inflammatory cytokine interleukin-10. Levodopa 39-45 tumor necrosis factor Rattus norvegicus 81-108 31335998-8 2019 Moreover, both compounds inhibited the l-dopa-induced microgliosis and excessive tumor necrosis factor-alpha in the striatum and substantia nigra reticulata, while restoring physiological levels of the anti-inflammatory cytokine interleukin-10. Levodopa 39-45 interleukin 10 Rattus norvegicus 229-243 31335998-9 2019 l-Dopa-induced angiogenesis was inhibited in both basal ganglia nuclei, and l-dopa-induced GLUR1 overexpression in the dorsolateral striatum was restored to normal levels. Levodopa 76-82 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 91-96 31799377-1 2019 Study objectives included testing whether presumed levodopa-unresponsive freezing of gait (FOG) in Parkinson"s disease (PD) actually persists in the presence of adequate dopaminergic dosing and to investigate whether the presence of other parkinsonian features and their responsiveness to therapy varies across patients without FOG (NO-FOG), with levodopa-responsive FOG (OFF-FOG), and with levodopa-unresponsive FOG (ONOFF-FOG). Levodopa 51-59 zinc finger protein, FOG family member 1 Homo sapiens 91-94 31701332-9 2021 We identified 19 cases with heterozygous NPC mutations in the literature who presented with a neurodegenerative disease, including levodopa-responsive PD, atypical parkinsonism (PSP, CBD), dystonia or dementia with a mean age at onset of about 57 years (range 8-87). Levodopa 131-139 NPC intracellular cholesterol transporter 1 Homo sapiens 41-44 31422483-1 2019 Preclinical evidence indicates that mGluR5 is a potential therapeutic target for Parkinson"s disease and L-DOPA-induced dyskinesia. Levodopa 105-111 glutamate receptor, ionotropic, kainate 1 Mus musculus 36-42 31419477-0 2019 Levodopa is effective in the treatment of three Chinese Tyrosine hydroxylase (TH) deficiency children. Levodopa 0-8 tyrosine hydroxylase Homo sapiens 56-76 31419477-0 2019 Levodopa is effective in the treatment of three Chinese Tyrosine hydroxylase (TH) deficiency children. Levodopa 0-8 tyrosine hydroxylase Homo sapiens 78-80 31419477-2 2019 TH converts tyrosine into L-DOPA, which is the direct precursor of catecholamine biosynthesis. Levodopa 26-32 tyrosine hydroxylase Homo sapiens 0-2 31252260-5 2019 The sensitivity towards the L-dopa detection is estimated to be 1.868 muA muM-1 cm-2 in the linear concentration of 0.05-7.0 mumol L-1 and 0.778 muA muM-1 cm-2 in the linear concentration of 7.00-100 mumol L-1, respectively. Levodopa 28-34 PWWP domain containing 3A, DNA repair factor Homo sapiens 76-81 30590075-0 2019 Immunoreactivity of a G protein-coupled l-DOPA receptor GPR143, in Lewy bodies. Levodopa 40-46 G protein-coupled receptor 143 Homo sapiens 56-62 30590075-3 2019 Recently, the ocular albinism 1 gene product, OA1/GPR143 (GPR143), was identified as a receptor for l-DOPA. Levodopa 100-106 G protein-coupled receptor 143 Homo sapiens 14-31 30590075-3 2019 Recently, the ocular albinism 1 gene product, OA1/GPR143 (GPR143), was identified as a receptor for l-DOPA. Levodopa 100-106 G protein-coupled receptor 143 Homo sapiens 46-56 30590075-3 2019 Recently, the ocular albinism 1 gene product, OA1/GPR143 (GPR143), was identified as a receptor for l-DOPA. Levodopa 100-106 G protein-coupled receptor 143 Homo sapiens 50-56 31279520-4 2019 Based on the broad substrate spectrum, tyrosinase has been used in bioremediation of phenolic pollutants, constructing biosensors for identifying phenolic compounds, and L-DOPA synthesis. Levodopa 170-176 tyrosinase Homo sapiens 39-49 31279520-6 2019 Accordingly, tyrosinase might be a potential biocatalyst for industrial applications (e.g., electroenzymatic L-DOPA production, but its long-term stability and reusability should be further explored. Levodopa 109-115 tyrosinase Homo sapiens 13-23 31279520-7 2019 In this review, we emphasize the versatility of tyrosinase, which includes conventional applications, and suggest new perspectives as an industrial biocatalyst (e.g., electroenzymatic L-DOPA production). Levodopa 184-190 tyrosinase Homo sapiens 48-58 31136763-1 2019 Rat models based on viral vector-mediated overexpression of alpha-synuclein are regarded as highly valuable models that closely mimic cardinal features of human Parkinson"s disease (PD) such as L-DOPA-dependent motor impairment, dopaminergic neurodegeneration and alpha-synuclein inclusions. Levodopa 194-200 synuclein alpha Homo sapiens 60-75 31829066-3 2019 Mutated amino acid sequences in genes of DOPA such as TH, DDC, DBH, VMAT2, and NMDA (SET-1) have been implicated as major factors causing schizophrenia. Levodopa 41-45 dopamine beta-hydroxylase Homo sapiens 63-66 31829066-3 2019 Mutated amino acid sequences in genes of DOPA such as TH, DDC, DBH, VMAT2, and NMDA (SET-1) have been implicated as major factors causing schizophrenia. Levodopa 41-45 solute carrier family 18 member A2 Homo sapiens 68-73 31829066-3 2019 Mutated amino acid sequences in genes of DOPA such as TH, DDC, DBH, VMAT2, and NMDA (SET-1) have been implicated as major factors causing schizophrenia. Levodopa 41-45 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 85-90 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 regulator of G protein signaling 4 Homo sapiens 65-69 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 neuregulin 1 Homo sapiens 71-75 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 catechol-O-methyltransferase Homo sapiens 77-81 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 AKT serine/threonine kinase 1 Homo sapiens 83-87 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 dystrobrevin binding protein 1 Homo sapiens 92-98 31829066-4 2019 In addition mutations in genes other than the DOPA genes such as RGS4, NRG1, COMT, AKT1 and DTNBP1 (SET 2) have also been implicated in the pathogenesis of schizophrenia. Levodopa 46-50 SET domain containing 2, histone lysine methyltransferase Homo sapiens 100-105 31829066-11 2019 From the results it is observed that, the compoud has exhibited best dock score against all the selected targets than the clozapie except DBH and VMAT2 in SET-1 targets of DOPA genes. Levodopa 172-176 dopamine beta-hydroxylase Homo sapiens 138-141 31829066-11 2019 From the results it is observed that, the compoud has exhibited best dock score against all the selected targets than the clozapie except DBH and VMAT2 in SET-1 targets of DOPA genes. Levodopa 172-176 solute carrier family 18 member A2 Homo sapiens 146-151 31829066-11 2019 From the results it is observed that, the compoud has exhibited best dock score against all the selected targets than the clozapie except DBH and VMAT2 in SET-1 targets of DOPA genes. Levodopa 172-176 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 155-160 31272925-2 2019 Levodopa-responsive juvenile parkinsonism that is consistent with diagnostic criteria for Parkinson"s disease is most often caused by mutations in the PARK-Parkin, PARK-PINK1, or PARK-DJ1 genes. Levodopa 0-8 PTEN induced kinase 1 Homo sapiens 169-174 31405930-9 2019 We previously showed that abrogating native alpha-synuclein (alphaS) tetramers produces a close PD model, including dopaminergic and cortical fiber loss and a progressive motor disorder responsive to l-DOPA. Levodopa 200-206 synuclein alpha Homo sapiens 44-59 31494731-2 2019 Dyskinesia improvement with STN DBS is believed to result entirely from levodopa reduction. Levodopa 72-80 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 28-31 31494731-9 2019 Dyskinesias after STN DBS improved more than predicted by levodopa reduction alone. Levodopa 58-66 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 18-21 31351976-1 2019 Selective blockade of serotonin 2A (5-HT2A) receptors is a promising strategy to reduce L-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia and has shown efficacy in a Phase III clinical trial for dopaminergic psychosis in Parkinson"s disease (PD). Levodopa 88-116 5-hydroxytryptamine receptor 2A Rattus norvegicus 36-42 31351976-1 2019 Selective blockade of serotonin 2A (5-HT2A) receptors is a promising strategy to reduce L-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia and has shown efficacy in a Phase III clinical trial for dopaminergic psychosis in Parkinson"s disease (PD). Levodopa 118-124 5-hydroxytryptamine receptor 2A Rattus norvegicus 36-42 20301387-9 1993 Prevention of secondary complications: Prevention of L-dopa induced dyskinesias may include deep-brain stimulation, constant drug delivery/stimulation (CDD/CDS), reduction of levodopa doses, and the use of dopamine receptor agonists. Levodopa 53-59 CDP-diacylglycerol synthase 1 Homo sapiens 156-159 31433646-0 2019 Unique Hydrolysis of an Ester-Type Prodrug of Levodopa in Human Plasma: Relay-Type Role Sharing between Alpha-1 Acid Glycoprotein and Human Serum Albumin. Levodopa 46-54 albumin Homo sapiens 140-153 30977041-8 2019 Similar to 5-HT, L-DOPA decreased aggression in Lmx1b-/- mice. Levodopa 17-23 LIM homeobox transcription factor 1 beta Mus musculus 48-53 31554346-2 2019 Several papers postulated that large-fiber neuropathy (PNP) in PD is related to vitamin B12 deficiency and L-Dopa exposure. Levodopa 107-113 purine nucleoside phosphorylase Homo sapiens 55-58 31554346-5 2019 In the L-Dopa group, the frequency of PNP was 67.3% as compared to PNP in the non-L-Dopa group, where one subject had PNP (chi2 = 23.41, p < 0.01). Levodopa 7-13 purine nucleoside phosphorylase Homo sapiens 38-41 31554346-9 2019 (4) Conclusions: PNP is more frequent in L-Dopa-treated patients than in L-Dopa-naive patients. Levodopa 41-47 purine nucleoside phosphorylase Homo sapiens 17-20 31554346-9 2019 (4) Conclusions: PNP is more frequent in L-Dopa-treated patients than in L-Dopa-naive patients. Levodopa 73-79 purine nucleoside phosphorylase Homo sapiens 17-20 31554346-10 2019 The results imply that longer exposure to high doses of L-Dopa may cause vitamin B12 and folate imbalance and PNP, secondarily. Levodopa 56-62 purine nucleoside phosphorylase Homo sapiens 110-113 31252260-5 2019 The sensitivity towards the L-dopa detection is estimated to be 1.868 muA muM-1 cm-2 in the linear concentration of 0.05-7.0 mumol L-1 and 0.778 muA muM-1 cm-2 in the linear concentration of 7.00-100 mumol L-1, respectively. Levodopa 28-34 PWWP domain containing 3A, DNA repair factor Homo sapiens 157-162 31397975-5 2019 Moreover, ACE was able to inhibit in vitro tyrosinase activity (IC50 77.44 mug mL-1 ), l-DOPA auto-oxidation (IC50 39.58 mug mL-1 ) and in an in vivo model it exhibited bleaching effects on the pigmentation of zebrafish embryos (72 h post fertilization) without affecting their development and survival. Levodopa 87-93 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Danio rerio 10-13 31455727-0 2019 Role of striatal DeltaFosB in l-Dopa-induced dyskinesias of parkinsonian nonhuman primates. Levodopa 30-36 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 17-26 31584763-1 2019 Monoamine oxidase B inhibitors are used in the treatment of this disease concomitantly with levodopa or as monotherapy. Levodopa 92-100 monoamine oxidase B Mus musculus 0-19 31455727-2 2019 The transcription factor DeltaFosB that is highly up-regulated in the striatum following chronic l-Dopa exposure may participate in the mechanisms of altered neuronal responses to DA generating LID. Levodopa 97-103 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-34 31455727-4 2019 Elevated DeltaFosB levels led to consistent appearance of LID since the initial acute l-Dopa tests. Levodopa 86-92 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-18 31598163-6 2019 Furthermore, treatment with L-3, 4-dihydroxyphenylalanine (L-dopa), a drug approved for Parkinson"s disease, led to down-regulation of SYT12 and similar phenotypes to SYT12 knockdown cells. Levodopa 28-57 synaptotagmin 12 Homo sapiens 135-140 31332769-10 2019 Recently, there has been a resurgence of its use due to the US Food and Drug Administration approval of an extended-release (ER) amantadine formulation for treatment of L-dopa-induced dyskinesia. Levodopa 169-175 epiregulin Homo sapiens 125-127 31606330-5 2019 GPR143, the gene product of ocular albinism 1 (OA1), was identified as a receptor for l-DOPA. Levodopa 86-92 G protein-coupled receptor 143 Rattus norvegicus 0-6 31606330-9 2019 Overexpression of mouse GPR143 inhibited neurite outgrowth, and the effect was mitigated by l-DOPA cyclohexylester, an antagonist for l-DOPA. Levodopa 92-98 G protein-coupled receptor 143 Mus musculus 24-30 31606330-9 2019 Overexpression of mouse GPR143 inhibited neurite outgrowth, and the effect was mitigated by l-DOPA cyclohexylester, an antagonist for l-DOPA. Levodopa 134-140 G protein-coupled receptor 143 Mus musculus 24-30 31306812-0 2019 Pharmacological antagonism of histamine H2R ameliorated L-DOPA-induced dyskinesia via normalization of GRK3 and by suppressing FosB and ERK in PD. Levodopa 56-62 G protein-coupled receptor kinase 3 Mus musculus 103-107 31306812-0 2019 Pharmacological antagonism of histamine H2R ameliorated L-DOPA-induced dyskinesia via normalization of GRK3 and by suppressing FosB and ERK in PD. Levodopa 56-62 FBJ osteosarcoma oncogene B Mus musculus 127-131 31306812-0 2019 Pharmacological antagonism of histamine H2R ameliorated L-DOPA-induced dyskinesia via normalization of GRK3 and by suppressing FosB and ERK in PD. Levodopa 56-62 mitogen-activated protein kinase 1 Mus musculus 136-139 31306812-8 2019 Ranitidine, when given along with L-DOPA, normalized the expression of GRK3 in the dopamine-depleted striatum thereby inhibiting LID in mice. Levodopa 34-40 G protein-coupled receptor kinase 3 Mus musculus 71-75 31598163-6 2019 Furthermore, treatment with L-3, 4-dihydroxyphenylalanine (L-dopa), a drug approved for Parkinson"s disease, led to down-regulation of SYT12 and similar phenotypes to SYT12 knockdown cells. Levodopa 28-57 synaptotagmin 12 Homo sapiens 167-172 31598163-6 2019 Furthermore, treatment with L-3, 4-dihydroxyphenylalanine (L-dopa), a drug approved for Parkinson"s disease, led to down-regulation of SYT12 and similar phenotypes to SYT12 knockdown cells. Levodopa 59-65 synaptotagmin 12 Homo sapiens 135-140 31598163-6 2019 Furthermore, treatment with L-3, 4-dihydroxyphenylalanine (L-dopa), a drug approved for Parkinson"s disease, led to down-regulation of SYT12 and similar phenotypes to SYT12 knockdown cells. Levodopa 59-65 synaptotagmin 12 Homo sapiens 167-172 31598163-7 2019 Taken together, we concluded that SYT12 plays a significant role in OSCC progression via CAMK2N1 and CAMK2, and that L-dopa would be a new drug for OSCC treatment through the SYT12 expression. Levodopa 117-123 synaptotagmin 12 Homo sapiens 175-180 30894696-7 2019 Urinary L-DOPA and noradrenaline levels were significantly increased in sik1-/- mice fed a high-salt diet as compared with sik1-/- mice on a control diet. Levodopa 8-14 salt inducible kinase 1 Mus musculus 72-76 31029342-2 2019 The structural features of Fe3O4@CaAl-LDH@l-Dopa were characterized using XRD, SEM, TEM, EDX, FT-IR, VSM, TGA, XPS, zeta potential analysis and BET. Levodopa 42-48 T-box transcription factor 1 Homo sapiens 106-109 31344959-2 2019 Among the isolated compounds, 974-A was demonstrated for the first time to be a potent competitive inhibitor of mushroom tyrosinase activity towards l-tyrosine and l-DOPA (IC50 values = 1.57 +- 0.08 and 3.56 +- 0.22 microM, respectively). Levodopa 164-170 tyrosinase Mus musculus 121-131 30839077-10 2019 CONCLUSION: Patients with persistent OFFmotor symptoms after STN-DBS should be screened for levodopa-responsiveness, which can serve as a benchmark for best achievable motor benefit. Levodopa 92-100 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 61-64 31213404-0 2019 Residual signs of dopa-responsive dystonia with GCH1 mutation following levodopa treatment are uncommon in Korean patients. Levodopa 72-80 GTP cyclohydrolase 1 Homo sapiens 48-52 31213404-4 2019 This study was designed to investigate the residual signs following levodopa treatment in Korean DRD patients with GCH1 mutation. Levodopa 68-76 GTP cyclohydrolase 1 Homo sapiens 115-119 30716176-0 2019 l-3,4-dihydroxyphenylalanine (l-DOPA) modulates brain iron, dopaminergic neurodegeneration and motor dysfunction in iron overload and mutant alpha-synuclein mouse models of Parkinson"s disease. Levodopa 0-28 synuclein, alpha Mus musculus 141-156 31337633-4 2019 The patient clearly showed a dose-dependent paradoxical response to L-DOPA treatment with the emergence of severe FOG and postural instability. Levodopa 68-74 zinc finger protein, FOG family member 1 Homo sapiens 114-117 30963543-1 2019 OBJECTIVES: To evaluate whether the prescription of monoamine oxidase B inhibitors (MAOB-I), rasagiline and safinamide, contributes to the reduction of levodopa and/or dopamine agonists (DA) dose in order to minimize adverse effects. Levodopa 152-160 monoamine oxidase B Homo sapiens 52-71 30536670-1 2019 Tyrosine hydroxylase (TH), catalyzing the conversion of tyrosine into l-DOPA, is the rate-limiting enzyme in dopamine synthesis. Levodopa 70-76 tyrosine hydroxylase Rattus norvegicus 0-20 30536670-1 2019 Tyrosine hydroxylase (TH), catalyzing the conversion of tyrosine into l-DOPA, is the rate-limiting enzyme in dopamine synthesis. Levodopa 70-76 tyrosine hydroxylase Rattus norvegicus 22-24 30716176-0 2019 l-3,4-dihydroxyphenylalanine (l-DOPA) modulates brain iron, dopaminergic neurodegeneration and motor dysfunction in iron overload and mutant alpha-synuclein mouse models of Parkinson"s disease. Levodopa 30-36 synuclein, alpha Mus musculus 141-156 30484112-0 2019 Riluzole Attenuates L-DOPA-Induced Abnormal Involuntary Movements Through Decreasing CREB1 Activity: Insights from a Rat Model. Levodopa 20-26 cAMP responsive element binding protein 1 Rattus norvegicus 85-90 31275238-5 2019 Within the next 6 months and after several programming sessions, the patient reported "on" FoG occurring regularly 1 h after taking levodopa and lasting a few hours. Levodopa 132-140 zinc finger protein, FOG family member 1 Homo sapiens 91-94 31180686-1 2019 l-Type amino acid transporter 1 (LAT1), selectively expressed at the blood-brain barrier (BBB) and brain parenchymal cells, mediates brain delivery of drugs and prodrugs such as l-dopa and gabapentin. Levodopa 178-184 solute carrier family 7 member 5 Rattus norvegicus 0-31 31180686-1 2019 l-Type amino acid transporter 1 (LAT1), selectively expressed at the blood-brain barrier (BBB) and brain parenchymal cells, mediates brain delivery of drugs and prodrugs such as l-dopa and gabapentin. Levodopa 178-184 solute carrier family 7 member 5 Rattus norvegicus 33-37 31275238-6 2019 Accordingly, a repeated levodopa challenge showed that FoG resolved with either levodopa administration or STN stimulation alone, but the combination of both therapies induced recurrence of FoG in our patient. Levodopa 24-32 zinc finger protein, FOG family member 1 Homo sapiens 55-58 31275238-6 2019 Accordingly, a repeated levodopa challenge showed that FoG resolved with either levodopa administration or STN stimulation alone, but the combination of both therapies induced recurrence of FoG in our patient. Levodopa 80-88 zinc finger protein, FOG family member 1 Homo sapiens 55-58 31258461-0 2019 Effect of L-DOPA/Benserazide on Propagation of Pathological alpha-Synuclein. Levodopa 10-16 synuclein, alpha Mus musculus 60-75 31275144-0 2019 Levodopa/Benserazide PLGA Microsphere Prevents L-Dopa-Induced Dyskinesia via Lower beta-Arrestin2 in 6-Hydroxydopamine Parkinson"s Rats. Levodopa 0-8 arrestin, beta 2, pseudogene Rattus norvegicus 83-97 31098725-0 2019 Assessment of plasma creatine kinase as biomarker for levodopa-induced dyskinesia in Parkinson"s disease. Levodopa 54-62 cytidine/uridine monophosphate kinase 1 Homo sapiens 21-36 31275144-0 2019 Levodopa/Benserazide PLGA Microsphere Prevents L-Dopa-Induced Dyskinesia via Lower beta-Arrestin2 in 6-Hydroxydopamine Parkinson"s Rats. Levodopa 47-53 arrestin, beta 2, pseudogene Rattus norvegicus 83-97 31258461-5 2019 Notably, a significant reduction in the accumulation of phosphorylated alpha-synuclein was detected in substantia nigra of L-DOPA/benserazide (a dopamine decarboxylase inhibitor)-treated mice, compared with control mice. Levodopa 123-129 synuclein, alpha Mus musculus 71-86 31258461-6 2019 These results suggest that L-DOPA may slow the progression of PD in vivo by suppressing the aggregation of alpha-synuclein in dopaminergic neurons and the cell-to-cell propagation of abnormal alpha-synuclein. Levodopa 27-33 synuclein, alpha Mus musculus 107-122 31258461-6 2019 These results suggest that L-DOPA may slow the progression of PD in vivo by suppressing the aggregation of alpha-synuclein in dopaminergic neurons and the cell-to-cell propagation of abnormal alpha-synuclein. Levodopa 27-33 synuclein, alpha Mus musculus 192-207 31258461-7 2019 This is the first report describing the suppressing effect of L-DOPA/benserazide on the propagation of pathological alpha-synuclein. Levodopa 62-68 synuclein, alpha Mus musculus 116-131 31098725-1 2019 We tested in a translational approach the usefulness of plasma creatine kinase (CK) as an objective biomarker for levodopa-induced dyskinesia (LID). Levodopa 114-122 cytidine/uridine monophosphate kinase 1 Homo sapiens 63-78 31098725-1 2019 We tested in a translational approach the usefulness of plasma creatine kinase (CK) as an objective biomarker for levodopa-induced dyskinesia (LID). Levodopa 114-122 cytidine/uridine monophosphate kinase 1 Homo sapiens 80-82 30777652-0 2019 PDE10A mutation in two sisters with a hyperkinetic movement disorder - Response to levodopa. Levodopa 83-91 phosphodiesterase 10A Homo sapiens 0-6 30066121-1 2019 PURPOSE: Modulation of presynaptic metabotropic glutamate receptor 4 (mGlu4) by an allosteric ligand has been proposed as a promising therapeutic target in Parkinson"s disease and levodopa-induced dyskinesia. Levodopa 180-188 glutamate metabotropic receptor 4 Homo sapiens 35-68 30259400-0 2019 Genetic Knockdown of mGluR5 in Striatal D1R-Containing Neurons Attenuates L-DOPA-Induced Dyskinesia in Aphakia Mice. Levodopa 74-80 glutamate receptor, ionotropic, kainate 1 Mus musculus 21-27 30259400-10 2019 Downregulating mGluR5 or nicotine treatment after L-DOPA decreased ERK and histone 3 activation, and FosB expression. Levodopa 50-56 glutamate receptor, ionotropic, kainate 1 Mus musculus 15-21 30259400-10 2019 Downregulating mGluR5 or nicotine treatment after L-DOPA decreased ERK and histone 3 activation, and FosB expression. Levodopa 50-56 Eph receptor B2 Mus musculus 67-70 30762089-0 2019 Chronic administration of the histamine H3 receptor agonist immepip decreases L-Dopa-induced dyskinesias in 6-hydroxydopamine-lesioned rats. Levodopa 78-84 histamine receptor H3 Rattus norvegicus 30-51 30796964-1 2019 L-Dopa decarboxylase (DDC) catalyzes the decarboxylation of L-Dopa to dopamine and 5-hydroxytryptophan (5-HTP) to serotonin. Levodopa 0-6 dopa decarboxylase Homo sapiens 22-25 31139367-3 2019 At 18 months of age, c-rel-/- mice showed nigrostriatal degeneration and accumulation of alpha-synuclein aggregates associated with a motor impairment responsive to L-DOPA administration. Levodopa 165-171 reticuloendotheliosis oncogene Mus musculus 21-26 31139367-3 2019 At 18 months of age, c-rel-/- mice showed nigrostriatal degeneration and accumulation of alpha-synuclein aggregates associated with a motor impairment responsive to L-DOPA administration. Levodopa 165-171 synuclein, alpha Mus musculus 89-104 31017021-9 2019 In patients, concomitant inhibition of monoamine oxidase-B caused less increase of levodopa dosages over five years. Levodopa 83-91 monoamine oxidase B Homo sapiens 39-58 30692049-0 2019 Craniocervical dystonia with levodopa-responsive parkinsonism co-segregating with a pathogenic ANO3 mutation in a Taiwanese family. Levodopa 29-37 anoctamin 3 Homo sapiens 95-99 30876866-1 2019 OBJECTIVE: We hypothesized that DA and L-DOPA derived from nutritional tyrosine and the resultant observed postprandial plasma excursions of L-DOPA and DA might affect glucose tolerance via their ability to be taken-up by beta cells and inhibit glucose-stimulated beta-cell insulin secretion. Levodopa 39-45 insulin Homo sapiens 274-281 30876866-1 2019 OBJECTIVE: We hypothesized that DA and L-DOPA derived from nutritional tyrosine and the resultant observed postprandial plasma excursions of L-DOPA and DA might affect glucose tolerance via their ability to be taken-up by beta cells and inhibit glucose-stimulated beta-cell insulin secretion. Levodopa 141-147 insulin Homo sapiens 274-281 30876866-8 2019 DA and L-DOPA derived from nutritional tyrosine may serve to defend against hypoglycemia via inhibition of glucose-stimulated beta-cell insulin secretion as proposed by the anti-incretin hypothesis. Levodopa 7-13 insulin Homo sapiens 136-143 30723034-4 2019 Interestingly, BDNF and phosphorylated TrkB levels were positively correlated with disease duration, UPDRS score, Hoehn-Yahr staging, as well as L-DOPA medication in PD patients. Levodopa 145-151 brain derived neurotrophic factor Homo sapiens 15-19 30723034-4 2019 Interestingly, BDNF and phosphorylated TrkB levels were positively correlated with disease duration, UPDRS score, Hoehn-Yahr staging, as well as L-DOPA medication in PD patients. Levodopa 145-151 neurotrophic receptor tyrosine kinase 2 Homo sapiens 39-43 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 brain derived neurotrophic factor Homo sapiens 66-70 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 neurotrophic receptor tyrosine kinase 2 Homo sapiens 71-75 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 brain derived neurotrophic factor Homo sapiens 208-212 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 neurotrophic receptor tyrosine kinase 2 Homo sapiens 213-217 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 brain derived neurotrophic factor Homo sapiens 208-212 30723034-5 2019 These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication. Levodopa 368-374 neurotrophic receptor tyrosine kinase 2 Homo sapiens 213-217 31031602-2 2019 Previously, we reported that the ghrelin receptor agonist, HM01 normalized the decreased 4-h fecal output and levodopa-inhibited gastric emptying in 6-OHDA rats, and activated selective areas in brain and spinal cord. Levodopa 110-118 ghrelin and obestatin prepropeptide Rattus norvegicus 33-40 30814443-0 2019 [Analysis of PEG-J associated complications in 14 adult patients treated with levodopa-carbidopa intestinal gel]. Levodopa 78-86 progestagen associated endometrial protein Homo sapiens 13-16 30967567-8 2019 In a final round, we discovered that deletion of heme oxygenase (HMX1) increases total heme concentration and increases L-DOPA production, using dopamine measurement as a proxy. Levodopa 120-126 Hmx1p Saccharomyces cerevisiae S288C 65-69 29995172-3 2019 Tyrosine hydroxylase (TH), tetrahydrobiopterin (BH4)-dependent and iron-containing monooxygenase, catalyzes the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the initial and rate-limiting step in the biosynthesis of catecholamines (DA, noradrenaline, and adrenaline). Levodopa 140-168 tyrosine hydroxylase Homo sapiens 0-20 29995172-3 2019 Tyrosine hydroxylase (TH), tetrahydrobiopterin (BH4)-dependent and iron-containing monooxygenase, catalyzes the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the initial and rate-limiting step in the biosynthesis of catecholamines (DA, noradrenaline, and adrenaline). Levodopa 140-168 tyrosine hydroxylase Homo sapiens 22-24 29995172-3 2019 Tyrosine hydroxylase (TH), tetrahydrobiopterin (BH4)-dependent and iron-containing monooxygenase, catalyzes the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the initial and rate-limiting step in the biosynthesis of catecholamines (DA, noradrenaline, and adrenaline). Levodopa 170-176 tyrosine hydroxylase Homo sapiens 0-20 29995172-3 2019 Tyrosine hydroxylase (TH), tetrahydrobiopterin (BH4)-dependent and iron-containing monooxygenase, catalyzes the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the initial and rate-limiting step in the biosynthesis of catecholamines (DA, noradrenaline, and adrenaline). Levodopa 170-176 tyrosine hydroxylase Homo sapiens 22-24 30867591-2 2019 LAT1, an antiporter of the amino acid-polyamine-organocation superfamily, also catalyses the permeation of thyroid hormones, pharmaceutical drugs, and hormone precursors such as L-3,4-dihydroxyphenylalanine across membranes2-6. Levodopa 178-206 solute carrier family 7 member 5 Homo sapiens 0-4 30030752-7 2019 Additionally, altered striatal responses to L-DOPA injection were observed after prolonged acupuncture and MCH treatments, which suggests that these treatment modalities influenced the compensatory mechanisms of LID. Levodopa 44-50 modifier of chinchilla Mus musculus 107-110 30030752-8 2019 In summary, present study demonstrated that acupuncture decreased LID via hypothalamic MCH using L-DOPA-administered ak/ak and 6-OHDA mouse models and that MCH administration resulted in novel antidyskinetic effects in these models. Levodopa 97-103 modifier of chinchilla Mus musculus 87-90 30645726-0 2019 Differential Expression of Striatal DeltaFosB mRNA and FosB mRNA After Different Levodopa Treatment Regimens in a Rat Model of Parkinson"s Disease. Levodopa 81-89 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 41-45 30645726-2 2019 While the overexpression of DeltaFosB transcription factor is related to the development of LID, few studies have been undertaken on fosB gene transcriptional regulation induced by levodopa in vivo. Levodopa 181-189 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 133-137 30645726-3 2019 The aim of this study is to evaluate the expression of DeltaFosB mRNA and FosB mRNA in the striatum after acute, chronic, and subchronic levodopa treatment in rats with unilateral 6-OHDA-lesion in the medial forebrain bundle. Levodopa 137-145 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 60-64 30645726-4 2019 qRT-PCR was used to compare the levels of DeltaFosB and FosB mRNA expression in the dopamine-denervated striatum following levodopa treatment. Levodopa 123-131 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 47-51 30645726-5 2019 While the results obtained after a single levodopa dose indicate a significant increase of FosB mRNA expression in the striatum 1 h post-injection, the levels returned to baseline values after 24 h. After subchronic levodopa treatment, the levels of FosB and FosB mRNA expression were lower 1 h post-administration of levodopa in comparison with acute effect. Levodopa 42-50 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-96 30645726-5 2019 While the results obtained after a single levodopa dose indicate a significant increase of FosB mRNA expression in the striatum 1 h post-injection, the levels returned to baseline values after 24 h. After subchronic levodopa treatment, the levels of FosB and FosB mRNA expression were lower 1 h post-administration of levodopa in comparison with acute effect. Levodopa 217-225 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-96 30645726-5 2019 While the results obtained after a single levodopa dose indicate a significant increase of FosB mRNA expression in the striatum 1 h post-injection, the levels returned to baseline values after 24 h. After subchronic levodopa treatment, the levels of FosB and FosB mRNA expression were lower 1 h post-administration of levodopa in comparison with acute effect. Levodopa 217-225 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-96 30645726-6 2019 However, after chronic levodopa treatment, FosB mRNA expression in the striatum persisted in dyskinetic rats only, and positive correlation was found between the levels of FosB mRNA expression 1 h after levodopa administration and the level of dyskinetic severity. Levodopa 23-31 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 44-48 30645726-6 2019 However, after chronic levodopa treatment, FosB mRNA expression in the striatum persisted in dyskinetic rats only, and positive correlation was found between the levels of FosB mRNA expression 1 h after levodopa administration and the level of dyskinetic severity. Levodopa 23-31 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 174-178 30645726-6 2019 However, after chronic levodopa treatment, FosB mRNA expression in the striatum persisted in dyskinetic rats only, and positive correlation was found between the levels of FosB mRNA expression 1 h after levodopa administration and the level of dyskinetic severity. Levodopa 205-213 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 174-178 30645726-7 2019 In summary, acute levodopa treatment led to highly increased levels of FosB mRNA expression in the striatum. Levodopa 18-26 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 72-76 30645726-8 2019 While repeated administration induced a partial desensitization of the fosB gene in the striatum, it did not suppress its activity completely, which could explain why dyskinesia appears after chronic levodopa treatment. Levodopa 200-208 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 71-75 30837649-6 2019 Therefore, our findings demonstrate that ALDH1A1-synthesized RA is required for postsynaptic MOR1 expression in the postnatal and adult dorsal striatum, supporting potential therapeutic benefits of RA supplementation in moderating L-DOPA-induced dyskinesia. Levodopa 231-237 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 41-48 30907884-8 2019 In melanogenesis, tyrosinase catalyzes the rate-limiting step that converts L-tyrosine into 3,4-dihydroxyphenylalanine (L-DOPA) and then into dopaquinone. Levodopa 120-126 tyrosinase Homo sapiens 18-28 30907884-10 2019 In cultured melanocytes, tyrosinase activity can be quantified by adding L-DOPA as a substrate and measuring dopaquinone production by spectrophotometry. Levodopa 73-79 tyrosinase Homo sapiens 25-35 30352709-9 2019 CONCLUSIONS: Patients with NKX2-1 gene mutations should be investigated for RLS, which, similarly to chorea, can sometimes be ameliorated by Levodopa. Levodopa 141-149 NK2 homeobox 1 Homo sapiens 27-33 30350722-0 2019 S-nitrosylation of Src by NR2B-nNOS signal causes Src activation and NR2B tyrosine phosphorylation in levodopa-induced dyskinetic rat model. Levodopa 102-110 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 19-22 30350722-0 2019 S-nitrosylation of Src by NR2B-nNOS signal causes Src activation and NR2B tyrosine phosphorylation in levodopa-induced dyskinetic rat model. Levodopa 102-110 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 26-30 30350722-0 2019 S-nitrosylation of Src by NR2B-nNOS signal causes Src activation and NR2B tyrosine phosphorylation in levodopa-induced dyskinetic rat model. Levodopa 102-110 nitric oxide synthase 1 Rattus norvegicus 31-35 30350722-0 2019 S-nitrosylation of Src by NR2B-nNOS signal causes Src activation and NR2B tyrosine phosphorylation in levodopa-induced dyskinetic rat model. Levodopa 102-110 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 50-53 30350722-0 2019 S-nitrosylation of Src by NR2B-nNOS signal causes Src activation and NR2B tyrosine phosphorylation in levodopa-induced dyskinetic rat model. Levodopa 102-110 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 69-73 30350722-1 2019 Abnormality in Src PSD-95 NR2B signaling complex assemble occurs in levodopa-induced dyskinesia (LID). Levodopa 68-76 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 15-18 30350722-1 2019 Abnormality in Src PSD-95 NR2B signaling complex assemble occurs in levodopa-induced dyskinesia (LID). Levodopa 68-76 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 26-30 30350722-7 2019 The results demonstrated that chronic levodopa treatment resulted in downregulation of p-nNOS-S847, one marker of nNOS overactivation. Levodopa 38-46 nitric oxide synthase 1 Rattus norvegicus 89-93 30350722-7 2019 The results demonstrated that chronic levodopa treatment resulted in downregulation of p-nNOS-S847, one marker of nNOS overactivation. Levodopa 38-46 nitric oxide synthase 1 Rattus norvegicus 114-118 30350722-9 2019 Conversely, administration of 7-NI, one nNOS inhibitor, reversed all these effects of levodopa treatment. Levodopa 86-94 nitric oxide synthase 1 Rattus norvegicus 40-44 30823626-4 2019 When assessing the effect of HTHQ on oxidative stress-related signaling pathways, HTHQ inhibited l-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). Levodopa 97-103 mitogen activated protein kinase 3 Rattus norvegicus 181-187 29992529-0 2019 MTOR Pathway-Based Discovery of Genetic Susceptibility to L-DOPA-Induced Dyskinesia in Parkinson"s Disease Patients. Levodopa 58-64 mechanistic target of rapamycin kinase Homo sapiens 0-4 29992529-4 2019 We screened 64 single nucleotide polymorphisms (SNPs) mapping to 57 genes of the mTOR pathway in a retrospective cohort of 401 PD cases treated with L-DOPA (70 PD with moderate/severe LID and 331 with no/mild LID). Levodopa 149-155 mechanistic target of rapamycin kinase Homo sapiens 81-85 30823626-4 2019 When assessing the effect of HTHQ on oxidative stress-related signaling pathways, HTHQ inhibited l-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). Levodopa 97-103 mitogen activated protein kinase 14 Rattus norvegicus 190-226 30823626-5 2019 HTHQ also normalized l-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival. Levodopa 21-27 BCL2 associated X, apoptosis regulator Rattus norvegicus 93-119 30823626-6 2019 Taken together, HTHQ exhibits protective effects against l-DOPA-induced cell death through modulation of the ERK1/2-p38MAPK-JNK1/2-Bad-Bax signaling pathway in PC12 cells. Levodopa 57-63 mitogen activated protein kinase 3 Rattus norvegicus 109-115 30823626-6 2019 Taken together, HTHQ exhibits protective effects against l-DOPA-induced cell death through modulation of the ERK1/2-p38MAPK-JNK1/2-Bad-Bax signaling pathway in PC12 cells. Levodopa 57-63 BCL2 associated X, apoptosis regulator Rattus norvegicus 135-138 30554648-0 2019 Simultaneous synthesis of l-DOPA and oxidation of d-amino acid by specific coupling of a peroxidase to d-amino acid oxidase. Levodopa 26-32 D-amino acid oxidase Homo sapiens 103-123 30554648-12 2019 For the sybthesis of l-DOPA from l-tyrosine, the catalytic efficiency of HDP&DAAO is 1.58 times that of HDP. Levodopa 21-27 D-amino acid oxidase Homo sapiens 81-85 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 184-190 solute carrier family 6 member 3 Homo sapiens 116-120 30353564-7 2019 CONCLUSIONS: Clinical and demographic characteristics of Brazilian PD patients and differences in DRD2 and DAT1 genes may to determine individual variations in the therapeutic response to L-DOPA in the Brazilian PD patients. Levodopa 188-194 dopamine receptor D2 Homo sapiens 98-102 30353564-0 2019 The influence of SLC6A3 and DRD2 polymorphisms on levodopa-therapy in patients with sporadic Parkinson"s disease. Levodopa 50-58 dopamine receptor D2 Homo sapiens 28-32 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 174-182 dopamine receptor D2 Homo sapiens 82-86 30353564-7 2019 CONCLUSIONS: Clinical and demographic characteristics of Brazilian PD patients and differences in DRD2 and DAT1 genes may to determine individual variations in the therapeutic response to L-DOPA in the Brazilian PD patients. Levodopa 188-194 solute carrier family 6 member 3 Homo sapiens 107-111 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 174-182 ankyrin repeat and kinase domain containing 1 Homo sapiens 87-92 30316985-7 2019 Also based on a logistic regression analysis, the 10R/10R and the A carrier allele of the rs393795 polymorphisms of the DAT gene, could reduce the susceptibility to develop LID during levodopa therapy adjusted by demographical and clinical variables (OR = 0.19; 95% CI, 0.05-0.69). Levodopa 184-192 solute carrier family 6 member 3 Homo sapiens 120-123 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 174-182 solute carrier family 6 member 3 Homo sapiens 109-115 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 174-182 solute carrier family 6 member 3 Homo sapiens 116-120 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 184-190 dopamine receptor D2 Homo sapiens 82-86 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 184-190 ankyrin repeat and kinase domain containing 1 Homo sapiens 87-92 30353564-1 2019 OBJECTIVES: The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L-DOPA)-therapy in patients with Parkinson"s disease (PD). Levodopa 184-190 solute carrier family 6 member 3 Homo sapiens 109-115 30316985-4 2019 Genotyping of the 40-bp VNTR (rs28363170) and rs393795 (A/C) polymorphisms of the DAT gene was performed in a well-characterized cohort of 181 Italian PD patients in treatment with L-DOPA for 3 years or more. Levodopa 181-187 solute carrier family 6 member 3 Homo sapiens 82-85 30316985-6 2019 However, the combination of the two genotypes 10R/10R (rs28363170) and A carrier (rs393795) of the DAT gene reduces the risk of LID occurrence during long-term therapy with l-DOPA with respect to the PD subjects who did not carry these alleles (OR = 0.31; 95% CI, 0.09-0.88). Levodopa 173-179 solute carrier family 6 member 3 Homo sapiens 99-102 30261284-7 2019 Moreover, this study demonstrates for the first time that 5AR inhibitors are able to prevent key events in the appearance of dyskinesia, such as L-DOPA-induced upregulation of striatal D1R-related cAMP/PKA/ERK signaling pathways and D1R-D3R coimmunoprecipitation, an index of heteromer formation. Levodopa 145-151 ferredoxin reductase Rattus norvegicus 59-61 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 27-33 catechol-O-methyltransferase Homo sapiens 88-116 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 27-33 catechol-O-methyltransferase Homo sapiens 118-122 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 27-33 monoamine oxidase B Homo sapiens 128-153 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 180-186 catechol-O-methyltransferase Homo sapiens 88-116 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 180-186 catechol-O-methyltransferase Homo sapiens 118-122 31258092-2 2019 To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine. Levodopa 180-186 monoamine oxidase B Homo sapiens 128-153 30326223-2 2019 In this study, we evaluated the dual effect of pyrogallol on tyrosinase as an inhibitor in the presence of L-DOPA simultaneously via integrating methods of enzyme kinetics and computational molecular dynamics (MD) simulations. Levodopa 107-113 tyrosinase Homo sapiens 61-71 30326223-3 2019 Pyrogallol was found to be a reversible inhibitor of tyrosinase in the presence of L-DOPA and its induced mechanism was the parabolic non-competitive inhibition type (IC50 = 0.772 +- 0.003 mM and Ki = 0.529 +- 0.022 mM). Levodopa 83-89 tyrosinase Homo sapiens 53-63 31322578-7 2019 We suggest that in Alzheimer"s disease patients with PSEN1 mutation, parkinsonism may be relieved by L-dopa when it is associated with presynaptic dopaminergic deficit. Levodopa 101-107 presenilin 1 Homo sapiens 53-58 30808844-14 2019 HBH, a specific DDC inhibitor; BCH, a LAT2 inhibitor; and Sch 23397, a specific D1R antagonist, totally suppressed the inhibition of Na+/K+-ATPase activity due to L-dopa or L-tyr administration, as indicated in the figures. Levodopa 163-169 NK2 homeobox 1 Homo sapiens 31-34 30808844-15 2019 CONCLUSION: The results indicate that DA formed mainly from luminal L-tyr or L-dopa uptake by LAT2, can inhibit the Na+/K+-ATPase. Levodopa 77-83 linker for activation of T cells family member 2 Homo sapiens 94-98 30189294-3 2019 The drug L-DOPA efficiently and specifically crosses the BBB via the large neutral amino acid transporter (LAT)-1 protein to enter the brain. Levodopa 9-15 solute carrier family 7 member 5 Homo sapiens 107-113 30130562-0 2019 Tat-Src reduced NR2B tyrosine phosphorylation and its interaction with NR2B in levodopa-induced dyskinetic rats model. Levodopa 79-87 tyrosine aminotransferase Rattus norvegicus 0-3 30130562-0 2019 Tat-Src reduced NR2B tyrosine phosphorylation and its interaction with NR2B in levodopa-induced dyskinetic rats model. Levodopa 79-87 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 4-7 30130562-0 2019 Tat-Src reduced NR2B tyrosine phosphorylation and its interaction with NR2B in levodopa-induced dyskinetic rats model. Levodopa 79-87 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 16-20 30130562-0 2019 Tat-Src reduced NR2B tyrosine phosphorylation and its interaction with NR2B in levodopa-induced dyskinetic rats model. Levodopa 79-87 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 71-75 30130562-5 2019 The data showed that in dyskinetic rats model intraperitoneal microinjection of Tat-Src improved dyskinetic behaviors and decreased NR2B tyrosine phosphorylation and the interactions of Src with NR2B induced by chronic levodopa treatment. Levodopa 219-227 tyrosine aminotransferase Rattus norvegicus 80-83 30130562-5 2019 The data showed that in dyskinetic rats model intraperitoneal microinjection of Tat-Src improved dyskinetic behaviors and decreased NR2B tyrosine phosphorylation and the interactions of Src with NR2B induced by chronic levodopa treatment. Levodopa 219-227 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 84-87 30130562-5 2019 The data showed that in dyskinetic rats model intraperitoneal microinjection of Tat-Src improved dyskinetic behaviors and decreased NR2B tyrosine phosphorylation and the interactions of Src with NR2B induced by chronic levodopa treatment. Levodopa 219-227 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 186-189 30130562-5 2019 The data showed that in dyskinetic rats model intraperitoneal microinjection of Tat-Src improved dyskinetic behaviors and decreased NR2B tyrosine phosphorylation and the interactions of Src with NR2B induced by chronic levodopa treatment. Levodopa 219-227 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 195-199 31629395-3 2019 A DDC substrate, L-DOPA, combined with an inhibitor of the enzyme is still the most effective treatment for symptoms of Parkinson"s disease. Levodopa 17-23 dopa decarboxylase Homo sapiens 2-5 31031465-3 2019 AIM: This study aims to generate and evaluate the 3D structure of TrkA, SERT, and AQP proteins and their interaction with the ligands, namely Asiaticoside-D (AD) and levodopa (L-DOPA) the anti-NDD agents. Levodopa 166-174 neurotrophic receptor tyrosine kinase 1 Homo sapiens 66-70 31031465-3 2019 AIM: This study aims to generate and evaluate the 3D structure of TrkA, SERT, and AQP proteins and their interaction with the ligands, namely Asiaticoside-D (AD) and levodopa (L-DOPA) the anti-NDD agents. Levodopa 166-174 solute carrier family 6 member 4 Homo sapiens 72-76 31031465-3 2019 AIM: This study aims to generate and evaluate the 3D structure of TrkA, SERT, and AQP proteins and their interaction with the ligands, namely Asiaticoside-D (AD) and levodopa (L-DOPA) the anti-NDD agents. Levodopa 176-182 neurotrophic receptor tyrosine kinase 1 Homo sapiens 66-70 31031465-3 2019 AIM: This study aims to generate and evaluate the 3D structure of TrkA, SERT, and AQP proteins and their interaction with the ligands, namely Asiaticoside-D (AD) and levodopa (L-DOPA) the anti-NDD agents. Levodopa 176-182 solute carrier family 6 member 4 Homo sapiens 72-76 31031465-8 2019 Interactions of AD with the SERT, AQP-4, and TrkA showed the binding energies as -9.93, 8.88, and -7.58 of Kcal/mol, respectively, while for L-DOPA did show -3.93, -5.13, and -6.0 Kcal/mol, respectively. Levodopa 141-147 solute carrier family 6 member 4 Homo sapiens 28-32 31031465-8 2019 Interactions of AD with the SERT, AQP-4, and TrkA showed the binding energies as -9.93, 8.88, and -7.58 of Kcal/mol, respectively, while for L-DOPA did show -3.93, -5.13, and -6.0 Kcal/mol, respectively. Levodopa 141-147 neurotrophic receptor tyrosine kinase 1 Homo sapiens 45-49 32146463-3 2019 RESULTS: In this work, our results showed clear modifications in the expression of kinases involved in mTOR and PKR apoptosis pathways, in lymphocytes of PD patients treated or not with anti-PD treatment (levodopa), which confirmed the role played by apoptosis in the pathogenesis of this disease and the positive effect of treatment with medication on this parameter. Levodopa 205-213 mechanistic target of rapamycin kinase Homo sapiens 103-107 30261284-7 2019 Moreover, this study demonstrates for the first time that 5AR inhibitors are able to prevent key events in the appearance of dyskinesia, such as L-DOPA-induced upregulation of striatal D1R-related cAMP/PKA/ERK signaling pathways and D1R-D3R coimmunoprecipitation, an index of heteromer formation. Levodopa 145-151 Eph receptor B1 Rattus norvegicus 206-209 32146463-3 2019 RESULTS: In this work, our results showed clear modifications in the expression of kinases involved in mTOR and PKR apoptosis pathways, in lymphocytes of PD patients treated or not with anti-PD treatment (levodopa), which confirmed the role played by apoptosis in the pathogenesis of this disease and the positive effect of treatment with medication on this parameter. Levodopa 205-213 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 112-115 30261285-0 2019 NMDA receptor GluN2D subunit participates to levodopa-induced dyskinesia pathophysiology. Levodopa 45-53 glutamate ionotropic receptor NMDA type subunit 2D Rattus norvegicus 14-20 31311029-1 2019 OBJECTIVE: Parkinson"s disease (PD) patients are usually treated with L-dopa and/or dopaminergic agonists, which act by binding five types of dopaminergic receptors (DRD1-DRD5). Levodopa 70-76 dopamine receptor D1 Homo sapiens 166-170 30261285-6 2019 Our results show that GluN2D synaptic abundance is selectively augmented in the striatum of L-DOPA-treated male parkinsonian rats displaying a dyskinetic phenotype. Levodopa 92-98 glutamate ionotropic receptor NMDA type subunit 2D Rattus norvegicus 22-28 31311029-1 2019 OBJECTIVE: Parkinson"s disease (PD) patients are usually treated with L-dopa and/or dopaminergic agonists, which act by binding five types of dopaminergic receptors (DRD1-DRD5). Levodopa 70-76 dopamine receptor D5 Homo sapiens 171-175 30261285-9 2019 Notably, in vivo treatment with a well-characterized GluN2D antagonist ameliorates the severity of established dyskinesia in L-DOPA-treated animals. Levodopa 125-131 glutamate ionotropic receptor NMDA type subunit 2D Rattus norvegicus 53-59 30357936-6 2018 SNCA mutation carriers often have additional psychiatric symptoms, and although not exclusive to only LRRK2 or VPS35 mutation carriers, LRRK2 mutation carriers have a typical form of PD, and, lastly, VPS35 mutation carriers have good response to l-dopa. Levodopa 246-252 synuclein alpha Homo sapiens 0-4 30100483-2 2018 PPO was immobilised in agar containing l-DOPA as substrate and 3-methyl-2-benzothiazolinone hydrazone hydrochloride (MBTH) to enhance colour development. Levodopa 39-45 polyphenol oxidase, chloroplastic Malus domestica 0-3 30291173-2 2018 In addition to its selective and reversible monoamine oxidase B inhibition, safinamide through use-dependent sodium channel blockade reduces overactive glutamatergic transmission in basal ganglia, which is believed to contribute to motor symptoms and complications including levodopa-induced dyskinesia (LID). Levodopa 275-283 monoamine oxidase B Rattus norvegicus 44-63 30357936-6 2018 SNCA mutation carriers often have additional psychiatric symptoms, and although not exclusive to only LRRK2 or VPS35 mutation carriers, LRRK2 mutation carriers have a typical form of PD, and, lastly, VPS35 mutation carriers have good response to l-dopa. Levodopa 246-252 VPS35 retromer complex component Homo sapiens 200-205 30285025-0 2018 l-Dopa and dopamine conjugated naphthalenediimides modulate amyloid beta toxicity. Levodopa 0-6 amyloid beta precursor protein Homo sapiens 60-72 30102999-10 2018 More specifically, our study suggest that SERT increase may be underpinned by an increased density of serotonergic fibers after MPTP and the first l-DOPA period, and by an elevation of SERT itself after MDMA and the second l-DOPA period. Levodopa 147-153 solute carrier family 6 member 4 Homo sapiens 42-46 30102999-10 2018 More specifically, our study suggest that SERT increase may be underpinned by an increased density of serotonergic fibers after MPTP and the first l-DOPA period, and by an elevation of SERT itself after MDMA and the second l-DOPA period. Levodopa 223-229 solute carrier family 6 member 4 Homo sapiens 42-46 30290160-10 2018 Opicapone fills the unmet need for a compound with sustained COMT inhibition which will improve levodopa bioavailability in patients with Parkinson"s disease. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 61-65 30290201-10 2018 Amitriptyline administered alone or jointly with L-DOPA had no effect on DAT binding on the lesioned side, significantly decreased SERT binding in the striatum and SN while NET binding only in the SN. Levodopa 49-55 solute carrier family 6 member 4 Rattus norvegicus 131-135 30290201-11 2018 Since in the DA-denervated striatum, SERT is mainly responsible for reuptake of L-DOPA-derived DA while in the SN, SERT and NET are involved, the inhibition of these transporters by antidepressant drugs may improve dopaminergic transmission and consequently motor behavior. Levodopa 80-86 solute carrier family 6 member 4 Rattus norvegicus 37-41 30253174-1 2018 Istradefylline, an adenosine A2A receptor (A2AR) antagonist, is effective as an adjunct to levodopa and can alleviate "off" time and motor symptoms in patients with Parkinson"s disease (PD). Levodopa 91-99 adenosine A2a receptor Homo sapiens 43-47 30285025-6 2018 Among the designed NDI-conjugates, l-dopa and dopamine derivatives (NLD and NDP, respectively) showed excellent aggregation modulation efficiency (inhibition and dissolution), as shown by the thioflavin T (ThT) binding assays, dot blot analysis and in cellulo studies. Levodopa 35-41 norrin cystine knot growth factor NDP Homo sapiens 76-79 30485908-9 2018 In the dopamine-depleted striatum, Vilazodone-l-dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced l-dopa-induced c-Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D1 receptor-mediated direct pathway overactivity. Levodopa 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 189-194 30142538-0 2018 Modulation of CaMKIIa-GluN2B interaction in levodopa-induced dyskinesia in 6-OHDA-lesioned Parkinson"s rats. Levodopa 44-52 calcium/calmodulin-dependent protein kinase II alpha Rattus norvegicus 14-21 30142538-0 2018 Modulation of CaMKIIa-GluN2B interaction in levodopa-induced dyskinesia in 6-OHDA-lesioned Parkinson"s rats. Levodopa 44-52 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 22-28 30142538-3 2018 In this study, we found that CaMKIIa was found to form complexes with GluN2B after chronic administration of L-dopa in adult rat striatal neurons. Levodopa 109-115 calcium/calmodulin-dependent protein kinase II alpha Rattus norvegicus 29-36 30142538-3 2018 In this study, we found that CaMKIIa was found to form complexes with GluN2B after chronic administration of L-dopa in adult rat striatal neurons. Levodopa 109-115 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 70-76 30142538-5 2018 In parallel, intrastriatal injection of MK-801 significantly alleviated the level of CaMKIIa in GluN2B precipitates compared to LID group (p < 0.01), and this is accompanied by realizing improvement of the Global ALO AIM score also without affect the efficacy of L-dopa. Levodopa 263-269 calcium/calmodulin-dependent protein kinase II alpha Rattus norvegicus 85-92 29569037-9 2018 Treatment with MAO-B inhibitors is advantageous as it enables sparing of dopamine agonist and levodopa dosing. Levodopa 94-102 monoamine oxidase B Homo sapiens 15-20 30485908-2 2018 To date, targeting serotonin transporters or serotonin receptor subtype 1A (5-HT1A ) reduces l-dopa-induced dyskinesia in animal models; however, these strategies have failed to translate clinically. Levodopa 93-99 5-hydroxytryptamine receptor 1A Rattus norvegicus 76-82 30063931-1 2018 The kinetic action of tyrosinase on l-tyrosine and l-Dopa as substrates in the presence of cinnamic acid and some of its derivatives has been characterized. Levodopa 51-57 tyrosinase Homo sapiens 22-32 29569037-5 2018 This discussion does not consider, that levodopa, respectively, dopamine agonists, are substrates, respectively, inhibitors of the ABCB1 (P-gp, MDR1, and CD243) transporter system. Levodopa 40-48 ATP binding cassette subfamily B member 1 Homo sapiens 131-136 29569037-5 2018 This discussion does not consider, that levodopa, respectively, dopamine agonists, are substrates, respectively, inhibitors of the ABCB1 (P-gp, MDR1, and CD243) transporter system. Levodopa 40-48 phosphoglycolate phosphatase Homo sapiens 138-142 29569037-5 2018 This discussion does not consider, that levodopa, respectively, dopamine agonists, are substrates, respectively, inhibitors of the ABCB1 (P-gp, MDR1, and CD243) transporter system. Levodopa 40-48 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 29569037-5 2018 This discussion does not consider, that levodopa, respectively, dopamine agonists, are substrates, respectively, inhibitors of the ABCB1 (P-gp, MDR1, and CD243) transporter system. Levodopa 40-48 ATP binding cassette subfamily B member 1 Homo sapiens 154-159 30485908-9 2018 In the dopamine-depleted striatum, Vilazodone-l-dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced l-dopa-induced c-Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D1 receptor-mediated direct pathway overactivity. Levodopa 46-52 prodynorphin Rattus norvegicus 199-214 30337665-1 2018 Increasing evidence supports a close relationship between Ras-ERK1/2 activation in the striatum and L-DOPA-induced dyskinesia (LID). Levodopa 100-106 mitogen-activated protein kinase 3 Mus musculus 62-68 30337665-2 2018 ERK1/2 activation by L-DOPA takes place through the crosstalk between D1R/AC/PKA/DARPP-32 pathway and NMDA/Ras pathway. Levodopa 21-27 mitogen-activated protein kinase 3 Mus musculus 0-6 30337665-2 2018 ERK1/2 activation by L-DOPA takes place through the crosstalk between D1R/AC/PKA/DARPP-32 pathway and NMDA/Ras pathway. Levodopa 21-27 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 81-89 30308173-0 2018 Abrogating Native alpha-Synuclein Tetramers in Mice Causes a L-DOPA-Responsive Motor Syndrome Closely Resembling Parkinson"s Disease. Levodopa 61-67 synuclein, alpha Mus musculus 18-33 30216534-3 2018 Modulation of metabotropic glutamate receptor 4 represents a promising antiparkinsonian approach in combination with l-dopa, but it has not been demonstrated in primates. Levodopa 117-123 glutamate metabotropic receptor 4 Homo sapiens 14-47 30187305-12 2018 This is the first report of mutation in the C-terminal domain of Synaptojanin 1 protein causing mild juvenile PD with generalized seizures, cognitive impairment, and good respond to levodopa treatment. Levodopa 182-190 synaptojanin 1 Homo sapiens 65-79 30216534-10 2018 CONCLUSIONS: This work provides a demonstration that a positive allosteric modulator of metabotropic glutamate receptor 4 can alleviate the motor symptoms of PD and the motor complications induced by l-dopa in primates. Levodopa 200-206 glutamate metabotropic receptor 4 Homo sapiens 88-121 30306626-0 2018 SPG11-related parkinsonism: Clinical profile, molecular imaging and l-dopa response. Levodopa 68-74 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 0-5 29936234-7 2018 CB1 receptor expression was upregulated in the putamen, GPe and STN during the active phase of dyskinesia and downregulated in the same nuclei and in the SN when dyskinetic animals were OFF levodopa. Levodopa 190-198 cannabinoid receptor 1 Homo sapiens 0-3 30026036-8 2018 We further hypothesize that the peculiar pattern of alpha-synuclein pathology may contribute to differences in the clinical phenotype, with a greater proportion of neuronal inclusions in the putamen being associated to a milder, "PD-like" phenotype with sustained levodopa response and slower disease progression. Levodopa 264-272 synuclein alpha Homo sapiens 52-67 30016498-8 2018 We find that downregulation of JhI-21, but not Mnd, reduced the sensitivity to L-DOPA as measured by sleep loss. Levodopa 79-85 Juvenile hormone Inducible-21 Drosophila melanogaster 31-37 30055889-2 2018 The resulting prodrug, dopa-CBT, inhibited the uptake of the LAT1 substrate [14C]-l-leucine in LAT1-expressing MCF-7 cells with an IC50 value of 28 microM, which was 3.5-times lower than that of the gold standard for dopamine replacement therapy, l-dopa (IC50 ca. Levodopa 247-253 solute carrier family 7 member 5 Homo sapiens 61-65 30262788-5 2018 In this review, an overview will be given on the therapeutically most important classes of pharmacokinetic enhancers like beta-lactamase inhibitors, inhibitors of CYP (cytochrome P450) enzymes in HIV therapy and hepatitis C, boosters for fluoropyrimidine-type anticancer agents, compounds utilized for enabling therapy of Parkinson"s disease with levodopa, and others. Levodopa 347-355 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 168-183 30220990-13 2018 In agreement with the clinical trial results, we found that minocycline and levodopa treatment of Ube3a mice did not show any sign of improved performance in our test battery. Levodopa 76-84 ubiquitin protein ligase E3A Mus musculus 98-103 30255159-5 2018 It is interesting to point out that the expression of miR-155-5p was modified by levodopa treatment, in fact a down-regulation of miR-155-5p in PD patients with the highest dosage was observed. Levodopa 81-89 microRNA 155 Homo sapiens 54-61 30255159-5 2018 It is interesting to point out that the expression of miR-155-5p was modified by levodopa treatment, in fact a down-regulation of miR-155-5p in PD patients with the highest dosage was observed. Levodopa 81-89 microRNA 155 Homo sapiens 130-137 30255159-7 2018 The role of levodopa in modulating the levels of miRNA 155 requires further studies. Levodopa 12-20 microRNA 155 Homo sapiens 49-58 30063943-8 2018 Additionally, the IL-1 level was significantly higher in patients who received a levodopa dosage of >250 mg than in their counterparts who received <=250 mg, and the IL-1 level was higher in patients with an H-Y stage of >2 and UPDRS III of >27 than in their counterparts with an H-Y stage of <=2 and UPDRS III of <=27. Levodopa 81-89 interleukin 1 alpha Homo sapiens 18-22 30271338-0 2018 Effects of mGluR5 Antagonists on Parkinson"s Patients With L-Dopa-Induced Dyskinesia: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Levodopa 59-65 glutamate receptor, ionotropic, kainate 1 Mus musculus 11-17 30271338-1 2018 Background: Modulation of Metabotropic glutamate receptor 5 (mGluR5) may be a novel therapeutic approach to manage Parkinson"s disease (PD) Patients with L-dopa-induced dyskinesia (LID). Levodopa 154-160 glutamate metabotropic receptor 5 Homo sapiens 26-59 30271338-1 2018 Background: Modulation of Metabotropic glutamate receptor 5 (mGluR5) may be a novel therapeutic approach to manage Parkinson"s disease (PD) Patients with L-dopa-induced dyskinesia (LID). Levodopa 154-160 glutamate receptor, ionotropic, kainate 1 Mus musculus 61-67 29734446-3 2018 L-DOPA (100 and 200 microM) induced sustained phosphorylation of extracellular signal-regulated kinases (ERK1/2) for 6 h, which were significantly decreased by cotreatments with ombuoside (1, 5, and 10 microM). Levodopa 0-6 mitogen activated protein kinase 3 Rattus norvegicus 105-120 30233336-6 2018 We found that Meis1KO share most of the tested behavioral properties with their wild type (WT) controls, including the modulation of the thermal pain withdrawal reflex by morphine, L-DOPA and D3 receptor (D3R) agonists and antagonists. Levodopa 181-187 Meis homeobox 1 Mus musculus 14-21 29998409-4 2018 Our aim was to determine whether HAT inhibitors such as anacardic acid, garcinol, and curcumin from natural plants reduce severity of L-DOPA-induced dyskinesia using a unilaterally 6-hydroxydopamine (6-OHDA)-lesioned PD mouse model. Levodopa 134-140 histocompatibility 49 Mus musculus 33-36 29998409-5 2018 Anacardic acid 2 mg/kg, garcinol 5 mg/kg, or curcumin 100 mg/kg co-treatment with L-DOPA significantly reduced the axial, limb, and orofacial (ALO) score indicating less dyskinesia with administration of HAT inhibitors in 6-OHDA-lesioned mice. Levodopa 82-88 histocompatibility 49 Mus musculus 204-207 29998409-8 2018 Our findings indicate that HAT inhibitor co-treatment with L-DOPA may have therapeutic potential for management of L-DOPA-induced dyskinesia in patients with PD. Levodopa 59-65 transmembrane serine protease 11D Homo sapiens 27-30 29998409-8 2018 Our findings indicate that HAT inhibitor co-treatment with L-DOPA may have therapeutic potential for management of L-DOPA-induced dyskinesia in patients with PD. Levodopa 115-121 transmembrane serine protease 11D Homo sapiens 27-30 29847694-10 2018 We also found all MAO-B inhibitors to be efficient when given together with levodopa. Levodopa 76-84 monoamine oxidase B Homo sapiens 18-23 29847694-13 2018 Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug. Levodopa 46-54 monoamine oxidase B Homo sapiens 77-82 29734446-4 2018 L-DOPA (100 and 200 microM) alone significantly increased c-Jun N-terminal kinase (JNK1/2) phosphorylation for 6 h and cleaved-caspase-3 expression for 24 h, both of which were partially, but significantly, blocked by ombuoside (1, 5, and 10 microM). Levodopa 0-6 caspase 3 Rattus norvegicus 127-136 29734446-5 2018 In addition, ombuoside (1, 5, and 10 microM) significantly restored the L-DOPA-induced (100 and 200 microM) decrease in superoxide dismutase (SOD) activity for 24 h. Taken together, these findings indicate that ombuoside protects against L-DOPA-induced neurotoxicity by inhibiting L-DOPA-induced increases in sustained ERK1/2 and JNK1/2 phosphorylation and caspase-3 expression and L-DOPA-induced decrease in SOD activity in PC12 cells. Levodopa 72-78 mitogen activated protein kinase 3 Rattus norvegicus 319-325 29734446-5 2018 In addition, ombuoside (1, 5, and 10 microM) significantly restored the L-DOPA-induced (100 and 200 microM) decrease in superoxide dismutase (SOD) activity for 24 h. Taken together, these findings indicate that ombuoside protects against L-DOPA-induced neurotoxicity by inhibiting L-DOPA-induced increases in sustained ERK1/2 and JNK1/2 phosphorylation and caspase-3 expression and L-DOPA-induced decrease in SOD activity in PC12 cells. Levodopa 72-78 caspase 3 Rattus norvegicus 357-366 30077198-3 2018 To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed. Levodopa 30-36 monoamine oxidase B Homo sapiens 108-127 29492662-4 2018 Experimental animal models of PD identified in DA D1/ERK-signaling pathway aberrant activation, occurring in striatal projection neurons, coupled with structural spines abnormalities, the molecular and neuronal basis of L-DOPA-induced dyskinesia (LIDs) occurrence. Levodopa 220-226 mitogen-activated protein kinase 1 Homo sapiens 53-56 29353394-1 2018 PURPOSE: The aims of the present study are to evaluate the effect of L-dopa on the secretion of cortisol and adrenocorticotropic hormone (ACTH) in short children and compare the performance of this test with the insulin tolerance test (ITT) in a large number of patients. Levodopa 69-75 proopiomelanocortin Homo sapiens 109-136 29353394-1 2018 PURPOSE: The aims of the present study are to evaluate the effect of L-dopa on the secretion of cortisol and adrenocorticotropic hormone (ACTH) in short children and compare the performance of this test with the insulin tolerance test (ITT) in a large number of patients. Levodopa 69-75 proopiomelanocortin Homo sapiens 138-142 30077198-3 2018 To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed. Levodopa 30-36 monoamine oxidase B Homo sapiens 129-134 29936243-1 2018 Individually, D1 and D3 dopamine receptors (D1R and D3R, respectively) have been implicated in L-DOPA-induced dyskinesia (LID). Levodopa 95-101 dopamine receptor D3 Rattus norvegicus 14-47 29940207-8 2018 Hemiparkinsonian alpha5-KO mice exhibited attenuated rotational behavior after amphetamine injection and attenuated levodopa-induced dyskinesia. Levodopa 116-124 laminin, alpha 5 Mus musculus 17-23 29857029-6 2018 In addition, this protein can also bind to and activate striatal mTORC1, one of the key players in l-DOPA-induced dyskinesia in rodent models of Parkinson"s disease. Levodopa 99-105 CREB regulated transcription coactivator 1 Mus musculus 65-71 29801899-5 2018 RESULTS: Logistic regression models controlling for age at diagnosis, sex, disease duration, and L-dopa dose revealed that 123I-FP-CIT binding in the putamen and striatum significantly predicted FOG (OR = 0.02, p = 0.03; OR = 0.01, p = 0.04; respectively) but not falls. Levodopa 97-103 zinc finger protein, FOG family member 1 Homo sapiens 195-198 30013350-0 2018 The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson"s rats. Levodopa 57-65 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 31-36 30042723-1 2018 Mutations of PLA2G6 gene are responsible for PARK14, an autosomal recessive L-DOPA responsive dystonia/parkinsonism with early/adult onset. Levodopa 76-82 phospholipase A2 group VI Homo sapiens 13-19 30042723-1 2018 Mutations of PLA2G6 gene are responsible for PARK14, an autosomal recessive L-DOPA responsive dystonia/parkinsonism with early/adult onset. Levodopa 76-82 phospholipase A2 group VI Homo sapiens 45-51 30013350-14 2018 The interaction between D1R and Shp-2 in the normal rats was kept stable after the long-term use of l-DOPA. Levodopa 100-106 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 32-37 30013350-15 2018 Moreover, we found that the pulsatile levodopa administration induced hyperphosphorylation of Shp-2, ERK1/2 and mTOR, while the coadministration of l-DOPA and D1R antagonist, SCH23390, did not induce the hyperphosphorylation of these proteins. Levodopa 38-46 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 94-99 30013350-15 2018 Moreover, we found that the pulsatile levodopa administration induced hyperphosphorylation of Shp-2, ERK1/2 and mTOR, while the coadministration of l-DOPA and D1R antagonist, SCH23390, did not induce the hyperphosphorylation of these proteins. Levodopa 38-46 mitogen activated protein kinase 3 Rattus norvegicus 101-107 30013350-15 2018 Moreover, we found that the pulsatile levodopa administration induced hyperphosphorylation of Shp-2, ERK1/2 and mTOR, while the coadministration of l-DOPA and D1R antagonist, SCH23390, did not induce the hyperphosphorylation of these proteins. Levodopa 38-46 mechanistic target of rapamycin kinase Rattus norvegicus 112-116 29968767-9 2018 Interestingly, FosB/ FosB induction by L-DOPA treatment occurred preferentially in cluster-2 dSPNs. Levodopa 39-45 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 15-19 29968767-9 2018 Interestingly, FosB/ FosB induction by L-DOPA treatment occurred preferentially in cluster-2 dSPNs. Levodopa 39-45 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 21-25 29530712-0 2018 Genetic disruption of the nuclear receptor Nur77 (Nr4a1) in rat reduces dopamine cell loss and l-Dopa-induced dyskinesia in experimental Parkinson"s disease. Levodopa 95-101 nuclear receptor subfamily 4, group A, member 1 Mus musculus 43-48 29924742-0 2018 Sudlow site II of human serum albumin remains functional after gold nanocluster encapsulation: a fluorescence-based drug binding study of L-Dopa. Levodopa 138-144 albumin Homo sapiens 24-37 29578580-0 2018 MAO-B and COMT Genetic Variations Associated With Levodopa Treatment Response in Patients With Parkinson"s Disease. Levodopa 50-58 monoamine oxidase B Homo sapiens 0-5 29578580-0 2018 MAO-B and COMT Genetic Variations Associated With Levodopa Treatment Response in Patients With Parkinson"s Disease. Levodopa 50-58 catechol-O-methyltransferase Homo sapiens 10-14 29578580-3 2018 In our study we investigated the possible relation among selected single-nucleotide polymorphisms (SNPs) in the MAO-B (rs1799836) and COMT (rs4680) genes and the therapeutic response to levodopa (l-dopa). Levodopa 186-194 monoamine oxidase B Homo sapiens 112-117 29578580-3 2018 In our study we investigated the possible relation among selected single-nucleotide polymorphisms (SNPs) in the MAO-B (rs1799836) and COMT (rs4680) genes and the therapeutic response to levodopa (l-dopa). Levodopa 186-194 catechol-O-methyltransferase Homo sapiens 134-138 29578580-3 2018 In our study we investigated the possible relation among selected single-nucleotide polymorphisms (SNPs) in the MAO-B (rs1799836) and COMT (rs4680) genes and the therapeutic response to levodopa (l-dopa). Levodopa 196-202 monoamine oxidase B Homo sapiens 112-117 29578580-8 2018 We observed that patients carrying MAO-B (rs1799836) A and AA genotypes and COMT (rs4680) LL genotype suffered more frequently from levodopa-induced-dyskinesia. Levodopa 132-140 monoamine oxidase B Homo sapiens 35-40 29578580-8 2018 We observed that patients carrying MAO-B (rs1799836) A and AA genotypes and COMT (rs4680) LL genotype suffered more frequently from levodopa-induced-dyskinesia. Levodopa 132-140 catechol-O-methyltransferase Homo sapiens 76-80 29578580-9 2018 In addition, we found an increased risk of 2.84-fold for male individuals carrying the MAO-B G allele to be treated with higher doses of levodopa (P = .04). Levodopa 137-145 monoamine oxidase B Homo sapiens 87-92 29039022-10 2018 Metformin globally normalized the increased glycogen synthase kinase 3beta activity induced by chronic treatment of L-DOPA in a manner associated with Akt activation in unilaterally 6-OHDA-lesioned mice. Levodopa 116-122 glycogen synthase kinase 3 beta Mus musculus 44-74 29039022-10 2018 Metformin globally normalized the increased glycogen synthase kinase 3beta activity induced by chronic treatment of L-DOPA in a manner associated with Akt activation in unilaterally 6-OHDA-lesioned mice. Levodopa 116-122 thymoma viral proto-oncogene 1 Mus musculus 151-154 29907754-6 2018 The obtained results concluded that CeO2 NP fit best in the active site of alpha-synuclein with good contacts and interaction, and potentially inhibited the PD against L-DOPA drug selected as positive control in the designed PD biochemical pathway. Levodopa 168-174 synuclein alpha Homo sapiens 75-90 29530712-0 2018 Genetic disruption of the nuclear receptor Nur77 (Nr4a1) in rat reduces dopamine cell loss and l-Dopa-induced dyskinesia in experimental Parkinson"s disease. Levodopa 95-101 nuclear receptor subfamily 4, group A, member 1 Mus musculus 50-55 29530712-7 2018 Genetic disruption of Nr4a1 in rat reduced neurotoxin-induced dopamine cell loss and l-Dopa-induced dyskinesia, whereas virally-driven striatal overexpression of Nr4a1 enhanced or partially restored involuntary movements induced by chronic l-Dopa in wild type and Nr4a1-deficient rats, respectively. Levodopa 85-91 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 22-27 29530712-8 2018 Collectively, these results suggest that Nr4a1 is involved in dopamine cell loss and l-Dopa-induced dyskinesia in experimental PD. Levodopa 85-91 nuclear receptor subfamily 4, group A, member 1 Mus musculus 41-46 29447969-4 2018 In accordance with the kinetic profile, molecular docking results show that PMI-5 is able to interact favorably with the tyrosinase active site containing the substrate molecule, L-DOPA, interacting with Val-247, Phe-263 and Val-282 residues. Levodopa 179-185 tyrosinase Homo sapiens 121-131 29479807-4 2018 7,8,4 -Trihydroxyflavone was found to strongly inhibit the oxidation of l-DOPA by tyrosinase with an IC50 value of 10.31 +- 0.41 muM. Levodopa 72-78 tyrosinase Homo sapiens 82-92 29369408-7 2018 Molecular docking results show that levedopa binds differentially and obtained less number of hydrogen bonds in compared with wild type LRRK2. Levodopa 36-44 leucine rich repeat kinase 2 Homo sapiens 136-141 29889613-1 2018 The aim of this study was to evaluate the stability of levodopa liposomes co-loaded with three different antioxidants (curcumin, ascorbic acid, and superoxide dismutase (SOD)). Levodopa 55-63 superoxide dismutase 1 Homo sapiens 148-168 29889613-1 2018 The aim of this study was to evaluate the stability of levodopa liposomes co-loaded with three different antioxidants (curcumin, ascorbic acid, and superoxide dismutase (SOD)). Levodopa 55-63 superoxide dismutase 1 Homo sapiens 170-173 28840468-0 2018 The Kinase Fyn As a Novel Intermediate in L-DOPA-Induced Dyskinesia in Parkinson"s Disease. Levodopa 42-48 Fyn proto-oncogene Mus musculus 11-14 29243232-0 2018 A de novo loss-of-function DYNC1H1 mutation in a patient with parkinsonian features and a favourable response to levodopa. Levodopa 113-121 dynein cytoplasmic 1 heavy chain 1 Homo sapiens 27-34 29496635-4 2018 Here, Pink1 -/- rats were treated with an oral dose of levodopa and limb motor and vocal communication behaviors were measured. Levodopa 55-63 PTEN induced kinase 1 Rattus norvegicus 6-11 29427634-3 2018 L-dopa is a natural inhibitor of prolactin (PRL) hormone which is required to maintain lactation in women but it"s over production (hyperprolactinemia) plays critical role in advancement of breast cancer. Levodopa 0-6 prolactin Homo sapiens 33-42 29427634-3 2018 L-dopa is a natural inhibitor of prolactin (PRL) hormone which is required to maintain lactation in women but it"s over production (hyperprolactinemia) plays critical role in advancement of breast cancer. Levodopa 0-6 prolactin Homo sapiens 44-47 29633651-0 2018 Age/disease duration influence on activities of daily living and quality of life after levodopa-carbidopa intestinal gel in Parkinson"s disease. Levodopa 87-95 renin binding protein Homo sapiens 0-3 29633651-1 2018 AIM: To determine if age and Parkinson"s disease duration at therapy initiation influence the efficacy of levodopa-carbidopa intestinal gel (LCIG) on quality of life and activities of daily living. Levodopa 106-114 renin binding protein Homo sapiens 21-24 29707715-0 2018 Effects of bovine lactoferrin on l-DOPA absorption and metabolism in mice. Levodopa 33-39 lactotransferrin Bos taurus 18-29 29452071-0 2018 CaMKII inhibition ameliorated levodopa-induced dyskinesia by downregulating tyrosine hydroxylase activity in an experimental model of Parkinson"s disease. Levodopa 30-38 tyrosine hydroxylase Rattus norvegicus 76-96 29452071-13 2018 Moreover, KN-93 treatment reduced the expression of Arc and Penk, two immediate early genes, induced by chronic L-dopa. Levodopa 112-118 nucleolar protein 3 Rattus norvegicus 52-55 29452071-13 2018 Moreover, KN-93 treatment reduced the expression of Arc and Penk, two immediate early genes, induced by chronic L-dopa. Levodopa 112-118 proenkephalin Rattus norvegicus 60-64 29243232-1 2018 Graphical summary of "A de novo loss-of-function DYNC1H1 mutation in a patient with parkinsonian features and a favourable response to levodopa" by Szczaluba et al.. Levodopa 135-143 dynein cytoplasmic 1 heavy chain 1 Homo sapiens 49-56 29508924-0 2018 A Selective Phosphodiesterase 10A Inhibitor Reduces L-Dopa-Induced Dyskinesias in Parkinsonian Monkeys. Levodopa 52-58 phosphodiesterase 10A Homo sapiens 12-33 29921400-11 2018 The levels of CD4+, CD8+, CD3+, and CD4+/CD8+ in PD patients treated with L-DOPA were higher than those of PD patients without L-DOPA treatment (P less than 0.05). Levodopa 74-80 CD4 molecule Homo sapiens 14-17 29921400-11 2018 The levels of CD4+, CD8+, CD3+, and CD4+/CD8+ in PD patients treated with L-DOPA were higher than those of PD patients without L-DOPA treatment (P less than 0.05). Levodopa 74-80 CD8a molecule Homo sapiens 20-23 29921400-11 2018 The levels of CD4+, CD8+, CD3+, and CD4+/CD8+ in PD patients treated with L-DOPA were higher than those of PD patients without L-DOPA treatment (P less than 0.05). Levodopa 74-80 CD4 molecule Homo sapiens 36-39 29921400-11 2018 The levels of CD4+, CD8+, CD3+, and CD4+/CD8+ in PD patients treated with L-DOPA were higher than those of PD patients without L-DOPA treatment (P less than 0.05). Levodopa 74-80 CD8a molecule Homo sapiens 41-44 29508924-2 2018 Phosphodiesterase 10A regulates cyclic adenosine monophosphate and cyclic guanosine monophosphate, which mediate responses to dopamine receptor activation, and the levels of these cyclic nucleotides are decreased in experimental models of l-dopa-induced dyskinesia. Levodopa 239-245 phosphodiesterase 10A Homo sapiens 0-21 29508924-3 2018 The elevation of cyclic adenosine monophosphate/cyclic guanosine monophosphate levels by phosphodiesterase 10A inhibition may thus be targeted to reduce l-dopa-induced dyskinesia. Levodopa 153-159 phosphodiesterase 10A Homo sapiens 89-110 29508924-15 2018 CONCLUSIONS: Results show that regulation of striatal cyclic nucleotides by phosphodiesterase 10A inhibition could be a useful therapeutic approach for l-dopa-induced dyskinesia, and therefore data support further studies of selective phosphodiesterase 10A inhibitors for PD therapy. Levodopa 152-158 phosphodiesterase 10A Homo sapiens 76-97 29508924-15 2018 CONCLUSIONS: Results show that regulation of striatal cyclic nucleotides by phosphodiesterase 10A inhibition could be a useful therapeutic approach for l-dopa-induced dyskinesia, and therefore data support further studies of selective phosphodiesterase 10A inhibitors for PD therapy. Levodopa 152-158 phosphodiesterase 10A Homo sapiens 235-256 29407218-3 2018 There is a loss of the DAT in Parkinson"s disease affecting release of levodopa implicated in levodopa-induced dyskinesias. Levodopa 71-79 solute carrier family 6 member 3 Rattus norvegicus 23-26 29407218-3 2018 There is a loss of the DAT in Parkinson"s disease affecting release of levodopa implicated in levodopa-induced dyskinesias. Levodopa 94-102 solute carrier family 6 member 3 Rattus norvegicus 23-26 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 nuclear factor, erythroid derived 2, like 2 Mus musculus 195-199 29572645-0 2018 Effects of the Serotonin 5-HT1A Receptor Biased Agonists, F13714 and F15599, on Striatal Neurotransmitter Levels Following L-DOPA Administration in Hemi-Parkinsonian Rats. Levodopa 123-129 5-hydroxytryptamine receptor 1A Rattus norvegicus 15-40 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 heme oxygenase 1 Mus musculus 200-204 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 glucagon Mus musculus 214-219 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 advanced glycosylation end product-specific receptor Mus musculus 300-304 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 transforming growth factor, beta 1 Mus musculus 306-315 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 tumor necrosis factor Mus musculus 317-326 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 interleukin 10 Mus musculus 328-333 29410018-5 2018 RESULTS: The combination of l-dopa/Carbidopa and linagliptin in a dose-dependent manner resulted in significant improvement of the behavioural changes, striatal dopamine, antioxidant parameters, Nrf2/HO-1 content, GLP-1, ATP and mitochondrial complex I activity with significant decrease in striatal RAGE, TGF-beta1, TNF-alpha, IL-10, TLR4 and alleviated the immunohistochemical changes better than the groups that received either l-dopa/Carbidopa or linagliptin alone. Levodopa 28-34 toll-like receptor 4 Mus musculus 335-339 29483281-13 2018 These results further consolidate the fidelity of the Pitx3-/- mouse as a PD model in which to study the morphological and physiological remodeling of striatal projection neurons by administration of l-DOPA and other drugs. Levodopa 200-206 paired-like homeodomain transcription factor 3 Mus musculus 54-59 29345156-1 2018 INTRODUCTION: Opicapone (OPC) is a novel, potent, reversible, and purely peripheral third-generation COMT inhibitor, which provides an enhancement in levodopa (L-Dopa) availability. Levodopa 150-158 catechol-O-methyltransferase Homo sapiens 101-105 30042645-12 2018 Chronic L-dopa treatment further increased SG2 levels in denervated striatum. Levodopa 8-14 secretogranin II Rattus norvegicus 43-46 29232769-1 2018 BACKGROUND AND PURPOSE: We previously showed that nociceptin/orphanin FQ opioid peptide (NOP) receptor agonists attenuate the expression of levodopa-induced dyskinesia in animal models of Parkinson"s disease. Levodopa 140-148 prepronociceptin Rattus norvegicus 50-60 29232769-9 2018 AT-403 reduced the ERK phosphorylation induced by SKF38393 in vitro and by levodopa in vivo. Levodopa 75-83 Eph receptor B1 Rattus norvegicus 19-22 29670409-8 2018 This inhibitor of peripheral catechol-O-methyltransferase supports continuous brain delivery of levodopa and, thus, the continuous dopaminergic stimulation concept. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 29-57 29339052-1 2018 Recently, the biased and highly selective 5-HT1A agonists, NLX-112, F13714 and F15599, have been shown to alleviate dyskinesia in rodent and primate models of Parkinson"s disease, while marginally interfering with antiparkinsonian effects of levodopa. Levodopa 242-250 5-hydroxytryptamine receptor 1A Homo sapiens 42-48 29350074-8 2018 The BDNF concentration was negatively correlated with age at PD onset and positively associated with disease duration, severity of PD symptoms, and treatment with L-DOPA. Levodopa 163-169 brain derived neurotrophic factor Homo sapiens 4-8 28375049-2 2018 Catechol-O-methyltransferase (COMT) is involved in the O-methylation of l-DOPA, dopamine, and other catechols. Levodopa 72-78 catechol-O-methyltransferase Mus musculus 0-28 28375049-2 2018 Catechol-O-methyltransferase (COMT) is involved in the O-methylation of l-DOPA, dopamine, and other catechols. Levodopa 72-78 catechol-O-methyltransferase Mus musculus 30-34 29558440-7 2018 The apparent permeability (Pe) values of encapsulated dopamine in functionalized and unfunctionalized liposomes showed that transferrin functionalized nanocarriers could represent appealing non-toxic candidates for brain delivery, thus improving benefits and decreasing complications to patients subjected to L-dopa chronical treatment. Levodopa 309-315 transferrin Homo sapiens 124-135 29345156-1 2018 INTRODUCTION: Opicapone (OPC) is a novel, potent, reversible, and purely peripheral third-generation COMT inhibitor, which provides an enhancement in levodopa (L-Dopa) availability. Levodopa 160-166 catechol-O-methyltransferase Homo sapiens 101-105 29345156-10 2018 It significantly decreases COMT activity, with half-life of COMT inhibition in human erythrocytes of 61.6 h and increases systemic exposure to L-Dopa. Levodopa 143-149 catechol-O-methyltransferase Homo sapiens 27-31 29241709-0 2018 Regulation of Pleiotrophin and Fyn in the striatum of rats undergoing L-DOPA-induced dyskinesia. Levodopa 70-76 pleiotrophin Rattus norvegicus 14-26 29341046-1 2018 The purpose of the study was to evaluate the relationship between arginine-levodopa-induced growth hormone (GH) secretion and nonalcoholic fatty liver disease (NAFLD) in obese children. Levodopa 75-83 growth hormone 1 Homo sapiens 92-106 29241709-0 2018 Regulation of Pleiotrophin and Fyn in the striatum of rats undergoing L-DOPA-induced dyskinesia. Levodopa 70-76 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 31-34 29241709-3 2018 In previous publications, we have shown that Pleiotrophin (PTN), a developmentally regulated trophic factor, is up-regulated by L-DOPA in the striatum of dopamine denervated rats. Levodopa 128-134 pleiotrophin Rattus norvegicus 45-57 29241709-3 2018 In previous publications, we have shown that Pleiotrophin (PTN), a developmentally regulated trophic factor, is up-regulated by L-DOPA in the striatum of dopamine denervated rats. Levodopa 128-134 pleiotrophin Rattus norvegicus 59-62 29241709-5 2018 The PTN-RPTPzeta/beta intracellular pathway has not been fully explored and it might be implicated in the striatal plastic changes triggered by L-DOPA treatment. Levodopa 144-150 pleiotrophin Rattus norvegicus 4-7 29241709-5 2018 The PTN-RPTPzeta/beta intracellular pathway has not been fully explored and it might be implicated in the striatal plastic changes triggered by L-DOPA treatment. Levodopa 144-150 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 8-21 29241709-7 2018 In this study, we evaluated the changes in PTN and Fyn protein levels and Fyn phosphorylation status in the 6-OHDA rat model of PD rendered dyskinetic with L-DOPA. Levodopa 156-162 pleiotrophin Rattus norvegicus 43-46 29416937-4 2018 Work-up revealed a novel pathogenic mutation in the Fibroblast Growth Factor 14 gene, and symptoms improved with amantadine and levodopa. Levodopa 128-136 fibroblast growth factor 14 Homo sapiens 52-79 29406893-0 2018 Dopamine transporter imaging predicts motor responsiveness to levodopa challenge in patients with Parkinson"s disease: A pilot study of DATSCAN for subthalamic deep brain stimulation. Levodopa 62-70 solute carrier family 6 member 3 Homo sapiens 0-20 29406886-1 2018 OBJECTIVE: To determine the impact of levodopa-carbidopa intestinal gel (LCIG) infusion on different subtypes of freezing of gait (FoG) classified according to levodopa responsiveness in advanced Parkinson disease (PD) patients. Levodopa 38-46 zinc finger protein, FOG family member 1 Homo sapiens 131-134 29246844-0 2018 SPG7 with parkinsonism responsive to levodopa and dopaminergic deficit. Levodopa 37-45 SPG7 matrix AAA peptidase subunit, paraplegin Homo sapiens 0-4 29246844-3 2018 She developed parkinsonism responsive to levodopa, expanding the phenotype of complex SPG7. Levodopa 41-49 SPG7 matrix AAA peptidase subunit, paraplegin Homo sapiens 86-90 29614697-5 2018 Peripheral catechol-O-methyltransferase (COMT) inhibition improves the bioavailability of levodopa and results in a prolonged response. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 11-39 29217686-4 2018 Interestingly, NSC loss in alpha-SYN-deficient mice can be prevented by viral delivery of human alpha-SYN into their sustantia nigra or by treatment with l-DOPA, suggesting that alpha-SYN regulates dopamine availability to NSCs. Levodopa 154-160 synuclein alpha Homo sapiens 27-36 29120941-5 2018 Gynosaponin TN-2 at 0.5 and 1.0 muM also reduced L-DOPA (100 and 200 muM)-induced JNK1/2 phosphorylation and cleaved caspase-3 expression. Levodopa 49-55 caspase 3 Rattus norvegicus 117-126 30439288-0 2018 L-DOPA-Induced Motor Impairment and Overexpression of Corticostriatal Synaptic Components Are Improved by the mGluR5 Antagonist MPEP in 6-OHDA-Lesioned Rats. Levodopa 0-6 glutamate receptor, ionotropic, kainate 1 Mus musculus 110-116 30439288-7 2018 Finally, MPEP reduced overexpression of the two postsynaptic proteins (PSD-95 and SAP102) induced by L-DOPA treatment. Levodopa 101-107 discs large MAGUK scaffold protein 4 Rattus norvegicus 71-77 30439288-7 2018 Finally, MPEP reduced overexpression of the two postsynaptic proteins (PSD-95 and SAP102) induced by L-DOPA treatment. Levodopa 101-107 discs large MAGUK scaffold protein 3 Rattus norvegicus 82-88 29697034-5 2018 MATERIALS & METHODS: Based on the roles of COMT and MAO in the metabolism of L-dopa and dopamine, the present study attempts to discover novel dual inhibitors of these enzymes. Levodopa 81-87 catechol-O-methyltransferase Homo sapiens 47-51 29233065-5 2018 The mechanisms of L-DOPA toxicity involve oxidative stress, L-DOPA oxidation to quinone, mitochondrial dysfunction, and alpha-synuclein. Levodopa 18-24 synuclein alpha Homo sapiens 120-135 29091814-2 2018 The aim of this work was to assess alterations in the urinary L-dopa/dopamine ratio over three time periods in rats with insulin resistance induced by fructose overload and its correlation with blood pressure levels and the presence of microalbuminuria and reduced nephrin expression as markers of renal structural damage. Levodopa 62-68 NPHS1 adhesion molecule, nephrin Rattus norvegicus 265-272 29091814-4 2018 A significant increase of the urinary L-dopa/dopamine ratio was found in FO rats since week 4, which positively correlated to the development of hypertension and preceded in time the onset of microalbuminuria and reduced nephrin expression observed on week 12 of treatment. Levodopa 38-44 NPHS1 adhesion molecule, nephrin Rattus norvegicus 221-228 29383286-7 2018 It dose-dependently inhibited the activity of tyrosinase, with the IC50 values 6.2 +- 2.0 microM and 10.3 +- 5.4 microM on tyrosine and L-Dopa formation, respectively. Levodopa 136-142 tyrosinase Homo sapiens 46-56 28843018-4 2018 They make a simple extract of the apple tissue and measure the activity of PPO using 3,4-dihydroxy-l-phenylalanine (l-DOPA) as substrate. Levodopa 85-114 polyphenol oxidase, chloroplastic Malus domestica 75-78 28843018-4 2018 They make a simple extract of the apple tissue and measure the activity of PPO using 3,4-dihydroxy-l-phenylalanine (l-DOPA) as substrate. Levodopa 116-122 polyphenol oxidase, chloroplastic Malus domestica 75-78 28843453-1 2018 Role of CB1 and CB2 receptors and relevance for Alzheimer"s disease and levodopa-induced dyskinesia. Levodopa 72-80 cannabinoid receptor 1 Rattus norvegicus 8-11 28843453-1 2018 Role of CB1 and CB2 receptors and relevance for Alzheimer"s disease and levodopa-induced dyskinesia. Levodopa 72-80 cannabinoid receptor 2 Rattus norvegicus 16-19 28843453-11 2018 Expression of CB1-CB2Hets was increased in the striatum from rats rendered dyskinetic by chronic levodopa treatment. Levodopa 97-105 cannabinoid receptor 1 Rattus norvegicus 14-17 28843453-11 2018 Expression of CB1-CB2Hets was increased in the striatum from rats rendered dyskinetic by chronic levodopa treatment. Levodopa 97-105 cannabinoid receptor 2 Rattus norvegicus 18-21 29697034-2 2018 L-Dopa is extensively decarboxylated in the gastrointestinal tract and peripheral tissues by Aromatic L-Amino Acid Decarboxylase (AADC), and AADC inhibitors are thus frequently combined with L-dopa therapy. Levodopa 0-6 dopa decarboxylase Homo sapiens 93-128 29697034-2 2018 L-Dopa is extensively decarboxylated in the gastrointestinal tract and peripheral tissues by Aromatic L-Amino Acid Decarboxylase (AADC), and AADC inhibitors are thus frequently combined with L-dopa therapy. Levodopa 0-6 dopa decarboxylase Homo sapiens 130-134 29697034-2 2018 L-Dopa is extensively decarboxylated in the gastrointestinal tract and peripheral tissues by Aromatic L-Amino Acid Decarboxylase (AADC), and AADC inhibitors are thus frequently combined with L-dopa therapy. Levodopa 191-197 dopa decarboxylase Homo sapiens 93-128 29697034-2 2018 L-Dopa is extensively decarboxylated in the gastrointestinal tract and peripheral tissues by Aromatic L-Amino Acid Decarboxylase (AADC), and AADC inhibitors are thus frequently combined with L-dopa therapy. Levodopa 191-197 dopa decarboxylase Homo sapiens 130-134 29697034-2 2018 L-Dopa is extensively decarboxylated in the gastrointestinal tract and peripheral tissues by Aromatic L-Amino Acid Decarboxylase (AADC), and AADC inhibitors are thus frequently combined with L-dopa therapy. Levodopa 191-197 dopa decarboxylase Homo sapiens 141-145 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 129-135 dopa decarboxylase Homo sapiens 5-9 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 129-135 catechol-O-methyltransferase Homo sapiens 52-80 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 129-135 catechol-O-methyltransferase Homo sapiens 82-86 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 129-135 catechol-O-methyltransferase Homo sapiens 141-145 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 194-200 dopa decarboxylase Homo sapiens 5-9 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 194-200 catechol-O-methyltransferase Homo sapiens 52-80 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 194-200 catechol-O-methyltransferase Homo sapiens 82-86 29697034-3 2018 When AADC is inhibited, 3-Omethylation Catalysed by Catechol-O-Methyltransferase (COMT) becomes a dominant metabolic pathway for L-dopa, and COMT inhibitors may thus also be used as adjuncts to L-dopa in Parkinson"s disease. Levodopa 194-200 catechol-O-methyltransferase Homo sapiens 141-145 29614697-5 2018 Peripheral catechol-O-methyltransferase (COMT) inhibition improves the bioavailability of levodopa and results in a prolonged response. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 41-45 29422851-3 2017 The patient was treated with bilateral STN DBS after developing side effects related to L-dopa. Levodopa 88-94 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 39-42 30075828-0 2018 Polymorphisms of Catechol-O-Methyl Transferase (COMT) Gene in Vulnerability to Levodopa-Induced Dyskinesia. Levodopa 79-87 catechol-O-methyltransferase Homo sapiens 17-46 30075828-0 2018 Polymorphisms of Catechol-O-Methyl Transferase (COMT) Gene in Vulnerability to Levodopa-Induced Dyskinesia. Levodopa 79-87 catechol-O-methyltransferase Homo sapiens 48-52 29055799-0 2018 Altered mGluR5 binding potential and glutamine concentration in the 6-OHDA rat model of acute Parkinson"s disease and levodopa-induced dyskinesia. Levodopa 118-126 glutamate receptor, ionotropic, kainate 1 Mus musculus 8-14 29055799-1 2018 Several lines of evidence point to alterations in glutamatergic signaling in Parkinson"s disease (PD) and levodopa-induced dyskinesia (LID), involving the metabotropic glutamate receptor type 5 (mGluR5). Levodopa 106-114 glutamate receptor, ionotropic, kainate 1 Mus musculus 195-201 29055799-6 2018 However, following L-DOPA, an increase in relative mGluR5 uptake was present in the contralateral motor cortex and somatosensory cortex. Levodopa 19-25 glutamate receptor, ionotropic, kainate 1 Mus musculus 51-57 29055799-9 2018 Relative mGluR5 uptake in the CP of levodopa-treated rats was also found positively correlated with abnormal involuntary movement scores. Levodopa 36-44 glutamate receptor, ionotropic, kainate 1 Mus musculus 9-15 27779245-0 2018 Association between DRD2 and DRD3 gene polymorphisms and gastrointestinal symptoms induced by levodopa therapy in Parkinson"s disease. Levodopa 94-102 dopamine receptor D2 Homo sapiens 20-24 27779245-0 2018 Association between DRD2 and DRD3 gene polymorphisms and gastrointestinal symptoms induced by levodopa therapy in Parkinson"s disease. Levodopa 94-102 dopamine receptor D3 Homo sapiens 29-33 27779245-4 2018 The aim of this study was to investigate the relationship of DRD2 rs1799732 and DRD3 rs6280 gene polymorphisms with gastrointestinal (GI) symptoms induced by levodopa in PD patients. Levodopa 158-166 dopamine receptor D2 Homo sapiens 61-65 27779245-4 2018 The aim of this study was to investigate the relationship of DRD2 rs1799732 and DRD3 rs6280 gene polymorphisms with gastrointestinal (GI) symptoms induced by levodopa in PD patients. Levodopa 158-166 dopamine receptor D3 Homo sapiens 80-84 27779245-8 2018 The analyses showed that DRD2 Ins/Ins (prevalence ratio (PR)=2.374, 95% confidence interval (CI): 1.105-5.100; P=0.027) and DRD3 Ser/Ser genotypes (PR=1.677, 95% CI 1.077-2.611; P=0.022) were independent and predictors of gastrointestinal symptoms associated with levodopa therapy. Levodopa 264-272 dopamine receptor D2 Homo sapiens 25-29 27779245-8 2018 The analyses showed that DRD2 Ins/Ins (prevalence ratio (PR)=2.374, 95% confidence interval (CI): 1.105-5.100; P=0.027) and DRD3 Ser/Ser genotypes (PR=1.677, 95% CI 1.077-2.611; P=0.022) were independent and predictors of gastrointestinal symptoms associated with levodopa therapy. Levodopa 264-272 dopamine receptor D3 Homo sapiens 124-128 29375464-0 2017 A Meta-Analysis of Adenosine A2A Receptor Antagonists on Levodopa-Induced Dyskinesia In Vivo. Levodopa 57-65 adenosine A2a receptor Homo sapiens 19-41 32264500-4 2017 The gold cluster was then modified with Levodopa (l-dopa), to utilize the large amino acid transporter 1 (LAT1) pathways to enhance brain entry. Levodopa 40-48 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 106-110 28823933-0 2017 Rabphilin 3A: A novel target for the treatment of levodopa-induced dyskinesias. Levodopa 50-58 rabphilin 3A Rattus norvegicus 0-12 28823933-2 2017 Changes in NMDAR subunit composition have been documented in brain disorders such as Parkinson"s disease (PD) and levodopa (L-DOPA)-induced dyskinesias (LIDs), where an increase of NMDAR GluN2A/GluN2B subunit ratio at striatal synapses has been observed. Levodopa 114-122 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 187-193 28823933-2 2017 Changes in NMDAR subunit composition have been documented in brain disorders such as Parkinson"s disease (PD) and levodopa (L-DOPA)-induced dyskinesias (LIDs), where an increase of NMDAR GluN2A/GluN2B subunit ratio at striatal synapses has been observed. Levodopa 114-122 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 194-200 28823933-2 2017 Changes in NMDAR subunit composition have been documented in brain disorders such as Parkinson"s disease (PD) and levodopa (L-DOPA)-induced dyskinesias (LIDs), where an increase of NMDAR GluN2A/GluN2B subunit ratio at striatal synapses has been observed. Levodopa 124-130 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 187-193 28823933-2 2017 Changes in NMDAR subunit composition have been documented in brain disorders such as Parkinson"s disease (PD) and levodopa (L-DOPA)-induced dyskinesias (LIDs), where an increase of NMDAR GluN2A/GluN2B subunit ratio at striatal synapses has been observed. Levodopa 124-130 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 194-200 28823933-6 2017 Considering that protein-protein interactions govern the synaptic retention of NMDARs, the purpose of this work was to analyse the role of Rph3A and Rph3A/NMDAR complex in PD and LIDs, and to modulate Rph3A/GluN2A interaction to counteract the aberrant motor behaviour associated to chronic L-DOPA administration. Levodopa 291-297 rabphilin 3A Rattus norvegicus 139-144 29186917-5 2017 Lazabemide is a monoamine oxidase (MAO)-B inhibitor, a class of compounds that slows the depletion of dopamine stores in Parkinson"s disease and elevates dopamine levels produced by exogenously administered l-dopa. Levodopa 207-213 monoamine oxidase B Mus musculus 16-41 29325386-0 2017 [The protective effect of the activation of NMDAR1/ERK1/2 signal pathway induced by levodopa on visual cortical neurons in monocular deprivation rats]. Levodopa 84-92 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 44-50 29325386-0 2017 [The protective effect of the activation of NMDAR1/ERK1/2 signal pathway induced by levodopa on visual cortical neurons in monocular deprivation rats]. Levodopa 84-92 mitogen activated protein kinase 3 Rattus norvegicus 51-57 29325386-1 2017 Objective: To investigate the protection effects of the activation of NMDAR1(NMDA receptor 1)/ERK1/2 signal pathway on visual cortex nerve cells induced by levodopa in amblyopia rats. Levodopa 156-164 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 70-76 29325386-1 2017 Objective: To investigate the protection effects of the activation of NMDAR1(NMDA receptor 1)/ERK1/2 signal pathway on visual cortex nerve cells induced by levodopa in amblyopia rats. Levodopa 156-164 mitogen activated protein kinase 3 Rattus norvegicus 94-100 29325386-17 2017 Conclusion: Levodopa played a protective role in visual cortex nerve cells of amblyopia rats at least partially through activation of NMDA-ERK1/2 signal pathway. Levodopa 12-20 mitogen activated protein kinase 3 Rattus norvegicus 139-145 29144589-6 2017 In addition, C2C12 cells culured on nanopatterned PUA-L-DOPA-S1P has well-oriented and organized myodubes formed with greater expression of myogenic regulatory factors such as MyoD and MyoG comapred to flat PUA groups. Levodopa 54-60 myogenic differentiation 1 Mus musculus 176-180 29144589-6 2017 In addition, C2C12 cells culured on nanopatterned PUA-L-DOPA-S1P has well-oriented and organized myodubes formed with greater expression of myogenic regulatory factors such as MyoD and MyoG comapred to flat PUA groups. Levodopa 54-60 myogenin Mus musculus 185-189 29201000-0 2017 Striatal Galphaolf/cAMP Signal-Dependent Mechanism to Generate Levodopa-Induced Dyskinesia in Parkinson"s Disease. Levodopa 63-71 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 9-18 29201000-6 2017 Based on the evidence obtained from parkinsonian mice, we hypothesized that in the DA-denervated striatum with D1R hypersensitivity, a repeated and pulsatile exposure to levodopa might cause a usage-induced degradation of Galphaolf proteins in striatal MSNs, resulting in increased and decreased levels of Galphaolf protein in the striatonigral and striatopallidal MSNs, respectively. Levodopa 170-178 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 222-231 29201000-6 2017 Based on the evidence obtained from parkinsonian mice, we hypothesized that in the DA-denervated striatum with D1R hypersensitivity, a repeated and pulsatile exposure to levodopa might cause a usage-induced degradation of Galphaolf proteins in striatal MSNs, resulting in increased and decreased levels of Galphaolf protein in the striatonigral and striatopallidal MSNs, respectively. Levodopa 170-178 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 306-315 32264500-4 2017 The gold cluster was then modified with Levodopa (l-dopa), to utilize the large amino acid transporter 1 (LAT1) pathways to enhance brain entry. Levodopa 50-56 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 74-104 32264500-4 2017 The gold cluster was then modified with Levodopa (l-dopa), to utilize the large amino acid transporter 1 (LAT1) pathways to enhance brain entry. Levodopa 50-56 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 106-110 28631864-9 2017 The ceftriaxone-treated l-dopa group had significantly increased striatal GLT-1 expression and glutamate uptake. Levodopa 24-30 solute carrier family 1 member 2 Rattus norvegicus 74-79 28958145-6 2017 Herein, we report on the development of a nanometric (100-135 nm) promising LAT1 selective liposomal drug carrier prepared from a novel l-3,4-dihydroxyphenylalanine (l-DOPA) functionalized amphiphile (Amphi-DOPA). Levodopa 136-164 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 76-80 28958145-6 2017 Herein, we report on the development of a nanometric (100-135 nm) promising LAT1 selective liposomal drug carrier prepared from a novel l-3,4-dihydroxyphenylalanine (l-DOPA) functionalized amphiphile (Amphi-DOPA). Levodopa 166-172 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 76-80 29251620-0 2017 [Effect of afobazole and levodopa on the activity of proline-specific proteinases and adenosine deaminase in blood serum and brain structures of rats with experimental Parkinson"s syndrome induced by systemic administration of rotenone]. Levodopa 25-33 adenosine deaminase Rattus norvegicus 86-105 29251620-3 2017 Afobazole and levodopa, which exhibit antiparkinsonian activity in this model of Parkinson"s syndrome, decrease elevated PREP activity in serum and increase reduced ADA activity in the prefrontal cortex of rats with the experimental pathology. Levodopa 14-22 prolyl endopeptidase Rattus norvegicus 121-125 29059133-0 2017 A Phase Ib Randomized Controlled Study to Evaluate the Effectiveness of a Single-Dose of the NR2B Selective N-Methyl-D-Aspartate Antagonist MK-0657 on Levodopa-Induced Dyskinesias and Motor Symptoms in Patients With Parkinson Disease. Levodopa 151-159 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 93-97 29059133-3 2017 The objective of this study was to evaluate the effects of the NR2B selective N-methyl-D-aspartate receptor antagonist MK-0657 on levodopa-induced dyskinesias and motor symptoms in PD patients. Levodopa 130-138 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 63-67 28757258-6 2017 Moreover, rats that over-expressed BDNF were more prone to develop LID and l-DOPA-induced rotations, compared to the GFP-treated control group. Levodopa 75-81 brain-derived neurotrophic factor Rattus norvegicus 35-39 28757258-7 2017 Finally, rats that over-expressed BDNF showed increased levels of striatal D1R-dependent signaling phospho-proteins in response to l-DOPA administration. Levodopa 131-137 brain-derived neurotrophic factor Rattus norvegicus 34-38 28757258-8 2017 This study suggests that BDNF over-expression, by inducing changes in pre-synaptic serotonin axonal trophism, is able to exacerbate maladaptive responses to l-DOPA administration. Levodopa 157-163 brain-derived neurotrophic factor Rattus norvegicus 25-29 28757258-0 2017 BDNF over-expression induces striatal serotonin fiber sprouting and increases the susceptibility to l-DOPA-induced dyskinesia in 6-OHDA-lesioned rats. Levodopa 100-106 brain-derived neurotrophic factor Rattus norvegicus 0-4 28757258-1 2017 In addition to its role in neuronal survival, the brain neurotrophic factor (BDNF) has been shown to influence serotonin transmission and synaptic plasticity, events strongly implicated in the appearance of l-DOPA-induced dyskinesia (LID), a motor complication occurring in parkinsonian patients after long-term treatment with the dopamine precursor. Levodopa 207-213 neurotrophin 3 Homo sapiens 56-75 28757258-1 2017 In addition to its role in neuronal survival, the brain neurotrophic factor (BDNF) has been shown to influence serotonin transmission and synaptic plasticity, events strongly implicated in the appearance of l-DOPA-induced dyskinesia (LID), a motor complication occurring in parkinsonian patients after long-term treatment with the dopamine precursor. Levodopa 207-213 brain derived neurotrophic factor Homo sapiens 77-81 29147684-7 2017 Variant filtering of all genes involved in the tetrahydrobiopterin pathway, required for levodopa synthesis, revealed an additional common variant in dihydrofolate reductase (DHFR, rs70991108). Levodopa 89-97 dihydrofolate reductase Homo sapiens 150-173 29147684-7 2017 Variant filtering of all genes involved in the tetrahydrobiopterin pathway, required for levodopa synthesis, revealed an additional common variant in dihydrofolate reductase (DHFR, rs70991108). Levodopa 89-97 dihydrofolate reductase Homo sapiens 175-179 29147684-10 2017 The common DHFR variant might have synergistic effects on production of tetrahydrobiopterin and levodopa, thereby increasing penetrance. Levodopa 96-104 dihydrofolate reductase Homo sapiens 11-15 29064509-6 2017 OBJECTIVES: The aim of the study was to: 1) explore the potential role for patient-driven N-of-1 studies as a tool for improving self-management in Parkinson"s disease (PD) using the example of managing levodopa-induced dyskinesia (LID) with nicotine, and 2) based on this example; identify some specific challenges of patient-driven N-of-1 studies. Levodopa 203-211 mitochondrial ribosomal protein L49 Homo sapiens 90-96 29064509-6 2017 OBJECTIVES: The aim of the study was to: 1) explore the potential role for patient-driven N-of-1 studies as a tool for improving self-management in Parkinson"s disease (PD) using the example of managing levodopa-induced dyskinesia (LID) with nicotine, and 2) based on this example; identify some specific challenges of patient-driven N-of-1 studies. Levodopa 203-211 mitochondrial ribosomal protein L49 Homo sapiens 334-340 28975571-3 2017 Long-term exposure to levodopa is no longer believed to solely induce LIDs, as studies have highlighted that PD patients who go on to develop LIDs exhibit elevated putaminal dopamine release before the initiation of levodopa treatment, suggesting the involvement of other mechanisms, including altered neuronal firing and abnormal levels of phosphodiesterase 10A. Levodopa 22-30 phosphodiesterase 10A Homo sapiens 341-362 29093677-0 2017 Levodopa/Benserazide Loaded Microspheres Alleviate L-dopa Induced Dyskinesia through Preventing the Over-Expression of D1R/Shp-2/ERK1/2 Signaling Pathway in a Rat Model of Parkinson"s Disease. Levodopa 0-8 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 123-128 29093677-0 2017 Levodopa/Benserazide Loaded Microspheres Alleviate L-dopa Induced Dyskinesia through Preventing the Over-Expression of D1R/Shp-2/ERK1/2 Signaling Pathway in a Rat Model of Parkinson"s Disease. Levodopa 0-8 mitogen activated protein kinase 3 Rattus norvegicus 129-135 29093677-0 2017 Levodopa/Benserazide Loaded Microspheres Alleviate L-dopa Induced Dyskinesia through Preventing the Over-Expression of D1R/Shp-2/ERK1/2 Signaling Pathway in a Rat Model of Parkinson"s Disease. Levodopa 51-57 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 123-128 29093677-0 2017 Levodopa/Benserazide Loaded Microspheres Alleviate L-dopa Induced Dyskinesia through Preventing the Over-Expression of D1R/Shp-2/ERK1/2 Signaling Pathway in a Rat Model of Parkinson"s Disease. Levodopa 51-57 mitogen activated protein kinase 3 Rattus norvegicus 129-135 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 39-47 mitogen activated protein kinase 3 Rattus norvegicus 137-178 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 39-47 mitogen activated protein kinase 3 Rattus norvegicus 180-186 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 49-55 mitogen activated protein kinase 3 Rattus norvegicus 137-178 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 49-55 mitogen activated protein kinase 3 Rattus norvegicus 180-186 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 257-263 mitogen activated protein kinase 3 Rattus norvegicus 137-178 29093677-1 2017 Background: The long-term intermittent Levodopa (L-dopa) stimulation contributes to an aberrant activation of D1 receptor (D1R) mediated extracellular signal-regulated kinases1/2 (ERK1/2) in the striatal medium spiny neurons, resulting in the occurrence of L-dopa induced dyskinesia (LID). Levodopa 257-263 mitogen activated protein kinase 3 Rattus norvegicus 180-186 29093677-8 2017 Intermittent L-dopa administration enhanced the expression of membrane D1R, and induced a robust increase of phosphorylation of Shp-2, Src, DARPP-32, and ERK1/2 in the 6-OHDA-lesioned striatum. Levodopa 13-19 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 128-133 29093677-8 2017 Intermittent L-dopa administration enhanced the expression of membrane D1R, and induced a robust increase of phosphorylation of Shp-2, Src, DARPP-32, and ERK1/2 in the 6-OHDA-lesioned striatum. Levodopa 13-19 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 135-138 29093677-8 2017 Intermittent L-dopa administration enhanced the expression of membrane D1R, and induced a robust increase of phosphorylation of Shp-2, Src, DARPP-32, and ERK1/2 in the 6-OHDA-lesioned striatum. Levodopa 13-19 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 140-148 29093677-8 2017 Intermittent L-dopa administration enhanced the expression of membrane D1R, and induced a robust increase of phosphorylation of Shp-2, Src, DARPP-32, and ERK1/2 in the 6-OHDA-lesioned striatum. Levodopa 13-19 mitogen activated protein kinase 3 Rattus norvegicus 154-160 28787702-0 2017 beta-asarone and levodopa coadministration increases striatal levels of dopamine and levodopa and improves behavioral competence in Parkinson"s rat by enhancing dopa decarboxylase activity. Levodopa 17-25 dopa decarboxylase Rattus norvegicus 161-179 28931752-3 2017 We here show that l-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, sensitizes the vascular adrenergic receptor alpha1 (ADRA1) through activation of L-DOPA receptor GPR143. Levodopa 18-46 adrenergic receptor, alpha 1d Mus musculus 140-145 28931752-3 2017 We here show that l-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, sensitizes the vascular adrenergic receptor alpha1 (ADRA1) through activation of L-DOPA receptor GPR143. Levodopa 18-46 G protein-coupled receptor 143 Mus musculus 185-191 28931752-3 2017 We here show that l-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, sensitizes the vascular adrenergic receptor alpha1 (ADRA1) through activation of L-DOPA receptor GPR143. Levodopa 48-54 adrenergic receptor, alpha 1d Mus musculus 140-145 28931752-3 2017 We here show that l-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, sensitizes the vascular adrenergic receptor alpha1 (ADRA1) through activation of L-DOPA receptor GPR143. Levodopa 48-54 G protein-coupled receptor 143 Mus musculus 185-191 28931752-6 2017 Specific knockout of Gpr143 in vascular smooth muscle cells (VSMCs) also showed a similar phenotype, indicating that L-DOPA directly modulates ADRA1 signaling in the VSMCs. Levodopa 117-123 G protein-coupled receptor 143 Mus musculus 21-27 28931752-6 2017 Specific knockout of Gpr143 in vascular smooth muscle cells (VSMCs) also showed a similar phenotype, indicating that L-DOPA directly modulates ADRA1 signaling in the VSMCs. Levodopa 117-123 adrenergic receptor, alpha 1d Mus musculus 143-148 28931752-11 2017 Taken together, our findings provide evidence for L-DOPA/GPR143 signaling that exerts precursor control of sympathetic neurotransmission through sensitizing vascular ADRA1. Levodopa 50-56 G protein-coupled receptor 143 Mus musculus 57-63 28931752-11 2017 Taken together, our findings provide evidence for L-DOPA/GPR143 signaling that exerts precursor control of sympathetic neurotransmission through sensitizing vascular ADRA1. Levodopa 50-56 adrenergic receptor, alpha 1d Mus musculus 166-171 28750831-8 2017 GBR12909, while having no effect on its own, blocked amphetamine-induced elevation of TH activity in dorsal striatum and nucleus accumbens, measured as increased tissue L-DOPA concentration. Levodopa 169-175 tyrosine hydroxylase Rattus norvegicus 86-88 28927418-8 2017 RESULTS: From 37 candidate studies on levodopa toxicity, 18 genes were found associated, of which, CAn STR 13, 14 (DRD2) was most significantly associated with dyskinesia, followed by rs1801133 (MTHFR) with hyper-homocysteinemia, and rs474559 (HOMER1) with hallucination. Levodopa 38-46 dopamine receptor D2 Homo sapiens 115-119 28927418-8 2017 RESULTS: From 37 candidate studies on levodopa toxicity, 18 genes were found associated, of which, CAn STR 13, 14 (DRD2) was most significantly associated with dyskinesia, followed by rs1801133 (MTHFR) with hyper-homocysteinemia, and rs474559 (HOMER1) with hallucination. Levodopa 38-46 homer scaffold protein 1 Homo sapiens 244-250 28682929-1 2017 BACKGROUND: Biogenic amines and monoamine oxidase inhibitors influence peripheral monoamine oxidase enzyme activity in chronic levodopa/dopa decarboxylase inhibitor-treated patients with Parkinson disease. Levodopa 127-135 dopa decarboxylase Homo sapiens 136-154 28236251-4 2017 A new extended-release (ER) carbidopa-levodopa capsule product (also referred to as IPX066) was developed and approved in the US as Rytary and in the EU as Numient . Levodopa 38-46 epiregulin Homo sapiens 24-26 28236251-6 2017 Phase III studies of this ER carbidopa-levodopa capsule formulation in patients with PD have shown a significant reduction in "off" time compared with IR carbidopa-levodopa and carbidopa-levodopa-entacapone. Levodopa 39-47 epiregulin Homo sapiens 26-28 28236251-7 2017 We present a review of the clinical pharmacokinetics and pharmacodynamics of this ER product of carbidopa-levodopa in healthy subjects and in patients with PD. Levodopa 106-114 epiregulin Homo sapiens 82-84 28777558-1 2017 Reduction of previously reported (ArL)FeCl with potassium graphite furnished a low-spin (S = 1/2) iron complex (ArL)Fe which features an intramolecular eta6-arene interaction and can be utilized as an FeI synthon (ArL = 5-mesityl-1,9-(2,4,6-Ph3C6H2)dipyrrin). Levodopa 34-37 spindlin 1 Homo sapiens 83-87 28687316-0 2017 Levodopa (L-DOPA) attenuates endoplasmic reticulum stress response and cell death signaling through DRD2 in SH-SY5Y neuronal cells under alpha-synuclein-induced toxicity. Levodopa 0-8 dopamine receptor D2 Homo sapiens 100-104 28687316-0 2017 Levodopa (L-DOPA) attenuates endoplasmic reticulum stress response and cell death signaling through DRD2 in SH-SY5Y neuronal cells under alpha-synuclein-induced toxicity. Levodopa 0-8 synuclein alpha Homo sapiens 137-152 28687316-0 2017 Levodopa (L-DOPA) attenuates endoplasmic reticulum stress response and cell death signaling through DRD2 in SH-SY5Y neuronal cells under alpha-synuclein-induced toxicity. Levodopa 10-16 dopamine receptor D2 Homo sapiens 100-104 28687316-0 2017 Levodopa (L-DOPA) attenuates endoplasmic reticulum stress response and cell death signaling through DRD2 in SH-SY5Y neuronal cells under alpha-synuclein-induced toxicity. Levodopa 10-16 synuclein alpha Homo sapiens 137-152 28687316-5 2017 In the present study, we investigated the effect of L-DOPA on SH-SY5Y neuronal cells under alpha-syn-induced toxicity. Levodopa 52-58 synuclein alpha Homo sapiens 91-100 28687316-8 2017 In conclusion, we suggest that L-DOPA may attenuate the neuropathology of PD by regulating signaling related to DRD2 in neuronal cells under alpha-syn-induced toxicity. Levodopa 31-37 dopamine receptor D2 Homo sapiens 112-116 28687316-8 2017 In conclusion, we suggest that L-DOPA may attenuate the neuropathology of PD by regulating signaling related to DRD2 in neuronal cells under alpha-syn-induced toxicity. Levodopa 31-37 synuclein alpha Homo sapiens 141-150 28716427-0 2017 Influence of L-dopa on subtle motor signs in heterozygous Parkin- and PINK1 mutation carriers. Levodopa 13-19 PTEN induced kinase 1 Homo sapiens 70-75 28716427-10 2017 (ii) The mild motor deficit present in a subgroup of heterozygous Parkin and PINK1 AMC appears to be non-progressive and responsive to L-dopa administration. Levodopa 135-141 PTEN induced kinase 1 Homo sapiens 77-82 28462804-1 2017 OBJECTIVE: We describe a Korean family in SCA2 with long-duration levodopa-responsive parkinsonism without cerebellar ataxia. Levodopa 66-74 ataxin 2 Homo sapiens 42-46 28698499-7 2017 The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Levodopa 33-39 annexin A1 Homo sapiens 152-162 28698499-7 2017 The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Levodopa 33-39 peroxiredoxin 6 Homo sapiens 164-179 28698499-7 2017 The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Levodopa 33-39 Parkinsonism associated deglycase Homo sapiens 184-189 28698499-7 2017 The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Levodopa 33-39 Parkinsonism associated deglycase Homo sapiens 190-194 28698499-7 2017 The cell surviving properties of L-DOPA and Edaravone against oxidative stress conditions rely on the alteration of a number of stress proteins such as Annexin A1, Peroxiredoxin-6 and PARK7/DJ-1 (Parkinson disease protein 7, also known as Protein deglycase DJ-1). Levodopa 33-39 Parkinsonism associated deglycase Homo sapiens 239-261 28698499-9 2017 Exposure to L-DOPA may result in hypoxia condition and further induction of ORP150 (150-kDa oxygen-regulated protein) with its concomitant cytoprotective effects but Edaravone seems to protect cells via direct induction of Peroxiredoxin-2 and inhibition of apoptosis. Levodopa 12-18 hypoxia up-regulated 1 Homo sapiens 76-116 28698499-9 2017 Exposure to L-DOPA may result in hypoxia condition and further induction of ORP150 (150-kDa oxygen-regulated protein) with its concomitant cytoprotective effects but Edaravone seems to protect cells via direct induction of Peroxiredoxin-2 and inhibition of apoptosis. Levodopa 12-18 peroxiredoxin 2 Homo sapiens 223-238 28580819-1 2017 INTRODUCTION: Opicapone is a third generation, highly potent and effective catechol O-methyltransferase (COMT) inhibitor that optimizes the pharmacokinetics and bioavailability of L-DOPA therapy. Levodopa 180-186 catechol-O-methyltransferase Homo sapiens 75-103 28580819-1 2017 INTRODUCTION: Opicapone is a third generation, highly potent and effective catechol O-methyltransferase (COMT) inhibitor that optimizes the pharmacokinetics and bioavailability of L-DOPA therapy. Levodopa 180-186 catechol-O-methyltransferase Homo sapiens 105-109 28583881-13 2017 L-DOPA treatment significantly increased A2AR binding in the affected striatum (BPND: 6.02 +- 0.91 L-DOPA vs. 4.90 +- 0.76 saline; + 23.4%; p = 0.02). Levodopa 0-6 adenosine A2a receptor Rattus norvegicus 41-45 28583881-15 2017 CONCLUSION: A2AR availability changed in drug-naive and in L-DOPA-treated PD rats. Levodopa 59-65 adenosine A2a receptor Rattus norvegicus 12-16 28855889-10 2017 l-DOPA improved gait significantly in patients with PD and particularly in patients with FOG mainly by reducing FOG duration and increasing specific spatiotemporal gait parameters. Levodopa 0-6 zinc finger protein, FOG family member 1 Homo sapiens 89-92 28855889-10 2017 l-DOPA improved gait significantly in patients with PD and particularly in patients with FOG mainly by reducing FOG duration and increasing specific spatiotemporal gait parameters. Levodopa 0-6 zinc finger protein, FOG family member 1 Homo sapiens 112-115 28855889-12 2017 Our study overall provides new information on the beneficial effect of l-DOPA on FOG severity and specific spatiotemporal gait parameters as objectively measured by a wearable sensory system. Levodopa 71-77 zinc finger protein, FOG family member 1 Homo sapiens 81-84 28769786-5 2017 We recently described that 18-month-old NF-kappaB/c-Rel deficient mice (c-rel-/-) develop a spontaneous late-onset PD-like phenotype encompassing L-DOPA-responsive motor impairment, nigrostriatal neuron degeneration, alpha-synuclein and iron accumulation. Levodopa 146-152 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 40-49 28769786-5 2017 We recently described that 18-month-old NF-kappaB/c-Rel deficient mice (c-rel-/-) develop a spontaneous late-onset PD-like phenotype encompassing L-DOPA-responsive motor impairment, nigrostriatal neuron degeneration, alpha-synuclein and iron accumulation. Levodopa 146-152 reticuloendotheliosis oncogene Mus musculus 50-55 28769786-5 2017 We recently described that 18-month-old NF-kappaB/c-Rel deficient mice (c-rel-/-) develop a spontaneous late-onset PD-like phenotype encompassing L-DOPA-responsive motor impairment, nigrostriatal neuron degeneration, alpha-synuclein and iron accumulation. Levodopa 146-152 reticuloendotheliosis oncogene Mus musculus 72-77 28566165-2 2017 PN has been demonstrated in some rare genetic forms of PD (e.g. PARK2 mutations) but has also been linked to levodopa exposure. Levodopa 109-117 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 0-2 28566165-10 2017 There is little evidence to support a direct link between levodopa treatment and the development of PN in idiopathic PD. Levodopa 58-66 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 100-102 28560461-0 2017 Increased SLC7A8 expression mediates L-DOPA uptake by renal tubular epithelial cells. Levodopa 37-43 solute carrier family 7 member 8 Rattus norvegicus 10-16 28560461-4 2017 The uptake of L-DOPA by cells of the proximal tubular epithelium of the kidney is controlled by the L-type amino acid transporter 2 (LAT2). Levodopa 14-20 solute carrier family 7 member 8 Rattus norvegicus 100-131 28560461-4 2017 The uptake of L-DOPA by cells of the proximal tubular epithelium of the kidney is controlled by the L-type amino acid transporter 2 (LAT2). Levodopa 14-20 solute carrier family 7 member 8 Rattus norvegicus 133-137 28560461-7 2017 The present study aimed to investigate the physiological role of the SLC7A8 gene in L-DOPA handling by kidney cells. Levodopa 84-90 solute carrier family 7 member 8 Rattus norvegicus 69-75 28560461-9 2017 In addition, L-DOPA uptake was determined using high performance liquid chromatography; NRK-52E cells expressing SLC7A8 exhibited increased uptake of L-DOPA. Levodopa 13-19 solute carrier family 7 member 8 Rattus norvegicus 113-119 28560461-9 2017 In addition, L-DOPA uptake was determined using high performance liquid chromatography; NRK-52E cells expressing SLC7A8 exhibited increased uptake of L-DOPA. Levodopa 150-156 solute carrier family 7 member 8 Rattus norvegicus 113-119 28560461-10 2017 The results of the present study suggested that SLC7A8 may serve a critical role in blood pressure control through regulating L-DOPA uptake in renal epithelial cells of the proximal tubule. Levodopa 126-132 solute carrier family 7 member 8 Rattus norvegicus 48-54 28764183-1 2017 Acquired coagulation factor VIII inhibitor leads to a rare disease i.e., acquired haemophilia which is idiopathic in majority of cases and is seen with autoimmune diseases, haematologic and solid tumours, infections, in the post-partum period and also with certain long-term use of drugs like penicillin and its derivatives, phenytoin, sulfa antibiotics, chloramphenicol, methyldopa, chlorpromazine, levodopa, interferon-alpha, fludarabine, clopidogrel. Levodopa 400-408 coagulation factor VIII Homo sapiens 9-32 28701947-4 2017 On the other hand, the protein-restricted diets including low-protein diet (LPD), protein-redistribution diet (PRD) and PRD with use of low-protein products can all improve the efficacy of levodopa in patients with motor fluctuations. Levodopa 189-197 acyl-CoA synthetase bubblegum family member 1 Homo sapiens 76-79 28342749-0 2017 Characterizing the differential roles of striatal 5-HT1A auto- and hetero-receptors in the reduction of l-DOPA-induced dyskinesia. Levodopa 104-110 5-hydroxytryptamine receptor 1A Rattus norvegicus 50-56 28625786-5 2017 RESULTS: We found that feeding D. melanogaster with the medium containing Levodopa or Chlorpromazine could induce depression-like phenotypes in both behavioral and biochemical biomarkers, including significantly decreased food intake, mating frequency, serotonin (5-HT) concentration, and increased malondialdehyde (MDA) concentration as well as reduced activity of superoxide dismutase (SOD). Levodopa 74-82 Superoxide dismutase 1 Drosophila melanogaster 366-386 28625786-5 2017 RESULTS: We found that feeding D. melanogaster with the medium containing Levodopa or Chlorpromazine could induce depression-like phenotypes in both behavioral and biochemical biomarkers, including significantly decreased food intake, mating frequency, serotonin (5-HT) concentration, and increased malondialdehyde (MDA) concentration as well as reduced activity of superoxide dismutase (SOD). Levodopa 74-82 Superoxide dismutase 1 Drosophila melanogaster 388-391 28223037-8 2017 Similarly, L-DOPA induced c-fos expression in both sensorimotor cortices, but only in the dopamine-depleted caudate-putamen. Levodopa 11-17 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 26-31 28540642-7 2017 We observed an upregulation trend for miR-30a-5p in L-dopa-treated PD patients and investigated candidate target genes by integrated in silico analyses. Levodopa 52-58 microRNA 30a Homo sapiens 38-45 28299453-1 2017 We determined monoamine oxidase-A (plasma) and -B (platelets) enzyme activity in chronic levodopa treated patients with Parkinson"s disease after first time intake of an irreversible monoamine oxidase-B inhibitor. Levodopa 89-97 monoamine oxidase A Homo sapiens 14-33 28550482-1 2017 Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD). Levodopa 130-138 monoamine oxidase B Homo sapiens 0-24 28550482-1 2017 Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD). Levodopa 130-138 monoamine oxidase B Homo sapiens 26-31 28550482-8 2017 However, MAO-B inhibitor use was associated with ~2-fold lower change in daily dose of levodopa (p < 0.001) and lower dyskinesia scores (p = 0.028) than non-users. Levodopa 87-95 monoamine oxidase B Homo sapiens 9-14 28550482-10 2017 Long-term use of MAO-B inhibitors resulted in a significant reduction in levodopa requirements and a lower frequency of dyskinesias in patients with PD. Levodopa 73-81 monoamine oxidase B Homo sapiens 17-22 28286180-0 2017 Dysregulation of BET proteins in levodopa-induced dyskinesia. Levodopa 33-41 delta/notch like EGF repeat containing Homo sapiens 17-20 28315782-1 2017 Catechol-O-methyltransferase (COMT) degrades dopamine and its precursor l-DOPA and plays a critical role in regulating synaptic dopamine actions. Levodopa 72-78 catechol-O-methyltransferase Mus musculus 0-28 28251464-6 2017 Patients with FOG showed lower proportion of male, longer disease duration, lower body mass index, lower concentrations of serum UA, higher total levodopa equivalent daily dosage, higher UPDRS III score, greater median H and Y stage, lower scores of FAB and MoCA, and higher frequencies of motor fluctuation, dyskinesia, falls, and festination compared to patients without FOG (P < 0.05). Levodopa 146-154 zinc finger protein, FOG family member 1 Homo sapiens 14-17 28315782-1 2017 Catechol-O-methyltransferase (COMT) degrades dopamine and its precursor l-DOPA and plays a critical role in regulating synaptic dopamine actions. Levodopa 72-78 catechol-O-methyltransferase Mus musculus 30-34 28315782-9 2017 Our results demonstrate that human COMT overexpression confers a heightened susceptibility to l-DOPA-induced dyskinesia and alters molecular and neurochemical responses in the lesioned striatum of mice. Levodopa 94-100 catechol-O-methyltransferase Homo sapiens 35-39 28772942-9 2017 Thus, the results suggest a potential use of the ARS-confined PEI/CMC films for constructing voltammetric sensors for L-dopa. Levodopa 118-124 RIEG2 Homo sapiens 49-52 28257907-6 2017 The inhibition constant of kojic acid to free tyrosinase (KI) and kojic acid to tyrosinase/L-DOPA complex (KIS) were calculated to be 36.64 and 74.35 muM, respectively, and the half-maximal inhibitory concentration (IC50) was determined to be 46.64 muM for kojic acid. Levodopa 91-97 tyrosinase Homo sapiens 80-90 28469105-12 2017 After L-DOPA treatment, Bmal1 decreased in the SCN compared with 6-OHDA group at 12:00 ( P < 0.01) and 24:00 ( P < 0.001). Levodopa 6-12 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 24-29 28490336-9 2017 Gabapentin and L-dopa as the substrates of LAT1 competitively inhibited the uptake of [14C] L-citrulline. Levodopa 15-21 solute carrier family 7 member 5 Homo sapiens 43-47 28437101-2 2017 Four-coordinate iron complexes of the type (ArL)FeX2 [ArL = 1,9-(2,4,6-Ph3C6H2)2-5-mesityldipyrromethene] with X = Cl or tBuO were prepared and found to be high-spin (S = 5/2), as determined by superconducting quantum interference device magnetometry, electron paramagnetic resonance, and 57Fe Mossbauer spectroscopy. Levodopa 44-47 stabilin 2 Homo sapiens 48-52 20301610-17 1993 Prevention of primary manifestations: Levodopa therapy from early infancy may prevent manifestations of some symptoms and signs in TH-deficient infantile parkinsonism with motor delay; however, no levodopa trials in the early postnatal period of infants with this type of TH deficiency and biallelic TH pathogenic variants have been reported. Levodopa 38-46 tyrosine hydroxylase Homo sapiens 131-133 20301610-17 1993 Prevention of primary manifestations: Levodopa therapy from early infancy may prevent manifestations of some symptoms and signs in TH-deficient infantile parkinsonism with motor delay; however, no levodopa trials in the early postnatal period of infants with this type of TH deficiency and biallelic TH pathogenic variants have been reported. Levodopa 38-46 tyrosine hydroxylase Homo sapiens 272-274 28469105-13 2017 In the striatum, the expression of Bmal1, Roralpha was lower than that in the 6-OHDA group at 18:00 (P < 0.05) and L-DOPA seemed to delay the peak of Per2 to 24:00. Levodopa 118-124 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 35-40 28469105-13 2017 In the striatum, the expression of Bmal1, Roralpha was lower than that in the 6-OHDA group at 18:00 (P < 0.05) and L-DOPA seemed to delay the peak of Per2 to 24:00. Levodopa 118-124 period circadian regulator 2 Rattus norvegicus 153-157 33429625-4 2017 We found that the ribbons functionalized with a solution of 3,4-dihydroxy-l-phenylalanine (DOPA) and then coated with poly-l-lysine (PLL) and fibronectin (FN) improve cell attachment and support the growth of C2C12. Levodopa 60-89 fibronectin 1 Mus musculus 142-153 28186666-6 2017 RESULTS: When compared with idiopathic PD and healthy subjects, leucine-rich repeat kinase 2 PD patients showed a remarkable reduction of short intracortical inhibition in both ON and in OFF l-dopa therapy. Levodopa 191-197 leucine rich repeat kinase 2 Homo sapiens 64-92 28186666-8 2017 Leucine-rich repeat kinase 2 PD showed abnormal long-term potentiation-like cortical plasticity in ON l-dopa therapy. Levodopa 102-108 leucine rich repeat kinase 2 Homo sapiens 0-28 28405611-8 2017 Daily duration of levodopa-induced dyskinesias significantly declined at 12 months in the AAV2-GAD group (P = 0.03; post-hoc Bonferroni test), while the sham group was unchanged. Levodopa 18-26 glutamate decarboxylase 1 Homo sapiens 95-98 26663864-0 2017 Synergetic effect of 3,4-dihydroxy-l-phenylalanine-modified poly(lactic-co-glycolic acid) nanopatterned patch with fibroblast growth factor-2 for skin wound regeneration. Levodopa 21-50 fibroblast growth factor 2 Homo sapiens 115-141 26663864-4 2017 Simple surface modification was applied using 3,4-dihydroxy-l-phenylalanine (LD), which has been reported as effective adhesion molecules with similar structure as mussel protein, to immobilize fibroblast growth factor-2 (FGF2) on PLGA patches. Levodopa 46-75 fibroblast growth factor 2 Homo sapiens 194-220 26663864-4 2017 Simple surface modification was applied using 3,4-dihydroxy-l-phenylalanine (LD), which has been reported as effective adhesion molecules with similar structure as mussel protein, to immobilize fibroblast growth factor-2 (FGF2) on PLGA patches. Levodopa 46-75 fibroblast growth factor 2 Homo sapiens 222-226 28377741-0 2017 Adenosine A2A Receptor Gene Knockout Prevents l-3,4-Dihydroxyphenylalanine-Induced Dyskinesia by Downregulation of Striatal GAD67 in 6-OHDA-Lesioned Parkinson"s Mice. Levodopa 46-74 adenosine A2a receptor Mus musculus 0-22 28256010-2 2017 Studies using D1 receptor drugs and genetically modified mice suggest that medium spiny neurons expressing D1 receptors play a primary role in l-dopa-induced dyskinesias. Levodopa 143-149 dopamine receptor D1 Mus musculus 14-25 28256089-9 2017 Postmortem tissue analysis revealed increased FosB expression, a molecular marker of l-dopa-induced dyskinesias, primarily in medium spiny neurons of the direct pathway in the dopamine-depleted hemisphere. Levodopa 85-91 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 46-50 27981510-0 2017 Aberrant CpG Methylation Mediates Abnormal Transcription of MAO-A Induced by Acute and Chronic L-3,4-Dihydroxyphenylalanine Administration in SH-SY5Y Neuronal Cells. Levodopa 95-123 monoamine oxidase A Homo sapiens 60-65 27981510-3 2017 Monoamine oxidase A (MAO-A) is one of the key enzymes in dopamine metabolism and therefore may be involved in L-dopa-induced side effects. Levodopa 110-116 monoamine oxidase A Homo sapiens 0-19 27981510-3 2017 Monoamine oxidase A (MAO-A) is one of the key enzymes in dopamine metabolism and therefore may be involved in L-dopa-induced side effects. Levodopa 110-116 monoamine oxidase A Homo sapiens 21-26 27981510-5 2017 To investigate the effects of L-dopa on MAO-A transcription and its underlying epigenetic mechanism, neuronal SH-SY5Y cells were treated with L-dopa for 24 h (acute) and for 7-21 days (chronic). Levodopa 30-36 monoamine oxidase A Homo sapiens 40-45 27981510-6 2017 Results showed that chronic L-dopa administration resulted in a dose-dependent and time-dependent downregulation of MAO-A, whereas acute L-dopa administration induced upregulation of MAO-A transcription and expression. Levodopa 28-34 monoamine oxidase A Homo sapiens 116-121 27981510-6 2017 Results showed that chronic L-dopa administration resulted in a dose-dependent and time-dependent downregulation of MAO-A, whereas acute L-dopa administration induced upregulation of MAO-A transcription and expression. Levodopa 137-143 monoamine oxidase A Homo sapiens 183-188 27981510-7 2017 Meanwhile, chronic L-dopa exposure induced CpG hypermethylation in MAO-A promoter, while acute L-dopa administration caused CpG hypomethylation. Levodopa 19-25 monoamine oxidase A Homo sapiens 67-72 27981510-9 2017 These results indicated that aberrant CpG methylation might play a key role in MAO-A transcriptional misregulation in L-dopa administration. Levodopa 118-124 monoamine oxidase A Homo sapiens 79-84 27981510-10 2017 In addition, results showed that acute L-dopa administration induced downregulation of DNA methyltransferase 3a (DNMT3a). Levodopa 39-45 DNA methyltransferase 3 alpha Homo sapiens 87-111 27981510-10 2017 In addition, results showed that acute L-dopa administration induced downregulation of DNA methyltransferase 3a (DNMT3a). Levodopa 39-45 DNA methyltransferase 3 alpha Homo sapiens 113-119 27981510-11 2017 Transcription of ten-eleven translocation 1 (TET1) were significantly downregulated in chronic L-dopa administration. Levodopa 95-101 tet methylcytosine dioxygenase 1 Homo sapiens 17-43 27981510-11 2017 Transcription of ten-eleven translocation 1 (TET1) were significantly downregulated in chronic L-dopa administration. Levodopa 95-101 tet methylcytosine dioxygenase 1 Homo sapiens 45-49 27981510-12 2017 These data indicated that in chronic L-dopa administration, TET1 downregulation might mediate CpG hypermethylation, which is responsible for the downregulation of MAO-A transcription. Levodopa 37-43 tet methylcytosine dioxygenase 1 Homo sapiens 60-64 27981510-12 2017 These data indicated that in chronic L-dopa administration, TET1 downregulation might mediate CpG hypermethylation, which is responsible for the downregulation of MAO-A transcription. Levodopa 37-43 monoamine oxidase A Homo sapiens 163-168 27981510-13 2017 In contrast, in acute L-dopa administration, DNMT3a downregulation might mediate hypomethylation, contributing to the MAO-A upregulation. Levodopa 22-28 DNA methyltransferase 3 alpha Homo sapiens 45-51 27981510-13 2017 In contrast, in acute L-dopa administration, DNMT3a downregulation might mediate hypomethylation, contributing to the MAO-A upregulation. Levodopa 22-28 monoamine oxidase A Homo sapiens 118-123 27981510-14 2017 In conclusion, our findings suggested that TET1 and DNMTs might mediate aberrant CpG methylation, associated with the misregulation of MAO-A in L-dopa administration, which might contribute to dopamine release abnormally leading to the side effects of L-dopa. Levodopa 144-150 tet methylcytosine dioxygenase 1 Homo sapiens 43-47 27981510-14 2017 In conclusion, our findings suggested that TET1 and DNMTs might mediate aberrant CpG methylation, associated with the misregulation of MAO-A in L-dopa administration, which might contribute to dopamine release abnormally leading to the side effects of L-dopa. Levodopa 144-150 monoamine oxidase A Homo sapiens 135-140 27981510-14 2017 In conclusion, our findings suggested that TET1 and DNMTs might mediate aberrant CpG methylation, associated with the misregulation of MAO-A in L-dopa administration, which might contribute to dopamine release abnormally leading to the side effects of L-dopa. Levodopa 252-258 tet methylcytosine dioxygenase 1 Homo sapiens 43-47 27981510-14 2017 In conclusion, our findings suggested that TET1 and DNMTs might mediate aberrant CpG methylation, associated with the misregulation of MAO-A in L-dopa administration, which might contribute to dopamine release abnormally leading to the side effects of L-dopa. Levodopa 252-258 monoamine oxidase A Homo sapiens 135-140 28077650-5 2017 In fact, synthetic melanin produced from tyrosine or 3-hydroxy-l-tyrosine inhibited abnormal PrP formation. Levodopa 53-73 prion protein Homo sapiens 93-96 28246328-3 2017 SV2C is emerging as a potentially relevant protein in Parkinson disease (PD), because it is a genetic modifier of sensitivity to l-DOPA and of nicotine neuroprotection in PD. Levodopa 129-135 synaptic vesicle glycoprotein 2c Mus musculus 0-4 28337120-11 2017 Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Levodopa 150-156 tyrosine hydroxylase Rattus norvegicus 0-20 28337120-11 2017 Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Levodopa 150-156 aryl hydrocarbon receptor nuclear translocator Rattus norvegicus 30-76 28337120-11 2017 Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Levodopa 150-156 aryl hydrocarbon receptor nuclear translocator Rattus norvegicus 78-82 28273866-5 2017 The anti-tyrosinase activities of the FTE and its principal phenolic compounds were investigated in l-3,4-dihydroxyphenylalanine (l-DOPA) oxidation by a mushroom tyrosinase. Levodopa 100-128 tyrosinase Rattus norvegicus 162-172 28273866-5 2017 The anti-tyrosinase activities of the FTE and its principal phenolic compounds were investigated in l-3,4-dihydroxyphenylalanine (l-DOPA) oxidation by a mushroom tyrosinase. Levodopa 130-136 tyrosinase Rattus norvegicus 9-19 28273866-5 2017 The anti-tyrosinase activities of the FTE and its principal phenolic compounds were investigated in l-3,4-dihydroxyphenylalanine (l-DOPA) oxidation by a mushroom tyrosinase. Levodopa 130-136 tyrosinase Rattus norvegicus 162-172 28253352-0 2017 Dopamine D2 receptor and beta-arrestin 2 mediate Amyloid-beta elevation induced by anti-parkinson"s disease drugs, levodopa and piribedil, in neuronal cells. Levodopa 115-123 dopamine receptor D2 Homo sapiens 0-20 28253352-0 2017 Dopamine D2 receptor and beta-arrestin 2 mediate Amyloid-beta elevation induced by anti-parkinson"s disease drugs, levodopa and piribedil, in neuronal cells. Levodopa 115-123 arrestin beta 2 Homo sapiens 25-40 28253352-9 2017 Here we present that both levodopa and piribedil enhance the generation of Abeta and the activity of gamma-secretase in human neuronal cells and primary neurons isolated from AD mouse. Levodopa 26-34 amyloid beta precursor protein Homo sapiens 75-80 28253352-12 2017 Moreover, the knockdown of beta-arrestin 2 attenuated the increases of Abeta generation and gamma-secretase activity mediated by levodopa or piribedil. Levodopa 129-137 arrestin beta 2 Homo sapiens 27-42 28253352-12 2017 Moreover, the knockdown of beta-arrestin 2 attenuated the increases of Abeta generation and gamma-secretase activity mediated by levodopa or piribedil. Levodopa 129-137 amyloid beta precursor protein Homo sapiens 71-76 27763682-10 2017 CONCLUSION: Opicapone, as once-daily oral evening regimen and/or 1 h apart from levodopa therapy, increases the bioavailability of levodopa associated with its pronounced, long-lasting and sustained catechol-O-methyltransferase inhibition. Levodopa 131-139 catechol-O-methyltransferase Homo sapiens 199-227 27869329-0 2017 Novel compound heterozygous synaptojanin-1 mutation causes l-dopa-responsive dystonia-parkinsonism syndrome. Levodopa 59-65 synaptojanin 1 Homo sapiens 28-42 28081695-6 2017 We further refined our analysis by evaluating the DNA methylation status of the maternally imprinted human gene encoding insulin-like growth factor 2 (IGF2) using bisulfite sequencing PCR (BSP) of DNA derived from 15 PD patients and 9 controls, taking into consideration different dosages of L-dopa. Levodopa 292-298 insulin like growth factor 2 Homo sapiens 121-149 28081695-6 2017 We further refined our analysis by evaluating the DNA methylation status of the maternally imprinted human gene encoding insulin-like growth factor 2 (IGF2) using bisulfite sequencing PCR (BSP) of DNA derived from 15 PD patients and 9 controls, taking into consideration different dosages of L-dopa. Levodopa 292-298 insulin like growth factor 2 Homo sapiens 151-155 28081695-7 2017 CONCLUSION: Our results demonstrated that methylation of IGF2 in PD patients was neither influenced by the dosage of L-dopa treatment nor by the disease itself. Levodopa 117-123 insulin like growth factor 2 Homo sapiens 57-61 28367136-0 2017 Reduced CA2-CA3 Hippocampal Subfield Volume Is Related to Depression and Normalized by l-DOPA in Newly Diagnosed Parkinson"s Disease. Levodopa 87-93 carbonic anhydrase 3 Homo sapiens 12-15 28234566-5 2017 Catechol-O-methyltransferase (COMT) inhibitors attain this goal by decreasing L-dopa peripheral metabolism. Levodopa 78-84 catechol-O-methyltransferase Homo sapiens 0-28 28234566-5 2017 Catechol-O-methyltransferase (COMT) inhibitors attain this goal by decreasing L-dopa peripheral metabolism. Levodopa 78-84 catechol-O-methyltransferase Homo sapiens 30-34 28239340-0 2017 Dopamine-Induced Changes in Galphaolf Protein Levels in Striatonigral and Striatopallidal Medium Spiny Neurons Underlie the Genesis of l-DOPA-Induced Dyskinesia in Parkinsonian Mice. Levodopa 135-141 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 28-37 28239340-7 2017 Using quantitative immunohistochemistry (IHC) and a dual-antigen recognition in situ proximity ligation assay (PLA), we here found that in the dopamine-depleted striatum, there appeared increased and decreased levels of Galphaolf protein in striatonigral and striatopallidal MSNs, respectively, after a daily pulsatile administration of l-DOPA. Levodopa 337-343 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 220-229 28239340-9 2017 Because Galphaolf protein levels serve as a determinant of cAMP signal-dependent activity in striatal MSNs, we suggest that l-DOPA-induced changes in striatal Galphaolf levels in the dopamine-depleted striatum could be a key event in generating LID. Levodopa 124-130 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 8-17 28239340-9 2017 Because Galphaolf protein levels serve as a determinant of cAMP signal-dependent activity in striatal MSNs, we suggest that l-DOPA-induced changes in striatal Galphaolf levels in the dopamine-depleted striatum could be a key event in generating LID. Levodopa 124-130 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 159-168 28132689-4 2017 In these six affected individuals, whole-exome sequencing (WES) identified biallelic mutations in DNAJC12, which encodes a heat shock co-chaperone family member that interacts with phenylalanine, tyrosine, and tryptophan hydroxylases catalyzing the BH4-activated conversion of phenylalanine into tyrosine, tyrosine into L-dopa (the precursor of dopamine), and tryptophan into 5-hydroxytryptophan (the precursor of serotonin), respectively. Levodopa 320-326 DnaJ heat shock protein family (Hsp40) member C12 Homo sapiens 98-105 28166239-1 2017 In Parkinson"s disease (PD), aromatic L-amino acid decarboxylase (AADC) is the rate-limiting enzyme in the conversion of L-DOPA (Sinemet) to dopamine (DA). Levodopa 121-127 dopa decarboxylase Homo sapiens 38-64 28166239-1 2017 In Parkinson"s disease (PD), aromatic L-amino acid decarboxylase (AADC) is the rate-limiting enzyme in the conversion of L-DOPA (Sinemet) to dopamine (DA). Levodopa 121-127 dopa decarboxylase Homo sapiens 66-70 28166239-2 2017 Previous studies in PD animal models demonstrated that lesion of dopaminergic neurons is associated with profound loss of AADC activity in the striatum, blocking efficient conversion of L-DOPA to DA. Levodopa 186-192 dopa decarboxylase Homo sapiens 122-126 28166239-11 2017 After L-DOPA administration in MPTP-treated NHP, very poor conversion to DA was detected, suggesting that AADC in NHP nigrostriatal fibers is mainly responsible for L-DOPA to DA conversion. Levodopa 6-12 dopa decarboxylase Rattus norvegicus 106-110 28166239-11 2017 After L-DOPA administration in MPTP-treated NHP, very poor conversion to DA was detected, suggesting that AADC in NHP nigrostriatal fibers is mainly responsible for L-DOPA to DA conversion. Levodopa 165-171 dopa decarboxylase Rattus norvegicus 106-110 27764702-4 2017 METHODS: The aim of the present study was to examine the impact of chronic administration of molsidomine (2mg/kg) and l-DOPA (25mg/kg), alone and in combination, on systolic (SBP) and diastolic (DBP) blood pressure in the anesthetized, unilaterally 6-OHDA-lesioned rats. Levodopa 118-124 spermine binding protein Rattus norvegicus 175-178 27840215-3 2017 Spectrophotometric analysis used to determine the inhibition capabilities of these compounds on tyrosinase catalyzing L-tyrosine (L-Tyr) and L-3,4-Dihydroxyphenylalanine (L-DOPA) as well. Levodopa 141-169 tyrosinase Homo sapiens 96-106 27840215-3 2017 Spectrophotometric analysis used to determine the inhibition capabilities of these compounds on tyrosinase catalyzing L-tyrosine (L-Tyr) and L-3,4-Dihydroxyphenylalanine (L-DOPA) as well. Levodopa 171-177 tyrosinase Homo sapiens 96-106 28112685-4 2017 Using the activatory Gq-coupled human M3 muscarinic receptor (hM3Dq), we found that chemogenetic stimulation of dSPNs mimicked, while stimulation of iSPNs abolished the therapeutic action of L-DOPA in PD mice. Levodopa 191-197 cholinergic receptor muscarinic 3 Homo sapiens 38-60 27941374-9 2017 Therefore, the dosage of dopa-decarboxylase inhibitor, increasing the L-dopa concentration, may contribute to GE delay and its consequent effect on drug delivery and efficacy. Levodopa 70-76 dopa decarboxylase Homo sapiens 25-43 28027332-1 2017 Importance: Catechol O-methyltransferase (COMT) inhibitors are an established treatment for end-of-dose motor fluctuations associated with levodopa therapy in patients with Parkinson disease (PD). Levodopa 139-147 catechol-O-methyltransferase Homo sapiens 12-40 28027332-1 2017 Importance: Catechol O-methyltransferase (COMT) inhibitors are an established treatment for end-of-dose motor fluctuations associated with levodopa therapy in patients with Parkinson disease (PD). Levodopa 139-147 catechol-O-methyltransferase Homo sapiens 42-46 27780818-0 2017 Gastrin stimulates renal dopamine production by increasing the renal tubular uptake of l-DOPA. Levodopa 87-93 gastrin Mus musculus 0-7 28062148-1 2017 BACKGROUND: Early-onset parkinsonism can be caused by PTEN-induced putative kinase 1 (PINK1) gene defects and is usually characterized by an age of onset in the fourth decade of life, slow disease progression, resting tremor, rigidity, bradykinesia, postural instability, and levodopa-induced dyskinesia. Levodopa 276-284 PTEN induced kinase 1 Homo sapiens 54-84 28062148-1 2017 BACKGROUND: Early-onset parkinsonism can be caused by PTEN-induced putative kinase 1 (PINK1) gene defects and is usually characterized by an age of onset in the fourth decade of life, slow disease progression, resting tremor, rigidity, bradykinesia, postural instability, and levodopa-induced dyskinesia. Levodopa 276-284 PTEN induced kinase 1 Homo sapiens 86-91 28956336-7 2017 New data on the efficacy of PDE10A inhibitors for reversing behavioral and electrophysiological correlates of L-DOPA-induced dyskinesias in a rat model of PD will also be presented. Levodopa 110-116 phosphodiesterase 10A Rattus norvegicus 28-34 27780818-4 2017 We show that in human and mouse renal proximal tubule cells (hRPTCs and mRPTCs, respectively), gastrin stimulates renal dopamine production by increasing the cellular uptake of l-DOPA via the l-type amino acid transporter (LAT) at the plasma membrane. Levodopa 177-183 gastrin Mus musculus 95-102 27780818-7 2017 The deficient renal cortical uptake of l-DOPA in C57Bl/6J mice may be due to decreased LAT-1 activity that is related to its decreased expression at the plasma membrane, relative to BALB/c mice. Levodopa 39-45 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 87-92 28124620-8 2017 When applied as monotherapy, MAO-B inhibitors provide a modest, but significant improvement of motor function and delay the need for levodopa. Levodopa 133-141 monoamine oxidase B Homo sapiens 29-34 28294055-8 2017 The selective MAO-B inhibitors are used with L-DOPA and/or dopamine agonists in the symptomatic treatment of Parkinson"s disease. Levodopa 45-51 monoamine oxidase B Homo sapiens 14-19 28124620-10 2017 As add-on to levodopa, MAO-B inhibitors significantly reduced off-time and were comparable in efficacy to COMT inhibitors. Levodopa 13-21 monoamine oxidase B Homo sapiens 23-28 27744056-0 2017 Fibrillogenesis of human serum albumin in the presence of levodopa - spectroscopic, calorimetric and microscopic studies. Levodopa 58-66 albumin Homo sapiens 25-38 27731537-6 2017 CONCLUSIONS: We suggested that the observed transcranial brain sonography features in patients with DRD might primarily be risk markers for particular clinical features (parkinsonism, dystonia) occurring in the specific genetic context (i.e. GCH1 mutations), or might reflect compensated neurodegenerative processes triggered by the long-lasting dopamine deficiency due to the profound delay in levodopa treatment in our patients with DRD. Levodopa 395-403 GTP cyclohydrolase 1 Homo sapiens 242-246 28123470-7 2017 These findings suggested that LEV was able to reduce steroid-induced bone cellular apoptosis, reduce the occurrence of necrosis of the femoral head and, through in vivo metabolism, it may promote the synthesis and release of IGF-1, which could be one of its biological pathways to prevent and treat SANFH. Levodopa 30-33 insulin-like growth factor I Oryctolagus cuniculus 225-230 26483399-0 2017 Dopamine D3 Receptor Modulates l-DOPA-Induced Dyskinesia by Targeting D1 Receptor-Mediated Striatal Signaling. Levodopa 31-37 dopamine receptor D3 Mus musculus 0-20 26483399-0 2017 Dopamine D3 Receptor Modulates l-DOPA-Induced Dyskinesia by Targeting D1 Receptor-Mediated Striatal Signaling. Levodopa 31-37 dopamine receptor D1 Mus musculus 70-81 27744056-3 2017 In the present study we have performed comprehensive biophysical and computational experiments showing levodopa not only significantly inhibits heat induced fibrillization of human serum albumin but also disaggregates preformed fibrils. Levodopa 103-111 albumin Homo sapiens 181-194 30566298-2 2017 Levodopa still remains the gold standard for the treatment of motor symptoms of PD in advanced stage, but dopamine agonists, monoamine oxidase B inhibitors and catechol-O-methyltransferase inhibitors have--also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to prevent and improve levodopa-induced motor complications, including wearing off phenomenon and peak-dose dyskinesia. Levodopa 327-335 catechol-O-methyltransferase Homo sapiens 160-188 29213160-1 2017 The kinetic (KIE) and solvent (SIE) isotope effect methods were used to investigate the mechanism of enzymatic hydroxylation of halogenated derivatives of l-tyrosine to l-DOPA catalyzed by the enzyme tyrosinase (EC 1.14.18.1). Levodopa 169-175 tyrosinase Homo sapiens 200-210 28005447-6 2017 These results suggest that GP-EX ameliorates habit learning memory deficits by activating dopaminergic neurons and spatial memory deficits by modulating NMDA receptor-ERK1/2-CREB system in MPTP-lesioned mice treated with L-DOPA. Levodopa 221-227 mitogen-activated protein kinase 3 Mus musculus 167-173 27796511-16 2017 Furthermore, L-DOPA significantly increased these peptide biomarkers, dynorphin and somatostatin, in Parkinson"s animals. Levodopa 13-19 somatostatin Homo sapiens 84-96 27647371-1 2016 To discover new molecules with an inhibitory activity of melanogenesis a hundred of scorpions, snakes, spiders and amphibians venoms were screened for their capacity to inhibit mushroom tyrosinase using 3,4-l-dihydroxyphenylalanine (l-DOPA) as substrate. Levodopa 233-239 tyrosinase Mus musculus 186-196 27685665-4 2016 These compounds represent a novel series of potent COMT inhibitors that might be further optimized to new drugs useful for the treatment of Parkinson"s disease, as adjuncts in levodopa based therapy, or for the treatment of schizophrenia. Levodopa 176-184 catechol-O-methyltransferase Homo sapiens 51-55 28195063-2 2016 COMT is involved in the O-methylation of L-DOPA, dopamine and other catechols. Levodopa 41-47 catechol-O-methyltransferase Mus musculus 0-4 27597528-1 2016 Ataxin-2 (ATXN2) polyglutamine domain expansions of large size result in an autosomal dominantly inherited multi-system-atrophy of the nervous system named spinocerebellar ataxia type 2 (SCA2), while expansions of intermediate size act as polygenic risk factors for motor neuron disease (ALS and FTLD) and perhaps also for Levodopa-responsive Parkinson"s disease (PD). Levodopa 323-331 ataxin 2 Homo sapiens 0-8 27597528-1 2016 Ataxin-2 (ATXN2) polyglutamine domain expansions of large size result in an autosomal dominantly inherited multi-system-atrophy of the nervous system named spinocerebellar ataxia type 2 (SCA2), while expansions of intermediate size act as polygenic risk factors for motor neuron disease (ALS and FTLD) and perhaps also for Levodopa-responsive Parkinson"s disease (PD). Levodopa 323-331 ataxin 2 Homo sapiens 10-15 27647371-4 2016 Our results demonstrate that ArgTX-636 reduced the mushroom tyrosinase activity in a dose-dependent way with a maximal half inhibitory concentration (IC50) value of 8.34muM, when l-DOPA is used as substrate. Levodopa 179-185 tyrosinase Mus musculus 60-70 27452719-6 2016 Protein analysis of striatal monoamine transporters in unilateral sham or 6-hydroxydopamine-lesioned rats treated with l-DOPA (0 or 6 mg/kg) showed lesion-induced DAT loss and l-DOPA-induced gain in SERT:DAT and NET:DAT ratios in lesioned rats which positively correlated with dyskinesia expression, suggesting functional shifts among monoamine transporters in the dyskinetic state. Levodopa 119-125 solute carrier family 6 member 3 Rattus norvegicus 163-166 27819409-25 2016 Three patients dropped out due to lethargy (2 patients), and drowsiness, syncope and fatigue (1 patient).Because of a short duration of action, rebound and augmentation were noted with levodopa treatment even though it conferred some benefit in reducing the symptoms of RLS. Levodopa 185-193 RLS1 Homo sapiens 270-273 27371992-2 2016 AADC catalyzes the synthesis of the neurotransmitters dopamine and serotonin from l-dopa and 5-HT respectively. Levodopa 82-88 dopa decarboxylase Homo sapiens 0-4 27491309-4 2016 This review discusses the historical overview of TH, BH4-, and other CA-related enzymes and their genes in relation to the pathophysiology of PD, the development of drugs, such as L-DOPA, and future prospects for drug and gene therapy for PD, especially the potential of induced pluripotent stem (iPS) cells. Levodopa 180-186 tyrosine hydroxylase Homo sapiens 49-51 27902448-4 2016 The guanosine triphosphatase Ras homolog enriched in the striatum (Rhes) inhibits dopaminergic signaling in the striatum, is implicated in HD and L-dopa-induced dyskinesia, and has a role in striatal motor control. Levodopa 146-152 RASD family, member 2 Mus musculus 67-71 27452719-0 2016 Monoamine transporter contributions to l-DOPA effects in hemi-parkinsonian rats. Levodopa 39-45 solute carrier family 18 member A2 Rattus norvegicus 0-21 27452719-5 2016 The current investigation sought to uncover the differential expression and function of DAT, SERT, and NET in the l-DOPA-treated hemi-parkinsonian rat. Levodopa 114-120 solute carrier family 6 member 3 Rattus norvegicus 88-91 27452719-5 2016 The current investigation sought to uncover the differential expression and function of DAT, SERT, and NET in the l-DOPA-treated hemi-parkinsonian rat. Levodopa 114-120 solute carrier family 6 member 4 Rattus norvegicus 93-97 27452719-6 2016 Protein analysis of striatal monoamine transporters in unilateral sham or 6-hydroxydopamine-lesioned rats treated with l-DOPA (0 or 6 mg/kg) showed lesion-induced DAT loss and l-DOPA-induced gain in SERT:DAT and NET:DAT ratios in lesioned rats which positively correlated with dyskinesia expression, suggesting functional shifts among monoamine transporters in the dyskinetic state. Levodopa 119-125 solute carrier family 6 member 4 Rattus norvegicus 199-203 27452719-6 2016 Protein analysis of striatal monoamine transporters in unilateral sham or 6-hydroxydopamine-lesioned rats treated with l-DOPA (0 or 6 mg/kg) showed lesion-induced DAT loss and l-DOPA-induced gain in SERT:DAT and NET:DAT ratios in lesioned rats which positively correlated with dyskinesia expression, suggesting functional shifts among monoamine transporters in the dyskinetic state. Levodopa 119-125 solute carrier family 6 member 3 Rattus norvegicus 204-207 27452719-6 2016 Protein analysis of striatal monoamine transporters in unilateral sham or 6-hydroxydopamine-lesioned rats treated with l-DOPA (0 or 6 mg/kg) showed lesion-induced DAT loss and l-DOPA-induced gain in SERT:DAT and NET:DAT ratios in lesioned rats which positively correlated with dyskinesia expression, suggesting functional shifts among monoamine transporters in the dyskinetic state. Levodopa 119-125 solute carrier family 6 member 3 Rattus norvegicus 204-207 27452719-9 2016 Overall, DA and DAT loss with l-DOPA treatment appear to precipitate gain in SERT and NET function. Levodopa 30-36 solute carrier family 6 member 3 Rattus norvegicus 16-19 27452719-9 2016 Overall, DA and DAT loss with l-DOPA treatment appear to precipitate gain in SERT and NET function. Levodopa 30-36 solute carrier family 6 member 4 Rattus norvegicus 77-81 27662331-7 2016 RESULTS: According to the available assessment tools severity of FOG is marked by one or a combination of multiple clinical expressions including frequency, duration, triggering circumstances, response to levodopa, association with falls and fear of falling, or need for assistance to avoid falls. Levodopa 205-213 zinc finger protein, FOG family member 1 Homo sapiens 65-68 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 59-65 tyrosinase Homo sapiens 82-92 27653922-8 2016 Subsequent ANCOVA analysis revealed that COMT genotype interacted with sex and daily levodopa equivalent dose (LED) to influence executive function. Levodopa 85-93 catechol-O-methyltransferase Homo sapiens 41-45 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 59-65 zinc finger RANBP2-type containing 3 Homo sapiens 127-130 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 59-65 tyrosinase Homo sapiens 265-275 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 59-65 zinc finger RANBP2-type containing 3 Homo sapiens 290-293 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 tyrosinase Homo sapiens 82-92 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 zinc finger RANBP2-type containing 3 Homo sapiens 127-130 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 tyrosinase Homo sapiens 265-275 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 zinc finger RANBP2-type containing 3 Homo sapiens 290-293 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 tyrosinase Homo sapiens 82-92 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 zinc finger RANBP2-type containing 3 Homo sapiens 127-130 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 tyrosinase Homo sapiens 265-275 27711193-1 2016 Hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by immobilized tyrosinase in the presence of ascorbic acid (AH2), which reduces DOPA-quinone to L-DOPA, is characterized by low reaction yields that are mainly caused by the suicide inactivation of tyrosinase by L-DOPA and AH2. Levodopa 163-169 zinc finger RANBP2-type containing 3 Homo sapiens 290-293 27711193-2 2016 The main aim of this work was to compare processes with native and immobilized tyrosinase to identify the conditions that limit suicide inactivation and produce substrate conversions to L-DOPA of above 50% using HPLC analysis. Levodopa 186-192 tyrosinase Homo sapiens 79-89 27711193-7 2016 A three-fold increase in the bound enzyme load achieved 95% conversion in two successive runs, but in the third one, tyrosinase lost its activity due to strong suicide inactivation caused by L-DOPA processing. Levodopa 191-197 tyrosinase Homo sapiens 117-127 27711193-8 2016 In this case, the cost of the immobilized enzyme preparation is not overcome by its reuse over time, and native tyrosinase may be more economically feasible for a single use in L-DOPA production. Levodopa 177-183 tyrosinase Homo sapiens 112-122 27111571-6 2016 The clinical characteristics of affected family members were similar to those described in PD families with other mutations in LRRK2 codon 1441 and included resting tremor, rigidity, bradykinesia, unilateral onset, and a good response to levodopa. Levodopa 238-246 leucine rich repeat kinase 2 Homo sapiens 127-132 27527415-4 2016 The results of fluorescence quenching experiment showed that the compound could interact with tyrosinase and the substrates (tyrosine and l-DOPA). Levodopa 138-144 tyrosinase Homo sapiens 94-104 27716431-10 2016 Pharmacological blockade of dopamine synthesis reduced severity of dystonia-like movements, whereas treatment with L-Dopa aggravated these but only in mutant mice suggesting a DYT1 related central component relevant to the development of abnormal involuntary movements. Levodopa 115-121 torsin family 1, member A (torsin A) Mus musculus 176-180 27165006-10 2016 For some patients, exome sequencing results had implications for treatment, exemplified by the favorable L-DOPA treatment in a patient with HSP due to ATP13A2 variants (Parkinson type 9). Levodopa 105-111 ATPase cation transporting 13A2 Homo sapiens 151-158 27498816-5 2016 The patient visited the hospital because of gait disturbances and DAT-scan showed a levodopa transducer decrease in the putamen. Levodopa 84-92 solute carrier family 6 member 3 Homo sapiens 66-69 27904494-6 2016 However, administration of Shudipingchan granule with levodopa reduced expression of phosphorylated extracellular signal-regulated kinase 1/2 and Bax, increased tyrosine hydroxylase and Bcl-2, reduced apoptosis in the substantia nigra, and markedly improved dyskinesia. Levodopa 54-62 BCL2 associated X, apoptosis regulator Rattus norvegicus 100-149 27904494-6 2016 However, administration of Shudipingchan granule with levodopa reduced expression of phosphorylated extracellular signal-regulated kinase 1/2 and Bax, increased tyrosine hydroxylase and Bcl-2, reduced apoptosis in the substantia nigra, and markedly improved dyskinesia. Levodopa 54-62 BCL2, apoptosis regulator Rattus norvegicus 186-191 27686972-7 2016 As it may exert anti-oxidative and ROS-scavenging functions, we studied whether it exerts such actions in human GCs and whether DOPA-decarboxylase (DDC), the enzyme converting L-DOPA to DA, is expressed in the human ovary. Levodopa 176-182 dopa decarboxylase Homo sapiens 128-146 27312773-11 2016 By contrast, mice sustaining the lesion at 23months of age showed a striking susceptibility to the dyskinetic effects of both l-DOPA and apomorphine, which was associated with a pronounced drug-induced upregulation of FosB in the ventrolateral striatum. Levodopa 126-132 FBJ osteosarcoma oncogene B Mus musculus 219-223 27320210-0 2016 l-DOPA-induced dyskinesia is associated with a deficient numerical downregulation of striatal tyrosine hydroxylase mRNA-expressing neurons. Levodopa 0-6 tyrosine hydroxylase Mus musculus 94-114 27613848-1 2016 Fluctuations of dopamine levels and upregulations of NR2B tyrosine phosphorylation in the striatum have been connected with levodopa (L-dopa)-induced dyskinesia (LID) in Parkinson"s disease (PD). Levodopa 124-132 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 53-57 27613848-1 2016 Fluctuations of dopamine levels and upregulations of NR2B tyrosine phosphorylation in the striatum have been connected with levodopa (L-dopa)-induced dyskinesia (LID) in Parkinson"s disease (PD). Levodopa 134-140 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 53-57 27320210-4 2016 Recent evidence suggests an involvement of striatal tyrosine hydroxylase (TH) protein-expressing neurons, as they are capable of endogenously producing l-DOPA and possibly dopamine. Levodopa 152-158 tyrosine hydroxylase Mus musculus 52-72 27320210-4 2016 Recent evidence suggests an involvement of striatal tyrosine hydroxylase (TH) protein-expressing neurons, as they are capable of endogenously producing l-DOPA and possibly dopamine. Levodopa 152-158 tyrosine hydroxylase Mus musculus 74-76 27320210-8 2016 Interestingly, similar changes were observed in intact non-deafferentiated striata, demonstrating an l-DOPA-responsive transcriptional TH regulation independently from nigrostriatal lesion severity. Levodopa 101-107 tyrosine hydroxylase Mus musculus 135-137 27622543-0 2016 l-3,4-Dihydroxyphenylalanine induces ptosis through a GPR143-independent mechanism in mice. Levodopa 0-28 G protein-coupled receptor 143 Mus musculus 54-60 27622543-1 2016 Through its conversion to dopamine by aromatic l-amino acid decarboxylase (AADC), l-3,4-dihydroxyphenylalanine (l-DOPA) replenishes depleted brain dopamine in Parkinson"s disease patients. Levodopa 82-110 dopa decarboxylase Homo sapiens 47-73 27622543-1 2016 Through its conversion to dopamine by aromatic l-amino acid decarboxylase (AADC), l-3,4-dihydroxyphenylalanine (l-DOPA) replenishes depleted brain dopamine in Parkinson"s disease patients. Levodopa 82-110 dopa decarboxylase Homo sapiens 75-79 27622543-1 2016 Through its conversion to dopamine by aromatic l-amino acid decarboxylase (AADC), l-3,4-dihydroxyphenylalanine (l-DOPA) replenishes depleted brain dopamine in Parkinson"s disease patients. Levodopa 112-118 dopa decarboxylase Homo sapiens 47-73 27622543-1 2016 Through its conversion to dopamine by aromatic l-amino acid decarboxylase (AADC), l-3,4-dihydroxyphenylalanine (l-DOPA) replenishes depleted brain dopamine in Parkinson"s disease patients. Levodopa 112-118 dopa decarboxylase Homo sapiens 75-79 27622543-2 2016 We recently identified GPR143 as a candidate receptor for l-DOPA. Levodopa 58-64 G protein-coupled receptor 143 Mus musculus 23-29 27622543-7 2016 l-DOPA-induced ptosis in Gpr143-deficient mice to a similar extent as in wt mice. Levodopa 0-6 G protein-coupled receptor 143 Mus musculus 25-31 27622543-8 2016 These results suggest that l-DOPA induces ptosis in a GPR143-independent fashion in mice. Levodopa 27-33 G protein-coupled receptor 143 Mus musculus 54-60 27178731-8 2016 Here we describe known effects of individual GRKs on dopamine receptors in cell culture and in the two in vivo models of dopamine-mediated signaling: behavioral response to psychostimulants and L-DOPA- induced dyskinesia. Levodopa 194-200 G protein-coupled receptor kinase 6 Homo sapiens 45-49 27214664-0 2016 A Phase 2A Trial of the Novel mGluR5-Negative Allosteric Modulator Dipraglurant for Levodopa-Induced Dyskinesia in Parkinson"s Disease. Levodopa 84-92 glutamate receptor, ionotropic, kainate 1 Mus musculus 30-36 27214664-1 2016 BACKGROUND: The metabotropic glutamate receptor 5-negative allosteric modulator dipraglurant reduces levodopa-induced dyskinesia in the MPTP-macaque model. Levodopa 101-109 glutamate metabotropic receptor 5 Homo sapiens 16-49 27287315-7 2016 These results confirm the role of VMAT2 in the protection of vulnerable nigrostriatal dopamine neurons and may also provide new insight into the side effects of L-DOPA treatments in Parkinson"s disease. Levodopa 161-167 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 34-39 27164322-0 2016 DAT versus D2 receptor binding in the rat striatum: l-DOPA-induced motor activity is better predicted by reuptake than release of dopamine. Levodopa 52-58 solute carrier family 6 member 3 Rattus norvegicus 0-3 27261334-4 2016 The use of l-DOPA, a small molecule drug shown to up-regulate VEGF in the Parkinsonian brain, can potentially resolve these issues by substituting for VEGF. Levodopa 11-17 vascular endothelial growth factor A Homo sapiens 62-66 27268039-2 2016 METHODS: We performed a cross-over, sham-controlled study of patients with severe PD, bilateral motor signs and debilitating, severe FoG, that was levodopa-sensitive but not controlled by optimal dopatherapy. Levodopa 147-155 zinc finger protein, FOG family member 1 Homo sapiens 133-136 27261334-4 2016 The use of l-DOPA, a small molecule drug shown to up-regulate VEGF in the Parkinsonian brain, can potentially resolve these issues by substituting for VEGF. Levodopa 11-17 vascular endothelial growth factor A Homo sapiens 151-155 26169221-7 2016 DOPA accumulation induced by preventing cAMP degradation with IBMX (iso-butyl-methylxantine, 1 mM) or by activating receptors for the vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating peptide (PACAP) with PACAP-27 (1 muM) was reduced (IBMX) or prevented (PACAP-27) by RAMH (100 nM). Levodopa 0-4 vasoactive intestinal peptide Rattus norvegicus 165-168 27485826-7 2016 An interaction network contained 17 genes was obtained and SORCS2 was involved in this network, interacted with nerve growth factor (NGF), nerve growth factor receptor (NGFR), dopa decarboxylase (L-dopa) and dopamine. Levodopa 196-202 sortilin related VPS10 domain containing receptor 2 Gallus gallus 59-65 27485826-8 2016 After knockdown of SORCS2, the mRNA levels of NGF, L-dopa and dopamine receptor genes DRD1, DRD2, DRD3 and DRD4 were significantly decreased (P < 0.05). Levodopa 51-57 sortilin related VPS10 domain containing receptor 2 Gallus gallus 19-25 27016022-6 2016 Treatment with l-dopa showed wearing-off over the course of the experiment in addition to development of abnormal involuntary movements and upregulated striatal VEGF level. Levodopa 15-21 vascular endothelial growth factor A Rattus norvegicus 161-165 27016022-7 2016 Treatment with ibuprofen or piroxicam in combination with l-dopa preserved the effect of l-dopa at the end of week 10, delayed the development of dyskinesia and decreased striatal COX-2 and VEGF levels. Levodopa 58-64 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 180-185 27016022-7 2016 Treatment with ibuprofen or piroxicam in combination with l-dopa preserved the effect of l-dopa at the end of week 10, delayed the development of dyskinesia and decreased striatal COX-2 and VEGF levels. Levodopa 58-64 vascular endothelial growth factor A Rattus norvegicus 190-194 27574484-9 2016 LID-induced hyper-phosphorylation of ERK1/2 and overexpression of FosB/DeltaFosB was markedly decreased in 6-OHDA-lesioned striatum of PA-5HT-treated mice, indicating that PA-5HT decreased the dopamine D1 receptor-hyperactivation induced by chronic treatment of L-DOPA in dopamine-denervated striatum. Levodopa 262-268 FBJ osteosarcoma oncogene B Mus musculus 66-70 26972524-2 2016 Here, we report clinical and genetic findings in a family with Turkish origin carrying a new DJ1 mutation and presenting with early-onset levodopa responsive parkinsonism and signs of amyotrophic lateral sclerosis (ALS). Levodopa 138-146 Parkinsonism associated deglycase Homo sapiens 93-96 27456338-1 2016 BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes. Levodopa 80-86 catechol-O-methyltransferase Homo sapiens 106-134 27456338-1 2016 BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes. Levodopa 80-86 catechol-O-methyltransferase Homo sapiens 136-140 27456338-1 2016 BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes. Levodopa 201-207 catechol-O-methyltransferase Homo sapiens 136-140 27456338-8 2016 Since some amount of entacapone can cross the blood-brain barrier, this reagent may enhance L-DOPA transportation by inhibiting COMT and increase the astrocyte-mediated neuroprotective effects of L-DOPA on dopaminergic neurons. Levodopa 92-98 catechol-O-methyltransferase Homo sapiens 128-132 26169221-7 2016 DOPA accumulation induced by preventing cAMP degradation with IBMX (iso-butyl-methylxantine, 1 mM) or by activating receptors for the vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating peptide (PACAP) with PACAP-27 (1 muM) was reduced (IBMX) or prevented (PACAP-27) by RAMH (100 nM). Levodopa 0-4 adenylate cyclase activating polypeptide 1 Rattus norvegicus 218-223 26169221-7 2016 DOPA accumulation induced by preventing cAMP degradation with IBMX (iso-butyl-methylxantine, 1 mM) or by activating receptors for the vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating peptide (PACAP) with PACAP-27 (1 muM) was reduced (IBMX) or prevented (PACAP-27) by RAMH (100 nM). Levodopa 0-4 adenylate cyclase activating polypeptide 1 Rattus norvegicus 230-235 26169221-7 2016 DOPA accumulation induced by preventing cAMP degradation with IBMX (iso-butyl-methylxantine, 1 mM) or by activating receptors for the vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating peptide (PACAP) with PACAP-27 (1 muM) was reduced (IBMX) or prevented (PACAP-27) by RAMH (100 nM). Levodopa 0-4 adenylate cyclase activating polypeptide 1 Rattus norvegicus 230-235 26830512-3 2016 Because AADC is a common enzyme catalyzing 5-hydroxytryptophan to serotonin and l-3,4-dihydroxyphenylalanine (l-dopa) to dopamine (DA), it seems likely that the ability of AADC cells using l-dopa to synthesize DA is also increased. Levodopa 80-108 dopa decarboxylase Rattus norvegicus 172-176 26830512-3 2016 Because AADC is a common enzyme catalyzing 5-hydroxytryptophan to serotonin and l-3,4-dihydroxyphenylalanine (l-dopa) to dopamine (DA), it seems likely that the ability of AADC cells using l-dopa to synthesize DA is also increased. Levodopa 110-116 dopa decarboxylase Rattus norvegicus 8-12 26830512-3 2016 Because AADC is a common enzyme catalyzing 5-hydroxytryptophan to serotonin and l-3,4-dihydroxyphenylalanine (l-dopa) to dopamine (DA), it seems likely that the ability of AADC cells using l-dopa to synthesize DA is also increased. Levodopa 189-195 dopa decarboxylase Rattus norvegicus 8-12 26830512-6 2016 However, following administration of a peripheral AADC inhibitor (carbidopa) with or without a monoamine oxidase inhibitor (pargyline) co-application, systemic administration of l-dopa resulted in ~94% of AADC cells becoming DA-immunopositive in the spinal cord below the lesion, whereas in normal or sham-operated rats none or very few of AADC cells became DA-immunopositive with the same treatment. Levodopa 178-184 dopa decarboxylase Rattus norvegicus 50-54 26830512-6 2016 However, following administration of a peripheral AADC inhibitor (carbidopa) with or without a monoamine oxidase inhibitor (pargyline) co-application, systemic administration of l-dopa resulted in ~94% of AADC cells becoming DA-immunopositive in the spinal cord below the lesion, whereas in normal or sham-operated rats none or very few of AADC cells became DA-immunopositive with the same treatment. Levodopa 178-184 dopa decarboxylase Rattus norvegicus 205-209 26830512-6 2016 However, following administration of a peripheral AADC inhibitor (carbidopa) with or without a monoamine oxidase inhibitor (pargyline) co-application, systemic administration of l-dopa resulted in ~94% of AADC cells becoming DA-immunopositive in the spinal cord below the lesion, whereas in normal or sham-operated rats none or very few of AADC cells became DA-immunopositive with the same treatment. Levodopa 178-184 dopa decarboxylase Rattus norvegicus 205-209 26991136-11 2016 In addition, the correlations of L-dopa or DA and P-gp or tight junction proteins respectively were significantly negative in co-administered- and beta-asarone-treated groups. Levodopa 33-39 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 50-54 27072528-0 2016 Enkephalin and dynorphin neuropeptides are differently correlated with locomotor hypersensitivity and levodopa-induced dyskinesia in parkinsonian rats. Levodopa 102-110 proenkephalin Rattus norvegicus 0-10 27190169-6 2016 Inasmuch as they increase synaptic dopamine levels, dopamine transporter (DAT) inhibitors, whether they are selective or have actions on noradrenaline or serotonin transporters, theoretically represent an attractive way to alleviate parkinsonism per se and potentially enhance l-DOPA antiparkinsonian action (provided that sufficient dopamine terminals remain within the striatum). Levodopa 277-283 solute carrier family 6 member 3 Homo sapiens 52-72 26991136-0 2016 beta-asarone and levodopa co-administration increase striatal dopamine level in 6-hydroxydopamine induced rats by modulating P-glycoprotein and tight junction proteins at the blood-brain barrier and promoting levodopa into the brain. Levodopa 17-25 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 125-139 27190169-6 2016 Inasmuch as they increase synaptic dopamine levels, dopamine transporter (DAT) inhibitors, whether they are selective or have actions on noradrenaline or serotonin transporters, theoretically represent an attractive way to alleviate parkinsonism per se and potentially enhance l-DOPA antiparkinsonian action (provided that sufficient dopamine terminals remain within the striatum). Levodopa 277-283 solute carrier family 6 member 3 Homo sapiens 74-77 27368041-12 2016 Scores at baseline, patients with Parkinson disease were more likely to experience FOG if: they were older, or from the countryside; had an akinetic-rigid style, anxiety, or higher NMSS scores; they used levodopa early or did not use amantadine or selegiline; their lower limbs were the site of onset; or they had more severe motor disability or higher HAMD scores at baseline. Levodopa 204-212 zinc finger protein, FOG family member 1 Homo sapiens 83-86 27224648-2 2016 18F-FDOPA is a large neutral amino acid biochemically resembling endogenous L-DOPA and taken up by the L-type amino acid transporters (LAT1 and LAT2). Levodopa 76-82 solute carrier family 7 member 5 Homo sapiens 135-139 27129930-0 2016 Levodopa and neuropathy risk in patients with Parkinson disease: Effect of COMT inhibition. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 75-79 27224648-2 2016 18F-FDOPA is a large neutral amino acid biochemically resembling endogenous L-DOPA and taken up by the L-type amino acid transporters (LAT1 and LAT2). Levodopa 76-82 linker for activation of T cells family member 2 Homo sapiens 144-148 27169991-0 2016 LRRK2 phosphorylation level correlates with abnormal motor behaviour in an experimental model of levodopa-induced dyskinesias. Levodopa 97-105 leucine rich repeat kinase 2 Homo sapiens 0-5 27169991-5 2016 Here we show that LRRK2 phosphorylation level at serine 935 correlates with LIDs induction and that inhibition of LRRK2 induces a significant increase in the dyskinetic score in L-DOPA treated parkinsonian animals. Levodopa 178-184 leucine rich repeat kinase 2 Homo sapiens 114-119 27173342-3 2016 Tyrosine hydroxylase (TH) expressed in substantia nigra neurons catalyzes the conversion of tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the rate-limiting step of DA biosynthesis. Levodopa 104-132 tyrosine hydroxylase Rattus norvegicus 0-20 27247854-3 2016 METHODS: Positron emission tomography (PET) with the GABA receptor alpha1/alpha5 subtype ligand [(11)C] Ro15-4513 was used to detect changes in GABA receptor availability after clinical oral doses of levodopa in a double blind controlled study. Levodopa 200-208 GABA type A receptor-associated protein Homo sapiens 53-66 27247854-3 2016 METHODS: Positron emission tomography (PET) with the GABA receptor alpha1/alpha5 subtype ligand [(11)C] Ro15-4513 was used to detect changes in GABA receptor availability after clinical oral doses of levodopa in a double blind controlled study. Levodopa 200-208 calcium voltage-gated channel subunit alpha1 A Homo sapiens 67-79 27247854-3 2016 METHODS: Positron emission tomography (PET) with the GABA receptor alpha1/alpha5 subtype ligand [(11)C] Ro15-4513 was used to detect changes in GABA receptor availability after clinical oral doses of levodopa in a double blind controlled study. Levodopa 200-208 GABA type A receptor-associated protein Homo sapiens 144-157 27173342-3 2016 Tyrosine hydroxylase (TH) expressed in substantia nigra neurons catalyzes the conversion of tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the rate-limiting step of DA biosynthesis. Levodopa 134-140 tyrosine hydroxylase Rattus norvegicus 0-20 26875664-7 2016 Whereas dopamine denervation in the dorsal striatum decreased Gadd45beta mRNA, chronic L-DOPA treatment significantly increased Gadd45beta mRNA expression in the 6-OHDA-lesioned striatum of wild-type mice. Levodopa 87-93 growth arrest and DNA-damage-inducible 45 beta Mus musculus 128-138 27163503-11 2016 It was concluded that OPC is a new COMT inhibitor that significantly decreased COMT activity and increased systemic exposure to levodopa in PD patients with motor fluctuations. Levodopa 128-136 catechol-O-methyltransferase Homo sapiens 35-39 26875664-0 2016 Gadd45beta ameliorates L-DOPA-induced dyskinesia in a Parkinson"s disease mouse model. Levodopa 23-29 growth arrest and DNA-damage-inducible 45 beta Mus musculus 0-10 26875664-10 2016 The deficiency of Gadd45beta in LID increased expression of DeltaFosB and c-Fos in the lesioned striatum 90 min after the last administration of L-DOPA following 11days of daily L-DOPA treatments. Levodopa 145-151 growth arrest and DNA-damage-inducible 45 beta Mus musculus 18-28 26875664-10 2016 The deficiency of Gadd45beta in LID increased expression of DeltaFosB and c-Fos in the lesioned striatum 90 min after the last administration of L-DOPA following 11days of daily L-DOPA treatments. Levodopa 178-184 growth arrest and DNA-damage-inducible 45 beta Mus musculus 18-28 26875664-11 2016 These data suggest that the increased expression of Gadd45beta induced by repeated administration of L-DOPA may be beneficial in patients with PD. Levodopa 101-107 growth arrest and DNA damage inducible beta Homo sapiens 52-62 27064915-1 2016 INTRODUCTION: Over recent years, several types of freezing of gait (FOG) have been described, mainly according to their response to levodopa. Levodopa 132-140 zinc finger protein, FOG family member 1 Homo sapiens 68-71 27231711-2 2016 Tyrosinase is the key cuproenzyme which initiates the pigment synthesis using its substrate amino acid tyrosine or L-DOPA (L-3, 4-dihydroxyphenylalanine). Levodopa 115-121 tyrosinase Mus musculus 0-10 27231711-2 2016 Tyrosinase is the key cuproenzyme which initiates the pigment synthesis using its substrate amino acid tyrosine or L-DOPA (L-3, 4-dihydroxyphenylalanine). Levodopa 123-152 tyrosinase Mus musculus 0-10 26871939-2 2016 Moreover, adenosine A2A receptor antagonists, such as preladenant, significantly increased l-dopa efficacy in PD without exacerbating dyskinetic-like behavior. Levodopa 91-97 adenosine A2a receptor Rattus norvegicus 10-32 27038906-6 2016 RESULTS: Cox10/DAT-cre mice showed decreased numbers of TH+ and DAT+ cells in the substantia nigra, early striatal dopamine depletion, motor defects reversible with L-DOPA treatment and hypersensitivity to L-DOPA with hyperkinetic behavior. Levodopa 165-171 heme A:farnesyltransferase cytochrome c oxidase assembly factor 10 Mus musculus 9-14 27038906-6 2016 RESULTS: Cox10/DAT-cre mice showed decreased numbers of TH+ and DAT+ cells in the substantia nigra, early striatal dopamine depletion, motor defects reversible with L-DOPA treatment and hypersensitivity to L-DOPA with hyperkinetic behavior. Levodopa 165-171 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 15-18 27038906-6 2016 RESULTS: Cox10/DAT-cre mice showed decreased numbers of TH+ and DAT+ cells in the substantia nigra, early striatal dopamine depletion, motor defects reversible with L-DOPA treatment and hypersensitivity to L-DOPA with hyperkinetic behavior. Levodopa 206-212 heme A:farnesyltransferase cytochrome c oxidase assembly factor 10 Mus musculus 9-14 27038906-6 2016 RESULTS: Cox10/DAT-cre mice showed decreased numbers of TH+ and DAT+ cells in the substantia nigra, early striatal dopamine depletion, motor defects reversible with L-DOPA treatment and hypersensitivity to L-DOPA with hyperkinetic behavior. Levodopa 206-212 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 15-18 26750488-3 2016 The hypersensitive D1-R-mediated transmission may be the culprit for the undesired expression of levodopa-induced dyskinesia, implying the involvement of Syt-IV and SP in the process. Levodopa 97-105 synaptotagmin 4 Rattus norvegicus 154-160 26871939-7 2016 Zif-268 was increased in the striatum of rats treated with l-dopa and l-dopa plus preladenant compared with vehicle. Levodopa 59-65 early growth response 1 Rattus norvegicus 0-7 26871939-7 2016 Zif-268 was increased in the striatum of rats treated with l-dopa and l-dopa plus preladenant compared with vehicle. Levodopa 70-76 early growth response 1 Rattus norvegicus 0-7 26871939-8 2016 In contrast, rats treated with eltoprazine (with or without preladenant) had lower zif-268 activation after chronic treatment in both the dyskinetic and l-dopa-non-primed groups. Levodopa 153-159 early growth response 1 Rattus norvegicus 83-90 26898243-0 2016 Shp-2 knockdown prevents l-dopa-induced dyskinesia in a rat model of Parkinson"s disease. Levodopa 25-31 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 0-5 26898243-3 2016 We recently identified the tyrosine phosphatase Shp-2 as a crucial effector transmitting D1 receptor signaling to extracellular signal-regulated protein kinases 1 and 2 activation and reported the involvement of the D1 receptor/Shp-2/extracellular signal-regulated protein kinases 1 and 2 pathway in the development of l-dopa-induced dyskinesia. Levodopa 319-325 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 48-53 26898243-3 2016 We recently identified the tyrosine phosphatase Shp-2 as a crucial effector transmitting D1 receptor signaling to extracellular signal-regulated protein kinases 1 and 2 activation and reported the involvement of the D1 receptor/Shp-2/extracellular signal-regulated protein kinases 1 and 2 pathway in the development of l-dopa-induced dyskinesia. Levodopa 319-325 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 228-233 26898243-4 2016 OBJECTIVES: In this study, the role of Shp-2 in l-dopa-induced dyskinesia development was investigated by in vivo silencing of Shp-2 in the striatum of the 6-hydroxy-dopamine rat model of PD. Levodopa 48-54 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 39-44 26898243-4 2016 OBJECTIVES: In this study, the role of Shp-2 in l-dopa-induced dyskinesia development was investigated by in vivo silencing of Shp-2 in the striatum of the 6-hydroxy-dopamine rat model of PD. Levodopa 48-54 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 127-132 26898243-7 2016 RESULTS: The results show that Shp-2 knockdown remarkably decreased extracellular signal-regulated protein kinases 1 and 2 phosphorylation and attenuated the severity of l-dopa-induced dyskinesia likely without compromising the therapeutic efficacy of l-dopa. Levodopa 170-176 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 31-36 26898243-7 2016 RESULTS: The results show that Shp-2 knockdown remarkably decreased extracellular signal-regulated protein kinases 1 and 2 phosphorylation and attenuated the severity of l-dopa-induced dyskinesia likely without compromising the therapeutic efficacy of l-dopa. Levodopa 252-258 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 31-36 26298063-0 2016 Dramatic Improvement in Juvenile Parkinsonism after Levodopa Treatment in a Patient Negative for the PANK2 Mutation. Levodopa 52-60 pantothenate kinase 2 Homo sapiens 101-106 26861200-8 2016 Antiparkinson drugs did not affect O&NS biomarkers, but levodopa+carbidopa significantly increased CRP. Levodopa 56-64 C-reactive protein Homo sapiens 99-102 26771081-0 2016 CART modulates the effects of levodopa in rat model of Parkinson"s disease. Levodopa 30-38 CART prepropeptide Rattus norvegicus 0-4 26997328-0 2016 Inhibition of Glycogen Synthase Kinase-3beta (GSK-3beta) as potent therapeutic strategy to ameliorates L-dopa-induced dyskinesia in 6-OHDA parkinsonian rats. Levodopa 103-109 glycogen synthase kinase 3 beta Rattus norvegicus 14-44 26997328-0 2016 Inhibition of Glycogen Synthase Kinase-3beta (GSK-3beta) as potent therapeutic strategy to ameliorates L-dopa-induced dyskinesia in 6-OHDA parkinsonian rats. Levodopa 103-109 glycogen synthase kinase 3 beta Rattus norvegicus 46-55 26997328-5 2016 TDZD8 reduced the phosphorylation levels of tau, DARPP32, ERK and PKA protein, which represent molecular markers of LID, as well as reduced L-dopa-induced FosB mRNA and PPEB mRNA levels in the lesioned striatum. Levodopa 140-146 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 155-159 26771081-8 2016 Prior treatment with CART via ICV route potentiated the anti-Parkinsonian effects of levodopa, while CART antibody produced opposite effects. Levodopa 85-93 CART prepropeptide Rattus norvegicus 21-25 26771081-10 2016 While CART-immunoreactivity in arcuate nucleus, paraventricular nucleus, striatum, substantia nigra, ventral tegmental area and locus coeruleus was reduced in the PD induced rats, levodopa treatment restored the expression of CART-immunoreactivity in these nuclei. Levodopa 180-188 CART prepropeptide Rattus norvegicus 226-230 26744332-0 2016 LRRK2 BAC transgenic rats develop progressive, L-DOPA-responsive motor impairment, and deficits in dopamine circuit function. Levodopa 47-53 leucine-rich repeat kinase 2 Rattus norvegicus 0-5 25146322-0 2016 Selective Inactivation of Striatal FosB/DeltaFosB-Expressing Neurons Alleviates L-DOPA-Induced Dyskinesia. Levodopa 80-86 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 35-39 25146322-0 2016 Selective Inactivation of Striatal FosB/DeltaFosB-Expressing Neurons Alleviates L-DOPA-Induced Dyskinesia. Levodopa 80-86 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 40-49 25146322-1 2016 BACKGROUND: DeltaFosB is a surrogate marker of L-DOPA-induced dyskinesia (LID), the unavoidable disabling consequence of Parkinson"s disease L-DOPA long-term treatment. Levodopa 47-53 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 12-21 25146322-6 2016 We then demonstrate that the selective, and reversible, inhibition of FosB/DeltaFosB-expressing striatal neurons with Daun02 decreases the severity of LID while improving the beneficial effect of L-DOPA. Levodopa 196-202 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 70-74 25146322-6 2016 We then demonstrate that the selective, and reversible, inhibition of FosB/DeltaFosB-expressing striatal neurons with Daun02 decreases the severity of LID while improving the beneficial effect of L-DOPA. Levodopa 196-202 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 75-84 25146322-7 2016 CONCLUSIONS: These results establish that FosB/DeltaFosB accumulation ultimately results in altered neuronal electrical properties sustaining maladaptive circuits leading not only to LID but also to a blunted response to L-DOPA. Levodopa 221-227 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 42-46 25146322-7 2016 CONCLUSIONS: These results establish that FosB/DeltaFosB accumulation ultimately results in altered neuronal electrical properties sustaining maladaptive circuits leading not only to LID but also to a blunted response to L-DOPA. Levodopa 221-227 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 47-56 25193242-0 2016 A Role for Mitogen- and Stress-Activated Kinase 1 in L-DOPA-Induced Dyskinesia and FosB Expression. Levodopa 53-59 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 11-49 25193242-1 2016 BACKGROUND: Abnormal regulation of extracellular signal-regulated kinases 1 and 2 has been implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkinson"s disease patients subjected to standard pharmacotherapy. Levodopa 105-134 mitogen-activated protein kinase 3 Homo sapiens 35-81 25193242-1 2016 BACKGROUND: Abnormal regulation of extracellular signal-regulated kinases 1 and 2 has been implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkinson"s disease patients subjected to standard pharmacotherapy. Levodopa 136-142 mitogen-activated protein kinase 3 Homo sapiens 35-81 25193242-8 2016 In line with this observation, the accumulation of FosB produced by chronic L-DOPA was reduced in MSK1 knockout. Levodopa 77-83 FBJ osteosarcoma oncogene B Mus musculus 52-56 25193242-8 2016 In line with this observation, the accumulation of FosB produced by chronic L-DOPA was reduced in MSK1 knockout. Levodopa 77-83 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 99-103 25442003-1 2016 BACKGROUND: A systematic search of brain nuclei putatively involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson"s disease shed light, notably, upon the lateral habenula (LHb), which displayed an overexpression of the FosB, ARC, and Zif268 immediate-early genes only in rats experiencing abnormal involuntary movements (AIMs). Levodopa 71-99 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 253-257 25442003-1 2016 BACKGROUND: A systematic search of brain nuclei putatively involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson"s disease shed light, notably, upon the lateral habenula (LHb), which displayed an overexpression of the FosB, ARC, and Zif268 immediate-early genes only in rats experiencing abnormal involuntary movements (AIMs). Levodopa 71-99 early growth response 1 Rattus norvegicus 268-274 25442003-1 2016 BACKGROUND: A systematic search of brain nuclei putatively involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson"s disease shed light, notably, upon the lateral habenula (LHb), which displayed an overexpression of the FosB, ARC, and Zif268 immediate-early genes only in rats experiencing abnormal involuntary movements (AIMs). Levodopa 101-107 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 253-257 25442003-1 2016 BACKGROUND: A systematic search of brain nuclei putatively involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson"s disease shed light, notably, upon the lateral habenula (LHb), which displayed an overexpression of the FosB, ARC, and Zif268 immediate-early genes only in rats experiencing abnormal involuntary movements (AIMs). Levodopa 101-107 early growth response 1 Rattus norvegicus 268-274 26524704-2 2016 A key cell type involved in AMD, the retinal pigment epithelium, expresses a G protein-coupled receptor that, in response to its ligand, L-DOPA, up-regulates pigment epithelia-derived factor, while down-regulating vascular endothelial growth factor. Levodopa 137-143 vascular endothelial growth factor A Homo sapiens 214-248 26810913-10 2016 CONCLUSIONS: Our results demonstrate that ICD+ patients have an increased CTh in limbic regions when compared with ICD- patients at the same disease stage and with an equal daily levodopa equivalent dose. Levodopa 179-187 V-set and immunoglobulin domain containing 2 Homo sapiens 74-77 26711621-0 2016 Role of the atypical vesicular glutamate transporter VGLUT3 in l-DOPA-induced dyskinesia. Levodopa 63-69 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8 Mus musculus 53-59 26711621-9 2016 Finally, the absence of VGLUT3 is accompanied by a reduction of l-DOPA-induced phosphorylation of ERK1/2, ribosomal subunit (rpS6) and GluA1. Levodopa 64-70 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8 Mus musculus 24-30 26711621-9 2016 Finally, the absence of VGLUT3 is accompanied by a reduction of l-DOPA-induced phosphorylation of ERK1/2, ribosomal subunit (rpS6) and GluA1. Levodopa 64-70 mitogen-activated protein kinase 3 Mus musculus 98-104 26711621-9 2016 Finally, the absence of VGLUT3 is accompanied by a reduction of l-DOPA-induced phosphorylation of ERK1/2, ribosomal subunit (rpS6) and GluA1. Levodopa 64-70 ribosomal protein S6 Mus musculus 125-129 26711621-9 2016 Finally, the absence of VGLUT3 is accompanied by a reduction of l-DOPA-induced phosphorylation of ERK1/2, ribosomal subunit (rpS6) and GluA1. Levodopa 64-70 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 135-140 26568446-1 2016 A homochiral MOF film grown on a functionalized substrate in a capillary column with high orientation and homogeneity was successfully prepared by using a layer-by-layer liquid phase epitaxial method; by introducing self-polymerized 3,4-dihydroxy-L-phenylalanine (poly(L-DOPA)) as a chiral substrate, the obtained enantiopure substrate mounted homochiral MOF thin film showed improved enantiomer separation. Levodopa 233-262 lysine acetyltransferase 8 Homo sapiens 13-16 26791104-8 2016 Clomipramine, the compound with the highest affinity for SERT was most effective in attenuating L-DOPA-induced dyskinesia without altering L-DOPA"s stimulatory effects. Levodopa 96-102 solute carrier family 6 member 4 Rattus norvegicus 57-61 26787846-0 2016 p11 modulates L-DOPA therapeutic effects and dyskinesia via distinct cell types in experimental Parkinsonism. Levodopa 14-20 S100 calcium binding protein A10 (calpactin) Mus musculus 0-3 26787846-3 2016 Subchronic L-DOPA increases levels of adaptor protein p11 (S100A10) in dopaminoceptive neurons of the striatum. Levodopa 11-17 S100 calcium binding protein A10 (calpactin) Mus musculus 54-57 26787846-8 2016 Mice lacking p11 in dopamine D2R-containing neurons have a reduced response to L-DOPA on the therapeutic parameters, but develop dyskinetic side effects. Levodopa 79-85 S100 calcium binding protein A10 (calpactin) Mus musculus 13-16 26787846-9 2016 In contrast, mice lacking p11 in dopamine D1R-containing neurons exhibit tremor and rotational responses toward L-DOPA, but develop less dyskinesia. Levodopa 112-118 S100 calcium binding protein A10 (calpactin) Mus musculus 26-29 26787846-12 2016 These data demonstrate that p11 located in ChAT or D2R-containing neurons is involved in regulating therapeutic actions in experimental PD, whereas p11 in D1R-containing neurons underlies the development of L-DOPA-induced dyskinesias. Levodopa 207-213 S100 calcium binding protein A10 (calpactin) Mus musculus 148-151 26787858-7 2016 Mice with unilateral lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists, and resulting rotational behaviors were significantly reduced after ipsilateral inhibition of dorsal striatal p11 expression. Levodopa 55-61 S100 calcium binding protein A10 (calpactin) Mus musculus 223-226 26787858-7 2016 Mice with unilateral lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists, and resulting rotational behaviors were significantly reduced after ipsilateral inhibition of dorsal striatal p11 expression. Levodopa 63-71 S100 calcium binding protein A10 (calpactin) Mus musculus 223-226 26787858-8 2016 Finally, p11 knockdown in the dorsal striatum dramatically reduced l-dopa-induced abnormal involuntary movements compared with control mice. Levodopa 67-73 S100 calcium binding protein A10 (calpactin) Mus musculus 9-12 26787858-9 2016 These data indicate that focal inhibition of p11 action in the dorsal striatum could be a promising PD therapeutic target to improve motor function while reducing l-dopa-induced dyskinesias. Levodopa 163-169 S100 calcium binding protein A10 (calpactin) Mus musculus 45-48 26363191-0 2016 L-DOPA modulates cell viability through the ERK-c-Jun system in PC12 and dopaminergic neuronal cells. Levodopa 0-6 Eph receptor B1 Rattus norvegicus 44-47 26363191-1 2016 L-DOPA causes neurotoxicity by modulating the Epac-ERK system in PC12 cells. Levodopa 0-6 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 46-50 26363191-1 2016 L-DOPA causes neurotoxicity by modulating the Epac-ERK system in PC12 cells. Levodopa 0-6 Eph receptor B1 Rattus norvegicus 51-54 26363191-2 2016 This study investigated the effects of a single treatment with L-DOPA and multiple treatments with L-DOPA (MT-LD) on ERK1/2 and JNK1/2-c-Jun systems. Levodopa 99-105 mitogen activated protein kinase 3 Rattus norvegicus 117-123 26363191-3 2016 In PC12 cells, a toxic L-DOPA concentration (200 muM) induced sustained ERK1/2 and JNK1/2 phosphorylation that was inhibited by the Epac inhibitor brefeldin A, but not by the PKA inhibitor H89. Levodopa 23-29 mitogen activated protein kinase 3 Rattus norvegicus 72-78 26363191-3 2016 In PC12 cells, a toxic L-DOPA concentration (200 muM) induced sustained ERK1/2 and JNK1/2 phosphorylation that was inhibited by the Epac inhibitor brefeldin A, but not by the PKA inhibitor H89. Levodopa 23-29 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 132-136 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 12-18 mitogen activated protein kinase 3 Rattus norvegicus 94-100 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 12-18 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 220-224 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 12-18 mitogen activated protein kinase 3 Rattus norvegicus 235-241 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 12-18 caspase 3 Rattus norvegicus 294-303 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 136-142 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 220-224 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 136-142 mitogen activated protein kinase 3 Rattus norvegicus 235-241 26363191-5 2016 A non-toxic L-DOPA concentration (20 muM) induced c-Jun phosphorylation (Ser73) via transient ERK1/2 phosphorylation, whereas the toxic L-DOPA concentration induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-sustained ERK1/2-JNK1/2 phosphorylation, which then enhanced cleaved caspase-3 expression. Levodopa 136-142 caspase 3 Rattus norvegicus 294-303 26779898-7 2016 A homogenous collagen type I and fibronectin coating was observed after L-DOPA functionalization. Levodopa 72-78 fibronectin 1 Homo sapiens 13-44 26528954-1 2016 OBJECTIVE: DNAJC6 mutations were recently described in two families with autosomal recessive juvenile parkinsonism (onset age < 11), prominent atypical signs, poor or absent response to levodopa, and rapid progression (wheelchair-bound within ~10 years from onset). Levodopa 189-197 DnaJ heat shock protein family (Hsp40) member C6 Homo sapiens 11-17 26363191-8 2016 However, L-DOPA administration (10 or 30 mg/kg) showed neurotoxicity through c-Jun phosphorylation (Ser63) and c-Jun expression via ERK1/2 phosphorylation for 3-4 weeks. Levodopa 9-15 mitogen activated protein kinase 3 Rattus norvegicus 132-138 26363191-10 2016 By contrast, toxic L-DOPA treatment or MT-LD (20 muM) induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-dependent sustained ERK1/2 and JNK1/2 phosphorylation, which subsequently led to cell death. Levodopa 19-25 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 117-121 26363191-10 2016 By contrast, toxic L-DOPA treatment or MT-LD (20 muM) induced c-Jun phosphorylation (Ser63) and c-Jun expression via Epac-dependent sustained ERK1/2 and JNK1/2 phosphorylation, which subsequently led to cell death. Levodopa 19-25 mitogen activated protein kinase 3 Rattus norvegicus 142-148 26363191-12 2016 Our data indicate that L-DOPA causes neurotoxicity via the ERK1/2-c-Jun system in dopaminergic neuronal cells. Levodopa 23-29 mitogen activated protein kinase 3 Rattus norvegicus 59-65 26568446-1 2016 A homochiral MOF film grown on a functionalized substrate in a capillary column with high orientation and homogeneity was successfully prepared by using a layer-by-layer liquid phase epitaxial method; by introducing self-polymerized 3,4-dihydroxy-L-phenylalanine (poly(L-DOPA)) as a chiral substrate, the obtained enantiopure substrate mounted homochiral MOF thin film showed improved enantiomer separation. Levodopa 233-262 lysine acetyltransferase 8 Homo sapiens 355-358 26755131-4 2016 Here we demonstrate that genetic or molecular impairment of PLA2g6-dependent Ca(2+) signalling is a trigger for autophagic dysfunction, progressive loss of dopaminergic (DA) neurons in substantia nigra pars compacta and age-dependent L-DOPA-sensitive motor dysfunction. Levodopa 234-240 phospholipase A2, group VI Mus musculus 60-66 26674175-2 2016 Taking inspiration from mussels that produce proteins rich in L-3,4-dihydroxyphenylalanine (DOPA) to adhere to a variety of organic and inorganic surfaces, the silk fibroin was functionalized with catechol groups. Levodopa 62-90 fibroin light chain Bombyx mori 165-172 26674175-2 2016 Taking inspiration from mussels that produce proteins rich in L-3,4-dihydroxyphenylalanine (DOPA) to adhere to a variety of organic and inorganic surfaces, the silk fibroin was functionalized with catechol groups. Levodopa 92-96 fibroin light chain Bombyx mori 165-172 25135633-5 2016 Similar to the DBH inhibitors, L-DOPA potentiated cocaine-induced dopamine release in the mPFC and suppressed cocaine-induced reinstatement of cocaine-seeking behaviour. Levodopa 31-37 dopamine beta-hydroxylase Rattus norvegicus 15-18 27493964-1 2016 Plasma homocysteine (Hcy) levels may increase in levodopa-treated patients with Parkinson"s disease (PD) as a consequence of levodopa methylation via catechol-O-methyltransferase (COMT). Levodopa 49-57 catechol-O-methyltransferase Homo sapiens 150-178 27413743-3 2016 Among them, mutations in the PTEN-induced kinase 1 (PINK1) gene were shown to be responsible for a phenotype characterized by early onset, good response to levodopa, and a benign course. Levodopa 156-164 PTEN induced kinase 1 Homo sapiens 29-50 27413743-3 2016 Among them, mutations in the PTEN-induced kinase 1 (PINK1) gene were shown to be responsible for a phenotype characterized by early onset, good response to levodopa, and a benign course. Levodopa 156-164 PTEN induced kinase 1 Homo sapiens 52-57 27493964-1 2016 Plasma homocysteine (Hcy) levels may increase in levodopa-treated patients with Parkinson"s disease (PD) as a consequence of levodopa methylation via catechol-O-methyltransferase (COMT). Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 150-178 27493964-2 2016 Results from previous studies that assessed the effect of COMT inhibitors on levodopa-induced hyperhomocysteinemia are conflicting. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 58-62 26293352-8 2016 Similarly, and particularly if a wearing-off symptom is present, COMT inhibitors smoothen and prolong the action of levodopa. Levodopa 116-124 catechol-O-methyltransferase Homo sapiens 65-69 27025882-2 2016 L-DOPA combined with an inhibitor of DOPA decarboxylase, a pyridoxal 5"-phosphate-dependent enzyme, is still the most effective treatment for symptoms of Parkinson"s disease. Levodopa 0-6 dopa decarboxylase Homo sapiens 37-55 27025882-3 2016 LDOPA increases synaptic dopamine, while the inhibitor of peripheral DOPA decarboxylase reduces the conversion of L-DOPA to dopamine in the systemic circulation, allowing for greater L-DOPA distribution into the central nervous system. Levodopa 114-120 dopa decarboxylase Homo sapiens 69-87 27025882-3 2016 LDOPA increases synaptic dopamine, while the inhibitor of peripheral DOPA decarboxylase reduces the conversion of L-DOPA to dopamine in the systemic circulation, allowing for greater L-DOPA distribution into the central nervous system. Levodopa 183-189 dopa decarboxylase Homo sapiens 69-87 26692288-2 2016 Carbidopa/levodopa ER capsules contain beads of carbidopa and levodopa, designed to release the drugs at different rates in the gastrointestinal tract and provide constant therapeutic levodopa concentrations that are maintained for 4-5 h (after an initial peak at 1 h). Levodopa 10-18 epiregulin Homo sapiens 19-21 26692288-2 2016 Carbidopa/levodopa ER capsules contain beads of carbidopa and levodopa, designed to release the drugs at different rates in the gastrointestinal tract and provide constant therapeutic levodopa concentrations that are maintained for 4-5 h (after an initial peak at 1 h). Levodopa 62-70 epiregulin Homo sapiens 19-21 26692288-3 2016 In randomized phase III trials, oral carbidopa/levodopa ER was significantly more effective than placebo with regard to improving motor symptoms and activities of daily living in patients with early PD after 30 weeks" treatment, and provided significantly greater reductions in daily "off-time" in patients with advanced PD than immediate-release (IR) carbidopa/levodopa or carbidopa/levodopa IR plus entacapone after a treatment period of 13 and 2 weeks, respectively, without increasing troublesome dyskinesia. Levodopa 47-55 epiregulin Homo sapiens 56-58 26635194-3 2016 Levodopa and monoamine oxidase inhibitors (rasagiline and selegiline) have shown effective improvement for FOG. Levodopa 0-8 zinc finger protein, FOG family member 1 Homo sapiens 107-110 26639458-8 2016 The brain molecular correlates of the long-term effect of mGlu5 negative allosteric modulators treatments with L-DOPA attenuating development of LID was shown to extend beyond mGlu5 receptors with normalization of glutamate activity in the basal ganglia of L-DOPA-induced changes of NMDA, AMPA, mGlu2/3 receptors and VGlut2 transporter. Levodopa 111-117 solute carrier family 17 member 6 Rattus norvegicus 317-323 26639458-9 2016 In the basal ganglia, mGlu5 receptor negative allosteric modulators also normalize the L-DOPA-induced changes of dopamine D2receptors, their associated signaling proteins (ERK1/2 and Akt/GSK3beta) and neuropeptides (preproenkephalin, preprodynorphin) as well as the adenosine A2A receptors expression. Levodopa 87-93 mitogen activated protein kinase 3 Rattus norvegicus 172-178 26639458-9 2016 In the basal ganglia, mGlu5 receptor negative allosteric modulators also normalize the L-DOPA-induced changes of dopamine D2receptors, their associated signaling proteins (ERK1/2 and Akt/GSK3beta) and neuropeptides (preproenkephalin, preprodynorphin) as well as the adenosine A2A receptors expression. Levodopa 87-93 AKT serine/threonine kinase 1 Rattus norvegicus 183-186 26639458-9 2016 In the basal ganglia, mGlu5 receptor negative allosteric modulators also normalize the L-DOPA-induced changes of dopamine D2receptors, their associated signaling proteins (ERK1/2 and Akt/GSK3beta) and neuropeptides (preproenkephalin, preprodynorphin) as well as the adenosine A2A receptors expression. Levodopa 87-93 glycogen synthase kinase 3 beta Rattus norvegicus 187-195 26639458-9 2016 In the basal ganglia, mGlu5 receptor negative allosteric modulators also normalize the L-DOPA-induced changes of dopamine D2receptors, their associated signaling proteins (ERK1/2 and Akt/GSK3beta) and neuropeptides (preproenkephalin, preprodynorphin) as well as the adenosine A2A receptors expression. Levodopa 87-93 prodynorphin Rattus norvegicus 234-249 26606044-0 2016 Levodopa-Induced Motor and Dopamine Receptor Changes in Caenorhabditis elegans Overexpressing Human Alpha-Synuclein. Levodopa 0-8 G_PROTEIN_RECEP_F1_2 domain-containing protein Caenorhabditis elegans 27-44 26754997-10 2016 STN DBS in patients with motor signs that are less responsive to levodopa results in shorter duration of clinical benefits. Levodopa 65-73 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 0-3 26606044-0 2016 Levodopa-Induced Motor and Dopamine Receptor Changes in Caenorhabditis elegans Overexpressing Human Alpha-Synuclein. Levodopa 0-8 synuclein alpha Homo sapiens 100-115 26480869-0 2016 Striatal NELF-mediated RNA polymerase II stalling controls L-dopa induced dyskinesia. Levodopa 59-65 NMDA receptor synaptonuclear signaling and neuronal migration factor Rattus norvegicus 9-13 26606044-5 2016 We aimed to study levodopa-induced changes in a Parkinson"s disease model of C. elegans expressing human alpha-synuclein. Levodopa 18-26 synuclein alpha Homo sapiens 105-120 26480869-4 2016 Such NELF-E reduced expression significantly attenuated the development of abnormal involuntary movements in response to chronic L-Dopa treatment. Levodopa 129-135 negative elongation factor complex member E Rattus norvegicus 5-11 26480869-6 2016 Repression of NELF-mediating RNA polymerase II stalling thus achieves both antidyskinetic and potentiation of antiparkinsonian L-Dopa effect, highlighting the role of transcriptional events in dyskinesia establishment, acute dyskinetic manifestation and in the therapeutic response to L-Dopa. Levodopa 127-133 NMDA receptor synaptonuclear signaling and neuronal migration factor Rattus norvegicus 14-18 26480869-6 2016 Repression of NELF-mediating RNA polymerase II stalling thus achieves both antidyskinetic and potentiation of antiparkinsonian L-Dopa effect, highlighting the role of transcriptional events in dyskinesia establishment, acute dyskinetic manifestation and in the therapeutic response to L-Dopa. Levodopa 285-291 NMDA receptor synaptonuclear signaling and neuronal migration factor Rattus norvegicus 14-18 26606044-6 2016 METHODS: We exposed the alpha-synuclein C. elegans to levodopa in continuous and alternating fashions. Levodopa 54-62 synuclein alpha Homo sapiens 24-39 26522958-0 2016 Genetic deletion of Rhes or pharmacological blockade of mTORC1 prevent striato-nigral neurons activation in levodopa-induced dyskinesia. Levodopa 108-116 RASD family, member 2 Mus musculus 20-24 26606044-9 2016 RESULTS: Chronic exposure to levodopa led to hyperactivity of the alpha-synuclein C. elegans without meaningful increase in motor activity. Levodopa 29-37 synuclein alpha Homo sapiens 66-81 26522958-0 2016 Genetic deletion of Rhes or pharmacological blockade of mTORC1 prevent striato-nigral neurons activation in levodopa-induced dyskinesia. Levodopa 108-116 CREB regulated transcription coactivator 1 Mus musculus 56-62 26606044-12 2016 CONCLUSIONS: This is the first report of changes in motor and dopamine receptors induced by levodopa in C. elegans overexpressing human alpha-synuclein. Levodopa 92-100 synuclein alpha Homo sapiens 136-151 26522958-2 2016 Rhes binding to mTORC1 is hypothesized to play a role in motor disorders such as levodopa-induced dyskinesia. Levodopa 81-89 RASD family, member 2 Mus musculus 0-4 27723713-8 2016 In patients with PD and GBA mutations, a slower escalation of levodopa dose should be recommended because of the high risk of complications of therapy. Levodopa 62-70 glucosylceramidase beta Homo sapiens 24-27 26522958-2 2016 Rhes binding to mTORC1 is hypothesized to play a role in motor disorders such as levodopa-induced dyskinesia. Levodopa 81-89 CREB regulated transcription coactivator 1 Mus musculus 16-22 26522958-4 2016 6-Hydroxydopamine-hemilesioned Rhes knockout mice and wild-type littermates were chronically treated with levodopa. Levodopa 106-114 RASD family, member 2 Mus musculus 31-35 26522958-10 2016 Levodopa also stimulated striatal glutamate in controls and Rhes knockouts but not in rapamycin-treated mice. Levodopa 0-8 RASD family, member 2 Mus musculus 60-64 26522958-11 2016 We conclude that both genetic deletion of Rhes and pharmacological blockade of mTORC1 significantly attenuate dyskinesia development by reducing the sensitization of striato-nigral medium-sized spiny neurons to levodopa. Levodopa 211-219 RASD family, member 2 Mus musculus 42-46 26522958-11 2016 We conclude that both genetic deletion of Rhes and pharmacological blockade of mTORC1 significantly attenuate dyskinesia development by reducing the sensitization of striato-nigral medium-sized spiny neurons to levodopa. Levodopa 211-219 CREB regulated transcription coactivator 1 Mus musculus 79-85 26642370-0 2016 Pharmacological treatment with L-DOPA may reduce striatal dopamine transporter binding in in vivo imaging studies. Levodopa 31-37 solute carrier family 6 member 3 Homo sapiens 58-78 26642370-4 2016 This paper gives an overview on those findings, which, so far, have been obtained on DAT binding in human Parkinson"s disease after treatment with L-DOPA. Levodopa 147-153 solute carrier family 6 member 3 Homo sapiens 85-88 26642370-6 2016 Results indicate that DAT imaging may be reduced in the striata of healthy animals, in the unlesioned striata of animal models of unilateral Parkinson"s disease and in less severly impaired striata of Parkinsonian patients, if animal or human subjects are under acute or subchronic treatment with L-DOPA. Levodopa 297-303 solute carrier family 6 member 3 Homo sapiens 22-25 26459303-10 2016 L-Dopa alone as well as the combined L-Dopa and OA treatment ameliorated the effects of 6-OHDA on catalase concentration. Levodopa 0-6 catalase Rattus norvegicus 98-106 26459303-10 2016 L-Dopa alone as well as the combined L-Dopa and OA treatment ameliorated the effects of 6-OHDA on catalase concentration. Levodopa 37-43 catalase Rattus norvegicus 98-106 26254863-5 2015 [3H]GR125743 specific binding to striatal and pallidal 5-HT1B receptors respectively were only increased in L-DOPA-treated MPTP monkeys (dyskinetic monkeys) as compared to controls, saline and L-DOPA+MPEP MPTP monkeys; dyskinesias scores correlated positively with this binding. Levodopa 108-114 5-hydroxytryptamine receptor 1B Homo sapiens 55-61 26295926-1 2015 Entacapone is an inhibitor of catechol-O-methyltransferase (COMT) and is being used to extend the therapeutic effect of levodopa in patients with advanced and fluctuating Parkinson"s disease. Levodopa 120-128 catechol-O-methyltransferase Homo sapiens 30-58 26295926-1 2015 Entacapone is an inhibitor of catechol-O-methyltransferase (COMT) and is being used to extend the therapeutic effect of levodopa in patients with advanced and fluctuating Parkinson"s disease. Levodopa 120-128 catechol-O-methyltransferase Homo sapiens 60-64 26363150-7 2015 M1 expression of two immediate-early genes (c-Fos and ARC) was strongly enhanced by either L-DOPA or SKF81297. Levodopa 91-97 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 44-49 26254863-5 2015 [3H]GR125743 specific binding to striatal and pallidal 5-HT1B receptors respectively were only increased in L-DOPA-treated MPTP monkeys (dyskinetic monkeys) as compared to controls, saline and L-DOPA+MPEP MPTP monkeys; dyskinesias scores correlated positively with this binding. Levodopa 193-199 5-hydroxytryptamine receptor 1B Homo sapiens 55-61 26643422-0 2015 [Association of VEGFR2 gene polymorphisms with the effect of L-dopa and dyskinesia complications]. Levodopa 61-67 kinase insert domain receptor Homo sapiens 16-22 25932606-13 2015 Levodopa treatment reversed MPTP-induced increases in mGlu2/3 receptors only in the GP. Levodopa 0-8 glutamate receptor, metabotropic 3 Mus musculus 54-61 25932606-14 2015 mGlu2/3 receptor-specific binding in the striatum and GP decreased bilaterally in the levodopa-treated, STN-lesioned MPTP monkeys compared with the other 3 groups. Levodopa 86-94 glutamate receptor, metabotropic 3 Mus musculus 0-7 26558771-0 2015 Loss of VGLUT3 Produces Circadian-Dependent Hyperdopaminergia and Ameliorates Motor Dysfunction and l-Dopa-Mediated Dyskinesias in a Model of Parkinson"s Disease. Levodopa 100-106 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8 Mus musculus 8-14 26415982-0 2015 The adenosine A2A receptor antagonist, istradefylline enhances anti-parkinsonian activity induced by combined treatment with low doses of L-DOPA and dopamine agonists in MPTP-treated common marmosets. Levodopa 138-144 LOW QUALITY PROTEIN: adenosine receptor A2a Callithrix jacchus 4-26 26415982-1 2015 The adenosine A2A receptor antagonist, istradefylline improves motor function in patients with advanced Parkinson"s disease (PD) optimally treated with a combination of L-DOPA and a dopamine agonist without increasing the risk of troublesome dyskinesia. Levodopa 169-175 adenosine A2a receptor Homo sapiens 4-26 26319690-0 2015 The preferential nNOS inhibitor 7-nitroindazole and the non-selective one N(G)-nitro-L-arginine methyl ester administered alone or jointly with L-DOPA differentially affect motor behavior and monoamine metabolism in sham-operated and 6-OHDA-lesioned rats. Levodopa 144-150 nitric oxide synthase 1 Rattus norvegicus 17-21 26319690-7 2015 In L-DOPA-treated group, 7-NI significantly enhanced the L-DOPA-derived tissue DA content in this system and decreased the level of the intracellular DA metabolite DOPAC produced by monoamine oxidase (MAO). Levodopa 3-9 monoamine oxidase A Rattus norvegicus 182-199 26319690-7 2015 In L-DOPA-treated group, 7-NI significantly enhanced the L-DOPA-derived tissue DA content in this system and decreased the level of the intracellular DA metabolite DOPAC produced by monoamine oxidase (MAO). Levodopa 3-9 monoamine oxidase A Rattus norvegicus 201-204 26319690-9 2015 It means that the differences in 7-NI and L-NAME-mediated modulation of L-DOPA-induced behavioral and biochemical effects resulted not only from the inhibition of NOS activity but also from differences in their ability to inhibit MAO. Levodopa 72-78 monoamine oxidase A Rattus norvegicus 230-233 26546233-0 2015 Selective toxicity of L-DOPA to dopamine transporter-expressing neurons and locomotor behavior in zebrafish larvae. Levodopa 22-28 solute carrier family 6 member 3 Danio rerio 32-52 26173746-0 2015 L-dopa increases alpha-synuclein DNA methylation in Parkinson"s disease patients in vivo and in vitro. Levodopa 0-6 synuclein alpha Homo sapiens 17-32 26173746-5 2015 alpha-Synuclein methylation was increased in sporadic PD patients with higher l-dopa dosage, and L-dopa specifically induced methylation of alpha-synuclein intron 1 in cultured mononuclear cells. Levodopa 78-84 synuclein alpha Homo sapiens 0-15 26173746-8 2015 The hypomethylation of alpha-synuclein in sporadic PD patients" blood already observed in previous studies was probably underestimated because of effect of L-dopa, which was not known previously. Levodopa 156-162 synuclein alpha Homo sapiens 23-38 26455457-6 2015 Specifically, stimulation of 5-HT1A receptors seems to be effective for multiple PD symptoms including parkinsonism, L-DOPA-induced dyskinesia, cognitive impairment, mood disorders and neurodegeneration of dopamine neurons. Levodopa 117-123 5-hydroxytryptamine receptor 1A Homo sapiens 29-35 26643422-1 2015 OBJECTIVE: To explore the association of VEGFR2 gene polymorphisms (rs2305948 and rs1870377) with the effect of levodopa (L-dopa) and dyskinesia in Chinese population and to provide theoretical basis for clinical treatment. Levodopa 112-120 kinase insert domain receptor Homo sapiens 41-47 26643422-1 2015 OBJECTIVE: To explore the association of VEGFR2 gene polymorphisms (rs2305948 and rs1870377) with the effect of levodopa (L-dopa) and dyskinesia in Chinese population and to provide theoretical basis for clinical treatment. Levodopa 122-128 kinase insert domain receptor Homo sapiens 41-47 26394059-2 2015 Because STN-DBS is effective in patients with PD whose motor symptoms are dramatically alleviated by L-3,4-dihydroxyphenylalanine (L-DOPA) treatment, the higher preoperative catecholamine levels might be related to the better clinical outcome after surgery. Levodopa 101-129 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 8-11 26579065-7 2015 The dTMS-induced significant improvements in motor, postural, and motivational symptoms of PD patients and may potentiate concurrent levodopa treatment. Levodopa 133-141 tms Drosophila melanogaster 4-8 26579065-8 2015 SIGNIFICANCE: The present study demonstrates that dTMS may have a much wider spectrum of beneficial effects than previously reported for TMS, including enhancement of levodopa effects, suggesting that future clinical trials with dTMS should include a broader range of symptom measurements. Levodopa 167-175 tms Drosophila melanogaster 50-54 26579065-8 2015 SIGNIFICANCE: The present study demonstrates that dTMS may have a much wider spectrum of beneficial effects than previously reported for TMS, including enhancement of levodopa effects, suggesting that future clinical trials with dTMS should include a broader range of symptom measurements. Levodopa 167-175 tms Drosophila melanogaster 51-54 26579065-8 2015 SIGNIFICANCE: The present study demonstrates that dTMS may have a much wider spectrum of beneficial effects than previously reported for TMS, including enhancement of levodopa effects, suggesting that future clinical trials with dTMS should include a broader range of symptom measurements. Levodopa 167-175 tms Drosophila melanogaster 229-233 26468205-6 2015 Subchronic l-DOPA treatment of TAAR1 KO mice unilaterally lesioned with 6-OHDA in the medial forebrain bundle resulted in more pronounced rotational behavior and dyskinesia than in their WT counterparts. Levodopa 11-17 trace amine-associated receptor 1 Mus musculus 31-36 26468205-7 2015 The enhanced behavioral sensitization to l-DOPA in TAAR1 KO mice was paralleled by increased phosphorylation of striatal GluA1 subunits of AMPA receptors. Levodopa 41-47 trace amine-associated receptor 1 Mus musculus 51-56 26468205-7 2015 The enhanced behavioral sensitization to l-DOPA in TAAR1 KO mice was paralleled by increased phosphorylation of striatal GluA1 subunits of AMPA receptors. Levodopa 41-47 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 121-126 26276013-1 2015 Tyrosine hydroxylase catalyses the hydroxylation of L-tyrosine to l-DOPA, the rate-limiting step in the synthesis of catecholamines. Levodopa 66-72 tyrosine hydroxylase Mus musculus 0-20 26622527-9 2015 In the rat plasma, TH and COMT peaked at 1 h, while AADC peaked at 5 h. In conclusion, the results of the present study indicate that the co-administration of L-dopa and beta-asarone may be used to maintain a stable striatal DA level within 48 h. In addition, this treatment may promote DA generation by AADC and reduce the metabolism of DA by COMT. Levodopa 159-165 catechol-O-methyltransferase Rattus norvegicus 26-30 26622527-9 2015 In the rat plasma, TH and COMT peaked at 1 h, while AADC peaked at 5 h. In conclusion, the results of the present study indicate that the co-administration of L-dopa and beta-asarone may be used to maintain a stable striatal DA level within 48 h. In addition, this treatment may promote DA generation by AADC and reduce the metabolism of DA by COMT. Levodopa 159-165 dopa decarboxylase Rattus norvegicus 52-56 26622527-9 2015 In the rat plasma, TH and COMT peaked at 1 h, while AADC peaked at 5 h. In conclusion, the results of the present study indicate that the co-administration of L-dopa and beta-asarone may be used to maintain a stable striatal DA level within 48 h. In addition, this treatment may promote DA generation by AADC and reduce the metabolism of DA by COMT. Levodopa 159-165 dopa decarboxylase Rattus norvegicus 304-308 26622527-9 2015 In the rat plasma, TH and COMT peaked at 1 h, while AADC peaked at 5 h. In conclusion, the results of the present study indicate that the co-administration of L-dopa and beta-asarone may be used to maintain a stable striatal DA level within 48 h. In addition, this treatment may promote DA generation by AADC and reduce the metabolism of DA by COMT. Levodopa 159-165 catechol-O-methyltransferase Rattus norvegicus 344-348 26036788-4 2015 We found that precoating with 3,4-dihydroxy-l-phenylalanine (DOPA) facilitated the immobilization of poly-l-lysine and fibronectin on PLGA substrates via bio-inspired catechol chemistry. Levodopa 30-59 fibronectin 1 Homo sapiens 119-130 26036788-4 2015 We found that precoating with 3,4-dihydroxy-l-phenylalanine (DOPA) facilitated the immobilization of poly-l-lysine and fibronectin on PLGA substrates via bio-inspired catechol chemistry. Levodopa 61-65 fibronectin 1 Homo sapiens 119-130 26036788-5 2015 The DOPA-coated nanopatterned substrates directed cellular alignment along the patterned grooves by contact guidance, leading to enhanced focal adhesion, skeletal protein reorganization, and neuronal differentiation of hNSCs as indicated by highly extended neurites from cell bodies and increased expression of neuronal markers (Tuj1 and MAP2). Levodopa 4-8 microtubule associated protein 2 Homo sapiens 338-342 26516604-7 2015 The case highlights the sometimes limited sensitivity of morphologic imaging for identifying the functional consequences of tissue damage and confirms that DaT imaging may serve as a predictor for levodopa responsiveness in Holmes" tremor. Levodopa 197-205 solute carrier family 6 member 3 Homo sapiens 156-159 26468205-11 2015 These data unveil a role for TAAR1 in modulating the degeneration of dopaminergic neurons, the behavioral response to l-DOPA, and presynaptic and postsynaptic glutamate neurotransmission in the striatum, supporting their relevance to the pathophysiology and, potentially, management of PD. Levodopa 118-124 trace amine-associated receptor 1 Mus musculus 29-34 26468205-15 2015 Here, we report that TAAR1 potentiates the degeneration of dopaminergic neurons and attenuates the behavioral response to l-DOPA and presynaptic and postsynaptic glutamate neurotransmission in the striatum, supporting the relevance of TAAR1 to the pathophysiology and, potentially, management of PD. Levodopa 122-128 trace amine-associated receptor 1 Mus musculus 21-26 26500815-4 2015 Enzyme kinetic analysis indicated that leaf aqueous extract acts as a mixed type inhibitor, while ethanolic extract shows a competitive inhibition effect on mushroom tyrosinase using L-DOPA as substrate. Levodopa 183-189 tyrosinase Mus musculus 166-176 26119916-0 2015 The combination of lithium and l-Dopa/Carbidopa reduces MPTP-induced abnormal involuntary movements (AIMs) via calpain-1 inhibition in a mouse model: Relevance for Parkinson s disease therapy. Levodopa 31-37 calpain 1 Mus musculus 111-120 26220941-2 2015 For instance, mutations in genes critical for the synthesis of dopamine, including GCH1 and TH cause l-DOPA-responsive dystonia. Levodopa 101-107 GTP cyclohydrolase 1 Mus musculus 83-87 26071982-2 2015 Modulation of serotonin 1A (5-HT1A) receptors is regarded as an effective way to alleviate dyskinesia, yet this approach has been marred by a reduction of the therapeutic effectiveness of L-DOPA. Levodopa 188-194 5-hydroxytryptamine receptor 1A Homo sapiens 28-34 26394059-13 2015 The preoperative plasma levels of L-DOPA had significantly negative correlations with postoperative UPDRS- III score in off phase three months after STN-DBS. Levodopa 34-40 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 149-152 26001615-0 2015 Intranigral administration of substance P receptor antagonist attenuated levodopa-induced dyskinesia in a rat model of Parkinson"s disease. Levodopa 73-81 tachykinin receptor 1 Rattus norvegicus 30-50 26417536-4 2015 The second patient presented with levodopa-responsive paroxysmal oculogyria, a finding never before reported in ATP1A3-related disorders. Levodopa 34-42 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 112-118 26253444-10 2015 The serotonin/dopamine transporter ratio might be a potential marker of disease progression and an indicator of risk for levodopa-induced dyskinesia in PD. Levodopa 121-129 solute carrier family 6 member 3 Homo sapiens 14-34 26253446-0 2015 Serotonin/dopamine transporter ratio as a predictor of L-dopa-induced dyskinesia. Levodopa 55-61 solute carrier family 6 member 3 Homo sapiens 10-30 24972960-5 2015 The fact that chronic levodopa treatment disrupted CB1R-CB2R heteromeric complexes should be taken into consideration when designing new drugs acting on cannabinoid receptor heteromers. Levodopa 22-30 cannabinoid receptor 1 Homo sapiens 51-60 26037043-0 2015 NLX-112, a novel 5-HT1A receptor agonist for the treatment of L-DOPA-induced dyskinesia: Behavioral and neurochemical profile in rat. Levodopa 62-68 5-hydroxytryptamine receptor 1A Rattus norvegicus 17-23 26037043-6 2015 potently and completely reversed haloperidol-induced catalepsy in intact rats and abolished L-DOPA-induced Abnormal Involuntary Movements (AIMs) in hemiparkinsonian rats, an effect that was reversed by the selective 5-HT1A antagonist, WAY100635. Levodopa 92-98 5-hydroxytryptamine receptor 1A Rattus norvegicus 216-222 25982926-8 2015 Analysis of Parkinson"s disease cases alone indicated that serpin-A5 and serpin-A13, and trypsin-2 expression in midbrain and cerebral cortex was different in cases with a high incidence of L-DOPA-induced dyskinesia and psychosis compared to those with low levels of these treatment-induced side effects. Levodopa 190-196 serpin family A member 5 Homo sapiens 59-68 25982926-8 2015 Analysis of Parkinson"s disease cases alone indicated that serpin-A5 and serpin-A13, and trypsin-2 expression in midbrain and cerebral cortex was different in cases with a high incidence of L-DOPA-induced dyskinesia and psychosis compared to those with low levels of these treatment-induced side effects. Levodopa 190-196 serpin family A member 13, pseudogene Homo sapiens 73-83 25982926-8 2015 Analysis of Parkinson"s disease cases alone indicated that serpin-A5 and serpin-A13, and trypsin-2 expression in midbrain and cerebral cortex was different in cases with a high incidence of L-DOPA-induced dyskinesia and psychosis compared to those with low levels of these treatment-induced side effects. Levodopa 190-196 serine protease 2 Homo sapiens 89-98 25939726-6 2015 FOG Questionnaire and UPDRS subscores related to gait and postural stability significantly improved during Levodopa-carbidopa intrajejunal gel infusion in all patients compared to O-LD treatment. Levodopa 107-115 zinc finger protein, FOG family member 1 Homo sapiens 0-3 26306801-4 2015 The H50Q SNCA mutation case had a clinical picture that mimicked late-onset idiopathic PD with a good and sustained levodopa response. Levodopa 116-124 synuclein alpha Homo sapiens 9-13 26283356-7 2015 These molecular and functional alterations lead to a severe feeding deficit in adult Foxa1/2 mutant mice, independently of motor control, which could be rescued by L-DOPA treatment. Levodopa 164-170 forkhead box A1 Mus musculus 85-92 26306801-5 2015 The SNCA duplication case presented with a clinical phenotype of frontotemporal dementia with marked behavioural changes, pyramidal signs, postural hypotension and transiently levodopa responsive parkinsonism. Levodopa 176-184 synuclein alpha Homo sapiens 4-8 26336641-6 2015 levodopa when given with adequate peripheral inhibition of DOPA decarboxylase. Levodopa 0-8 dopa decarboxylase Homo sapiens 59-77 26788349-4 2015 We present a case of inappropriate laughter lacking mirth as a levodopa OFF phenomenon in a patient with PD, whose laughter also worsened with STN-DBS in his non-medicated state. Levodopa 63-71 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 143-146 26308525-9 2015 The regression coefficients of baseline CRP for the two periods were 1.41 (95% confidence interval [CI] 0.21-2.61) and 2.62 (95% CI 0.25-4.98), respectively, after adjusting for sex, age, baseline UPDRS-III score, dementia, and incremental L-dopa equivalent dose. Levodopa 240-246 C-reactive protein Homo sapiens 40-43 26788349-6 2015 The case demonstrates pseudobulbar laughter as a levodopa OFF phenomenon that is also exacerbated by STN-DBS. Levodopa 49-57 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 101-104 25976300-2 2015 Motor symptoms of PD are most commonly controlled by L-3,4-dihydroxyphenylalanine (Levodopa, L-DOPA), a precursor of dopamine, plus a peripherally-acting aromatic-L-amino-acid decarboxylase (dopa decarboxylase) inhibitor, such as carbidopa. Levodopa 83-91 dopa decarboxylase Mus musculus 191-209 26235617-4 2015 Application of L-DOPA augmented the D2-receptor-mediated inhibitory postsynaptic current (IPSC) in dopamine neurons of the substantia nigra. Levodopa 15-21 dopamine receptor D2 Mus musculus 36-47 26235617-6 2015 Selective optogenetic stimulation of 5-HT terminals evoked dopamine release, producing D2-receptor-mediated IPSCs following treatment with L-DOPA. Levodopa 139-145 dopamine receptor D2 Mus musculus 87-98 26235617-7 2015 In the dorsal raphe, L-DOPA produced a long-lasting depression of the 5-HT1A-receptor-mediated IPSC in 5-HT neurons. Levodopa 21-27 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 70-85 26235617-8 2015 When D2 receptors were expressed in the dorsal raphe, application of L-DOPA resulted in a D2-receptor-mediated IPSC. Levodopa 69-75 dopamine receptor D2 Mus musculus 90-101 25960345-4 2015 Here we show that in normal wild-type (Pitx3WT) mice with adult-onset symmetric, bilateral 6-OHDA-induced DA lesion in the dorsal striatum, l-dopa induces normal horizontal movements and upward movements that are qualitatively identical to those in Pitx3Null mice. Levodopa 140-146 paired-like homeodomain transcription factor 3 Mus musculus 39-44 25962878-5 2015 At the behavioral level, ANR 94 and MSX-3 given alone significantly potentiated L-DOPA-induced turning behavior. Levodopa 80-86 msh homeobox 3 Rattus norvegicus 36-41 25962878-6 2015 Combination of either A2A R antagonists with MPEP synergistically increased L-DOPA-induced turning. Levodopa 76-82 adenosine A2a receptor Rattus norvegicus 22-27 25787808-4 2015 Consequently, inhibitors of MAPK signaling cascade that block the aberrant supersensitive response of direct pathway striatal neurons could provide a novel therapeutic adjunct to L-DOPA in the treatment of PD. Levodopa 179-185 mitogen activated protein kinase 3 Rattus norvegicus 28-32 25787808-8 2015 This lower AIM severity was related to a decrease in L-DOPA-induced increase in the following: (1) striatal pERK1/2 and (2) FosB levels. Levodopa 53-59 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 124-128 25914172-13 2015 These findings demonstrated that HSYA provided anti-dyskinetic relief against L-DOPA in a preclinical model of PD via regulating the expression of the dopamine D3 receptor. Levodopa 78-84 dopamine receptor D3 Rattus norvegicus 151-171 25960345-5 2015 Furthermore, after unilateral 6-OHDA lesion of the residual DA innervation in the striatum in Pitx3Null mice, l-dopa induces contraversive rotation that is similar to that in Pitx3WT mice with the classic unilateral 6-OHDA lesion. Levodopa 110-116 paired-like homeodomain transcription factor 3 Mus musculus 94-99 25960345-6 2015 These results indicate that in Pitx3Null mice, the bilateral symmetric DA denervation in the dorsal striatum is sufficient for expressing the l-dopa-induced motor phenotype and the perinatal timing of their DA loss is not a determining factor, providing further evidence that Pitx3Null mice are a convenient and suitable mouse model to study the consequences of DA loss and dopaminergic replacement therapy in Parkinson"s disease. Levodopa 142-148 paired-like homeodomain transcription factor 3 Mus musculus 31-36 25907446-0 2015 Effect of serotonin transporter blockade on L-DOPA-induced dyskinesia in animal models of Parkinson"s disease. Levodopa 44-50 solute carrier family 6 member 4 Rattus norvegicus 10-31 25907446-1 2015 Serotonin transporter blockade with selective serotonin reuptake inhibitors (SSRIs) was recently shown to counteract L-DOPA-induced dyskinesia in 6-hydroxydopamine (6-OHDA)-lesioned rats. Levodopa 117-123 solute carrier family 6 member 4 Rattus norvegicus 0-21 26009769-0 2015 Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson"s disease induced by L-DOPA? Levodopa 99-105 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 4-20 26217176-0 2015 NMDA receptor GluN2A/GluN2B subunit ratio as synaptic trait of levodopa-induced dyskinesias: from experimental models to patients. Levodopa 63-71 glutamate ionotropic receptor NMDA type subunit 2A Homo sapiens 14-20 26217176-0 2015 NMDA receptor GluN2A/GluN2B subunit ratio as synaptic trait of levodopa-induced dyskinesias: from experimental models to patients. Levodopa 63-71 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 21-27 26217176-4 2015 Here we demonstrate an altered ratio of synaptic GluN2A/GluN2B-containing NMDA receptors in the striatum of levodopa-treated dyskinetic rats and monkeys as well as in post-mortem tissue from dyskinetic PD patients. Levodopa 108-116 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 49-55 26217176-4 2015 Here we demonstrate an altered ratio of synaptic GluN2A/GluN2B-containing NMDA receptors in the striatum of levodopa-treated dyskinetic rats and monkeys as well as in post-mortem tissue from dyskinetic PD patients. Levodopa 108-116 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 56-62 26009769-9 2015 These results suggest that increased COX2 expression after L-DOPA long-term treatment in Parkinsonian-like rats could contribute to the development of dyskinesia. Levodopa 59-65 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 37-41 26010069-5 2015 RESULTS: The new p.L34R (c.101 T>G) FBXO7 mutation was detected in a homozygous state in two Turkish sibs with typical levodopa-responsive PD. Levodopa 119-127 F-box protein 7 Homo sapiens 36-41 25913862-2 2015 When the monophenolase and the diphenolase activities of tyrosinase on its physiological substrates l-dopa and/or l-tyrosine are measured in the presence of these compounds, the rate of action of the enzyme decreases. Levodopa 100-106 tyrosinase Homo sapiens 57-67 26112716-9 2015 Furthermore, the increase in Nurr1 mRNA expression was seen in DA agonist and L-dopa group. Levodopa 78-84 nuclear receptor subfamily 4 group A member 2 Homo sapiens 29-34 26112716-10 2015 Multivariate linear regression showed DA agonists, L-dopa, and DA agonists were independent predictors correlated with Nurr1 mRNA expression level in PBMC. Levodopa 51-57 nuclear receptor subfamily 4 group A member 2 Homo sapiens 119-124 26024204-1 2015 Tyrosine hydroxylase is a mononuclear non-heme iron monooxygenase found in the central nervous system that catalyzes the hydroxylation of tyrosine to yield L-3,4-dihydroxyphenylalanine, the rate-limiting step in the biosynthesis of catecholamine neurotransmitters. Levodopa 156-184 tyrosine hydroxylase Homo sapiens 0-20 25697393-0 2015 The NR2B antagonist, ifenprodil, corrects the l-DOPA-induced deficit of bilateral movement and reduces c-Fos expression in the subthalamic nucleus of hemiparkinsonian rats. Levodopa 46-52 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 4-8 25697393-5 2015 Next, in order to identify the brain area influenced by L-DOPA and ifenprodil, quantitative analysis of L-DOPA-induced c-Fos immunoreactivity was performed in various brain areas of hemi-PD following administration of L-dopa with and without ifenprodil. Levodopa 104-110 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 25697393-6 2015 Among brain areas with robust c-Fos expression within the motor loop circuit in dopamine-depleted hemispheres, co-administered ifenprodil markedly attenuated L-DOPA-induced c-Fos expression in only the subthalamic nucleus (STN), suggesting that the STN is the primary target for the anti-parkinsonian action of NR2B antagonists. Levodopa 158-164 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 173-178 25697393-6 2015 Among brain areas with robust c-Fos expression within the motor loop circuit in dopamine-depleted hemispheres, co-administered ifenprodil markedly attenuated L-DOPA-induced c-Fos expression in only the subthalamic nucleus (STN), suggesting that the STN is the primary target for the anti-parkinsonian action of NR2B antagonists. Levodopa 158-164 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 311-315 25772224-13 2015 These results shed light on the regulation of Galphaolf by dopamine signaling that could be involved in the pathophysiology of the maladaptive response to chronic l-dopa treatment in Parkinson"s disease. Levodopa 163-169 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 46-55 25813704-0 2015 Evidence for a role for alpha6(*) nAChRs in l-dopa-induced dyskinesias using Parkinsonian alpha6(*) nAChR gain-of-function mice. Levodopa 44-50 cholinergic receptor, nicotinic, alpha polypeptide 6 Mus musculus 24-39 25813704-10 2015 However, the nAChR antagonist mecamylamine (1mg/kg ip 30min before l-dopa) reduced l-dopa-induced AIMs in both alpha6L9S and WT mice. Levodopa 83-89 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 13-18 25442325-6 2015 The carbi and L-dopa treatments completely suppressed GH-releasing responses to GHRH in both male and female goats (P < 0.05). Levodopa 14-20 growth hormone Capra hircus 54-56 26043205-0 2015 GRK3 suppresses L-DOPA-induced dyskinesia in the rat model of Parkinson"s disease via its RGS homology domain. Levodopa 16-22 G protein-coupled receptor kinase 3 Rattus norvegicus 0-4 26043205-7 2015 Kinase-dead GRK3 and its separated RGS homology domain (RH) suppressed sensitization to L-DOPA, whereas GRK3 with disabled RH did not. Levodopa 88-94 G protein-coupled receptor kinase 3 Rattus norvegicus 12-16 26125041-0 2015 Differential involvement of Ras-GRF1 and Ras-GRF2 in L-DOPA-induced dyskinesia. Levodopa 53-59 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 28-36 26125041-0 2015 Differential involvement of Ras-GRF1 and Ras-GRF2 in L-DOPA-induced dyskinesia. Levodopa 53-59 RAS protein-specific guanine nucleotide-releasing factor 2 Mus musculus 41-49 26125041-1 2015 OBJECTIVE: Recent findings have shown that pharmacogenetic manipulations of the Ras-ERK pathway provide a therapeutic means to tackle l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID). Levodopa 134-162 mitogen-activated protein kinase 1 Mus musculus 84-87 26125041-1 2015 OBJECTIVE: Recent findings have shown that pharmacogenetic manipulations of the Ras-ERK pathway provide a therapeutic means to tackle l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID). Levodopa 164-170 mitogen-activated protein kinase 1 Mus musculus 84-87 26125041-2 2015 First, we investigated whether a prolonged l-DOPA treatment differentially affected ERK signaling in medium spiny neurons of the direct pathway (dMSNs) and in cholinergic aspiny interneurons (ChIs) and assessed the role of Ras-GRF1 in both subpopulations. Levodopa 43-49 mitogen-activated protein kinase 1 Mus musculus 84-87 26125041-10 2015 Accordingly, Ras-GRF1 but not Ras-GRF2 striatal gene-knockdown reduced l-DOPA-induced GABA and glutamate release in the substantia nigra pars reticulata, a neurochemical correlate of dyskinesia. Levodopa 71-77 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 13-21 25442325-6 2015 The carbi and L-dopa treatments completely suppressed GH-releasing responses to GHRH in both male and female goats (P < 0.05). Levodopa 14-20 somatoliberin Capra hircus 80-84 25442325-9 2015 The treatments with carbi and L-dopa significantly reduced TRH-induced PRL release in goats (P < 0.05). Levodopa 30-36 prolactin Capra hircus 71-74 25701434-8 2015 For example, a mixture of 1 muM PMHC with 10 muM L-DOPA causes 18-fold elongation of suppression time as compared to 1 muM PMHC used alone. Levodopa 49-55 latexin Homo sapiens 28-31 26164425-5 2015 In combination with levodopa, MAO-B inhibitors may improve motor fluctuations and allow for lower total doses of levodopa. Levodopa 113-121 monoamine oxidase B Homo sapiens 30-35 25701434-8 2015 For example, a mixture of 1 muM PMHC with 10 muM L-DOPA causes 18-fold elongation of suppression time as compared to 1 muM PMHC used alone. Levodopa 49-55 latexin Homo sapiens 45-48 25701434-8 2015 For example, a mixture of 1 muM PMHC with 10 muM L-DOPA causes 18-fold elongation of suppression time as compared to 1 muM PMHC used alone. Levodopa 49-55 latexin Homo sapiens 45-48 25645393-0 2015 Activity of serotonin 5-HT(1A) receptor "biased agonists" in rat models of Parkinson"s disease and L-DOPA-induced dyskinesia. Levodopa 99-105 5-hydroxytryptamine receptor 1A Rattus norvegicus 12-39 25645393-16 2015 Preferential activation of 5-HT1A autoreceptors could potentially translate to superior antidyskinetic and L-DOPA dose-sparing effects in PD patients. Levodopa 107-113 5-hydroxytryptamine receptor 1A Homo sapiens 27-33 25510857-4 2015 RESULTS: The COMT 158val allele was associated with an increased startle potentiation by unpleasant stimuli as compared with neutral stimuli irrespective of L-dopa or placebo intervention. Levodopa 157-163 catechol-O-methyltransferase Homo sapiens 13-17 25510857-5 2015 COMT 158met/met genotype carriers, while displaying no difference in startle magnitude in response to unpleasant or neutral pictures in the placebo condition, showed startle potentiation by unpleasant pictures under L-dopa administration only. Levodopa 216-222 catechol-O-methyltransferase Homo sapiens 0-4 25510857-6 2015 CONCLUSIONS: The present proof-of-concept study provides preliminary support for a complex, multilevel impact of the dopaminergic system on the emotion-potentiated startle reflex suggesting increased phasic dopamine transmission driven by the more active COMT 158val allele and/or a single dose of L-dopa to predispose to maladaptive emotional processing and thereby potentially also to anxiety-related psychopathological states. Levodopa 298-304 catechol-O-methyltransferase Homo sapiens 255-259 25805645-4 2015 The objective of the present study was to determine whether genetic variants of the dopamine transporter type 1-encoding gene (SLC6A3) are associated with differences in the response to treatment of motor symptoms and gait disorders with l-DOPA and methylphenidate (with respect to the demographic, the disease and the treatment parameters and the other genes involved in the dopaminergic neurotransmission). Levodopa 238-244 solute carrier family 6 member 3 Homo sapiens 127-133 25826232-2 2015 The particles are built up by enzymatic reaction of l-DOPA with tyrosinase. Levodopa 52-58 tyrosinase Homo sapiens 64-74 25938891-3 2015 The chemical oxidative polymerization of L-DOPA (PDC) by NaAuCl4 in GOx-containing neutral aqueous solution is used to immobilize GOx and gold nanoparticles (AuNPs). Levodopa 41-47 hydroxyacid oxidase 1 Homo sapiens 68-71 25938891-3 2015 The chemical oxidative polymerization of L-DOPA (PDC) by NaAuCl4 in GOx-containing neutral aqueous solution is used to immobilize GOx and gold nanoparticles (AuNPs). Levodopa 41-47 hydroxyacid oxidase 1 Homo sapiens 130-133 25918399-0 2015 Targeting beta-arrestin2 in the treatment of L-DOPA-induced dyskinesia in Parkinson"s disease. Levodopa 45-51 arrestin, beta 2 Mus musculus 10-24 25918399-5 2015 Here we show in a bilateral DA-depletion mouse model of Parkinson"s symptoms that genetic deletion of beta-arrestin2 significantly limits the beneficial locomotor effects while markedly enhancing the dyskinesia-like effects of acute or chronic L-DOPA treatment. Levodopa 244-250 arrestin, beta 2 Mus musculus 102-116 25805645-10 2015 The SLC6A3 variants were significantly associated with greater efficacy of l-DOPA for motor symptoms. Levodopa 75-81 solute carrier family 6 member 3 Homo sapiens 4-10 25805645-11 2015 The SLC6A3 variants were also associated with greater efficacy of methylphenidate for motor symptoms and gait disorders in the ON l-DOPA condition. Levodopa 130-136 solute carrier family 6 member 3 Homo sapiens 4-10 25805645-13 2015 Our preliminary results suggest that variants of SLC6A3 are genetic modifiers of the treatment response to l-DOPA and methylphenidate in Parkinson"s disease. Levodopa 107-113 solute carrier family 6 member 3 Homo sapiens 49-55 25649051-1 2015 BACKGROUND AND PURPOSE: Opicapone (OPC) is a novel third generation catechol-O-methyltransferase (COMT) inhibitor that enhances levodopa availability. Levodopa 128-136 catechol-O-methyltransferase Homo sapiens 68-96 25861706-8 2015 When the two therapies were combined, GPI-DBS prevented the L-DOPA induced increase in static sway and improved the accuracy of the dynamic task. Levodopa 60-66 glucose-6-phosphate isomerase Homo sapiens 38-41 25861706-9 2015 CONCLUSION: The findings demonstrate GPI-DBS and L-DOPA have differential effects on temporal and spatial aspects of postural control in IPD and that GPI-DBS counteracts some of the adverse effects of L-DOPA. Levodopa 201-207 glucose-6-phosphate isomerase Homo sapiens 150-153 25649051-1 2015 BACKGROUND AND PURPOSE: Opicapone (OPC) is a novel third generation catechol-O-methyltransferase (COMT) inhibitor that enhances levodopa availability. Levodopa 128-136 catechol-O-methyltransferase Homo sapiens 98-102 25649051-11 2015 CONCLUSIONS: OPC is a promising new COMT inhibitor that significantly decreased COMT activity, increased systemic exposure to levodopa and improved motor response. Levodopa 126-134 catechol-O-methyltransferase Homo sapiens 36-40 25840672-3 2015 RESULTS: The groups were similar in age, education, disease duration, levodopa equivalent daily dose, and Unified Parkinson"s Disease Rating Scale (UPDRS) II-IV; however, the LRRK2-PD showed less impairment on UPDRS-I (2.0 +- 1.7 vs. 4.2 +- 2.8, p = 0.003). Levodopa 70-78 leucine rich repeat kinase 2 Homo sapiens 175-180 25592335-2 2015 In vivo viral vector-mediated gene expression encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) provides a drug delivery strategy of DOPA with distinct advantages over pharmacotherapy. Levodopa 150-154 tyrosine hydroxylase Homo sapiens 55-75 25592335-2 2015 In vivo viral vector-mediated gene expression encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) provides a drug delivery strategy of DOPA with distinct advantages over pharmacotherapy. Levodopa 150-154 tyrosine hydroxylase Homo sapiens 77-79 25592335-2 2015 In vivo viral vector-mediated gene expression encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) provides a drug delivery strategy of DOPA with distinct advantages over pharmacotherapy. Levodopa 150-154 GTP cyclohydrolase 1 Homo sapiens 85-105 25592335-2 2015 In vivo viral vector-mediated gene expression encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) provides a drug delivery strategy of DOPA with distinct advantages over pharmacotherapy. Levodopa 150-154 GTP cyclohydrolase 1 Homo sapiens 107-111 25896846-6 2015 In addition, the increases in FosB expression and ERK1/2 phosphorylation in 6-OHDA-lesioned rats induced by L-DOPA administration were significantly reduced by co-treatment with GPS (25 and 50 mg/kg) or GP-EX (50 mg/kg). Levodopa 109-115 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 31-35 25896846-6 2015 In addition, the increases in FosB expression and ERK1/2 phosphorylation in 6-OHDA-lesioned rats induced by L-DOPA administration were significantly reduced by co-treatment with GPS (25 and 50 mg/kg) or GP-EX (50 mg/kg). Levodopa 109-115 mitogen activated protein kinase 3 Rattus norvegicus 51-57 25928000-7 2015 Insulin-like growth factor-1 (IGF-1) was 52.7 ng/ml, lower than the normal range (55 ~ 452 ng/ml) and the peak growth hormone level was 7.57 ng/ml at 90 minutes after taking moderate levodopa and pyridostigmine bromide. Levodopa 183-191 insulin like growth factor 1 Homo sapiens 0-28 25926720-5 2015 RESULTS: L-DOPA treatment enhanced surface levels of GluN1 expression and reduced its intracellular expression, but did not change total levels of GluN1 protein in the lesioned striatum. Levodopa 9-15 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 53-58 25926720-6 2015 In contrast, l-DOPA decreased GluN2A surface expression but increased its intracellular expression. Levodopa 13-19 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 30-36 25926720-7 2015 L-DOPA increased GluN2B expression preferentially in the surface compartment. Levodopa 0-6 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 17-23 25644418-9 2015 Our results show that chronic L-DOPA administration in rats with intra-nigral 6-OHDA-lesion caused significant increases in SWM deficit, nitrite levels and the immunoreactivity of 3-NT, iNOS and GFAP in the nigro-striatal-cortical pathway. Levodopa 30-36 nitric oxide synthase 2 Rattus norvegicus 186-190 25644418-9 2015 Our results show that chronic L-DOPA administration in rats with intra-nigral 6-OHDA-lesion caused significant increases in SWM deficit, nitrite levels and the immunoreactivity of 3-NT, iNOS and GFAP in the nigro-striatal-cortical pathway. Levodopa 30-36 glial fibrillary acidic protein Rattus norvegicus 195-199 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 57-88 G protein-coupled receptor 143 Homo sapiens 26-29 25409768-1 2015 BACKGROUND AND PURPOSE: Catechol-O-methyltransferase (COMT) is an important target in the levodopa treatment of Parkinson"s disease; however, the inhibitors available have problems, and not all patients benefit from their efficacy. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 24-52 25409768-1 2015 BACKGROUND AND PURPOSE: Catechol-O-methyltransferase (COMT) is an important target in the levodopa treatment of Parkinson"s disease; however, the inhibitors available have problems, and not all patients benefit from their efficacy. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 54-58 25409768-11 2015 CONCLUSIONS AND IMPLICATIONS: Opicapone has a prolonged inhibitory effect on peripheral COMT, which extends the bioavailability of levodopa, without inducing toxicity. Levodopa 131-139 catechol-O-methyltransferase Rattus norvegicus 88-92 25637802-6 2015 Synaptic filtering on the lesioned side was abolished by either l-DOPA or a D2 receptor agonist, but when combined with a CB1 receptor antagonist, l-DOPA or D2 agonists normalized both synaptic filtering and behavior. Levodopa 147-153 cannabinoid receptor 1 (brain) Mus musculus 122-125 25576192-7 2015 Immunoblots probing for the Ste2p-[Bio-DOPA]11-mer complex revealed that novobiocin markedly decreased cross-linking of the [Bio-DOPA]11-mer to the receptor, but cross-linking of the alpha-factor analog [Bio-DOPA]13-mer, which interacts with the orthosteric binding site of the receptor, was minimally altered. Levodopa 35-43 alpha-factor pheromone receptor STE2 Saccharomyces cerevisiae S288C 28-33 25576965-0 2015 NR2B antagonist CP-101,606 inhibits NR2B phosphorylation at tyrosine-1472 and its interactions with Fyn in levodopa-induced dyskinesia rat model. Levodopa 107-115 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 0-4 25576965-0 2015 NR2B antagonist CP-101,606 inhibits NR2B phosphorylation at tyrosine-1472 and its interactions with Fyn in levodopa-induced dyskinesia rat model. Levodopa 107-115 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 36-40 25576965-0 2015 NR2B antagonist CP-101,606 inhibits NR2B phosphorylation at tyrosine-1472 and its interactions with Fyn in levodopa-induced dyskinesia rat model. Levodopa 107-115 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 100-103 25576965-1 2015 The augmented tyrosine phosphorylation of NR2B subunit of N-methyl-d-aspartate receptors (NMDAR) dependent on Fyn kinase has been associated with levodopa (l-dopa)-induced dyskinesia (LID). Levodopa 146-154 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 42-46 25576965-1 2015 The augmented tyrosine phosphorylation of NR2B subunit of N-methyl-d-aspartate receptors (NMDAR) dependent on Fyn kinase has been associated with levodopa (l-dopa)-induced dyskinesia (LID). Levodopa 146-154 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 110-113 25576965-1 2015 The augmented tyrosine phosphorylation of NR2B subunit of N-methyl-d-aspartate receptors (NMDAR) dependent on Fyn kinase has been associated with levodopa (l-dopa)-induced dyskinesia (LID). Levodopa 156-162 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 42-46 25576965-1 2015 The augmented tyrosine phosphorylation of NR2B subunit of N-methyl-d-aspartate receptors (NMDAR) dependent on Fyn kinase has been associated with levodopa (l-dopa)-induced dyskinesia (LID). Levodopa 156-162 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 110-113 25576965-10 2015 In agreement with behavioral analysis, CP-101,606 reduced the augmented pNR2B-Tyr1472 and its interactions with Fyn triggered during the l-dopa administration in the lesioned striatum of parkinsonian rats. Levodopa 137-143 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 112-115 25669730-3 2015 Simultaneous activation of 5-HT1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine depletion, justifying a clinical study with eltoprazine, a 5-HT1A/B receptor agonist, against L-DOPA-induced dyskinesias in patients with Parkinson"s disease. Levodopa 74-80 5-hydroxytryptamine receptor 1A Homo sapiens 27-33 25669730-3 2015 Simultaneous activation of 5-HT1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine depletion, justifying a clinical study with eltoprazine, a 5-HT1A/B receptor agonist, against L-DOPA-induced dyskinesias in patients with Parkinson"s disease. Levodopa 224-230 5-hydroxytryptamine receptor 1A Homo sapiens 27-33 25687550-0 2015 Overexpression of GRK6 rescues L-DOPA-induced signaling abnormalities in the dopamine-depleted striatum of hemiparkinsonian rats. Levodopa 31-37 G protein-coupled receptor kinase 6 Rattus norvegicus 18-22 25687550-4 2015 Here we show that 2-fold lentivirus-mediated overexpression of GRK6 in the dopamine-depleted striatum in rats unilaterally lesioned with 6-hydroxydopamine ameliorated supersensitive ERK response to l-DOPA challenge caused by loss of dopamine. Levodopa 198-204 G protein-coupled receptor kinase 6 Rattus norvegicus 63-67 25687550-5 2015 A somewhat stronger effect of GRK6 was observed in drug-naive than in chronically l-DOPA-treated animals. Levodopa 82-88 G protein-coupled receptor kinase 6 Rattus norvegicus 30-34 25687550-6 2015 GRK6 reduced the responsiveness of p38 MAP kinase to l-DOPA challenge rendered supersensitive by dopamine depletion. Levodopa 53-59 G protein-coupled receptor kinase 6 Rattus norvegicus 0-4 25687550-6 2015 GRK6 reduced the responsiveness of p38 MAP kinase to l-DOPA challenge rendered supersensitive by dopamine depletion. Levodopa 53-59 mitogen activated protein kinase 14 Rattus norvegicus 35-38 25687550-9 2015 Finally, GRK6 reduced accumulation of DeltaFosB in the lesioned striatum, the effect that paralleled a decrease in locomotor sensitization to l-DOPA in GRK6-expressing rats. Levodopa 142-148 G protein-coupled receptor kinase 6 Rattus norvegicus 9-13 25687550-9 2015 Finally, GRK6 reduced accumulation of DeltaFosB in the lesioned striatum, the effect that paralleled a decrease in locomotor sensitization to l-DOPA in GRK6-expressing rats. Levodopa 142-148 G protein-coupled receptor kinase 6 Rattus norvegicus 152-156 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 57-88 G protein-coupled receptor 143 Homo sapiens 172-175 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 90-94 G protein-coupled receptor 143 Homo sapiens 26-29 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 90-94 G protein-coupled receptor 143 Homo sapiens 172-175 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 134-138 G protein-coupled receptor 143 Homo sapiens 26-29 25601010-3 2015 It has been reported that OA1 is a specific receptor for 3, 4-dihydroxy- L-phenylalanine (DOPA) in retinal pigmental epithelium where DOPA facilitates the pigmentation via OA1 stimulation. Levodopa 134-138 G protein-coupled receptor 143 Homo sapiens 172-175 25601010-4 2015 We have recently shown that OA1 mediates DOPA-induced depressor response in rat nucleus tractus solitarii. Levodopa 41-45 G protein-coupled receptor 143 Mus musculus 28-31 25601010-10 2015 The expression of OA1 in the nucleus tractus solitarii of medulla oblongata may support the reduction of blood pressure by the microinjection of DOPA into this region. Levodopa 145-149 G protein-coupled receptor 143 Homo sapiens 18-21 25790475-2 2015 The single RING finger type E3 ubiquitin-protein ligase PARK2 is mutated in a Parkinson"s disease (PD) variant and was found to interact with ATXN2, a protein where polyglutamine expansions cause Spinocerebellar ataxia type 2 (SCA2) or increase the risk for Levodopa-responsive PD and for the motor neuron disease Amyotrophic lateral sclerosis (ALS). Levodopa 258-266 parkin RBR E3 ubiquitin protein ligase Mus musculus 56-61 32262068-1 2015 High-intensity fluorescent carbon dots (CDs) coupled with tyrosinase (TYR) yielded hybrids, as a fluorescent probe, which were efficient, fast, stable and sensitive in the detection of levodopa (l-DOPA). Levodopa 185-193 tyrosinase Homo sapiens 58-68 32262068-1 2015 High-intensity fluorescent carbon dots (CDs) coupled with tyrosinase (TYR) yielded hybrids, as a fluorescent probe, which were efficient, fast, stable and sensitive in the detection of levodopa (l-DOPA). Levodopa 185-193 tyrosinase Homo sapiens 70-73 32262068-1 2015 High-intensity fluorescent carbon dots (CDs) coupled with tyrosinase (TYR) yielded hybrids, as a fluorescent probe, which were efficient, fast, stable and sensitive in the detection of levodopa (l-DOPA). Levodopa 195-201 tyrosinase Homo sapiens 58-68 32262068-1 2015 High-intensity fluorescent carbon dots (CDs) coupled with tyrosinase (TYR) yielded hybrids, as a fluorescent probe, which were efficient, fast, stable and sensitive in the detection of levodopa (l-DOPA). Levodopa 195-201 tyrosinase Homo sapiens 70-73 25790475-2 2015 The single RING finger type E3 ubiquitin-protein ligase PARK2 is mutated in a Parkinson"s disease (PD) variant and was found to interact with ATXN2, a protein where polyglutamine expansions cause Spinocerebellar ataxia type 2 (SCA2) or increase the risk for Levodopa-responsive PD and for the motor neuron disease Amyotrophic lateral sclerosis (ALS). Levodopa 258-266 ataxin 2 Mus musculus 142-147 25790475-2 2015 The single RING finger type E3 ubiquitin-protein ligase PARK2 is mutated in a Parkinson"s disease (PD) variant and was found to interact with ATXN2, a protein where polyglutamine expansions cause Spinocerebellar ataxia type 2 (SCA2) or increase the risk for Levodopa-responsive PD and for the motor neuron disease Amyotrophic lateral sclerosis (ALS). Levodopa 258-266 ataxin 2 Mus musculus 196-225 25790475-2 2015 The single RING finger type E3 ubiquitin-protein ligase PARK2 is mutated in a Parkinson"s disease (PD) variant and was found to interact with ATXN2, a protein where polyglutamine expansions cause Spinocerebellar ataxia type 2 (SCA2) or increase the risk for Levodopa-responsive PD and for the motor neuron disease Amyotrophic lateral sclerosis (ALS). Levodopa 258-266 ataxin 2 Mus musculus 227-231 25637699-8 2015 In synuclein overexpressing PC12 cells, levodopa and 5-hydroxytryptophan elicited pargyline-sensitive alpha-synuclein oligomerization. Levodopa 40-48 synuclein alpha Rattus norvegicus 102-117 25424835-0 2015 beta-asarone and levodopa co-administration protects against 6-hydroxydopamine-induced damage in parkinsonian rat mesencephalon by regulating autophagy: down-expression Beclin-1 and light chain 3B and up-expression P62. Levodopa 17-25 beclin 1 Rattus norvegicus 169-177 25424835-0 2015 beta-asarone and levodopa co-administration protects against 6-hydroxydopamine-induced damage in parkinsonian rat mesencephalon by regulating autophagy: down-expression Beclin-1 and light chain 3B and up-expression P62. Levodopa 17-25 KH RNA binding domain containing, signal transduction associated 1 Rattus norvegicus 215-218 25424835-10 2015 The results showed that Beclin-1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l-dopa, beta-asarone, and co-administered groups when compared with the 6-OHDA model. Levodopa 127-133 KH RNA binding domain containing, signal transduction associated 1 Rattus norvegicus 72-75 25648938-6 2015 Cox"s regression models showed that the urinary domain was associated with a higher probability of starting L-dopa (hazard ratio: 2.1; P = 0.002). Levodopa 108-114 cytochrome c oxidase subunit 8A Homo sapiens 0-3 27747611-10 2015 CONCLUSION: To avoid major drug-to-drug interactions, patients receiving preparations of levodopa and benserazide should be prescribed angiotensin-converting enzyme inhibitors, antagonists of AT1 receptor for angiotensin II, or antagonists of beta-adrenoreceptors (beta-adrenolytics) as the first-line agents of antihypertensive treatment. Levodopa 89-97 angiotensinogen Homo sapiens 209-223 25505120-7 2015 Nonbursty MSNs fired irregularly with marked pausing that increased in the on state in the MSN subset with a levodopa response compatible with dopamine D2 receptor activation (indirect pathway MSNs), although the pause increase was not sustained in some units during the appearance of dyskinesias. Levodopa 109-117 moesin Homo sapiens 10-13 25505120-7 2015 Nonbursty MSNs fired irregularly with marked pausing that increased in the on state in the MSN subset with a levodopa response compatible with dopamine D2 receptor activation (indirect pathway MSNs), although the pause increase was not sustained in some units during the appearance of dyskinesias. Levodopa 109-117 dopamine receptor D2 Homo sapiens 143-163 25866725-7 2015 MATERIALS AND METHODS: The inhibitory activities of hydroalcoholic extracts of plants against oxidation of L-Dopa (as a substrate) by mushroom tyrosinase were investigated. Levodopa 107-113 tyrosinase Homo sapiens 143-153 25578290-1 2015 OBJECTIVE: We report a prospective, open label study of 24 h levodopa-carbidopa intestinal gel (LCIG) as treatment for levodopa "unresponsive" freezing of gait (FOG) associated with Parkinson"s disease. Levodopa 61-69 zinc finger protein, FOG family member 1 Homo sapiens 161-164 25578290-1 2015 OBJECTIVE: We report a prospective, open label study of 24 h levodopa-carbidopa intestinal gel (LCIG) as treatment for levodopa "unresponsive" freezing of gait (FOG) associated with Parkinson"s disease. Levodopa 119-127 zinc finger protein, FOG family member 1 Homo sapiens 161-164 25578290-2 2015 METHOD: 5 patients with disabling FOG, documented as being levodopa "unresponsive", were commenced on continuous 24 h infusion LCIG therapy with the night-time rate at 50-80% of the daytime infusion rate. Levodopa 59-67 zinc finger protein, FOG family member 1 Homo sapiens 34-37 25596881-8 2015 However, once levodopa treatment was initiated, higher p-tau and p-tau/Abeta42 predicted subsequent decline on cognitive tasks involving both memory and executive functions. Levodopa 14-22 microtubule associated protein tau Homo sapiens 57-60 25596881-8 2015 However, once levodopa treatment was initiated, higher p-tau and p-tau/Abeta42 predicted subsequent decline on cognitive tasks involving both memory and executive functions. Levodopa 14-22 microtubule associated protein tau Homo sapiens 67-70 25603767-11 2015 Motor fluctuations (odds ratio (OR) 3.45; p = 0.036) and higher levodopa dose (OR 1.30/100 mg, p = 0.009) at baseline were independent risk factors of incident FOG. Levodopa 64-72 zinc finger protein, FOG family member 1 Homo sapiens 160-163 30363880-1 2015 MSA is a progressive neurodegenerative disorder characterized by autonomic failure and a variable combination of poor levodopa-responsive parkinsonism and cerebellar ataxia (CA). Levodopa 118-126 thyroid peroxidase Homo sapiens 0-3 25565255-1 2015 Negative allosteric modulators (NAMs) of metabotropic glutamate receptor 5 (mGlu5) have potential for the treatment of psychiatric diseases including depression, fragile X syndrome (FXS), anxiety, obsessive-compulsive disorders, and levodopa induced dyskinesia in Parkinson"s disease. Levodopa 233-241 glutamate metabotropic receptor 5 Rattus norvegicus 41-74 30363880-3 2015 Almost one third of MSA patients may benefit from l-dopa for the symptomatic treatment of parkinsonism, whereas physiotherapy remains the best therapeutic option for CA. Levodopa 50-56 thyroid peroxidase Homo sapiens 20-23 25503261-7 2015 Activation of somatodendritic 5-HT1A receptors in the dorsal raphe nucleus has an important role in the alleviation of extrapyramidal symptoms and levodopa-induced dyskinesia induced by antipsychotic treatment. Levodopa 147-155 5-hydroxytryptamine receptor 1A Homo sapiens 30-36 25303957-2 2015 We have previously demonstrated that the dopamine D4 receptor antagonist L-745,870 reduces the severity of L-DOPA-induced dyskinesia in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned macaque without compromising L-DOPA antiparkinsonian benefits. Levodopa 107-113 dopamine receptor D4 Rattus norvegicus 41-61 25303957-2 2015 We have previously demonstrated that the dopamine D4 receptor antagonist L-745,870 reduces the severity of L-DOPA-induced dyskinesia in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned macaque without compromising L-DOPA antiparkinsonian benefits. Levodopa 230-236 dopamine receptor D4 Rattus norvegicus 41-61 25414038-12 2015 The repetitive TMS experiments showed that a session of continuous but not intermittent or sham theta burst stimulation applied over the inferior frontal cortex was able to reduce the amount of dyskinesias induced by a supramaximal single dose of levodopa, suggesting that this area may play a key role in controlling the development of dyskinesias. Levodopa 247-255 PYD and CARD domain containing Homo sapiens 15-18 25559423-2 2015 This narrative review aims to discuss the role of COMT inhibitors on peripheral levodopa metabolism and continuous brain delivery of levodopa, and to describe their metabolic properties. Levodopa 80-88 catechol-O-methyltransferase Homo sapiens 50-54 25559423-2 2015 This narrative review aims to discuss the role of COMT inhibitors on peripheral levodopa metabolism and continuous brain delivery of levodopa, and to describe their metabolic properties. Levodopa 133-141 catechol-O-methyltransferase Homo sapiens 50-54 25559423-3 2015 Oral application of levodopa formulations with a dopa decarboxylase inhibitor (DDI) results in fluctuating levodopa plasma concentrations, predominantly due to the short half-life of levodopa and its slowing of gastric emptying. Levodopa 20-28 dopa decarboxylase Homo sapiens 49-67 25559423-3 2015 Oral application of levodopa formulations with a dopa decarboxylase inhibitor (DDI) results in fluctuating levodopa plasma concentrations, predominantly due to the short half-life of levodopa and its slowing of gastric emptying. Levodopa 107-115 dopa decarboxylase Homo sapiens 49-67 25559423-3 2015 Oral application of levodopa formulations with a dopa decarboxylase inhibitor (DDI) results in fluctuating levodopa plasma concentrations, predominantly due to the short half-life of levodopa and its slowing of gastric emptying. Levodopa 107-115 dopa decarboxylase Homo sapiens 49-67 25559423-6 2015 More continuous plasma behaviour was observed after the combination of levodopa/DDI formulations with COMT inhibitors. Levodopa 71-79 catechol-O-methyltransferase Homo sapiens 102-106 25559423-8 2015 These findings favour the concept of chronic levodopa/DDI application with concomitant inhibition of COMT and monoamine oxidase, since deamination of dopamine via this enzyme also generates free radicals. Levodopa 45-53 catechol-O-methyltransferase Homo sapiens 101-105 25546160-13 2015 Compared to MAO-B inhibitors, the HR for switching to levodopa was 0.38 (CI 0.34-0.43; p<0.001) for anticholinergics and 0.85 (CI 0.75-0.97; p=0.017) for nonergot DA. Levodopa 54-62 monoamine oxidase B Homo sapiens 12-17 25355370-3 2015 The peripheral metabolic pathways significantly decrease the amount of L-dopa reaching the brain; therefore, all of the current commercial formulations require an association with an inhibitor of dopa-decarboxylase, such as carbidopa. Levodopa 71-77 dopa decarboxylase Homo sapiens 196-214 25447236-9 2015 Furthermore, DAT-tg mice also show fine motor deficits on challenging beam traversal that are reversed with l-DOPA treatment. Levodopa 108-114 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 13-16 25486547-5 2015 In this study, we showed that the stimulation of peroxisome proliferator-activated receptors (PPAR), a family of transcription factors activated by anandamide, contributes to the anti-dyskinetic effects of URB+CPZ, and that the direct activation of the PPARgamma subtype by rosiglitazone (RGZ) alleviates levodopa-induced AIMs in 6-OHDA rats. Levodopa 305-313 peroxisome proliferator-activated receptor gamma Rattus norvegicus 94-98 25486547-6 2015 AIM reduction was associated with an attenuation of levodopa-induced increase of dynorphin, zif-268, and of ERK phosphorylation in the denervated striatum. Levodopa 52-60 Eph receptor B1 Rattus norvegicus 108-111 24906468-8 2015 The enhanced behavioral and neurochemical effects produced by D3-L-DOPA and the combination of selegiline/L-DOPA are attributed to decreased metabolism of released dopamine by MAO-B. Levodopa 65-71 monoamine oxidase B Rattus norvegicus 176-181 25196732-3 2015 Here, we investigated the ability of a daily co-treatment of the preferential neuronal NOS (nNOS) inhibitor, 7-nitroindazole (7-NI, 30 mg/kg), with L-DOPA (30 mg/kg) to counteract LID in unilaterally 6-OHDA-lesioned rats. Levodopa 148-154 nitric oxide synthase 1 Rattus norvegicus 78-90 25196732-3 2015 Here, we investigated the ability of a daily co-treatment of the preferential neuronal NOS (nNOS) inhibitor, 7-nitroindazole (7-NI, 30 mg/kg), with L-DOPA (30 mg/kg) to counteract LID in unilaterally 6-OHDA-lesioned rats. Levodopa 148-154 nitric oxide synthase 1 Rattus norvegicus 92-96 25196732-9 2015 At postsynaptic striatal sites, 7-NI prevented L-DOPA-induced Fos-B/DeltaFosB up-regulation in the motor cortex, nucleus accumbens and striatum. Levodopa 47-53 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 62-67 25486547-0 2015 Activation of PPAR gamma receptors reduces levodopa-induced dyskinesias in 6-OHDA-lesioned rats. Levodopa 43-51 peroxisome proliferator-activated receptor gamma Rattus norvegicus 14-24 24844602-0 2015 Derangement of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and extracellular signal-regulated kinase (ERK) dependent striatal plasticity in L-DOPA-induced dyskinesia. Levodopa 149-155 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 15-56 26180632-11 2015 However, levodopa"s effect on DA release differed significantly in a right midbrain region (p=0.002, corrected), where levodopa displaced RAC* by 59% in control subjects but increased BP ND by 74% in TS subjects. Levodopa 9-17 AKT serine/threonine kinase 1 Homo sapiens 138-142 26180632-11 2015 However, levodopa"s effect on DA release differed significantly in a right midbrain region (p=0.002, corrected), where levodopa displaced RAC* by 59% in control subjects but increased BP ND by 74% in TS subjects. Levodopa 119-127 AKT serine/threonine kinase 1 Homo sapiens 138-142 24857398-0 2015 Activation of DREAM (downstream regulatory element antagonistic modulator), a calcium-binding protein, reduces L-DOPA-induced dyskinesias in mice. Levodopa 111-117 Kv channel interacting protein 3, calsenilin Mus musculus 14-19 24857398-0 2015 Activation of DREAM (downstream regulatory element antagonistic modulator), a calcium-binding protein, reduces L-DOPA-induced dyskinesias in mice. Levodopa 111-117 Kv channel interacting protein 3, calsenilin Mus musculus 21-73 24844602-0 2015 Derangement of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and extracellular signal-regulated kinase (ERK) dependent striatal plasticity in L-DOPA-induced dyskinesia. Levodopa 149-155 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 58-66 24857398-1 2015 BACKGROUND: Previous studies have implicated the cyclic adenosine monophosphate/protein kinase A pathway as well as FosB and dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia. Levodopa 215-244 FBJ osteosarcoma oncogene B Mus musculus 116-120 24844602-0 2015 Derangement of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and extracellular signal-regulated kinase (ERK) dependent striatal plasticity in L-DOPA-induced dyskinesia. Levodopa 149-155 mitogen-activated protein kinase 1 Mus musculus 72-109 24857398-1 2015 BACKGROUND: Previous studies have implicated the cyclic adenosine monophosphate/protein kinase A pathway as well as FosB and dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia. Levodopa 215-244 dopamine receptor D1 Mus musculus 160-180 24857398-1 2015 BACKGROUND: Previous studies have implicated the cyclic adenosine monophosphate/protein kinase A pathway as well as FosB and dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia. Levodopa 246-252 dopamine receptor D1 Mus musculus 160-180 24844602-0 2015 Derangement of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and extracellular signal-regulated kinase (ERK) dependent striatal plasticity in L-DOPA-induced dyskinesia. Levodopa 149-155 mitogen-activated protein kinase 1 Mus musculus 111-114 24857398-7 2015 The impact of DREAM on L-DOPA efficacy was evaluated using the rotarod and the cylinder test after the establishment of dyskinesia and the molecular changes by immunohistochemistry and Western blot. Levodopa 23-29 Kv channel interacting protein 3, calsenilin Mus musculus 14-19 24857398-12 2015 CONCLUSIONS: The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated histone H3, and dynorphin-B in the striatum. Levodopa 56-62 Kv channel interacting protein 3, calsenilin Mus musculus 25-30 24844602-9 2015 Analysis of LTP in animals with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-independent, apparently stochastic involvement of ERK. Levodopa 111-117 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 147-155 24857398-12 2015 CONCLUSIONS: The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated histone H3, and dynorphin-B in the striatum. Levodopa 56-62 FBJ osteosarcoma oncogene B Mus musculus 131-135 25411385-7 2015 These results suggest that the overexpression of LAT1 in the renal cortex of the renalase KO mice might contribute to the enhanced l-DOPA availability/uptake and consequently to the activation of the renal dopaminergic system in the presence of renalase deficiency. Levodopa 131-137 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 49-53 24857398-12 2015 CONCLUSIONS: The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated histone H3, and dynorphin-B in the striatum. Levodopa 102-108 Kv channel interacting protein 3, calsenilin Mus musculus 25-30 24857398-12 2015 CONCLUSIONS: The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated histone H3, and dynorphin-B in the striatum. Levodopa 102-108 FBJ osteosarcoma oncogene B Mus musculus 131-135 24857398-13 2015 These data suggest that therapeutic approaches that activate DREAM may be useful to alleviate L-DOPA-induced dyskinesia without interfering with the therapeutic motor effects of L-DOPA. Levodopa 94-100 Kv channel interacting protein 3, calsenilin Mus musculus 61-66 25411385-7 2015 These results suggest that the overexpression of LAT1 in the renal cortex of the renalase KO mice might contribute to the enhanced l-DOPA availability/uptake and consequently to the activation of the renal dopaminergic system in the presence of renalase deficiency. Levodopa 131-137 renalase, FAD-dependent amine oxidase Mus musculus 81-89 24844602-9 2015 Analysis of LTP in animals with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-independent, apparently stochastic involvement of ERK. Levodopa 111-117 mitogen-activated protein kinase 1 Mus musculus 218-221 24844602-10 2015 CONCLUSIONS: These data not only demonstrate a central role for Ras-ERK signaling in striatal LTP, depotentiation, and LTP restored after L-DOPA treatment but also disclose multifaceted synaptic adaptations occurring in response to dopaminergic denervation and pulsatile administration of L-DOPA. Levodopa 138-144 mitogen-activated protein kinase 1 Mus musculus 68-71 24844602-10 2015 CONCLUSIONS: These data not only demonstrate a central role for Ras-ERK signaling in striatal LTP, depotentiation, and LTP restored after L-DOPA treatment but also disclose multifaceted synaptic adaptations occurring in response to dopaminergic denervation and pulsatile administration of L-DOPA. Levodopa 289-295 mitogen-activated protein kinase 1 Mus musculus 68-71 25445374-0 2015 Chronic levodopa treatment alters expression and function of dopamine D3 receptor in the MPTP/p mouse model of Parkinson"s disease. Levodopa 8-16 dopamine receptor D3 Mus musculus 61-81 25499739-1 2015 The adenosine A2A receptor antagonist, istradefylline, enhances anti-parkinsonian activity in patients with advanced Parkinson s disease (PD) already treated with combinations of L-DOPA and dopamine agonist drugs but who are still exhibiting prolonged "OFF" periods. Levodopa 179-185 adenosine A2a receptor Homo sapiens 4-26 26393346-0 2015 L-Dopa Stimulates Cortisol Secretion through Adrenocorticotropic Hormone Release in Short Children. Levodopa 0-6 proopiomelanocortin Homo sapiens 45-72 25046277-9 2015 [(3)H]-ketanserin specific binding to striatal and pallidal 5-HT2A receptors was increased in L-DOPA-treated MPTP monkeys as compared to controls, saline and L-DOPA+MPEP MPTP monkeys and no difference between the latter groups was observed; dyskinesia scores correlated positively with this binding. Levodopa 94-100 5-hydroxytryptamine receptor 2A Homo sapiens 60-66 25568106-0 2015 Gene expression analyses identify Narp contribution in the development of L-DOPA-induced dyskinesia. Levodopa 74-80 neuronal pentraxin 2 Mus musculus 34-38 25568106-8 2015 We confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-PCR in independent experiments. Levodopa 46-52 neuronal pentraxin 2 Mus musculus 23-28 25568106-9 2015 Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp knock-out mice compared with their wild-type littermates or after overexpression of a dominant-negative form of Narp in the striatum. Levodopa 20-26 neuronal pentraxin 2 Mus musculus 72-76 25568106-9 2015 Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp knock-out mice compared with their wild-type littermates or after overexpression of a dominant-negative form of Narp in the striatum. Levodopa 20-26 neuronal pentraxin 2 Mus musculus 189-193 25866756-2 2015 Both levodopa responsive Parkinson disease (PD) like phenotype and atypical parkinsonism have been described especially in SCA2, SCA3, and SCA17 with geographic differences in prevalence. Levodopa 5-13 ataxin 2 Homo sapiens 123-127 25866756-2 2015 Both levodopa responsive Parkinson disease (PD) like phenotype and atypical parkinsonism have been described especially in SCA2, SCA3, and SCA17 with geographic differences in prevalence. Levodopa 5-13 ataxin 3 Homo sapiens 129-133 25866756-2 2015 Both levodopa responsive Parkinson disease (PD) like phenotype and atypical parkinsonism have been described especially in SCA2, SCA3, and SCA17 with geographic differences in prevalence. Levodopa 5-13 ataxin 7 Homo sapiens 139-144 26393346-2 2015 Herein, we examined whether adrenocorticotropic hormone (ACTH) is implicated in the mechanism by which cortisol is stimulated during the L-Dopa test. Levodopa 137-143 proopiomelanocortin Homo sapiens 28-55 26393346-2 2015 Herein, we examined whether adrenocorticotropic hormone (ACTH) is implicated in the mechanism by which cortisol is stimulated during the L-Dopa test. Levodopa 137-143 proopiomelanocortin Homo sapiens 57-61 26393346-7 2015 Among the children with a normal response in ACTH, its concentration increased from a basal value (mean +- standard deviation) of 23.3 +- 9.6 to 290.3 +- 221 pg/ml, almost always 90-120 min after L-Dopa administration. Levodopa 196-202 proopiomelanocortin Homo sapiens 45-49 25335824-3 2015 Dopa-decarboxylase inhibitors were the first such drugs that were developed, and their use in combination with L-dopa has become standard practice. Levodopa 111-117 dopa decarboxylase Homo sapiens 0-18 25274160-4 2015 Radioligands with limited affinity for the dopamine D2 receptor are sensitive to changes in the levels of synaptic dopamine and can accordingly provide helpful insights into the magnitude and time course of dopamine release after l-dopa. Levodopa 230-236 dopamine receptor D2 Homo sapiens 43-63 25281315-0 2015 Nitric oxide synthase inhibition decreases l-DOPA-induced dyskinesia and the expression of striatal molecular markers in Pitx3(-/-) aphakia mice. Levodopa 43-49 nitric oxide synthase 1, neuronal Mus musculus 0-21 25476691-6 2015 Novel enzyme inhibitors enhancing l-dopa efficacy and half-life are also still being developed, including a novel catechol-O-methyltransferase inhibitor with once-daily pharmacokinetics, and there are studies testing the effects of increasing the dose of amino acid decarboxylase inhibitors given concomitantly with l-dopa. Levodopa 34-40 catechol-O-methyltransferase Homo sapiens 114-142 25281315-6 2015 Moreover, 7-NI significantly reduced FosB and pAcH3 expression in the acutely and chronically l-DOPA-treated mice. Levodopa 94-100 FBJ osteosarcoma oncogene B Mus musculus 37-41 25785228-6 2015 FOG improved with levodopa in 21/27 patients with typical PD but did not improve in the 12 patients with atypical parkinsonism. Levodopa 18-26 zinc finger protein, FOG family member 1 Homo sapiens 0-3 25447229-6 2015 L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). Levodopa 0-6 glial fibrillary acidic protein Homo sapiens 93-124 25447229-6 2015 L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). Levodopa 0-6 glial fibrillary acidic protein Homo sapiens 126-130 25447229-6 2015 L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). Levodopa 0-6 integrin subunit alpha M Homo sapiens 179-184 25447229-6 2015 L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). Levodopa 0-6 nitric oxide synthase 2 Homo sapiens 323-327 26558134-10 2015 The impact of levodopa intake on vowel articulation changed with STN DBS: before surgery, levodopa impaired articulation, while it no longer had a negative effect after surgery. Levodopa 14-22 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 65-68 26558134-10 2015 The impact of levodopa intake on vowel articulation changed with STN DBS: before surgery, levodopa impaired articulation, while it no longer had a negative effect after surgery. Levodopa 90-98 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 65-68 26558134-12 2015 These results indicate that while STN DBS could lead to a direct deterioration in articulation, it may indirectly improve it by reducing the levodopa dose required to manage motor symptoms. Levodopa 141-149 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 34-37 25872644-0 2015 Is there a role for ADORA2A polymorphisms in levodopa-induced dyskinesia in Parkinson"s disease patients? Levodopa 45-53 adenosine A2a receptor Homo sapiens 20-27 25872644-4 2015 The aim of the present study was to investigate whether ADORA2A is associated with levodopa adverse effects. Levodopa 83-91 adenosine A2a receptor Homo sapiens 56-63 25565773-0 2015 Postsynaptic density protein 95-regulated NR2B tyrosine phosphorylation and interactions of Fyn with NR2B in levodopa-induced dyskinesia rat models. Levodopa 109-117 discs large MAGUK scaffold protein 4 Rattus norvegicus 0-31 25565773-12 2015 Meanwhile, PSD-95 ASO pretreatment decreased the level of PSD-95 protein expression and reduced both the augmented NR2B tyrosine phosphorylation and interactions of Fyn with NR2B triggered during the levodopa administration in the lesioned striatum of PD rats. Levodopa 200-208 discs large MAGUK scaffold protein 4 Rattus norvegicus 11-17 25869243-2 2015 The aim of this study was to investigate the biotransformation of salvianolic acid B (SAB) by catechol-O-methyltransferase (COMT) and its interaction with levodopa (l-DOPA) methylation in rats. Levodopa 155-163 SH3-domain binding protein 5 Rattus norvegicus 86-89 25869243-2 2015 The aim of this study was to investigate the biotransformation of salvianolic acid B (SAB) by catechol-O-methyltransferase (COMT) and its interaction with levodopa (l-DOPA) methylation in rats. Levodopa 155-163 catechol-O-methyltransferase Rattus norvegicus 94-122 25869243-2 2015 The aim of this study was to investigate the biotransformation of salvianolic acid B (SAB) by catechol-O-methyltransferase (COMT) and its interaction with levodopa (l-DOPA) methylation in rats. Levodopa 155-163 catechol-O-methyltransferase Rattus norvegicus 124-128 25869243-2 2015 The aim of this study was to investigate the biotransformation of salvianolic acid B (SAB) by catechol-O-methyltransferase (COMT) and its interaction with levodopa (l-DOPA) methylation in rats. Levodopa 165-171 SH3-domain binding protein 5 Rattus norvegicus 86-89 25869243-2 2015 The aim of this study was to investigate the biotransformation of salvianolic acid B (SAB) by catechol-O-methyltransferase (COMT) and its interaction with levodopa (l-DOPA) methylation in rats. Levodopa 165-171 catechol-O-methyltransferase Rattus norvegicus 124-128 25869243-6 2015 For l-DOPA, the effect of SAB inhibition on l-DOPA methylation was studied in vitro. Levodopa 44-50 SH3-domain binding protein 5 Rattus norvegicus 26-29 25869243-12 2015 SAB inhibited the methylation of l-DOPA with an IC50 value of 2.08 muM in vitro. Levodopa 33-39 SH3-domain binding protein 5 Rattus norvegicus 0-3 25869243-14 2015 Multiple doses of SAB given to rats also decreased the plasma concentration of 3-OMD, while SAB increased the plasma concentration of l-DOPA. Levodopa 134-140 SH3-domain binding protein 5 Rattus norvegicus 92-95 25565773-12 2015 Meanwhile, PSD-95 ASO pretreatment decreased the level of PSD-95 protein expression and reduced both the augmented NR2B tyrosine phosphorylation and interactions of Fyn with NR2B triggered during the levodopa administration in the lesioned striatum of PD rats. Levodopa 200-208 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 165-168 25565773-12 2015 Meanwhile, PSD-95 ASO pretreatment decreased the level of PSD-95 protein expression and reduced both the augmented NR2B tyrosine phosphorylation and interactions of Fyn with NR2B triggered during the levodopa administration in the lesioned striatum of PD rats. Levodopa 200-208 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 174-178 25565773-0 2015 Postsynaptic density protein 95-regulated NR2B tyrosine phosphorylation and interactions of Fyn with NR2B in levodopa-induced dyskinesia rat models. Levodopa 109-117 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 42-46 25565773-0 2015 Postsynaptic density protein 95-regulated NR2B tyrosine phosphorylation and interactions of Fyn with NR2B in levodopa-induced dyskinesia rat models. Levodopa 109-117 FYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 92-95 25565773-0 2015 Postsynaptic density protein 95-regulated NR2B tyrosine phosphorylation and interactions of Fyn with NR2B in levodopa-induced dyskinesia rat models. Levodopa 109-117 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 101-105 25565773-8 2015 Then, the effect of pretreatment with an intrastriatal injection of the PSD-95mRNA antisense oligonucleotides (PSD-95 ASO) on the rotational response to levodopa challenge was assessed. Levodopa 153-161 discs large MAGUK scaffold protein 4 Rattus norvegicus 72-78 25566000-0 2014 Relationship between L-DOPA-induced reduction in motor and exploratory activity and degree of DAT binding in the rat. Levodopa 21-27 solute carrier family 6 member 3 Rattus norvegicus 94-97 25566000-1 2014 PURPOSE: The present study assessed the influence of L-DOPA administration on neostriatal dopamine (DA) transporter (DAT) binding in relation to motor and exploratory behaviors in the rat. Levodopa 53-59 solute carrier family 6 member 3 Rattus norvegicus 117-120 25566000-5 2014 RESULTS: Both L-DOPA doses significantly reduced DAT binding and led to significantly less head-shoulder motility and more sitting relative to vehicle. Levodopa 14-20 solute carrier family 6 member 3 Rattus norvegicus 49-52 25566000-8 2014 CONCLUSIONS: The reductions of striatal DAT binding after L-DOPA challenges reflected elevated concentrations of synaptic DA. Levodopa 58-64 solute carrier family 6 member 3 Rattus norvegicus 40-43 25511986-5 2014 Moreover, we also showed L-dopa elicits profound alterations in the activity of three LID molecular markers, namely DR1/PKA/P-tau (ser396). Levodopa 25-31 down-regulator of transcription 1 Rattus norvegicus 116-119 25150543-0 2014 L-dopa reverses behavioral deficits in the Pitx3 mouse fetus. Levodopa 0-6 paired-like homeodomain transcription factor 3 Mus musculus 43-48 25150543-9 2014 Specific behavioral deficits observed in the Pitx3 mutants were reversed by L-dopa administration in a dose-dependent manner. Levodopa 76-82 paired-like homeodomain transcription factor 3 Mus musculus 45-50 25582874-2 2014 Levodopa-induced vitamin B12 deficiency has been discussed as a causal factor of PN in idiopathic Parkinson"s disease, but peripheral nervous system involvement might also be a consequence of the underlying neurodegenerative process. Levodopa 0-8 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 81-83 25311167-8 2014 Finally, we investigated whether myocilin was present on the exosomes released by RPE and whether l-DOPA stimulation of GPR143 caused recruitment of myocilin to the endocytic pathway, as we have previously observed using cultured cells. Levodopa 98-104 G protein-coupled receptor 143 Homo sapiens 120-126 25311167-8 2014 Finally, we investigated whether myocilin was present on the exosomes released by RPE and whether l-DOPA stimulation of GPR143 caused recruitment of myocilin to the endocytic pathway, as we have previously observed using cultured cells. Levodopa 98-104 myocilin Homo sapiens 149-157 25044243-0 2014 Multiple treatments with L-3,4-dihydroxyphenylalanine modulate dopamine biosynthesis and neurotoxicity through the protein kinase A-transient extracellular signal-regulated kinase and exchange protein activation by cyclic AMP-sustained extracellular signal-regulated kinase signaling pathways. Levodopa 25-53 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 115-131 25044243-11 2014 Our data demonstrate that L-DOPA can cause neurotoxicity by modulating the Epac-ERK pathways in neuronal and PC12 cells. Levodopa 26-32 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 75-79 25044243-11 2014 Our data demonstrate that L-DOPA can cause neurotoxicity by modulating the Epac-ERK pathways in neuronal and PC12 cells. Levodopa 26-32 Eph receptor B1 Rattus norvegicus 80-83 24705818-6 2014 Our results show that L-DOPA treatment induces an increase in DRD2 and DRD3 expression in the postcommissural putamen, but only DRD3 is correlated with the severity of LID. Levodopa 22-28 dopamine receptor D2 Homo sapiens 62-66 24705818-6 2014 Our results show that L-DOPA treatment induces an increase in DRD2 and DRD3 expression in the postcommissural putamen, but only DRD3 is correlated with the severity of LID. Levodopa 22-28 dopamine receptor D3 Homo sapiens 71-75 24705818-8 2014 In contrast, activation of the DRD2-signaling pathway, visible in the levels of Akt phosphorylated on Thr308 and GSK3beta on Ser9, is associated with L-DOPA treatment, independently of the presence of dyskinesias. Levodopa 150-156 dopamine receptor D2 Homo sapiens 31-35 24705818-8 2014 In contrast, activation of the DRD2-signaling pathway, visible in the levels of Akt phosphorylated on Thr308 and GSK3beta on Ser9, is associated with L-DOPA treatment, independently of the presence of dyskinesias. Levodopa 150-156 glycogen synthase kinase 3 beta Homo sapiens 113-121 25329528-7 2014 The utility of these methods is illustrated in the synthesis of protected forms of (R)-beta(3)-DOPA and L-DOPA from the same aziridine, the former by SmI2-mediated reductive opening at C-2 and the latter by palladium-mediated reductive opening at C-3. Levodopa 104-110 complement C2 Homo sapiens 185-188 25327342-0 2014 New ghrelin agonist, HM01 alleviates constipation and L-dopa-delayed gastric emptying in 6-hydroxydopamine rat model of Parkinson"s disease. Levodopa 54-60 ghrelin and obestatin prepropeptide Rattus norvegicus 4-11 24912720-7 2014 Moreover, molecular docking results suggested that morin competitively bound to the active site of tyrosinase with the substrate levodopa. Levodopa 129-137 tyrosinase Homo sapiens 99-109 25208966-0 2014 Norepinephrine transporter inhibition with desipramine exacerbates L-DOPA-induced dyskinesia: role for synaptic dopamine regulation in denervated nigrostriatal terminals. Levodopa 67-73 solute carrier family 6 member 2 Rattus norvegicus 0-26 25209359-0 2014 Binding studies of L-3,4-dihydroxyphenylalanine with human serum albumin. Levodopa 19-47 albumin Homo sapiens 59-72 25209359-2 2014 The binding interaction between L-dopa (phytochemical) and human serum albumin (HSA) under simulated physiological conditions was investigated by spectroscopic and molecular modeling methods. Levodopa 32-38 albumin Homo sapiens 65-78 25452081-6 2014 However, expressions of isozyme phosphodiesterase-1B and -10A highly and specifically located in the basal ganglia were not changed after levodopa in dyskinetic and eukinetic animals: accordingly, selective inhibitors of phosphodiesterase-1B and -10A were ineffective on levodopa dyskinesias. Levodopa 271-279 phosphodiesterase 1B Rattus norvegicus 32-61 25452081-6 2014 However, expressions of isozyme phosphodiesterase-1B and -10A highly and specifically located in the basal ganglia were not changed after levodopa in dyskinetic and eukinetic animals: accordingly, selective inhibitors of phosphodiesterase-1B and -10A were ineffective on levodopa dyskinesias. Levodopa 271-279 phosphodiesterase 1B Rattus norvegicus 221-250 25446341-4 2014 Pharmacologic subtypes of FOG include those that are responsive and unresponsive to levodopa. Levodopa 84-92 zinc finger protein, FOG family member 1 Homo sapiens 26-29 25446341-5 2014 OBJECTIVE: To determine whether executive and visuospatial dysfunction are associated specifically with the levodopa unresponsive subtype of FOG. Levodopa 108-116 zinc finger protein, FOG family member 1 Homo sapiens 141-144 25329528-7 2014 The utility of these methods is illustrated in the synthesis of protected forms of (R)-beta(3)-DOPA and L-DOPA from the same aziridine, the former by SmI2-mediated reductive opening at C-2 and the latter by palladium-mediated reductive opening at C-3. Levodopa 104-110 complement C3 Homo sapiens 247-250 25203713-0 2014 POLG1-related levodopa-responsive parkinsonism. Levodopa 14-22 DNA polymerase gamma, catalytic subunit Homo sapiens 0-5 25395834-3 2014 L-DOPA has also been found to modify the two key signaling cascades, protein kinase A/dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), in striatal neurons, which are thought to play a pivotal role in forming motor complications. Levodopa 0-6 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 141-149 25395834-3 2014 L-DOPA has also been found to modify the two key signaling cascades, protein kinase A/dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), in striatal neurons, which are thought to play a pivotal role in forming motor complications. Levodopa 0-6 mitogen activated protein kinase 3 Rattus norvegicus 155-201 25395834-3 2014 L-DOPA has also been found to modify the two key signaling cascades, protein kinase A/dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), in striatal neurons, which are thought to play a pivotal role in forming motor complications. Levodopa 0-6 mitogen activated protein kinase 3 Rattus norvegicus 203-209 25395834-8 2014 Similarly, chronic injections of WIN-55,212-2 influence the L-DOPA-induced alteration of DARPP-32 and ERK1/2 phosphorylation status in striatal neurons. Levodopa 60-66 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 89-97 25233866-2 2014 LID results in part from l-DOPA-induced activation of extracellular signal-regulated kinase (ERK) in the dopamine-denervated striatum. Levodopa 25-31 mitogen-activated protein kinase 1 Mus musculus 54-91 25233866-2 2014 LID results in part from l-DOPA-induced activation of extracellular signal-regulated kinase (ERK) in the dopamine-denervated striatum. Levodopa 25-31 mitogen-activated protein kinase 1 Mus musculus 93-96 25233866-5 2014 The absence of MSK1 had no effect on the lesion or l-DOPA-induced ERK activation, but reduced l-DOPA-induced phosphorylation of histone H3 and FosB accumulation in the dopamine-denervated striatum. Levodopa 94-100 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 15-19 25233866-5 2014 The absence of MSK1 had no effect on the lesion or l-DOPA-induced ERK activation, but reduced l-DOPA-induced phosphorylation of histone H3 and FosB accumulation in the dopamine-denervated striatum. Levodopa 94-100 FBJ osteosarcoma oncogene B Mus musculus 143-147 25233866-8 2014 In conclusion, l-DOPA-induced activation of MSK1 contributes to histone H3 phosphorylation, induction of FosB, and Galphaolf up-regulation but appears not to be necessary for the development of LID. Levodopa 15-21 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 44-48 25233866-8 2014 In conclusion, l-DOPA-induced activation of MSK1 contributes to histone H3 phosphorylation, induction of FosB, and Galphaolf up-regulation but appears not to be necessary for the development of LID. Levodopa 15-21 FBJ osteosarcoma oncogene B Mus musculus 105-109 25233866-8 2014 In conclusion, l-DOPA-induced activation of MSK1 contributes to histone H3 phosphorylation, induction of FosB, and Galphaolf up-regulation but appears not to be necessary for the development of LID. Levodopa 15-21 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 115-124 25395834-8 2014 Similarly, chronic injections of WIN-55,212-2 influence the L-DOPA-induced alteration of DARPP-32 and ERK1/2 phosphorylation status in striatal neurons. Levodopa 60-66 mitogen activated protein kinase 3 Rattus norvegicus 102-108 25172808-13 2014 The improved motor response to l-DOPA after subthalamotomy in the parkinsonian monkeys investigated may be associated with an increased synthesis and expression of D1 receptors ipsilateral to STN lesion of the direct pathway. Levodopa 31-37 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 192-195 25303896-10 2014 Droxidopa is a synthetic amino acid that is converted to norepinephrine by dopa-decarboxylase, the same enzyme that converts levodopa into dopamine in the treatment of Parkinson disease. Levodopa 125-133 dopa decarboxylase Homo sapiens 75-93 25160895-10 2014 Interestingly, animals treated with both candesartan and l-dopa displayed significantly lower levels of VEGF, IL-1beta and dyskinesia than those treated with l-dopa alone. Levodopa 57-63 vascular endothelial growth factor A Rattus norvegicus 104-108 25160895-10 2014 Interestingly, animals treated with both candesartan and l-dopa displayed significantly lower levels of VEGF, IL-1beta and dyskinesia than those treated with l-dopa alone. Levodopa 57-63 interleukin 1 alpha Rattus norvegicus 110-118 25173217-0 2014 Adenosine A1 receptor stimulation reduces D1 receptor-mediated GABAergic transmission from striato-nigral terminals and attenuates l-DOPA-induced dyskinesia in dopamine-denervated mice. Levodopa 131-137 adenosine A1 receptor Mus musculus 0-21 25297374-4 2014 The aim of the present study was to examine if arbutin could suppress the hydroxyl radical generation via tyrosinase reaction with its substrates, L-tyrosine and L-DOPA. Levodopa 162-168 tyrosinase Homo sapiens 106-116 24770794-0 2014 Fewer fluctuations, higher maximum concentration and better motor response of levodopa with catechol-O-methyltransferase inhibition. Levodopa 78-86 catechol-O-methyltransferase Homo sapiens 92-120 24770794-1 2014 Catechol-O-methyltransferase inhibitor addition to levodopa/carbidopa formulations improves motor symptoms and reduces levodopa fluctuations in patients with Parkinson"s disease. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 0-28 24770794-1 2014 Catechol-O-methyltransferase inhibitor addition to levodopa/carbidopa formulations improves motor symptoms and reduces levodopa fluctuations in patients with Parkinson"s disease. Levodopa 119-127 catechol-O-methyltransferase Homo sapiens 0-28 24770794-5 2014 Catechol-O-methyltransferase inhibition caused less fluctuations and higher baseline levels of levodopa after the first intake and less 3-O-methyldopa appearance. Levodopa 95-103 catechol-O-methyltransferase Homo sapiens 0-28 24770794-6 2014 The maximum levodopa concentrations were higher after the second levodopa intake, particularly with catechol-O-methyltransferase inhibition. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 100-128 24770794-6 2014 The maximum levodopa concentrations were higher after the second levodopa intake, particularly with catechol-O-methyltransferase inhibition. Levodopa 65-73 catechol-O-methyltransferase Homo sapiens 100-128 24770794-7 2014 The motor response to levodopa was better with catechol-O-methyltransferase inhibition than without, tolcapone was superior to entacapone. Levodopa 22-30 catechol-O-methyltransferase Homo sapiens 47-75 24917201-0 2014 Improvement of the Rett syndrome phenotype in a MeCP2 mouse model upon treatment with levodopa and a dopa-decarboxylase inhibitor. Levodopa 86-94 methyl CpG binding protein 2 Mus musculus 48-53 25130058-5 2014 In the presence of a catalytic amount of l-dopa, human tyrosinase, which can oxidize l-tyrosine but not d-tyrosine, was found to oxidize both R(-)- and S(+)-RD to give RD-catechol and its oxidation products. Levodopa 41-47 tyrosinase Homo sapiens 55-65 25297374-0 2014 Alleviation effect of arbutin on oxidative stress generated through tyrosinase reaction with L-tyrosine and L-DOPA. Levodopa 108-114 tyrosinase Homo sapiens 68-78 23733911-6 2014 Levodopa reinstated physiological gamma-gamma coupling from lPM to SMA and significantly strengthened coupling in the feedback connection from M1 to lPM expressed as beta-beta as well as theta-beta coupling. Levodopa 0-8 survival of motor neuron 1, telomeric Homo sapiens 67-70 24770794-8 2014 More continuous levodopa brain delivery and lower 3-O-methyldopa bioavailability caused a better motor response during catechol-O-methyltransferase inhibition. Levodopa 16-24 catechol-O-methyltransferase Homo sapiens 119-147 25171793-8 2014 A symptomatic dose of l-DOPA restored bidirectional plasticity on both pathways to levels comparable to naive animals (Indirect pathway: LTP protocol: 124.4+-22.0% and LTD protocol: 52.1+-18.5% of baseline. Levodopa 22-28 liver transport protein Mus musculus 137-140 25171793-10 2014 In dyskinesia, in the presence of l-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9+-21.3% and LTD protocol 52.0+-14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6+-13.2% and LTD protocol 166.7+-15.8% of baseline). Levodopa 34-40 liver transport protein Mus musculus 188-191 25171793-10 2014 In dyskinesia, in the presence of l-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9+-21.3% and LTD protocol 52.0+-14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6+-13.2% and LTD protocol 166.7+-15.8% of baseline). Levodopa 34-40 liver transport protein Mus musculus 188-191 25343491-5 2014 We provide evidence that, in addition to tyrosine hydroxylase (TH) that synthesizes L-DOPA, neurons within the A11 region of the mouse contain aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-DOPA to dopamine. Levodopa 84-90 tyrosine hydroxylase Mus musculus 41-61 25343491-5 2014 We provide evidence that, in addition to tyrosine hydroxylase (TH) that synthesizes L-DOPA, neurons within the A11 region of the mouse contain aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-DOPA to dopamine. Levodopa 212-218 annexin A11, opposite strand Mus musculus 111-114 25343491-5 2014 We provide evidence that, in addition to tyrosine hydroxylase (TH) that synthesizes L-DOPA, neurons within the A11 region of the mouse contain aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-DOPA to dopamine. Levodopa 212-218 dopa decarboxylase Mus musculus 152-178 25297374-5 2014 RESULTS: The hydroxyl radical, which was determined by an electron spin resonance-spin trapping technique, was generated by the addition of not only L-tyrosine but L-DOPA to tyrosinase in a concentration dependent manner. Levodopa 164-170 tyrosinase Homo sapiens 174-184 25080285-9 2014 Task-specific regional activations in Parkinson"s disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. Levodopa 142-150 microtubule associated protein tau Homo sapiens 226-230 25080285-9 2014 Task-specific regional activations in Parkinson"s disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. Levodopa 142-150 apolipoprotein E Homo sapiens 311-315 25034405-1 2014 Previous studies in Parkinsonian rats and monkeys have shown that beta2-selective nicotinic acetylcholine receptor (nAChR) agonists reduce l-Dopa-induced dyskinesias (LIDs), a serious complication of l-Dopa therapy for Parkinson"s disease. Levodopa 139-145 cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus 116-121 25220836-4 2014 Therapeutic manipulation of VMAT2 level or function has the potential to improve efficacy of dopamine derived from administered levodopa, increase dopamine neurotransmission from remaining midbrain dopamine neurons and protect against neurotoxic insults. Levodopa 128-136 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 28-33 25034405-1 2014 Previous studies in Parkinsonian rats and monkeys have shown that beta2-selective nicotinic acetylcholine receptor (nAChR) agonists reduce l-Dopa-induced dyskinesias (LIDs), a serious complication of l-Dopa therapy for Parkinson"s disease. Levodopa 200-206 cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus 116-121 25154960-1 2014 BACKGROUND: Levodopa (l-dopa) therapy in Parkinson"s disease (PD) increases serum homocysteine levels because of its metabolism via catechol O-methyltransferase, which may lead to endothelial dysfunction. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 132-160 25154960-1 2014 BACKGROUND: Levodopa (l-dopa) therapy in Parkinson"s disease (PD) increases serum homocysteine levels because of its metabolism via catechol O-methyltransferase, which may lead to endothelial dysfunction. Levodopa 22-28 catechol-O-methyltransferase Homo sapiens 132-160 24842650-6 2014 Finally, we determined the effect of the repeated administration of 1BnTIQ on the L-DOPA-induced elevation of caspase-3 activity in the hippocampus. Levodopa 82-88 caspase 3 Rattus norvegicus 110-119 24842650-10 2014 Additionally, we found that chronic administration of 1BnTIQ completely blocked the L-DOPA-induced increase in caspase-3 activity in the hippocampus. Levodopa 84-90 caspase 3 Rattus norvegicus 111-120 24997271-2 2014 The aim of this study was to test our hypothesis that DA is synthesized by monoenzymatic neurons, i.e. l-3,4-dihydroxyphenylalanine (l-DOPA), which produced in the monoenzymatic TH neurons is transported in the monoenzymatic AADC neurons for DA synthesis. Levodopa 133-139 dopa decarboxylase Rattus norvegicus 225-229 24969021-4 2014 In situ hybridisation revealed that repeated l-DOPA/benserazide treatment caused an elevation of RGS4 mRNA levels in the striatum, predominantly in the lateral regions. Levodopa 45-51 regulator of G-protein signaling 4 Rattus norvegicus 97-101 24969021-6 2014 We found that suppressing the elevation of RGS4 mRNA in the striatum by continuous infusion of RGS4 antisense oligonucleotides, via implanted osmotic mini-pumps, during l-DOPA priming, reduced the induction of AIMs. Levodopa 169-175 regulator of G-protein signaling 4 Rattus norvegicus 43-47 24969021-6 2014 We found that suppressing the elevation of RGS4 mRNA in the striatum by continuous infusion of RGS4 antisense oligonucleotides, via implanted osmotic mini-pumps, during l-DOPA priming, reduced the induction of AIMs. Levodopa 169-175 regulator of G-protein signaling 4 Rattus norvegicus 95-99 24969021-7 2014 Moreover, ex vivo analyses of the rostral dorsolateral striatum showed that RGS4 antisense infusion attenuated l-DOPA-induced elevations of PPE-B mRNA and dopamine-stimulated [(35)S]GTPgammaS binding, a marker used for measuring dopamine receptor super-sensitivity. Levodopa 111-117 regulator of G-protein signaling 4 Rattus norvegicus 76-80 24969021-8 2014 Taken together, these data suggest that (i) RGS4 proteins play an important pathophysiological role in the development and expression of LID and (ii) suppressing the elevation of RGS4 mRNA levels in l-DOPA priming attenuates the associated pathological changes in LID, dampening its physiological expression. Levodopa 199-205 regulator of G-protein signaling 4 Rattus norvegicus 44-48 24969021-8 2014 Taken together, these data suggest that (i) RGS4 proteins play an important pathophysiological role in the development and expression of LID and (ii) suppressing the elevation of RGS4 mRNA levels in l-DOPA priming attenuates the associated pathological changes in LID, dampening its physiological expression. Levodopa 199-205 regulator of G-protein signaling 4 Rattus norvegicus 179-183 24836728-4 2014 The general nAChR agonist nicotine, as well as several nAChR agonists (varenicline, ABT-089 and ABT-894), reduces l-dopa-induced abnormal involuntary movements or dyskinesias up to 60% in parkinsonian nonhuman primates and rodents. Levodopa 114-120 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 12-17 25073474-4 2014 l-DOPA is routinely coadministered with levodopa metabolism inhibitors (dopa-decarboxylase and cathechol-O-methyl transferase inhibitors) that share structural similarity with levodopa. Levodopa 0-6 dopa decarboxylase Mus musculus 72-90 25073474-4 2014 l-DOPA is routinely coadministered with levodopa metabolism inhibitors (dopa-decarboxylase and cathechol-O-methyl transferase inhibitors) that share structural similarity with levodopa. Levodopa 40-48 dopa decarboxylase Mus musculus 72-90 25073474-4 2014 l-DOPA is routinely coadministered with levodopa metabolism inhibitors (dopa-decarboxylase and cathechol-O-methyl transferase inhibitors) that share structural similarity with levodopa. Levodopa 176-184 dopa decarboxylase Mus musculus 72-90 25073474-7 2014 L-Leucine and L-arginine competed with levodopa across the luminal enterocyte membrane as expected for b(0,+)AT-rBAT substrates, whereas dopa-decarboxylase and cathechol-O-methyl transferase inhibitors had no effect. Levodopa 39-47 solute carrier family 7 (cationic amino acid transporter, y+ system), member 9 Mus musculus 103-111 25073474-7 2014 L-Leucine and L-arginine competed with levodopa across the luminal enterocyte membrane as expected for b(0,+)AT-rBAT substrates, whereas dopa-decarboxylase and cathechol-O-methyl transferase inhibitors had no effect. Levodopa 39-47 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 112-116 25073474-8 2014 The presence of amino acids in the basolateral compartment mimicking the postprandial phase increased transepithelial levodopa transport by stimulating basolateral efflux via the antiporter LAT2-4F2 (SLC7A8-SLC3A2). Levodopa 118-126 solute carrier family 7 (cationic amino acid transporter, y+ system), member 8 Mus musculus 200-206 25073474-8 2014 The presence of amino acids in the basolateral compartment mimicking the postprandial phase increased transepithelial levodopa transport by stimulating basolateral efflux via the antiporter LAT2-4F2 (SLC7A8-SLC3A2). Levodopa 118-126 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 207-213 25073474-9 2014 Additionally, the aromatic amino acid uniporter TAT1 (SLC16A10) was shown to play a major role in l-DOPA efflux from intestinal enterocytes. Levodopa 98-104 solute carrier family 16 (monocarboxylic acid transporters), member 10 Mus musculus 48-52 25073474-9 2014 Additionally, the aromatic amino acid uniporter TAT1 (SLC16A10) was shown to play a major role in l-DOPA efflux from intestinal enterocytes. Levodopa 98-104 solute carrier family 16 (monocarboxylic acid transporters), member 10 Mus musculus 54-62 24997271-2 2014 The aim of this study was to test our hypothesis that DA is synthesized by monoenzymatic neurons, i.e. l-3,4-dihydroxyphenylalanine (l-DOPA), which produced in the monoenzymatic TH neurons is transported in the monoenzymatic AADC neurons for DA synthesis. Levodopa 103-131 dopa decarboxylase Rattus norvegicus 225-229 24997271-3 2014 Incubation of MBH in Krebs-Ringer solution with l-leucine, a competitive inhibitor of l-DOPA uptake, was used to prevent a hypothetical l-DOPA capture into AADC-containing neurons. Levodopa 136-142 dopa decarboxylase Rattus norvegicus 156-160 24997271-6 2014 This conclusion was supported by an observation of higher concentration of l-DOPA in the incubation medium under perfusion of MBH with Krebs-Ringer solution containing tolcapone, an inhibitor of catechol-O-methyltransferase, and l-leucine than under perfusion with the same solution, but without l-leucine. Levodopa 75-81 catechol-O-methyltransferase Rattus norvegicus 195-223 24910244-7 2014 In addition, plasma and striatal COMT levels decreased after coadministration of beta-asarone and l-dopa, whereas there were no significant differences in MAO-B concentrations among groups. Levodopa 98-104 catechol-O-methyltransferase Rattus norvegicus 33-37 25188235-2 2014 Since cortical astrocytes express neutral amino acid transporter (LAT) and DA transporter (DAT), the uptake and metabolism of L-DOPA and DA in striatal astrocytes may influence their availability in the dopaminergic system of PD. Levodopa 126-132 linker for activation of T cells Rattus norvegicus 66-69 25188235-2 2014 Since cortical astrocytes express neutral amino acid transporter (LAT) and DA transporter (DAT), the uptake and metabolism of L-DOPA and DA in striatal astrocytes may influence their availability in the dopaminergic system of PD. Levodopa 126-132 solute carrier family 6 member 3 Rattus norvegicus 75-89 25188235-2 2014 Since cortical astrocytes express neutral amino acid transporter (LAT) and DA transporter (DAT), the uptake and metabolism of L-DOPA and DA in striatal astrocytes may influence their availability in the dopaminergic system of PD. Levodopa 126-132 solute carrier family 6 member 3 Rattus norvegicus 91-94 25188235-4 2014 Repeated injections of L-DOPA induced apparent L-DOPA- and DA-immunoreactivities and marked expression of DAT in reactive astrocytes on the lesioned side of the striatum in hemi-parkinsonian rats. Levodopa 23-29 solute carrier family 6 member 3 Rattus norvegicus 106-109 24910244-9 2014 Altogether, beta-asarone affects the conversion of l-dopa to DA by modulating COMT activity and DA metabolism. Levodopa 51-57 catechol-O-methyltransferase Rattus norvegicus 78-82 24925090-15 2014 CONCLUSION: Opicapone, a novel third generation COMT inhibitor, when compared to entacapone, provides a superior response upon the bioavailability of levodopa associated to more pronounced, long-lasting, and sustained COMT inhibition. Levodopa 150-158 catechol-O-methyltransferase Homo sapiens 48-52 24925090-2 2014 The purpose of this study was to compare the levodopa pharmacokinetic profile throughout a day driven by the COMT inhibition either following repeated doses of opicapone or concomitant administration with entacapone. Levodopa 45-53 catechol-O-methyltransferase Homo sapiens 109-113 24925090-15 2014 CONCLUSION: Opicapone, a novel third generation COMT inhibitor, when compared to entacapone, provides a superior response upon the bioavailability of levodopa associated to more pronounced, long-lasting, and sustained COMT inhibition. Levodopa 150-158 catechol-O-methyltransferase Homo sapiens 218-222 24806705-5 2014 In humans, patients treated with L-dopa or catecholaminergic agonists showed a significant increase of a MPC-like population (CD45-CD31-CD34-CD105+) in their peripheral blood. Levodopa 33-39 protein tyrosine phosphatase receptor type C Homo sapiens 126-130 24993959-2 2014 Loss-of-function mutations in GCH1 result in severe reduction of dopamine synthesis in nigrostriatal cells and are the most common cause of DOPA-responsive dystonia, a rare disease that classically presents in childhood with generalized dystonia and a dramatic long-lasting response to levodopa. Levodopa 286-294 GTP cyclohydrolase 1 Homo sapiens 30-34 24798695-8 2014 Moreover, we show that PARK13 and PINK1 protein levels accumulate in response to H2 O2 and L-DOPA treatments in a subcellular fashion and that both proteins show relocation to the cytoskeleton in response to H2 O2 . Levodopa 91-97 HtrA serine peptidase 2 Homo sapiens 23-29 24798695-8 2014 Moreover, we show that PARK13 and PINK1 protein levels accumulate in response to H2 O2 and L-DOPA treatments in a subcellular fashion and that both proteins show relocation to the cytoskeleton in response to H2 O2 . Levodopa 91-97 PTEN induced kinase 1 Homo sapiens 34-39 24806705-5 2014 In humans, patients treated with L-dopa or catecholaminergic agonists showed a significant increase of a MPC-like population (CD45-CD31-CD34-CD105+) in their peripheral blood. Levodopa 33-39 platelet and endothelial cell adhesion molecule 1 Homo sapiens 131-135 24806705-5 2014 In humans, patients treated with L-dopa or catecholaminergic agonists showed a significant increase of a MPC-like population (CD45-CD31-CD34-CD105+) in their peripheral blood. Levodopa 33-39 CD34 molecule Homo sapiens 136-140 25170965-6 2014 Electron microscopic analysis revealed that the M6PR-positive swollen vacuoles were multi-layered and contained melanized granules, and they produced melanin when L-DOPA was applied, indicating that these vacuoles were still capable of producing melanin, but the inner conditions were not compatible with melanin production. Levodopa 163-169 mannose-6-phosphate receptor, cation dependent Homo sapiens 48-52 25164669-7 2014 The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Levodopa 54-60 adenylate cyclase 5 Mus musculus 64-67 25164669-7 2014 The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Levodopa 54-60 mitogen-activated protein kinase 1 Mus musculus 151-154 25164669-7 2014 The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Levodopa 54-60 mitogen-activated protein kinase 3 Mus musculus 156-198 25164669-7 2014 The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Levodopa 54-60 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 200-204 25164669-7 2014 The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Levodopa 54-60 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 206-252 25164669-8 2014 Consistently, FosB/DeltaFosB expression, which was induced by long-term L-DOPA treatment in the lesioned striatum, was also decreased in AC5-KO mice. Levodopa 72-78 FBJ osteosarcoma oncogene B Mus musculus 14-18 25164669-8 2014 Consistently, FosB/DeltaFosB expression, which was induced by long-term L-DOPA treatment in the lesioned striatum, was also decreased in AC5-KO mice. Levodopa 72-78 adenylate cyclase 5 Mus musculus 137-140 24837745-0 2014 Effects of noradrenergic denervation by anti-DBH-saporin on behavioral responsivity to L-DOPA in the hemi-parkinsonian rat. Levodopa 87-93 dopamine beta-hydroxylase Rattus norvegicus 45-48 24754803-6 2014 After levodopa/benserazide treatment, we found a significant reduction of cytotoxic T-cells (CD3+ CD8+ ) in the ischemic hemisphere together with reduced levels of T-cell-associated cytokine IL-5, while other T-cell populations (CD3+, CD3+ CD4+, CD3+ CD4+ CD25+) were unchanged compared with vehicle-treated rats. Levodopa 6-14 interleukin 5 Rattus norvegicus 191-195 24631324-4 2014 We investigated the effects of low-frequency repetitive transcranial magnetic stimulation (rTMS) of the SMA on levodopa-induced dyskinesias (LID) and motor performance in PD. Levodopa 111-119 survival of motor neuron 1, telomeric Homo sapiens 104-107 24396010-11 2014 STN-DBS-induced benefits on FOG were mostly mediated by baseline levodopa equivalent dose, altered medication-intake and reduced motor fluctuations. Levodopa 65-73 zinc finger protein, FOG family member 1 Homo sapiens 28-31 24754803-7 2014 Moreover, a reduced number of cells was associated with reduced levels of intercellular adhesion molecule 1, expressed in endothelial cells, in the infarct core of levodopa/benserazide-treated animals. Levodopa 164-172 intercellular adhesion molecule 1 Rattus norvegicus 74-107 24960254-4 2014 A potential strategy, currently under investigation, is the coadministration of metabotropic glutamate receptor 5 (mGluR5) negative allosteric modulators (NAMs) and L-DOPA; a treatment that results in the improvement of dyskinesia symptoms and that permits reductions in l-DOPA dosage frequency. Levodopa 271-277 glutamate metabotropic receptor 5 Homo sapiens 80-113 24960254-4 2014 A potential strategy, currently under investigation, is the coadministration of metabotropic glutamate receptor 5 (mGluR5) negative allosteric modulators (NAMs) and L-DOPA; a treatment that results in the improvement of dyskinesia symptoms and that permits reductions in l-DOPA dosage frequency. Levodopa 271-277 glutamate receptor, ionotropic, kainate 1 Mus musculus 115-121 24960254-7 2014 EXPERT OPINION: Interaction between mGluR5 NAM and L-DOPA is an area of interest in PD research as concomitant treatment results in the improvement of LID symptoms in humans, thus enhancing the patient"s quality of life. Levodopa 51-57 glutamate receptor, ionotropic, kainate 1 Mus musculus 36-42 24960254-7 2014 EXPERT OPINION: Interaction between mGluR5 NAM and L-DOPA is an area of interest in PD research as concomitant treatment results in the improvement of LID symptoms in humans, thus enhancing the patient"s quality of life. Levodopa 51-57 SH3 and cysteine rich domain 3 Homo sapiens 43-46 24815018-7 2014 Wnt3a increased the population of TRP-1(+) cells, the number of L-3,4-dihydroxyphenylalanine (DOPA)(+) cells and dendrite formation in NC explant cultures. Levodopa 64-92 Wnt family member 3A Homo sapiens 0-5 24815018-7 2014 Wnt3a increased the population of TRP-1(+) cells, the number of L-3,4-dihydroxyphenylalanine (DOPA)(+) cells and dendrite formation in NC explant cultures. Levodopa 94-98 Wnt family member 3A Homo sapiens 0-5 24632468-0 2014 H2O2- or l-DOPA-injured dopaminergic neurons trigger the release of soluble mediators that up-regulate striatal GDNF through different signalling pathways. Levodopa 9-15 glial cell derived neurotrophic factor Homo sapiens 112-116 24632468-2 2014 We have previously shown that H2O2- or l-3,4-dihydroxyphenylalanine (l-DOPA)-challenged dopaminergic neurons trigger the release of soluble factors that signal ventral midbrain astrocytes to increase GDNF expression. Levodopa 39-67 glial cell derived neurotrophic factor Homo sapiens 200-204 24632468-2 2014 We have previously shown that H2O2- or l-3,4-dihydroxyphenylalanine (l-DOPA)-challenged dopaminergic neurons trigger the release of soluble factors that signal ventral midbrain astrocytes to increase GDNF expression. Levodopa 69-75 glial cell derived neurotrophic factor Homo sapiens 200-204 24632468-4 2014 Our data showed that soluble mediators released upon H2O2- or l-DOPA-induced dopaminergic injury up-regulated GDNF in striatal cells, with different temporal patterns depending on the oxidative agent used. Levodopa 62-68 glial cell derived neurotrophic factor Homo sapiens 110-114 24632468-7 2014 Both phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways were involved in striatal GDNF up-regulation triggered by H2O2-induced dopaminergic injury, while diffusible factors released in the presence of l-DOPA-challenged dopaminergic neurons induced GDNF expression in striatal cells through the activation of the MAPK pathway. Levodopa 240-246 glial cell derived neurotrophic factor Homo sapiens 121-125 24754803-6 2014 After levodopa/benserazide treatment, we found a significant reduction of cytotoxic T-cells (CD3+ CD8+ ) in the ischemic hemisphere together with reduced levels of T-cell-associated cytokine IL-5, while other T-cell populations (CD3+, CD3+ CD4+, CD3+ CD4+ CD25+) were unchanged compared with vehicle-treated rats. Levodopa 6-14 Cd4 molecule Rattus norvegicus 240-243 24754803-6 2014 After levodopa/benserazide treatment, we found a significant reduction of cytotoxic T-cells (CD3+ CD8+ ) in the ischemic hemisphere together with reduced levels of T-cell-associated cytokine IL-5, while other T-cell populations (CD3+, CD3+ CD4+, CD3+ CD4+ CD25+) were unchanged compared with vehicle-treated rats. Levodopa 6-14 Cd4 molecule Rattus norvegicus 251-254 24794108-1 2014 DOPA decarboxylase (DDC) is responsible for the decarboxylation of l-DOPA and related aromatic amino acids and correlates closely with a number of clinical disorders. Levodopa 67-73 dopa decarboxylase Homo sapiens 0-18 24865335-1 2014 BACKGROUND: Blocking metabotropic glutamate receptor type 5 (mGluR5) has been proposed as a target for levodopa-induced dyskinesias (LID) in Parkinson"s disease (PD). Levodopa 103-111 glutamate receptor, ionotropic, kainate 1 Mus musculus 61-67 24768615-9 2014 Levodopa tended to decrease FoG and falls with or without dual tasking. Levodopa 0-8 zinc finger protein, FOG family member 1 Homo sapiens 28-31 24809448-0 2014 The influence of dopamine beta-hydroxylase gene polymorphism rs1611115 on levodopa/carbidopa treatment for cocaine dependence: a preliminary study. Levodopa 74-82 dopamine beta-hydroxylase Homo sapiens 17-42 24809448-2 2014 Here we hypothesized that response to levodopa/carbidopa treatment would be greater in patients with genetically determined low levels of the dopamine metabolizing enzyme dopamine beta-hydroxylase (DbetaH). Levodopa 38-46 dopamine beta-hydroxylase Homo sapiens 171-196 24809448-2 2014 Here we hypothesized that response to levodopa/carbidopa treatment would be greater in patients with genetically determined low levels of the dopamine metabolizing enzyme dopamine beta-hydroxylase (DbetaH). Levodopa 38-46 dopamine beta-hydroxylase Homo sapiens 198-204 24809448-4 2014 Our results showed that for patients with the low DbetaH activity genotypes (CT/TT) who received levodopa, the odds of having cocaine-positive urine decreased significantly over treatment compared with placebo-treated patients with the CT/TT genotypes (P=0.004). Levodopa 97-105 dopamine beta-hydroxylase Homo sapiens 50-56 24794108-1 2014 DOPA decarboxylase (DDC) is responsible for the decarboxylation of l-DOPA and related aromatic amino acids and correlates closely with a number of clinical disorders. Levodopa 67-73 dopa decarboxylase Homo sapiens 20-23 24126708-0 2014 Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson"s disease patients. Levodopa 59-67 homer scaffold protein 1 Homo sapiens 42-48 24633632-0 2014 Sequence variants in SLC6A3, DRD2, and BDNF genes and time to levodopa-induced dyskinesias in Parkinson"s disease. Levodopa 62-70 solute carrier family 6 member 3 Homo sapiens 21-27 24633632-0 2014 Sequence variants in SLC6A3, DRD2, and BDNF genes and time to levodopa-induced dyskinesias in Parkinson"s disease. Levodopa 62-70 brain derived neurotrophic factor Homo sapiens 39-43 24633632-5 2014 After adjusting for gender, age at PD onset, duration of symptoms prior to levodopa exposure, and multiple testing correction, one SNP in SLC6A3 (with 81 % genotyping success) was significantly associated with LID latency: the C allele of the rs393795 extended the time to LID onset, time ratio = 4.96 (95 % CI, 2.3-10.9; p = 4.1 x 10(-5)). Levodopa 75-83 solute carrier family 6 member 3 Homo sapiens 138-144 24687897-6 2014 The annual decline in the mini-mental state examination score was 0.4 +- 1.7 with impaired attention and executive function and a higher levodopa equivalent dose at baseline being the predictors of a faster global cognitive decline after STN DBS. Levodopa 137-145 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 238-241 24126708-3 2014 This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. Levodopa 148-156 homer scaffold protein 1 Homo sapiens 53-59 24126708-7 2014 Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. Levodopa 93-101 homer scaffold protein 1 Homo sapiens 22-28 25024584-1 2014 Aromatic L-amino acid decarboxylase (AADC), a vitamin B6-requiring enzyme that converts L-dopa to dopamine and 5-hydroxytryptophan to serotonin. Levodopa 88-94 dopa decarboxylase Homo sapiens 37-41 24905513-7 2014 Prolactin response to stress in NAL-treated rats was blocked by l-DOPA administration. Levodopa 64-70 prolactin Rattus norvegicus 0-9 24948886-7 2014 However, the differences in aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio of 500 mg/kg levodopa nanocomposite (0.32 +- 0.12) and 500 mg/kg LDH nanocomposite (0.34 +- 0.12) were statistically significant (p < 0.05) compared to the control (0.51 +- 0.07). Levodopa 109-117 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 81-84 24830331-2 2014 Entacapone, a peripheral inhibitor of catechol-O-methyltransferase (COMT), reduces this motor complication by prolonging the effect of levodopa. Levodopa 135-143 catechol-O-methyltransferase Homo sapiens 38-66 24830331-2 2014 Entacapone, a peripheral inhibitor of catechol-O-methyltransferase (COMT), reduces this motor complication by prolonging the effect of levodopa. Levodopa 135-143 catechol-O-methyltransferase Homo sapiens 68-72 24637127-4 2014 Accordingly, we determined if treatment with a SP NK1 receptor antagonist reduced the onset of L-DOPA induced dyskinesia (LID) in the hemi-parkinsonian rodent model. Levodopa 95-101 tachykinin receptor 1 Rattus norvegicus 50-62 24904309-4 2014 Systemic administration of L-DOPA alleviated parkinsonian motor signs and decreased abnormal neuronal oscillations (8-15 Hz) in the internal (GPi) and external (GPe) segments of the globus pallidus and the subthalamic nucleus (STN). Levodopa 27-33 glucose-6-phosphate isomerase Homo sapiens 142-145 24670480-11 2014 Incubation of PC12 cells with L-DOPA markedly increased intracellular DOPAL content and promoted alpha-synuclein dimerization. Levodopa 30-36 synuclein alpha Rattus norvegicus 97-112 24670480-12 2014 Co-incubation with Cu(2+) amplified (p=0.01), while monoamine oxidase inhibition prevented, L-DOPA-related dimerization of alpha-synuclein (p=0.01). Levodopa 92-98 synuclein alpha Rattus norvegicus 123-138 23769604-0 2014 L-DOPA treatment selectively restores spine density in dopamine receptor D2-expressing projection neurons in dyskinetic mice. Levodopa 0-6 dopamine receptor D2 Mus musculus 55-75 23769604-9 2014 Chronic L-DOPA treatment, which induced dyskinesia and aberrant FosB expression, restored spine density in D2R-MSNs but not in D1R-MSNs. Levodopa 8-14 FBJ osteosarcoma oncogene B Mus musculus 64-68 23769604-9 2014 Chronic L-DOPA treatment, which induced dyskinesia and aberrant FosB expression, restored spine density in D2R-MSNs but not in D1R-MSNs. Levodopa 8-14 dopamine receptor D2 Mus musculus 107-110 23769604-12 2014 CONCLUSIONS: Chronic L-DOPA induces abnormal spine re-growth exclusively in D2R-MSNs and robust supersensitization to D1R-activated excitability in denervated striatal MSNs. Levodopa 21-27 dopamine receptor D2 Mus musculus 76-79 24756517-6 2014 RESULTS: Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged <60 years) other medications (eg, monoamine oxidase type B inhibitors [MAOBIs], amantadine, anticholinergics, beta-blockers, or dopamine agonists) may be initiated first to avoid levodopa-related motor complications. Levodopa 18-26 monoamine oxidase B Homo sapiens 250-274 24471650-1 2014 Dopamine, a biogenic amine with important biological functions, is produced from l-DOPA by DOPA decarboxylase (DDC). Levodopa 81-87 dopa decarboxylase Homo sapiens 91-109 24471650-1 2014 Dopamine, a biogenic amine with important biological functions, is produced from l-DOPA by DOPA decarboxylase (DDC). Levodopa 81-87 dopa decarboxylase Homo sapiens 111-114 24333147-0 2014 Buspirone anti-dyskinetic effect is correlated with temporal normalization of dysregulated striatal DRD1 signalling in L-DOPA-treated rats. Levodopa 119-125 dopamine receptor D1 Rattus norvegicus 100-104 24361601-4 2014 RESULTS: p-FOG patients showed higher power in the high-beta band (F=11.6, p=0.002) that was significantly reduced after l-dopa administration along with suppression of FOG (F=4.6, p=0.042). Levodopa 121-127 zinc finger protein, FOG family member 1 Homo sapiens 11-14 24361601-4 2014 RESULTS: p-FOG patients showed higher power in the high-beta band (F=11.6, p=0.002) that was significantly reduced after l-dopa administration along with suppression of FOG (F=4.6, p=0.042). Levodopa 121-127 zinc finger protein, FOG family member 1 Homo sapiens 169-172 24456747-8 2014 Striatal preproenkephalin/preprodynorphin mRNA levels and phosphorylated ERK1/2 and Akt/GSK3beta levels increased only in L-DOPA-treated MPTP monkeys as compared to controls, saline treated-MPTP and l-DOPA + MPEP treated MPTP monkeys. Levodopa 122-128 proenkephalin Homo sapiens 9-25 24456747-8 2014 Striatal preproenkephalin/preprodynorphin mRNA levels and phosphorylated ERK1/2 and Akt/GSK3beta levels increased only in L-DOPA-treated MPTP monkeys as compared to controls, saline treated-MPTP and l-DOPA + MPEP treated MPTP monkeys. Levodopa 122-128 mitogen-activated protein kinase 3 Homo sapiens 73-79 24271646-1 2014 PURPOSE: Opicapone (OPC) is a novel catechol-O-methyltransferase (COMT) inhibitor to be used as adjunctive therapy in levodopa-treated patients with Parkinson"s disease. Levodopa 118-126 catechol-O-methyltransferase Homo sapiens 66-70 24456747-8 2014 Striatal preproenkephalin/preprodynorphin mRNA levels and phosphorylated ERK1/2 and Akt/GSK3beta levels increased only in L-DOPA-treated MPTP monkeys as compared to controls, saline treated-MPTP and l-DOPA + MPEP treated MPTP monkeys. Levodopa 122-128 AKT serine/threonine kinase 1 Homo sapiens 84-87 24456747-8 2014 Striatal preproenkephalin/preprodynorphin mRNA levels and phosphorylated ERK1/2 and Akt/GSK3beta levels increased only in L-DOPA-treated MPTP monkeys as compared to controls, saline treated-MPTP and l-DOPA + MPEP treated MPTP monkeys. Levodopa 122-128 glycogen synthase kinase 3 beta Homo sapiens 88-96 24599591-5 2014 We identify several hundred genes, the expression of which is correlated with levodopa dose, many of which are under the control of activator protein-1 and ERK signaling. Levodopa 78-86 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-151 24599591-5 2014 We identify several hundred genes, the expression of which is correlated with levodopa dose, many of which are under the control of activator protein-1 and ERK signaling. Levodopa 78-86 mitogen-activated protein kinase 1 Homo sapiens 156-159 24599591-6 2014 Despite homeostatic adaptations involving several signaling modulators, activator protein-1-dependent gene expression remains highly dysregulated in direct pathway SPNs upon chronic levodopa treatment. Levodopa 182-190 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-91 24650244-0 2014 Gastrodia elata Blume alleviates L-DOPA-induced dyskinesia by normalizing FosB and ERK activation in a 6-OHDA-lesioned Parkinson"s disease mouse model. Levodopa 33-39 FBJ osteosarcoma oncogene B Mus musculus 74-78 24650244-0 2014 Gastrodia elata Blume alleviates L-DOPA-induced dyskinesia by normalizing FosB and ERK activation in a 6-OHDA-lesioned Parkinson"s disease mouse model. Levodopa 33-39 mitogen-activated protein kinase 1 Mus musculus 83-86 24407024-1 2014 Mammalian Dopa decarboxylase catalyzes the conversion of L-Dopa and L-5-hydroxytryptophan to dopamine and serotonin, respectively. Levodopa 57-63 dopa decarboxylase Homo sapiens 10-28 24974674-10 2014 It seems that L-dopa could be effective in the treatment of dystonia due to VPS13A mutations. Levodopa 14-20 vacuolar protein sorting 13 homolog A Homo sapiens 76-82 24389502-0 2014 May stimulation of the pre-SMA become a new therapeutic target for PD patients with levodopa-induced dyskinesias? Levodopa 84-92 survival of motor neuron 1, telomeric Homo sapiens 27-30 24614670-0 2014 Unusual case of levodopa-responsive camptocormia in a patient with negative dopamine transporter scan and normal DYT 5 gene. Levodopa 16-24 solute carrier family 6 member 3 Homo sapiens 76-96 24614670-0 2014 Unusual case of levodopa-responsive camptocormia in a patient with negative dopamine transporter scan and normal DYT 5 gene. Levodopa 16-24 GTP cyclohydrolase 1 Homo sapiens 113-118 24614670-2 2014 METHODS: We present a case of camptocormia with a sustained excellent response to levodopa in a patient with negative dopamine transporter and no DYT 5 genetic mutations. Levodopa 82-90 solute carrier family 6 member 3 Homo sapiens 118-138 24716406-1 2014 Catechol O-methyltransferase (COMT) is an important enzyme involved in the metabolism of levodopa (L-dopa) which is clinically used to treat Parkinson"s disease through boosting the concentration of dopamine in the brain. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 0-28 24412491-2 2014 Experimental and clinical data have indicated that adenosine A2A receptor antagonists can provide symptomatic improvement by potentiating L-DOPA efficacy and minimizing its side effects. Levodopa 138-144 adenosine A2a receptor Rattus norvegicus 51-73 24412491-5 2014 We investigated the expression of A2A-CB1-D2 receptor heteromers in the striatum of both naive and hemiparkinsonian rats (HPD-rats) bearing a unilateral 6-hydroxydopamine (6-OHDA) lesion, and assessed how receptor heteromer expression and biochemical properties were affected by L-DOPA treatment. Levodopa 279-285 spectrin, alpha, non-erythrocytic 1 Rattus norvegicus 34-37 24716406-2 2014 Development of COMT inhibitors can efficiently increase the bioavailability of L-dopa. Levodopa 79-85 catechol-O-methyltransferase Homo sapiens 15-19 24487825-0 2014 Paroxysmal exercise-induced dystonia due to GLUT1 mutation can be responsive to levodopa: a case report. Levodopa 80-88 solute carrier family 2 member 1 Homo sapiens 44-49 24716406-1 2014 Catechol O-methyltransferase (COMT) is an important enzyme involved in the metabolism of levodopa (L-dopa) which is clinically used to treat Parkinson"s disease through boosting the concentration of dopamine in the brain. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 30-34 24716406-1 2014 Catechol O-methyltransferase (COMT) is an important enzyme involved in the metabolism of levodopa (L-dopa) which is clinically used to treat Parkinson"s disease through boosting the concentration of dopamine in the brain. Levodopa 99-105 catechol-O-methyltransferase Homo sapiens 0-28 24716406-1 2014 Catechol O-methyltransferase (COMT) is an important enzyme involved in the metabolism of levodopa (L-dopa) which is clinically used to treat Parkinson"s disease through boosting the concentration of dopamine in the brain. Levodopa 99-105 catechol-O-methyltransferase Homo sapiens 30-34 24366652-0 2014 SPG15: a cause of juvenile atypical levodopa responsive parkinsonism. Levodopa 36-44 zinc finger FYVE-type containing 26 Homo sapiens 0-5 24361037-4 2014 Tyrosinase assay and L-3,4-dihydroxyphenylalanine (L-DOPA) gel staining assay revealed that tyrosinase activity in eyes of pale ear mutants was greatly reduced in early postnatal stages and increased gradually after postnatal day 7 (P7). Levodopa 21-49 tyrosinase Mus musculus 92-102 24361037-4 2014 Tyrosinase assay and L-3,4-dihydroxyphenylalanine (L-DOPA) gel staining assay revealed that tyrosinase activity in eyes of pale ear mutants was greatly reduced in early postnatal stages and increased gradually after postnatal day 7 (P7). Levodopa 51-57 tyrosinase Mus musculus 92-102 24148813-1 2014 OBJECTIVE: The present study aimed at evaluating the effect of opicapone, a third generation nitrocatechol catechol-O-methyltransferase (COMT) inhibitor, on the systemic and central bioavailability of 3,4-dihydroxy-l-phenylalanine (levodopa) and related metabolites in the cynomolgus monkey. Levodopa 201-230 catechol O-methyltransferase Macaca fascicularis 107-135 23680795-5 2014 We have therefore used Rosetta to guide the introduction of an oxidizable crosslinking NCAA, l-3,4-dihydroxyphenylalanine (l-DOPA), into the CDRs of the anti-protective antigen scFv antibody M18, and have measured crosslinking to its cognate antigen, domain 4 of the anthrax protective antigen. Levodopa 93-121 immunglobulin heavy chain variable region Homo sapiens 177-181 23680795-5 2014 We have therefore used Rosetta to guide the introduction of an oxidizable crosslinking NCAA, l-3,4-dihydroxyphenylalanine (l-DOPA), into the CDRs of the anti-protective antigen scFv antibody M18, and have measured crosslinking to its cognate antigen, domain 4 of the anthrax protective antigen. Levodopa 123-129 immunglobulin heavy chain variable region Homo sapiens 177-181 24067924-5 2014 Therefore the current endeavor sought to mimic a prolonged regimen of SERT inhibition in L-DOPA-primed and -naive hemi-parkinsonian rats. Levodopa 89-95 solute carrier family 6 member 4 Rattus norvegicus 70-74 24067924-9 2014 Neurochemical analysis of striatal tissue indicated that a 3 week SERT blockade increased DA levels in L-DOPA-treated rats. Levodopa 103-109 solute carrier family 6 member 4 Rattus norvegicus 66-70 24067924-11 2014 Collectively, these findings demonstrate that prolonged SERT inhibition provides enduring anti-dyskinetic effects in part via 5-HT(1A) receptors while maintaining L-DOPA"s anti-parkinsonian efficacy by enhancing striatal DA levels. Levodopa 163-169 solute carrier family 6 member 4 Rattus norvegicus 56-60 24140894-0 2014 Oleoylethanolamide reduces L-DOPA-induced dyskinesia via TRPV1 receptor in a mouse model of Parkinson s disease. Levodopa 27-33 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 57-62 24140894-9 2014 We found that OEA antidyskinetic properties were mediated by TRPV1 receptor, as pretreatment with capsaicin, a TRPV1 agonist, blocked OEA antidyskinetic actions, as well as the reduction in FosB- and pAcH3-overexpression induced by L-DOPA. Levodopa 232-238 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 61-66 24148813-1 2014 OBJECTIVE: The present study aimed at evaluating the effect of opicapone, a third generation nitrocatechol catechol-O-methyltransferase (COMT) inhibitor, on the systemic and central bioavailability of 3,4-dihydroxy-l-phenylalanine (levodopa) and related metabolites in the cynomolgus monkey. Levodopa 201-230 catechol O-methyltransferase Macaca fascicularis 137-141 24148813-10 2014 CONCLUSIONS: Opicapone behaved as long-acting COMT inhibitor that markedly increased systemic and central levodopa bioavailability. Levodopa 106-114 catechol O-methyltransferase Macaca fascicularis 46-50 24148813-11 2014 Opicapone is a strong candidate to fill the unmet need for COMT inhibitors that lead to more sustained levodopa levels in Parkinson"s disease patients. Levodopa 103-111 catechol-O-methyltransferase Homo sapiens 59-63 25230230-3 2014 TH is responsible for catalyzing the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine. Levodopa 65-93 tyrosine hydroxylase Homo sapiens 0-2 24182522-0 2014 Oculogyric crises induced by levodopa in PLA2G6 parkinsonism-dystonia. Levodopa 29-37 phospholipase A2 group VI Homo sapiens 41-47 24182523-1 2014 UNLABELLED: Deep brain stimulation of the subthalamic nuclei (STN-DBS) for the treatment of levodopa-induced motor complications in advanced Parkinson"s disease (APD) has been associated with neuropsychiatric disorders. Levodopa 92-100 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 62-65 24216088-0 2014 Dopa-decarboxylase gene polymorphisms affect the motor response to L-dopa in Parkinson"s disease. Levodopa 67-73 dopa decarboxylase Homo sapiens 0-18 24216088-2 2014 The major pathway for dopamine synthesis from L-dopa is decarboxylation by aromatic L-amino acid decarboxylase (AAAD, encoded by the DDC gene). Levodopa 46-52 dopa decarboxylase Homo sapiens 75-110 24216088-2 2014 The major pathway for dopamine synthesis from L-dopa is decarboxylation by aromatic L-amino acid decarboxylase (AAAD, encoded by the DDC gene). Levodopa 46-52 dopa decarboxylase Homo sapiens 112-116 24216088-2 2014 The major pathway for dopamine synthesis from L-dopa is decarboxylation by aromatic L-amino acid decarboxylase (AAAD, encoded by the DDC gene). Levodopa 46-52 dopa decarboxylase Homo sapiens 133-136 24216088-3 2014 OBJECTIVE: To determine the motor response to L-dopa in PD patients as a function of the DDC gene promoter polymorphisms (rs921451 T > C polymorphism (DDC(T/C)) and rs3837091 AGAG del (DDC(AGAG/-))). Levodopa 46-52 dopa decarboxylase Homo sapiens 89-92 24216088-3 2014 OBJECTIVE: To determine the motor response to L-dopa in PD patients as a function of the DDC gene promoter polymorphisms (rs921451 T > C polymorphism (DDC(T/C)) and rs3837091 AGAG del (DDC(AGAG/-))). Levodopa 46-52 dopa decarboxylase Homo sapiens 151-154 24216088-3 2014 OBJECTIVE: To determine the motor response to L-dopa in PD patients as a function of the DDC gene promoter polymorphisms (rs921451 T > C polymorphism (DDC(T/C)) and rs3837091 AGAG del (DDC(AGAG/-))). Levodopa 46-52 dopa decarboxylase Homo sapiens 151-154 24216088-8 2014 RESULTS: When adjusted for the L-dopa dose, the AUCDeltaUPDRS was significantly lower in DDC(CC/CT) patients (n = 14) than in DDC(TT) patients (n = 19) and significantly lower in DDC(-/- or AGAG/-) patients (n = 8) than in DDC(AGAG/AGAG) patients (n = 25). Levodopa 31-37 dopa decarboxylase Homo sapiens 89-92 24216088-10 2014 DISCUSSION: The rs921451 and rs3837091 polymorphisms of the DDC gene promoter influence the motor response to L-dopa but do not significantly change peripheral pharmacokinetic parameters for L-dopa and dopamine. Levodopa 110-116 dopa decarboxylase Homo sapiens 60-63 24216088-10 2014 DISCUSSION: The rs921451 and rs3837091 polymorphisms of the DDC gene promoter influence the motor response to L-dopa but do not significantly change peripheral pharmacokinetic parameters for L-dopa and dopamine. Levodopa 191-197 dopa decarboxylase Homo sapiens 60-63 24216088-11 2014 Our results suggest that DDC may be a genetic modifier of the l-dopa response in Parkinson"s disease. Levodopa 62-68 dopa decarboxylase Homo sapiens 25-28 24369987-0 2014 Imaging of the dopamine transporter predicts pattern of disease progression and response to levodopa in patients with schizophrenia and parkinsonism: a 2-year follow-up multicenter study. Levodopa 92-100 solute carrier family 6 member 3 Homo sapiens 15-35 24369987-10 2014 Functional imaging of the dopamine transporter can be helpful to select this patient sub-group that might benefit from levodopa therapy. Levodopa 119-127 solute carrier family 6 member 3 Homo sapiens 26-46 24321617-8 2014 Furthermore, abnormal expression of FosB, the immediate early gene of L-dopa induced dyskinesia (LID), was mitigated in the striatum by the combination treatment. Levodopa 70-76 FBJ osteosarcoma oncogene B Mus musculus 36-40 25197640-4 2014 Such mutations in ATP13A2, also named PARK9, were first identified in 2006 in a Chilean family and are associated with a juvenile-onset, levodopa-responsive type of Parkinsonism called Kufor-Rakeb syndrome (KRS). Levodopa 137-145 ATPase cation transporting 13A2 Homo sapiens 18-25 25197640-4 2014 Such mutations in ATP13A2, also named PARK9, were first identified in 2006 in a Chilean family and are associated with a juvenile-onset, levodopa-responsive type of Parkinsonism called Kufor-Rakeb syndrome (KRS). Levodopa 137-145 ATPase cation transporting 13A2 Homo sapiens 38-43 24681641-0 2014 Adenosine A2A-receptor antagonist istradefylline enhances the motor response of L-DOPA without worsening dyskinesia in MPTP-treated common marmosets. Levodopa 80-86 LOW QUALITY PROTEIN: adenosine receptor A2a Callithrix jacchus 0-22 25175964-1 2014 Dopamine replacement therapy using the dopamine precursor, l-3,4-dihydroxyphenylalanine (l-DOPA), with a peripheral dopa decarboxylase inhibitor is the most effective treatment currently available for the symptoms of Parkinson"s disease (PD). Levodopa 59-87 dopa decarboxylase Homo sapiens 116-134 25175964-1 2014 Dopamine replacement therapy using the dopamine precursor, l-3,4-dihydroxyphenylalanine (l-DOPA), with a peripheral dopa decarboxylase inhibitor is the most effective treatment currently available for the symptoms of Parkinson"s disease (PD). Levodopa 89-95 dopa decarboxylase Homo sapiens 116-134 25042502-10 2014 FOG in off-periods were observed in 2/3 patients treated with levodopa, 1/3 of patients did not relate FOG with the periods of levodopa action. Levodopa 62-70 zinc finger protein, FOG family member 1 Homo sapiens 0-3 24008922-0 2014 Influence of single nucleotide polymorphisms in COMT, MAO-A and BDNF genes on dyskinesias and levodopa use in Parkinson"s disease. Levodopa 94-102 brain derived neurotrophic factor Homo sapiens 64-68 24008922-8 2014 The possibility that combined COMT and MAO-A genotype is a significant factor in determining an individual"s lifetime levodopa exposure warrants further investigation. Levodopa 118-126 catechol-O-methyltransferase Homo sapiens 30-34 24008922-8 2014 The possibility that combined COMT and MAO-A genotype is a significant factor in determining an individual"s lifetime levodopa exposure warrants further investigation. Levodopa 118-126 monoamine oxidase A Homo sapiens 39-44 24376341-1 2013 BACKGROUND: Recent studies have shown that expression of G protein-coupled receptor kinase 6 (GRK6) and beta-arrestin1 in the striatum is closely associated with hyperactive dopamine receptors in rats with levodopa-induced dyskinesia (LID). Levodopa 206-214 G protein-coupled receptor kinase 6 Rattus norvegicus 57-92 24376341-1 2013 BACKGROUND: Recent studies have shown that expression of G protein-coupled receptor kinase 6 (GRK6) and beta-arrestin1 in the striatum is closely associated with hyperactive dopamine receptors in rats with levodopa-induced dyskinesia (LID). Levodopa 206-214 G protein-coupled receptor kinase 6 Rattus norvegicus 94-98 24376341-0 2013 Effect of Tianqi antitremor granules on behavioral manifestations and expression of G protein-coupled receptor kinase 6 and beta-arrestin1 in levodopa-induced dyskinesia in a rat model of Parkinson"s disease. Levodopa 142-150 G protein-coupled receptor kinase 6 Rattus norvegicus 84-119 24376341-1 2013 BACKGROUND: Recent studies have shown that expression of G protein-coupled receptor kinase 6 (GRK6) and beta-arrestin1 in the striatum is closely associated with hyperactive dopamine receptors in rats with levodopa-induced dyskinesia (LID). Levodopa 206-214 arrestin, beta 1 Rattus norvegicus 104-118 24376341-0 2013 Effect of Tianqi antitremor granules on behavioral manifestations and expression of G protein-coupled receptor kinase 6 and beta-arrestin1 in levodopa-induced dyskinesia in a rat model of Parkinson"s disease. Levodopa 142-150 arrestin, beta 1 Rattus norvegicus 124-138 24376341-11 2013 In accordance with changed behavior, GRK6 and beta-arrestin1 expression was decreased in rats with PD and was persistently low in rats with LID, but this decrease was prevented by coadministration of levodopa and Tianqi antitremor granules. Levodopa 200-208 G protein-coupled receptor kinase 6 Rattus norvegicus 37-41 24376341-11 2013 In accordance with changed behavior, GRK6 and beta-arrestin1 expression was decreased in rats with PD and was persistently low in rats with LID, but this decrease was prevented by coadministration of levodopa and Tianqi antitremor granules. Levodopa 200-208 arrestin, beta 1 Rattus norvegicus 46-60 24532988-4 2013 In the review pharmacogenetic aspects of levodopa, dopamine agonists and COMT inhibitors are discussed. Levodopa 41-49 catechol-O-methyltransferase Homo sapiens 73-77 24367353-5 2013 In one patient levodopa treatment was initialized which was somewhat successful to relieve FOG. Levodopa 15-23 zinc finger protein, FOG family member 1 Homo sapiens 91-94 24029003-0 2013 Modulating mGluR5 and 5-HT1A/1B receptors to treat l-DOPA-induced dyskinesia: effects of combined treatment and possible mechanisms of action. Levodopa 51-57 glutamate receptor, ionotropic, kainate 1 Mus musculus 11-17 24029003-0 2013 Modulating mGluR5 and 5-HT1A/1B receptors to treat l-DOPA-induced dyskinesia: effects of combined treatment and possible mechanisms of action. Levodopa 51-57 5-hydroxytryptamine receptor 1A Rattus norvegicus 22-28 24234932-0 2013 Association Between Catechol-O-Methyltransferase (COMT) Gene Polymorphisms, Parkinson"s Disease, and Levodopa Efficacy. Levodopa 101-109 catechol-O-methyltransferase Homo sapiens 20-48 24144882-4 2013 Furthermore, this pathway is also dysfunctional and pathogenically linked to mTOR signaling in L-DOPA-induced dyskinesias (LID). Levodopa 95-101 mechanistic target of rapamycin kinase Homo sapiens 77-81 23982164-1 2013 PURPOSE: The effect of clinical L-3,4-dihydroxyphenylalanine (L-DOPA) doses on the binding of [121I]N-Omega-fluoropropyl-2beta-carbomethoxy-3beta-(4-iodophenyl)nortropane (121[I]FP-CIT) to the rat dopamine transporter (DAT) was investigated using small animal single-photon emission computed tomography. Levodopa 62-68 solute carrier family 6 member 3 Rattus norvegicus 197-217 23982164-1 2013 PURPOSE: The effect of clinical L-3,4-dihydroxyphenylalanine (L-DOPA) doses on the binding of [121I]N-Omega-fluoropropyl-2beta-carbomethoxy-3beta-(4-iodophenyl)nortropane (121[I]FP-CIT) to the rat dopamine transporter (DAT) was investigated using small animal single-photon emission computed tomography. Levodopa 62-68 solute carrier family 6 member 3 Rattus norvegicus 219-222 23982164-7 2013 After 5 mg/kg L-DOPA/benserazide, DAT binding was inversely correlated with sitting duration (1-5 min) and sitting frequency (10-15 min). Levodopa 14-20 solute carrier family 6 member 3 Rattus norvegicus 34-37 23982164-9 2013 CONCLUSION: Challenge with 5 and 10 mg/kg L-DOPA/benserazide led to mean reductions in DAT binding by 34 and 20%, respectively. Levodopa 42-48 solute carrier family 6 member 3 Rattus norvegicus 87-90 24234932-0 2013 Association Between Catechol-O-Methyltransferase (COMT) Gene Polymorphisms, Parkinson"s Disease, and Levodopa Efficacy. Levodopa 101-109 catechol-O-methyltransferase Homo sapiens 50-54 24234932-1 2013 OBJECTIVES: We investigated the association between catechol-O-methyltransferase (COMT) gene polymorphisms and Parkinson"s disease (PD) susceptibility, severity of disease, and levodopa (L-Dopa) efficacy. Levodopa 177-185 catechol-O-methyltransferase Homo sapiens 52-80 24348138-2 2013 In the current work, we analyzed the effects of L-DOPA on the growth, the activities of phenylalanine ammonia-lyase (PAL), tyrosine ammonia-lyase (TAL), and peroxidase (POD), and the contents of phenylalanine, tyrosine, and lignin in maize (Zea mays) roots. Levodopa 48-54 phenylalanine ammonia-lyase Zea mays 117-120 23932066-5 2013 RESULTS: At week 24, the mean dose of ropinirole PR was 11.4 mg/day with a mean reduction of L-dopa from 506.6 to 411.6 mg/day. Levodopa 93-99 transmembrane protein 37 Homo sapiens 49-51 23992249-0 2013 Increased L-DOPA-derived dopamine following selective MAO-A or -B inhibition in rat striatum depleted of dopaminergic and serotonergic innervation. Levodopa 10-16 monoamine oxidase A Rattus norvegicus 54-59 23992249-1 2013 BACKGROUND AND PURPOSE: Selective MAO type B (MAO-B) inhibitors are effective in potentiation of the clinical effect of L-DOPA in Parkinson"s disease, but dopamine (DA) is deaminated mainly by MAO type A (MAO-A) in rat brain. Levodopa 120-126 monoamine oxidase B Rattus norvegicus 34-44 23992249-1 2013 BACKGROUND AND PURPOSE: Selective MAO type B (MAO-B) inhibitors are effective in potentiation of the clinical effect of L-DOPA in Parkinson"s disease, but dopamine (DA) is deaminated mainly by MAO type A (MAO-A) in rat brain. Levodopa 120-126 monoamine oxidase B Rattus norvegicus 46-51 23992249-10 2013 CONCLUSIONS AND IMPLICATIONS: In striatum devoid of dopaminergic and serotonergic inputs, most deamination of L-DOPA-derived DA is mediated by MAO-A in MSN and a smaller amount by MAO-B in both MSN and glia. Levodopa 110-116 monoamine oxidase A Rattus norvegicus 143-148 23992249-10 2013 CONCLUSIONS AND IMPLICATIONS: In striatum devoid of dopaminergic and serotonergic inputs, most deamination of L-DOPA-derived DA is mediated by MAO-A in MSN and a smaller amount by MAO-B in both MSN and glia. Levodopa 110-116 monoamine oxidase B Rattus norvegicus 180-185 23992249-10 2013 CONCLUSIONS AND IMPLICATIONS: In striatum devoid of dopaminergic and serotonergic inputs, most deamination of L-DOPA-derived DA is mediated by MAO-A in MSN and a smaller amount by MAO-B in both MSN and glia. Levodopa 110-116 moesin Rattus norvegicus 194-197 23932066-11 2013 CONCLUSIONS: This study demonstrated for the first time in Chinese subjects that ropinirole PR improved Parkinson"s disease symptoms, permitting a reduction in L-dopa dose. Levodopa 160-166 transmembrane protein 37 Homo sapiens 92-94 23831952-3 2013 In addition, nicotine and nAChR drugs improve L-dopa-induced dyskinesias, a debilitating side effect of L-dopa therapy which remains the gold-standard treatment for Parkinson"s disease. Levodopa 46-52 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 26-31 24237242-1 2013 Negative allosteric modulators of metabotropic glutamate receptor 5 (mGlu5) have been actively pursued for over a decade as a potential treatment for anxiety, depression, substance abuse, pain, levodopa-induced dyskinesia in Parkinson"s disease, fragile X Syndrome, autism, gastroesophageal reflux disease and lower-urinary-tract disorders. Levodopa 194-202 glutamate metabotropic receptor 5 Homo sapiens 34-67 23831952-3 2013 In addition, nicotine and nAChR drugs improve L-dopa-induced dyskinesias, a debilitating side effect of L-dopa therapy which remains the gold-standard treatment for Parkinson"s disease. Levodopa 104-110 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 26-31 23831952-5 2013 One approach to identify the subtypes specifically involved in L-dopa-induced dyskinesias is through the use of nAChR subunit null mutant mice. Levodopa 63-69 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 112-117 23831952-6 2013 Previous work with beta2 and alpha6 nAChR knockout mice has shown that alpha6beta2* nAChRs were necessary for the development/maintenance of L-dopa-induced abnormal involuntary movements (AIMs). Levodopa 141-147 hemoglobin, beta adult minor chain Mus musculus 19-24 23831952-6 2013 Previous work with beta2 and alpha6 nAChR knockout mice has shown that alpha6beta2* nAChRs were necessary for the development/maintenance of L-dopa-induced abnormal involuntary movements (AIMs). Levodopa 141-147 cholinergic receptor, nicotinic, alpha polypeptide 6 Mus musculus 29-41 23831952-9 2013 In contrast to the studies with alpha4 and alpha6 knockout mice, nicotine treatment did reduce L-dopa-induced AIMs in parkinsonian alpha7 nAChR knockout mice. Levodopa 95-101 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 131-143 24082892-8 2013 Our results show that all synthesized compounds have inhibitory effect on tyrosinase activity for the oxidation of L-DOPA. Levodopa 115-121 tyrosinase Homo sapiens 74-84 23916724-7 2013 STN-DBS could remarkably reduce levodopa equivalent daily dose at 7 years. Levodopa 32-40 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 0-3 23631981-1 2013 A previous clinical trial studied the effect of long-term treatment with levodopa (LD) or the dopamine agonist pramipexole (PPX) on disease progression in Parkinson disease using SPECT with the dopamine transporter (DAT)-radioligand [(123)I]beta-CIT as surrogate marker. Levodopa 73-81 solute carrier family 6 member 3 Homo sapiens 194-214 23631981-1 2013 A previous clinical trial studied the effect of long-term treatment with levodopa (LD) or the dopamine agonist pramipexole (PPX) on disease progression in Parkinson disease using SPECT with the dopamine transporter (DAT)-radioligand [(123)I]beta-CIT as surrogate marker. Levodopa 73-81 solute carrier family 6 member 3 Homo sapiens 216-219 23902940-13 2013 These data suggest that nAChR agonists may be useful for the management of dyskinesias in l-DOPA-treated Parkinson"s disease patients. Levodopa 90-96 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 24-29 23896526-3 2013 Alterations of Akt/GSK3 have been observed and may contribute to the neurodegenerative processes and the development of L-DOPA-induced dyskinesia. Levodopa 120-126 AKT serine/threonine kinase 1 Homo sapiens 15-18 23896526-5 2013 L-DOPA and dopamine agonist dose-dependently and differentially modulated Akt and GSK3 expression and phosphorylation when added alone or combined. Levodopa 0-6 AKT serine/threonine kinase 1 Homo sapiens 74-77 23937977-8 2013 These findings could be exploited to design diverse and selective novel chemical libraries for the treatment of diseases and conditions where the alpha4beta2 nAChR is disrupted, such as Alzheimer disease, Parkinson"s disease and l-dopa-induced dyskinesia (LID). Levodopa 229-235 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 158-163 23481547-6 2013 This excitatory response was strongly attenuated by CNQX (10 muM), pointing to the involvement of TOPA quinone, an auto-oxidation product of L-DOPA and a potent activator of AMPA/kainate receptors. Levodopa 141-147 latexin Homo sapiens 61-64 24132839-7 2013 The depletion of motor and cognitive reserves and an increasingly complex response to levodopa with disease progression will also have an impact on the emergence of FOG episodes. Levodopa 86-94 zinc finger protein, FOG family member 1 Homo sapiens 165-168 23360800-12 2013 L-DOPA treatment increased GluR2-flip mRNA expression in the lesioned striatum of both groups; this was blocked by the Ca(2+)-permeable AMPA receptor antagonist IEM 1460. Levodopa 0-6 glutamate ionotropic receptor AMPA type subunit 2 Rattus norvegicus 27-32 23664961-3 2013 Here we investigated if the activation of astrocytic dopamine receptors (D1 and D2) regulates the expression of glial cell line-derived neurotrophic factor (GDNF) after combined in vitro hypoxia/aglycemia (H/A) and studied the expression of GDNF in the ischemic brain after treatment with levodopa/benserazide following transient occlusion of the middle cerebral artery (tMCAO) in the rat. Levodopa 289-297 glial cell derived neurotrophic factor Rattus norvegicus 157-161 23664961-7 2013 In addition, treatment with levodopa/benserazide significantly increased GDNF levels in the infarct core and peri-infarct area after tMCAO without affecting the expression of glial fibrillar acidic protein (GFAP), an intermediate filament and marker of reactive gliosis. Levodopa 28-36 glial cell derived neurotrophic factor Rattus norvegicus 73-77 24108333-2 2013 Although the P300 component has been used to assess cognitive changes induced by levodopa and deep brain stimulation (DBS), the effects caused by unilateral pallidotomy remain unknown. Levodopa 81-89 E1A binding protein p300 Homo sapiens 13-17 23664961-8 2013 After stroke, GDNF levels increase in the ischemic hemisphere in rats treated with levodopa, implicating GDNF in the mechanisms of tissue reorganization and plasticity and in l-DOPA enhanced recovery of lost brain function. Levodopa 83-91 glial cell derived neurotrophic factor Rattus norvegicus 14-18 23664961-8 2013 After stroke, GDNF levels increase in the ischemic hemisphere in rats treated with levodopa, implicating GDNF in the mechanisms of tissue reorganization and plasticity and in l-DOPA enhanced recovery of lost brain function. Levodopa 83-91 glial cell derived neurotrophic factor Rattus norvegicus 105-109 23664961-8 2013 After stroke, GDNF levels increase in the ischemic hemisphere in rats treated with levodopa, implicating GDNF in the mechanisms of tissue reorganization and plasticity and in l-DOPA enhanced recovery of lost brain function. Levodopa 175-181 glial cell derived neurotrophic factor Rattus norvegicus 14-18 23884809-3 2013 Also, mutations in mitochondrial DNA polymerase gamma result in multiple mitochondrial DNA deletions that can be associated with levodopa-responsive parkinsonism and severe substantia nigra pars compacta dopaminergic neurodegeneration. Levodopa 129-137 polymerase (DNA directed), gamma Mus musculus 19-53 23881105-0 2013 Exome sequencing expands the mutational spectrum of SPG8 in a family with spasticity responsive to L-DOPA treatment. Levodopa 99-105 WASH complex subunit 5 Homo sapiens 52-56 23917951-6 2013 Thus adenosine A2A antagonists, safinamide, and the antiepileptic agent zonisamide can extend the duration of action of levodopa. Levodopa 120-128 immunoglobulin kappa variable 2D-29 Homo sapiens 15-18 23616567-3 2013 The candidate transport systems for L-DOPA, the source for dopamine, include the sodium-dependent systems B(0), B(0,+), and y(+)L, and the sodium-independent systems L (LAT1 and LAT2) and b(0,+). Levodopa 36-42 linker for activation of T cells family, member 2 Rattus norvegicus 178-182 23616567-4 2013 Renal LAT2 is overexpressed in the prehypertensive spontaneously hypertensive rat (SHR), which might contribute to enhanced L-DOPA uptake in the proximal tubule and increased dopamine production, as an attempt to overcome the defect in D1 receptor function. Levodopa 124-130 linker for activation of T cells family, member 2 Rattus norvegicus 6-10 23241013-0 2013 Drebrin immunoreactivity in the striatum of a rat model of levodopa-induced dyskinesia. Levodopa 59-67 drebrin 1 Rattus norvegicus 0-7 23241013-4 2013 The cross-sectional area of drebrin-immunoreactive organelles, putative spines, in the dopamine-denervated striatum of the levodopa-induced dyskinesia model was greater than that of the Parkinson"s disease model. Levodopa 123-131 drebrin 1 Rattus norvegicus 28-35 23241013-5 2013 Immunoelectron microscopic examinations confirmed that drebrin-immunoreactive spines became enlarged in the dopamine-denervated striatum of the levodopa-induced dyskinesia model, but not in the Parkinson"s disease model. Levodopa 144-152 drebrin 1 Rattus norvegicus 55-62 24018429-2 2013 The content of L-dihydroxyphenylalanine (L-DOPA) was assessed in the frontal lobe, thalamus, hypothalamus and brain stem of rats by high-pressure chromatography with electrochemical detection (HPLC/ED) after administration of 5-HT3 receptor ligands. Levodopa 15-39 5-hydroxytryptamine receptor 3A Rattus norvegicus 226-240 23583932-0 2013 alpha4beta2 Nicotinic receptors play a role in the nAChR-mediated decline in L-dopa-induced dyskinesias in parkinsonian rats. Levodopa 77-83 cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus 51-56 23583932-10 2013 A series of beta2* nAChR compounds, including TC-2696, TI-10165, TC-8831, TC-10600 and sazetidine reduced l-dopa-induced AIMs in these rats by 23-32%. Levodopa 106-112 UDP glucuronosyltransferase 1 family, polypeptide A7C Rattus norvegicus 12-17 23583932-10 2013 A series of beta2* nAChR compounds, including TC-2696, TI-10165, TC-8831, TC-10600 and sazetidine reduced l-dopa-induced AIMs in these rats by 23-32%. Levodopa 106-112 cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus 19-24 23228187-7 2013 An independent association was also found with the severity of motor symptoms (Hoehn-Yahr stage, OR 1 48 (95 % CI 1 00, 2 55); P= 0 049) and levodopa dose (OR 1 16 (95 % CI 1 04, 1 31) mg/kg per d; P= 0 009). Levodopa 141-149 olfactory receptor family 7 subfamily E member 2 pseudogene Homo sapiens 156-163 23861813-0 2013 DAT1 polymorphism determines L-DOPA effects on learning about others" prosociality. Levodopa 29-35 solute carrier family 6 member 3 Homo sapiens 0-4 23607456-8 2013 The increase in PRL concentration after isolation was abolished by pre-injection of L-DOPA. Levodopa 84-90 prolactin Bos taurus 16-19 23607456-0 2013 L-DOPA attenuates prolactin secretion in response to isolation stress in Holstein steers. Levodopa 0-6 prolactin Bos taurus 18-27 23524988-8 2013 Levodopa is less preferred for treating daily RLS due to its high risk of augmentation. Levodopa 0-8 RLS1 Homo sapiens 46-49 23237479-9 2013 CONCLUSIONS: In line with the model of non-linear effects of l-dopa on cortical plasticity high dopaminergic prefrontal activity mediated by COMT Val158Met polymorphism predicts a detrimental effect of anodal tDCS on cognitive flexibility. Levodopa 61-67 catechol-O-methyltransferase Homo sapiens 141-145 23887222-0 2013 Effects of Levodopa loaded chitosan nanoparticles on cell viability and caspase-3 expression in PC12 neural like cells. Levodopa 11-19 caspase 3 Rattus norvegicus 72-81 23363854-0 2013 Polymorphisms in the dopamine transporter gene are associated with visual hallucinations and levodopa equivalent dose in Brazilians with Parkinson"s disease. Levodopa 93-101 solute carrier family 6 member 3 Homo sapiens 21-41 23363854-3 2013 Polymorphisms in the DAT1 gene might affect the reuptake of dopamine in the synaptic cleft, but the influence of this variability on adverse effects or levodopa equivalent dose on PD patients is still poorly investigated. Levodopa 152-160 solute carrier family 6 member 3 Homo sapiens 21-25 23363854-4 2013 Therefore, the aim of the present study was to investigate DAT1 gene polymorphisms on levodopa equivalent dose and visual hallucination occurrence in PD patients. Levodopa 86-94 solute carrier family 6 member 3 Homo sapiens 59-63 23363854-10 2013 Our results support an effect of DAT1 polymorphisms in adverse effects of anti-Parkinsonian drugs and in levodopa equivalent dose usage. Levodopa 105-113 solute carrier family 6 member 3 Homo sapiens 33-37 24403689-9 2013 This case study shows a person with PD demonstrating decreased cerebral oxygenation during FOG, which may be based on his variable response to levodopa medication or may be attributable to as yet unidentified physiologic mechanisms. Levodopa 143-151 zinc finger protein, FOG family member 1 Homo sapiens 91-94 23524988-9 2013 For intermittent RLS, it is levodopa or dopamine agonists or low-potency opioids or benzodiazepines. Levodopa 28-36 RLS1 Homo sapiens 17-20 22926528-8 2013 In conclusion ET-PD patients differed from PD patients, showing more frequent familial tremor histories and lower levodopa responsiveness. Levodopa 114-122 major facilitator superfamily domain containing 11 Homo sapiens 14-16 23776585-1 2013 Tyrosinase, which catalyzes both the hydroxylation of tyrosine and consequent oxidation of L-DOPA to form melanin in melanocytes, is also expressed in the brain, and oxidizes L-DOPA and dopamine. Levodopa 91-97 tyrosinase Mus musculus 0-10 23776585-1 2013 Tyrosinase, which catalyzes both the hydroxylation of tyrosine and consequent oxidation of L-DOPA to form melanin in melanocytes, is also expressed in the brain, and oxidizes L-DOPA and dopamine. Levodopa 175-181 tyrosinase Mus musculus 0-10 23762458-0 2013 Motivational disturbances and effects of L-dopa administration in neurofibromatosis-1 model mice. Levodopa 41-47 neurofibromin 1 Mus musculus 66-85 23776585-5 2013 Transplantation of tyrosinase cDNA-transfected hepatoma cells, which constitutively produce L-DOPA, resulted in marked amelioration of the asymmetric apomorphine-induced rotation in hemi-parkinsonian mice and the effect was present up to 2 months. Levodopa 92-98 tyrosinase Mus musculus 19-29 22887993-2 2013 Moreover, MAO-B inhibitors are used in the treatment of idiopathic Parkinson disease as preliminary monotherapy or adjunct therapy with L-dopa. Levodopa 136-142 monoamine oxidase B Homo sapiens 10-15 23328768-0 2013 Persistent activation of the D1R/Shp-2/Erk1/2 pathway in l-DOPA-induced dyskinesia in the 6-hydroxy-dopamine rat model of Parkinson"s disease. Levodopa 57-63 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 33-38 23328768-0 2013 Persistent activation of the D1R/Shp-2/Erk1/2 pathway in l-DOPA-induced dyskinesia in the 6-hydroxy-dopamine rat model of Parkinson"s disease. Levodopa 57-63 mitogen activated protein kinase 3 Rattus norvegicus 39-45 23328768-6 2013 In these animals, the chronic activation of D1R either by l-DOPA or by the selective D1R agonist SKF 38393 induced both dyskinesia and Shp-2/Erk1/2 activation. Levodopa 58-64 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 135-140 23328768-6 2013 In these animals, the chronic activation of D1R either by l-DOPA or by the selective D1R agonist SKF 38393 induced both dyskinesia and Shp-2/Erk1/2 activation. Levodopa 58-64 mitogen activated protein kinase 3 Rattus norvegicus 141-147 23328768-8 2013 Interestingly, we found that D1R-mediated Shp-2-Erk1/2 activation was persistently detected in the striatum of dyskinetic rats during l-DOPA washout, with a close correlation between LID severity and the extent of long term activation of both Shp-2 and Erk1/2. Levodopa 134-140 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 42-47 23328768-8 2013 Interestingly, we found that D1R-mediated Shp-2-Erk1/2 activation was persistently detected in the striatum of dyskinetic rats during l-DOPA washout, with a close correlation between LID severity and the extent of long term activation of both Shp-2 and Erk1/2. Levodopa 134-140 mitogen activated protein kinase 3 Rattus norvegicus 48-54 23328768-9 2013 Taken together, our data show that in hemiparkinsonian rats developing dyskinesia, the aberrant phosphorylation of Shp-2 by D1R activation, represents an upstream molecular event leading to the persistent phosphorylation of Erk1/2 and therefore a novel therapeutic target to counteract LID development and maintenance during l-DOPA therapy. Levodopa 325-331 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 115-120 23328768-9 2013 Taken together, our data show that in hemiparkinsonian rats developing dyskinesia, the aberrant phosphorylation of Shp-2 by D1R activation, represents an upstream molecular event leading to the persistent phosphorylation of Erk1/2 and therefore a novel therapeutic target to counteract LID development and maintenance during l-DOPA therapy. Levodopa 325-331 mitogen activated protein kinase 3 Rattus norvegicus 224-230 23539311-5 2013 However, both concentrations of berberine in 6-OHDA-lesioned groups treated with L-DOPA aggravated the numbers of TH-immunopositive neurons in the substantia nigra and the levels of dopamine, norepinephrine, DOPAC and HVA in the striatum as compared to rats not treated with berberine. Levodopa 81-87 tyrosine hydroxylase Rattus norvegicus 114-116 23611155-0 2013 GluN2A and GluN2B NMDA receptor subunits differentially modulate striatal output pathways and contribute to levodopa-induced abnormal involuntary movements in dyskinetic rats. Levodopa 108-116 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 0-6 23439215-0 2013 Task-dependent interactions between dopamine D2 receptor polymorphisms and L-DOPA in patients with Parkinson"s disease. Levodopa 75-81 dopamine receptor D2 Homo sapiens 36-56 23439215-2 2013 In the current study, we determined whether a dopamine D2 receptor DNA sequence polymorphism interacts with L-DOPA during motor tasks in patients with Parkinson"s disease (PD). Levodopa 108-114 dopamine receptor D2 Homo sapiens 46-66 23439215-5 2013 For motor sequence learning, DRD2 genotype mediated L-DOPA effects such that L-DOPA associated improvements were only observed in the minor T allele carriers (associated with lower D2 receptor availability, t10=-2.71, p=0.022), whereas G homozygotes showed no performance change with L-DOPA. Levodopa 52-58 dopamine receptor D2 Homo sapiens 29-33 23439215-5 2013 For motor sequence learning, DRD2 genotype mediated L-DOPA effects such that L-DOPA associated improvements were only observed in the minor T allele carriers (associated with lower D2 receptor availability, t10=-2.71, p=0.022), whereas G homozygotes showed no performance change with L-DOPA. Levodopa 77-83 dopamine receptor D2 Homo sapiens 29-33 23439215-5 2013 For motor sequence learning, DRD2 genotype mediated L-DOPA effects such that L-DOPA associated improvements were only observed in the minor T allele carriers (associated with lower D2 receptor availability, t10=-2.71, p=0.022), whereas G homozygotes showed no performance change with L-DOPA. Levodopa 77-83 dopamine receptor D2 Homo sapiens 29-33 23658034-5 2013 A mutation was detected in TITF1 (c.825delC) in both of them and clinical improvement was observed in the response to treatment with low doses of levodopa-carbidopa. Levodopa 146-154 NK2 homeobox 1 Homo sapiens 27-32 23611155-0 2013 GluN2A and GluN2B NMDA receptor subunits differentially modulate striatal output pathways and contribute to levodopa-induced abnormal involuntary movements in dyskinetic rats. Levodopa 108-116 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 11-17 23613810-10 2013 Individually, DRD2/ANKK1 genotype was significantly associated with motor learning (p = .02) and its modulation by L-Dopa (p<.0001), but not with any TMS measures. Levodopa 115-121 dopamine receptor D2 Homo sapiens 14-18 23403028-0 2013 L-Dopa synthesis catalyzed by tyrosinase immobilized in poly(ethyleneoxide) conducting polymers. Levodopa 0-6 tyrosinase Homo sapiens 30-40 23403028-2 2013 In this study, with regards to the synthesis of L-Dopa two types of biosensors were designed by immobilizing tyrosinase on conducting polymers: thiophene capped poly(ethyleneoxide)/polypyrrole (PEO-co-PPy) and 3-methylthienyl methacrylate-co-p-vinylbenzyloxy poly(ethyleneoxide)/polypyrrole (CP-co-PPy). Levodopa 48-54 tyrosinase Homo sapiens 109-119 23453891-6 2013 The PN may be linked to use of high-dose levodopa, promoting high levels of homocysteine and methylmalonic acid or reduced absorption of vitamins essential for homocysteine metabolism. Levodopa 41-49 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 4-6 23237247-5 2013 Also, hBMMSCs cultured on DOPA-coated plates exhibited a higher degree of osteogenic differentiation than did hBMMSCs cultured on noncoated plates, as evaluated with alkaline phosphate (ALP) activity, calcium content, and the mRNA expression of runt-related transcription factor 2, ALP, and osteocalcin. Levodopa 26-30 RUNX family transcription factor 2 Homo sapiens 245-280 23237247-5 2013 Also, hBMMSCs cultured on DOPA-coated plates exhibited a higher degree of osteogenic differentiation than did hBMMSCs cultured on noncoated plates, as evaluated with alkaline phosphate (ALP) activity, calcium content, and the mRNA expression of runt-related transcription factor 2, ALP, and osteocalcin. Levodopa 26-30 bone gamma-carboxyglutamate protein Homo sapiens 291-302 23428503-9 2013 FosB/DeltaFosB expression in lateral striatum was correlated with l-DOPA-induced dyskinesia. Levodopa 66-72 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-4 23613810-10 2013 Individually, DRD2/ANKK1 genotype was significantly associated with motor learning (p = .02) and its modulation by L-Dopa (p<.0001), but not with any TMS measures. Levodopa 115-121 ankyrin repeat and kinase domain containing 1 Homo sapiens 19-24 23261515-2 2013 Dopamine is produced first by hydroxylalation of l-tyrosine to l-dihydroxyphenylalanine (l-dopa) and subsequently by the decarboxylation of l-dopa to dopamine catalysed by the enzymes tyrosine hydroxylase and aromatic l-amino acid decarboxylase (AADC) respectively. Levodopa 89-95 dopa decarboxylase Homo sapiens 246-250 23357114-0 2013 Parallel dopamine D1 receptor activity dependence of l-Dopa-induced normal movement and dyskinesia in mice. Levodopa 53-59 dopamine receptor D1 Mus musculus 18-29 23357114-7 2013 These results also indicate that l-dopa stimulated both normal and dyskinetic movements primarily via D1 receptor activation and that proper D1 agonism is potentially an efficacious therapy for PD motor deficits. Levodopa 33-39 dopamine receptor D1 Mus musculus 102-113 23515972-3 2013 Levodopa still remains the gold standard for the treatment of motor symptoms of PD but dopamine agonists (DAs), catechol-O-methyltransferase (COMT) inhibitors and monoamine oxidase B (MAO-B) inhibitors have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes and decrease the risk of levodopa-induced motor complications. Levodopa 356-364 monoamine oxidase B Homo sapiens 184-189 23261515-2 2013 Dopamine is produced first by hydroxylalation of l-tyrosine to l-dihydroxyphenylalanine (l-dopa) and subsequently by the decarboxylation of l-dopa to dopamine catalysed by the enzymes tyrosine hydroxylase and aromatic l-amino acid decarboxylase (AADC) respectively. Levodopa 89-95 dopa decarboxylase Homo sapiens 209-244 23593219-8 2013 STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson"s disease. Levodopa 12-18 adrenoceptor beta 1 Rattus norvegicus 223-228 23593219-8 2013 STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson"s disease. Levodopa 12-18 adrenoceptor beta 1 Rattus norvegicus 248-274 23196068-4 2013 Since l-dopa could be decarboxylated by aromatic amino acid decarboxylase (AADC) present within both dopamine and serotonin neurons, it was hypothesized that serotonin neurons convert l-dopa into dopamine to generate excessive reactive oxygen species and quinoproteins that ultimately lead to serotonin neuron death. Levodopa 6-12 dopa decarboxylase Rattus norvegicus 75-79 23196068-4 2013 Since l-dopa could be decarboxylated by aromatic amino acid decarboxylase (AADC) present within both dopamine and serotonin neurons, it was hypothesized that serotonin neurons convert l-dopa into dopamine to generate excessive reactive oxygen species and quinoproteins that ultimately lead to serotonin neuron death. Levodopa 184-190 dopa decarboxylase Rattus norvegicus 75-79 23196068-10 2013 The MAO inhibitor, pargyline, also attenuated cell death and ROS after l-dopa treatment. Levodopa 71-77 monoamine oxidase A Rattus norvegicus 4-7 23261515-2 2013 Dopamine is produced first by hydroxylalation of l-tyrosine to l-dihydroxyphenylalanine (l-dopa) and subsequently by the decarboxylation of l-dopa to dopamine catalysed by the enzymes tyrosine hydroxylase and aromatic l-amino acid decarboxylase (AADC) respectively. Levodopa 140-146 dopa decarboxylase Homo sapiens 209-244 23261515-2 2013 Dopamine is produced first by hydroxylalation of l-tyrosine to l-dihydroxyphenylalanine (l-dopa) and subsequently by the decarboxylation of l-dopa to dopamine catalysed by the enzymes tyrosine hydroxylase and aromatic l-amino acid decarboxylase (AADC) respectively. Levodopa 140-146 dopa decarboxylase Homo sapiens 246-250 23261515-7 2013 The same concentration of l-dopa was also found to increase intracellular GSH in SH-SY5Y cells, however when AADC was inhibited this affect was abolished. Levodopa 26-32 dopa decarboxylase Homo sapiens 109-113 23281915-1 2013 L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is a complication of dopaminergic treatment in Parkinson"s disease. Levodopa 30-36 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 0-3 23395217-1 2013 BACKGROUND: Subthalamic Nucleus Deep Brain Stimulation (STN-DBS) represents a valid therapeutic option for advanced Parkinson"s disease (PD), leading to a significant amelioration of motor fluctuations and levodopa-induced involuntary movements (IM). Levodopa 206-214 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 56-59 23265352-8 2013 Moreover, the beneficial effect was observed only in patients with levodopa-resistant FOG. Levodopa 67-75 zinc finger protein, FOG family member 1 Homo sapiens 86-89 23339054-1 2013 BACKGROUND: Adenosine A2A receptor antagonists reduce or prevent the development of dyskinesia in animal models of levodopa-induced dyskinesia. Levodopa 115-123 adenosine A2a receptor Homo sapiens 12-34 23658969-0 2010 Discovery of a novel metabotropic glutamate receptor 4 (mGlu4) positive allosteric modulator (PAM) extended probe: Characterization of ML292, a potent and selective mGlu4 PAM which produces efficacy alone or in combination with L-DOPA in preclinical rodent models of Parkinson"s disease ML292 was identified through a medicinal chemistry campaign that was designed to improve the in vivo characteristics of ML128 and ML182. Levodopa 228-234 glutamate metabotropic receptor 4 Rattus norvegicus 21-54 23420105-5 2013 Moreover, in the 1-methyl-4-phenyl-1,2,4,6-tetrahydropyridine (MPTP) mouse model, dopamine deficiency caused increased phosphorylation of both Tyr15-Cdk5 and Thr75-DARPP-32 in the striatum, which could be attenuated by administration of L-3,4-dihydroxyphenylalanine and imatinib (STI-571), a selective c-Abl inhibitor. Levodopa 237-265 cyclin-dependent kinase 5 Mus musculus 143-153 23423244-5 2013 Thus, 5-HT(1A) agonists improve the various motor disorders associated with dopaminergic deficits, dyskinesia induced by chronic L-DOPA treatment, mood disturbances (anxiety and depression) and dopamine agonist-induced emesis. Levodopa 129-135 5-hydroxytryptamine receptor 1A Homo sapiens 6-13 23413259-5 2013 This study shows that (i) although rare, C9orf72 repeat expansions may be associated with clinically typical Parkinson"s disease and also with other parkinsonism; (ii) in several patients, parkinsonism was levodopa-responsive and remained pure, without associated dementia, for >10 years and (iii) interestingly, all C9orf72 repeat expansion carriers had positive family histories of parkinsonism, degenerative dementias or amyotrophic lateral sclerosis. Levodopa 206-214 C9orf72-SMCR8 complex subunit Homo sapiens 41-48 23413259-5 2013 This study shows that (i) although rare, C9orf72 repeat expansions may be associated with clinically typical Parkinson"s disease and also with other parkinsonism; (ii) in several patients, parkinsonism was levodopa-responsive and remained pure, without associated dementia, for >10 years and (iii) interestingly, all C9orf72 repeat expansion carriers had positive family histories of parkinsonism, degenerative dementias or amyotrophic lateral sclerosis. Levodopa 206-214 C9orf72-SMCR8 complex subunit Homo sapiens 317-324 22491024-0 2013 Synergy between L-DOPA and a novel positive allosteric modulator of metabotropic glutamate receptor 4: implications for Parkinson"s disease treatment and dyskinesia. Levodopa 16-22 glutamate metabotropic receptor 4 Rattus norvegicus 68-101 23206800-5 2013 While both tea catechins and quercetin strongly inhibit human liver catechol-O-methyltransferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+)-catechin exerts a significant inhibition of L-DOPA methylation in both peripheral compartment and striatum in rats. Levodopa 130-136 catechol-O-methyltransferase Homo sapiens 68-96 23206800-5 2013 While both tea catechins and quercetin strongly inhibit human liver catechol-O-methyltransferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+)-catechin exerts a significant inhibition of L-DOPA methylation in both peripheral compartment and striatum in rats. Levodopa 130-136 catechol-O-methyltransferase Homo sapiens 98-102 23206800-5 2013 While both tea catechins and quercetin strongly inhibit human liver catechol-O-methyltransferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+)-catechin exerts a significant inhibition of L-DOPA methylation in both peripheral compartment and striatum in rats. Levodopa 200-206 catechol-O-methyltransferase Homo sapiens 98-102 23265352-9 2013 This result supports our hypothesis, at least in patients with levodopa-resistant FOG, and shows that the co-administration of L-DOPS and entacapone could be a new strategy for FOG treatment. Levodopa 63-71 zinc finger protein, FOG family member 1 Homo sapiens 82-85 23265352-9 2013 This result supports our hypothesis, at least in patients with levodopa-resistant FOG, and shows that the co-administration of L-DOPS and entacapone could be a new strategy for FOG treatment. Levodopa 63-71 zinc finger protein, FOG family member 1 Homo sapiens 177-180 23159831-3 2013 Functionally, while having no detectable motor effect in wild type mice, the 5-HT2R agonist 2,5-dimethoxy-4-iodoamphetamine increased both the baseline and l-dopa-induced normal ambulatory and dyskinetic movements in Pitx3 mutant mice, whereas the selective 5-HT2AR blocker volinanserin had the opposite effects. Levodopa 156-162 paired-like homeodomain transcription factor 3 Mus musculus 217-222 24459666-0 2013 Immobilization of bone morphogenetic protein on DOPA- or dopamine-treated titanium surfaces to enhance osseointegration. Levodopa 48-52 bone morphogenetic protein 1 Homo sapiens 18-44 24312874-0 2013 Dampening of Serotonergic System through 5HT1A Receptors is a Promising Target for Treatment of Levodopa Induced Motor Problems. Levodopa 96-104 5-hydroxytryptamine receptor 1A Homo sapiens 41-46 24312874-5 2013 With respect to the role of serotonergic projection in Parkinson"s disease and importance of 5HT1A receptors in motor activity it seems that inactivation of these neurons by stimulation of 5HT1A receptors could provide benefits in treatment of Levodopa induced motor impairments. Levodopa 244-252 5-hydroxytryptamine receptor 1A Homo sapiens 93-98 24312874-5 2013 With respect to the role of serotonergic projection in Parkinson"s disease and importance of 5HT1A receptors in motor activity it seems that inactivation of these neurons by stimulation of 5HT1A receptors could provide benefits in treatment of Levodopa induced motor impairments. Levodopa 244-252 5-hydroxytryptamine receptor 1A Homo sapiens 189-194 23010244-1 2013 Tyrosine hydroxylase (TH) is the rate-limiting step in dopamine (DA) synthesis, oxidizing tyrosine to l-DOPA, which is further metabolized to DA. Levodopa 102-108 tyrosine hydroxylase Homo sapiens 0-20 23010244-1 2013 Tyrosine hydroxylase (TH) is the rate-limiting step in dopamine (DA) synthesis, oxidizing tyrosine to l-DOPA, which is further metabolized to DA. Levodopa 102-108 tyrosine hydroxylase Homo sapiens 22-24 24054140-6 2013 It means that l-3,4-dihydroxyphenylalanine (l-DOPA) synthesized from l-tyrosine in monoenzymatic TH neurons is transported to monoenzymatic AADC neurons for DA synthesis. Levodopa 14-42 dopa decarboxylase Homo sapiens 140-144 24054140-6 2013 It means that l-3,4-dihydroxyphenylalanine (l-DOPA) synthesized from l-tyrosine in monoenzymatic TH neurons is transported to monoenzymatic AADC neurons for DA synthesis. Levodopa 44-50 dopa decarboxylase Homo sapiens 140-144 24459666-1 2013 Titanium was treated with 3,4-dihydroxy-L-phenylalanine (DOPA) or dopamine to immobilize bone morphogenetic protein-2 (BMP2), a biomolecule. Levodopa 26-55 bone morphogenetic protein 2 Homo sapiens 89-117 24024214-4 2013 Analyses of effects of pharmacological treatments suggested significantly higher BDNF serum levels in patients taking mood stabilizers/antiepileptics (P = 0.009) and L-DOPA (P < 0.001) and significant reductions in patients taking benzodiazepines (P = 0.020). Levodopa 166-172 brain derived neurotrophic factor Homo sapiens 81-85 24459666-1 2013 Titanium was treated with 3,4-dihydroxy-L-phenylalanine (DOPA) or dopamine to immobilize bone morphogenetic protein-2 (BMP2), a biomolecule. Levodopa 26-55 bone morphogenetic protein 2 Homo sapiens 119-123 24459666-11 2013 Thus, the present study demonstrates that titanium treated with DOPA or dopamine can become bioactive via the surface immobilization of BMP2, which induces specific signal transduction. Levodopa 64-68 bone morphogenetic protein 2 Homo sapiens 136-140 23938307-0 2013 mTOR inhibition alleviates L-DOPA-induced dyskinesia in parkinsonian rats. Levodopa 27-33 mechanistic target of rapamycin kinase Rattus norvegicus 0-4 23391905-8 2013 LCa/Mg diet-induced catalepsy was improved by the administration of L-DOPA (50-200 mg/kg i.p.) Levodopa 68-74 clathrin, light polypeptide (Lca) Mus musculus 0-3 23821384-5 2013 After treatment with L-DOPA, both the CD95/CD3 ratio, assumed to represent an antigen marker characteristic of apoptotic cells, and the number of cells dead due to apoptotic processes were found to be decreased. Levodopa 21-27 Fas cell surface death receptor Homo sapiens 38-42 22592937-0 2013 The effect of piribedil on L-DOPA-induced dyskinesias in a rat model of Parkinson"s disease: differential role of alpha(2) adrenergic mechanisms. Levodopa 27-33 UDP glucuronosyltransferase 1 family, polypeptide A7C Rattus norvegicus 51-52 23781496-0 2013 Interaction of human Dopa decarboxylase with L-Dopa: spectroscopic and kinetic studies as a function of pH. Levodopa 45-51 dopa decarboxylase Homo sapiens 21-39 23781496-4 2013 During the reaction of hDDC with L-Dopa, monitored by stopped-flow spectrophotometry, a 420 nm band attributed to the 4"-N-protonated external aldimine first appears, and its decrease parallels the emergence of a 390 nm peak, assigned to the 4"-N-unprotonated external aldimine. Levodopa 33-39 dopa decarboxylase Homo sapiens 23-27 23569367-4 2013 METHODS: In this study, we investigated the effect of 6-hydroxydopamine lesions in dopaminergic neurons and chronic treatment with levodopa on expression of G protein-coupled receptor kinase 6 and beta-arrestin-1, two key regulators of G protein-coupled receptors, in the rat striatum. Levodopa 131-139 G protein-coupled receptor kinase 6 Rattus norvegicus 157-192 23569367-4 2013 METHODS: In this study, we investigated the effect of 6-hydroxydopamine lesions in dopaminergic neurons and chronic treatment with levodopa on expression of G protein-coupled receptor kinase 6 and beta-arrestin-1, two key regulators of G protein-coupled receptors, in the rat striatum. Levodopa 131-139 arrestin, beta 1 Rattus norvegicus 197-212 23569367-7 2013 In addition, coadministration of the N-methyl-D-aspartate receptor antagonist, MK-801, and levodopa reversed the reduction of G protein-coupled receptor kinase 6 and beta-arrestin-1 in the striatum. Levodopa 91-99 G protein-coupled receptor kinase 6 Rattus norvegicus 126-161 23569367-7 2013 In addition, coadministration of the N-methyl-D-aspartate receptor antagonist, MK-801, and levodopa reversed the reduction of G protein-coupled receptor kinase 6 and beta-arrestin-1 in the striatum. Levodopa 91-99 arrestin, beta 1 Rattus norvegicus 166-181 23569367-9 2013 CONCLUSION: These data indicate that G protein-coupled receptor kinase 6 and beta-arrestin-1 in striatal neurons are sensitive to dopamine depletion and are downregulated in rats with Parkinson"s disease and in levodopa-treated rats with the disease. Levodopa 211-219 G protein-coupled receptor kinase 6 Rattus norvegicus 37-72 23569367-9 2013 CONCLUSION: These data indicate that G protein-coupled receptor kinase 6 and beta-arrestin-1 in striatal neurons are sensitive to dopamine depletion and are downregulated in rats with Parkinson"s disease and in levodopa-treated rats with the disease. Levodopa 211-219 arrestin, beta 1 Rattus norvegicus 77-92 23646697-9 2013 The enzymatic assay using L-DOPA and mushroom tyrosinase demonstrated that H2-Silica restrained UVA-mediated melanin formation owing to down-regulation of tyrosinase activity, which could be attributed to scavenging of free radicals and inhibition of L-DOPA-to-dopachrome oxidation by hydrogen released from H2-Silica. Levodopa 26-32 tyrosinase Homo sapiens 155-165 23646697-9 2013 The enzymatic assay using L-DOPA and mushroom tyrosinase demonstrated that H2-Silica restrained UVA-mediated melanin formation owing to down-regulation of tyrosinase activity, which could be attributed to scavenging of free radicals and inhibition of L-DOPA-to-dopachrome oxidation by hydrogen released from H2-Silica. Levodopa 251-257 tyrosinase Homo sapiens 46-56 23646697-9 2013 The enzymatic assay using L-DOPA and mushroom tyrosinase demonstrated that H2-Silica restrained UVA-mediated melanin formation owing to down-regulation of tyrosinase activity, which could be attributed to scavenging of free radicals and inhibition of L-DOPA-to-dopachrome oxidation by hydrogen released from H2-Silica. Levodopa 251-257 tyrosinase Homo sapiens 155-165 23948989-2 2013 Oral levodopa has been widely used for over 40 years, often in combination with a dopa-decarboxylase inhibitor (DDCI), which reduces many treatment complications, extending its half-life and increasing levodopa availability to the brain. Levodopa 5-13 dopa decarboxylase Homo sapiens 82-100 23948989-2 2013 Oral levodopa has been widely used for over 40 years, often in combination with a dopa-decarboxylase inhibitor (DDCI), which reduces many treatment complications, extending its half-life and increasing levodopa availability to the brain. Levodopa 202-210 dopa decarboxylase Homo sapiens 82-100 23948989-3 2013 Entacapone, a catechol-O-methyltransferase inhibitor, can also be used to improve the bioavailability of levodopa, especially when used in conjunction with a DDCI. Levodopa 105-113 catechol-O-methyltransferase Homo sapiens 14-42 22858180-6 2013 dPD subjects were younger at onset (p < 0.0001), had more psychosis (p: 0.038), were receiving higher levodopa equivalent daily doses (p: 0.02), were predominantly left-handed (p: 0.048), and had greater frequency of left-sided onset (p: 0.015) compared to cPD subjects. Levodopa 102-110 dachs Drosophila melanogaster 0-3 22538235-3 2013 Because previous research has shown that levodopa and DBS variably influence beta LFP activity (8-20 Hz), we designed this study to find out how they affect low-frequency (LF) oscillations (2-7 Hz). Levodopa 41-49 lamin A/C Homo sapiens 82-85 23526936-5 2013 L-Dopa, but not dopamine nor any other catecholamine, appears in pigmented retina as soon as tyrosinase is expressed in RPE at E10.5. Levodopa 0-6 tyrosinase Mus musculus 93-103 23994933-2 2013 The aim of the study was to verify whether a combination of levodopa with DOPA decarboxylase and catechol-O-methyltransferase inhibitors (stalevo) could delay the development of dyskinesia compared to the standard two-component drug due to the more stable concentration levodopa in the blood that provided the persistent stimulation of dopamine receptors in the striatum. Levodopa 270-278 dopa decarboxylase Homo sapiens 74-92 23994933-2 2013 The aim of the study was to verify whether a combination of levodopa with DOPA decarboxylase and catechol-O-methyltransferase inhibitors (stalevo) could delay the development of dyskinesia compared to the standard two-component drug due to the more stable concentration levodopa in the blood that provided the persistent stimulation of dopamine receptors in the striatum. Levodopa 270-278 catechol-O-methyltransferase Homo sapiens 97-125 23223310-4 2012 D2-like receptor (D2R) agonists are a powerful clinical option as an alternative to L-DOPA, especially in the early stages of the disease, being associated to a reduced risk of dyskinesia development. Levodopa 84-90 dopamine receptor D2 Homo sapiens 18-21 23223310-5 2012 D2R agonists also find considerable application in the advanced stages of PD, in conjunction with L-DOPA, which is used in this context at lower dosages, to delay the appearance and the extent of the motor complications. Levodopa 98-104 dopamine receptor D2 Homo sapiens 0-3 21968930-5 2012 Administration of a therapeutic dose of L-dopa reverted the hypodopaminergic state in the NAcc of iuGC animals, normalized Drd2 expression and prevented morphine-induced hypermethylation of the Drd2 promoter. Levodopa 40-46 dopamine receptor D2 Rattus norvegicus 123-127 23143301-7 2012 These findings demonstrate the complex effects of UBE3A loss on dopamine signaling in subcortical motor pathways that may inform ongoing clinical trials of L-DOPA therapy in patients with AS. Levodopa 156-162 ubiquitin protein ligase E3A Homo sapiens 50-55 21968930-5 2012 Administration of a therapeutic dose of L-dopa reverted the hypodopaminergic state in the NAcc of iuGC animals, normalized Drd2 expression and prevented morphine-induced hypermethylation of the Drd2 promoter. Levodopa 40-46 dopamine receptor D2 Rattus norvegicus 194-198 22759925-0 2012 Effects of L-DOPA and STN-HFS dyskinesiogenic treatments on NR2B regulation in basal ganglia in the rat model of Parkinson"s disease. Levodopa 11-17 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 60-64 22759925-4 2012 Here, we investigated the possible association between L-DOPA- and STN-HFS-induced dyskinesia and regulation of the NR2B subunit of NMDA receptors in the rodent model of PD. Levodopa 55-61 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 116-120 22759925-8 2012 Both STN-HFS and L-DOPA dyskinesiogenic treatments induced NR2B activation in the STN and EP, but only L-DOPA triggered NR2B hyperphosphorylation in the striatum. Levodopa 17-23 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 59-63 22759925-8 2012 Both STN-HFS and L-DOPA dyskinesiogenic treatments induced NR2B activation in the STN and EP, but only L-DOPA triggered NR2B hyperphosphorylation in the striatum. Levodopa 103-109 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 120-124 22940695-0 2012 Effect of chronic l-DOPA treatment on 5-HT(1A) receptors in parkinsonian monkey brain. Levodopa 18-24 5-hydroxytryptamine receptor 1A Homo sapiens 38-45 22759925-9 2012 Finally, the use of CP-101,606 exacerbated L-DOPA-induced motor behavior and associated NR2B hyperphosphorylation in the striatum, STN and EP. Levodopa 43-49 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 88-92 22940695-7 2012 An increase of 5-HT(1A) receptor specific binding was observed in the hippocampus of MPTP monkeys treated with l-DOPA regardless to their adjunct treatment. Levodopa 111-117 5-hydroxytryptamine receptor 1A Homo sapiens 15-32 22820144-6 2012 Interestingly, our experiments in aphakia mice, which lack Pitx3 expression in the brain, indicate that the L-DOPA-dependent increase in the number of TH-ir neurons is independent of Pitx3, a transcription factor necessary for the development of mesencephalic dopaminergic neurons. Levodopa 108-114 paired-like homeodomain transcription factor 3 Mus musculus 59-64 22940695-8 2012 Cortical 5-HT(1A) receptor specific binding was increased in the l-DOPA-treated MPTP monkeys alone or with DHA or naltrexone and this increase was prevented in low dyskinetic MPTP monkeys treated with l-DOPA and Ro 61-8048. Levodopa 65-71 5-hydroxytryptamine receptor 1A Homo sapiens 9-26 22940695-8 2012 Cortical 5-HT(1A) receptor specific binding was increased in the l-DOPA-treated MPTP monkeys alone or with DHA or naltrexone and this increase was prevented in low dyskinetic MPTP monkeys treated with l-DOPA and Ro 61-8048. Levodopa 201-207 5-hydroxytryptamine receptor 1A Homo sapiens 9-26 22940695-9 2012 These results highlight the importance of 5-HT(1A) receptor alterations in treatment of PD with l-DOPA. Levodopa 96-102 5-hydroxytryptamine receptor 1A Homo sapiens 42-59 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 21-27 dopa decarboxylase Homo sapiens 70-105 22859504-5 2012 In open field tests, Mfn2 mutants show severe, age-dependent motor deficits that can be rescued with L-3,4 dihydroxyphenylalanine. Levodopa 101-129 mitofusin 2 Mus musculus 21-25 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 21-27 dopa decarboxylase Homo sapiens 107-111 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 21-27 catechol-O-methyltransferase Homo sapiens 117-146 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 21-27 catechol-O-methyltransferase Homo sapiens 148-152 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 191-197 dopa decarboxylase Homo sapiens 70-105 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 191-197 dopa decarboxylase Homo sapiens 107-111 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 191-197 catechol-O-methyltransferase Homo sapiens 117-146 23020119-5 2012 Two major peripheral L-Dopa metabolic pathways, driven by the enzymes Aromatic L-amino acid decarboxylase (AADC) and catechol-O-methyl transferase (COMT), significantly deplete the amount of L-Dopa reaching the brain. Levodopa 191-197 catechol-O-methyltransferase Homo sapiens 148-152 23041629-0 2012 PSD-95 expression controls L-DOPA dyskinesia through dopamine D1 receptor trafficking. Levodopa 27-33 discs large MAGUK scaffold protein 4 Homo sapiens 0-6 23041629-0 2012 PSD-95 expression controls L-DOPA dyskinesia through dopamine D1 receptor trafficking. Levodopa 27-33 dopamine receptor D1 Homo sapiens 53-73 23041629-1 2012 L-DOPA-induced dyskinesia (LID), a detrimental consequence of dopamine replacement therapy for Parkinson"s disease, is associated with an alteration in dopamine D1 receptor (D1R) and glutamate receptor interactions. Levodopa 0-6 dopamine receptor D1 Homo sapiens 152-172 23110504-9 2012 Running and enriched environment refused to stimulate NG2-generation and oligodendrogenesis in MPTP-mice, an effect which could be reversed by pharmacological levodopa-induced rescue. Levodopa 159-167 chondroitin sulfate proteoglycan 4 Mus musculus 54-57 22729819-8 2012 L-dopa, 5-hydroxytryptophan, and BH(4) are supplemented in PTPS and GTPCH-deficient patients, whereas L-dopa, 5-hydroxytryptophan, folinic acid and diet are used in DHPR-deficient patients. Levodopa 0-6 6-pyruvoyltetrahydropterin synthase Homo sapiens 59-63 23115014-7 2012 The combination of the following four independent contributors provided the best explanatory model of FOG (R(2) = 0.49): nongait freezing; levodopa equivalent dose (LED); cognitive impairment; and falls and balance problems. Levodopa 139-147 zinc finger protein, FOG family member 1 Homo sapiens 102-105 22703868-2 2012 OBJECTIVE: To assess the impact of the LRRK2 Gly2019Ser (G2019S) carrier status on the time to the onset of levodopa-induced dyskinesias (LID). Levodopa 108-116 leucine rich repeat kinase 2 Homo sapiens 39-44 22569849-2 2012 Agonists at 5-HT1A-receptors attenuate levodopa-induced motor complications in non-human primates. Levodopa 39-47 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 12-18 22569849-3 2012 Mice with increased dopamine D2 receptor (DRD2) signalling due to the lack of expression of the regulator of G-protein signalling 9 (RGS9) also develop dyskinesia following levodopa treatment. Levodopa 173-181 dopamine receptor D2 Mus musculus 20-40 22569849-3 2012 Mice with increased dopamine D2 receptor (DRD2) signalling due to the lack of expression of the regulator of G-protein signalling 9 (RGS9) also develop dyskinesia following levodopa treatment. Levodopa 173-181 dopamine receptor D2 Mus musculus 42-46 22569849-3 2012 Mice with increased dopamine D2 receptor (DRD2) signalling due to the lack of expression of the regulator of G-protein signalling 9 (RGS9) also develop dyskinesia following levodopa treatment. Levodopa 173-181 regulator of G-protein signaling 9 Mus musculus 96-131 22569849-3 2012 Mice with increased dopamine D2 receptor (DRD2) signalling due to the lack of expression of the regulator of G-protein signalling 9 (RGS9) also develop dyskinesia following levodopa treatment. Levodopa 173-181 regulator of G-protein signaling 9 Mus musculus 133-137 23171335-0 2012 DRD2 haplotype is associated with dyskinesia induced by levodopa therapy in Parkinson"s disease patients. Levodopa 56-64 dopamine receptor D2 Homo sapiens 0-4 23171335-5 2012 CONCLUSION: Our data suggest an influence of the DRD2/ANKK1 gene region on levodopa-induced dyskinesia. Levodopa 75-83 dopamine receptor D2 Homo sapiens 49-53 23171335-5 2012 CONCLUSION: Our data suggest an influence of the DRD2/ANKK1 gene region on levodopa-induced dyskinesia. Levodopa 75-83 ankyrin repeat and kinase domain containing 1 Homo sapiens 54-59 22967858-8 2012 The development of NHP FOG was significantly associated with the severity of parkinsonism, as shown by high motor disability scores (>= 20) and levodopa-induced dyskinesia scores (p=0.01 and p=0.04, respectively). Levodopa 147-155 zinc finger protein, FOG family member 1 Homo sapiens 23-26 23083099-2 2012 The DDC gene encodes L-DOPA decarboxylase, an enzyme catalyzing the decarboxylation of L-DOPA to dopamine. Levodopa 21-27 dopa decarboxylase Homo sapiens 4-7 22938619-10 2012 This approach also allowed the determination of tyrosinase activity because tyrosinase catalyzes the conversion of l-tyrosine to L-DOPA. Levodopa 129-135 tyrosinase Homo sapiens 48-58 22938619-10 2012 This approach also allowed the determination of tyrosinase activity because tyrosinase catalyzes the conversion of l-tyrosine to L-DOPA. Levodopa 129-135 tyrosinase Homo sapiens 76-86 22859407-1 2012 Targeted deletion or selective pharmacological inhibition of alpha(2C)-adrenoceptors in mice results in increased brain tissue levels of dopamine and its precursor l-3,4-dihydroxyphenylalanine (l-DOPA), without significant changes in l-DOPA synthesis. Levodopa 164-192 adrenergic receptor, alpha 2c Mus musculus 61-69 22859407-1 2012 Targeted deletion or selective pharmacological inhibition of alpha(2C)-adrenoceptors in mice results in increased brain tissue levels of dopamine and its precursor l-3,4-dihydroxyphenylalanine (l-DOPA), without significant changes in l-DOPA synthesis. Levodopa 194-200 adrenergic receptor, alpha 2c Mus musculus 61-69 22859407-1 2012 Targeted deletion or selective pharmacological inhibition of alpha(2C)-adrenoceptors in mice results in increased brain tissue levels of dopamine and its precursor l-3,4-dihydroxyphenylalanine (l-DOPA), without significant changes in l-DOPA synthesis. Levodopa 234-240 adrenergic receptor, alpha 2c Mus musculus 61-69 22859407-3 2012 Since alpha(2C)-adrenoceptors may influence the transport of l-DOPA, we investigated the effect of alpha(2C)-adrenoceptor activation on l-DOPA uptake in a kidney cell line (opossum kidney cells). Levodopa 136-142 adrenergic receptor, alpha 2c Mus musculus 99-107 22859407-10 2012 In conclusion, in a kidney cell line, alpha(2C)-adrenoceptor activation inhibits l-DOPA uptake, and in mice, deletion or blockade of alpha(2C)-adrenoceptors increases l-DOPA kidney tissue levels. Levodopa 81-87 adrenergic receptor, alpha 2c Mus musculus 38-60 22859407-10 2012 In conclusion, in a kidney cell line, alpha(2C)-adrenoceptor activation inhibits l-DOPA uptake, and in mice, deletion or blockade of alpha(2C)-adrenoceptors increases l-DOPA kidney tissue levels. Levodopa 81-87 adrenergic receptor, alpha 2c Mus musculus 38-46 22859407-10 2012 In conclusion, in a kidney cell line, alpha(2C)-adrenoceptor activation inhibits l-DOPA uptake, and in mice, deletion or blockade of alpha(2C)-adrenoceptors increases l-DOPA kidney tissue levels. Levodopa 167-173 adrenergic receptor, alpha 2c Mus musculus 38-60 22859407-10 2012 In conclusion, in a kidney cell line, alpha(2C)-adrenoceptor activation inhibits l-DOPA uptake, and in mice, deletion or blockade of alpha(2C)-adrenoceptors increases l-DOPA kidney tissue levels. Levodopa 167-173 adrenergic receptor, alpha 2c Mus musculus 38-46 23196729-4 2012 However, mutations inATP13A2, PLA2G6 and FBX07 are often associated with rapidly progressive parkinsonism and with additional features including pyramidal signs, cognitive decline and loss of sustained Levodopa responsiveness.Clarifying the phenotypes of each of these autosomal-recessive parkinsonian-pyramidal syndromes and understanding the mechanism ot these causative gene products might illuminate the pathogenesis of dopaminergic neuronal degeneration also in the common forms of PD. Levodopa 202-210 phospholipase A2 group VI Homo sapiens 30-36 22815142-5 2012 Of 17 enrolled patients, 11 were treated with different doses of L-DOPA; in this group, we found that the levels of two spots, corresponding to ATP synthase subunit beta and proteasome subunit beta type-2, correlated linearly with the L-DOPA daily dose. Levodopa 65-71 proteasome 20S subunit beta 2 Homo sapiens 174-204 22815142-5 2012 Of 17 enrolled patients, 11 were treated with different doses of L-DOPA; in this group, we found that the levels of two spots, corresponding to ATP synthase subunit beta and proteasome subunit beta type-2, correlated linearly with the L-DOPA daily dose. Levodopa 235-241 proteasome 20S subunit beta 2 Homo sapiens 174-204 22324564-3 2012 [Correction added on 18 April 2012, after online publication: In the preceding statement, 55 instead of 54 patients with PD were evaluated, and FOG negative consisted of 34 instead of 33 patients] Furthermore, we examined rCBF in FOG-negative patients treated with levodopa with or without selegiline. Levodopa 265-273 zinc finger protein, FOG family member 1 Homo sapiens 230-233 23196729-4 2012 However, mutations inATP13A2, PLA2G6 and FBX07 are often associated with rapidly progressive parkinsonism and with additional features including pyramidal signs, cognitive decline and loss of sustained Levodopa responsiveness.Clarifying the phenotypes of each of these autosomal-recessive parkinsonian-pyramidal syndromes and understanding the mechanism ot these causative gene products might illuminate the pathogenesis of dopaminergic neuronal degeneration also in the common forms of PD. Levodopa 202-210 F-box protein 7 Homo sapiens 41-46 21821315-0 2012 Targeting NR2A-containing NMDA receptors reduces L-DOPA-induced dyskinesias. Levodopa 49-55 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 10-14 22915735-8 2012 Both locomotor and gait-related deficits recovered in c-rel(-/-) mice treated with l-3,4-dihydroxyphenylalanine. Levodopa 83-111 reticuloendotheliosis oncogene Mus musculus 54-59 22762478-0 2012 Serotonin transporter inhibition attenuates l-DOPA-induced dyskinesia without compromising l-DOPA efficacy in hemi-parkinsonian rats. Levodopa 44-50 solute carrier family 6 member 4 Rattus norvegicus 0-21 22979934-0 2012 [Effects of Chinese herbal medicine Tianqi Pingchan Granule on G protein-coupled receptor kinase 6 involved in the prevention of levodopa-induced dyskinesia in rats with Parkinson disease]. Levodopa 129-137 G protein-coupled receptor kinase 6 Rattus norvegicus 63-98 22579614-9 2012 To conclude, the similar declines in L-dopa-induced AIMs in nicotine-treated wildtype mice and in alpha6-/- mice treated with and without nicotine indicate an essential role for alpha6beta2* nAChRs in the maintenance of L-dopa-induced AIMs.These findings suggest that alpha6beta2* nAChR drugs have potential for reducing L-dopa-induced dyskinesias in Parkinson"s disease. Levodopa 37-43 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 191-196 22979934-7 2012 RESULTS: AIM score was increased and the expression of GRK6 protein in lesion side was decreased after the long-tern treatment with levodopa and benserazide in rats. Levodopa 132-140 G protein-coupled receptor kinase 6 Rattus norvegicus 55-59 22979934-9 2012 Immunohistochemical results showed that the number of GRK6-positive cells in medium- and high-dose TQPC Granule groups was increased as compared to that in the levodopa group (P<0.05). Levodopa 160-168 G protein-coupled receptor kinase 6 Rattus norvegicus 54-58 22979934-10 2012 The expression level of GRK6 protein was increased in medium-dose TQPC Granule group when compared with the levodopa group (P<0.01), which was observed by Western blotting. Levodopa 108-116 G protein-coupled receptor kinase 6 Rattus norvegicus 24-28 22753408-5 2012 These studies demonstrate that, in D1R-expressing MSNs, l-DOPA-induced activation of ERK and mTORC1 requires DARPP-32 and indicates the importance of the cAMP/DARPP-32 signaling cascade in dyskinesia. Levodopa 56-62 CREB regulated transcription coactivator 1 Mus musculus 93-99 22767596-6 2012 The S354G mutation at the active site enlarged the size of the hHDC substrate-binding pocket and resulted in a decreased affinity for histidine, but an acquired ability to bind and act on L-DOPA as a substrate. Levodopa 188-194 histidine decarboxylase Homo sapiens 63-67 22753408-1 2012 Dyskinesia, a motor complication caused by prolonged administration of the antiparkinsonian drug l-3,4-dihydroxyphenylalanine (l-DOPA), is accompanied by activation of cAMP signaling and hyperphosphorylation of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 97-125 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 215-268 22753408-5 2012 These studies demonstrate that, in D1R-expressing MSNs, l-DOPA-induced activation of ERK and mTORC1 requires DARPP-32 and indicates the importance of the cAMP/DARPP-32 signaling cascade in dyskinesia. Levodopa 56-62 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 109-117 22753408-1 2012 Dyskinesia, a motor complication caused by prolonged administration of the antiparkinsonian drug l-3,4-dihydroxyphenylalanine (l-DOPA), is accompanied by activation of cAMP signaling and hyperphosphorylation of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 97-125 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 270-278 22753408-1 2012 Dyskinesia, a motor complication caused by prolonged administration of the antiparkinsonian drug l-3,4-dihydroxyphenylalanine (l-DOPA), is accompanied by activation of cAMP signaling and hyperphosphorylation of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 127-133 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 215-268 22753408-5 2012 These studies demonstrate that, in D1R-expressing MSNs, l-DOPA-induced activation of ERK and mTORC1 requires DARPP-32 and indicates the importance of the cAMP/DARPP-32 signaling cascade in dyskinesia. Levodopa 56-62 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 159-167 22753408-1 2012 Dyskinesia, a motor complication caused by prolonged administration of the antiparkinsonian drug l-3,4-dihydroxyphenylalanine (l-DOPA), is accompanied by activation of cAMP signaling and hyperphosphorylation of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 127-133 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 270-278 22284852-6 2012 Voltammetric peak currents showed a linear response for L-Dopa concentration in the range of 3 to 100 muM, with a sensitivity of 4.43 muAcm(-2)/muM and a detection limit of 0.86 muM. Levodopa 56-62 latexin Homo sapiens 102-105 22753408-3 2012 Using mice in which DARPP-32 is selectively deleted in D1R-expressing MSNs, we demonstrate that this protein is required for l-DOPA-induced activation of the extracellular signal-regulated protein kinases 1 and 2 and the mammalian target of rapamycin complex 1 (mTORC1) pathways, which are implicated in dyskinesia. Levodopa 125-131 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 20-28 22753408-3 2012 Using mice in which DARPP-32 is selectively deleted in D1R-expressing MSNs, we demonstrate that this protein is required for l-DOPA-induced activation of the extracellular signal-regulated protein kinases 1 and 2 and the mammalian target of rapamycin complex 1 (mTORC1) pathways, which are implicated in dyskinesia. Levodopa 125-131 CREB regulated transcription coactivator 1 Mus musculus 262-268 22753408-4 2012 We also show that mutation of the phosphorylation site for cAMP-dependent protein kinase on DARPP-32 attenuates l-DOPA-induced dyskinesia and reduces the concomitant activations of ERK and mTORC1 signaling. Levodopa 112-118 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 92-100 22753408-4 2012 We also show that mutation of the phosphorylation site for cAMP-dependent protein kinase on DARPP-32 attenuates l-DOPA-induced dyskinesia and reduces the concomitant activations of ERK and mTORC1 signaling. Levodopa 112-118 CREB regulated transcription coactivator 1 Mus musculus 189-195 22753408-5 2012 These studies demonstrate that, in D1R-expressing MSNs, l-DOPA-induced activation of ERK and mTORC1 requires DARPP-32 and indicates the importance of the cAMP/DARPP-32 signaling cascade in dyskinesia. Levodopa 56-62 mitogen-activated protein kinase 1 Homo sapiens 85-88 22284852-6 2012 Voltammetric peak currents showed a linear response for L-Dopa concentration in the range of 3 to 100 muM, with a sensitivity of 4.43 muAcm(-2)/muM and a detection limit of 0.86 muM. Levodopa 56-62 latexin Homo sapiens 144-147 22284852-6 2012 Voltammetric peak currents showed a linear response for L-Dopa concentration in the range of 3 to 100 muM, with a sensitivity of 4.43 muAcm(-2)/muM and a detection limit of 0.86 muM. Levodopa 56-62 latexin Homo sapiens 144-147 22284852-7 2012 The related standard deviation for 10 determinations of 50 muM L-Dopa was 1.6%. Levodopa 63-69 latexin Homo sapiens 59-62 22537672-6 2012 Oral application of DOPA to workers led to DOPA uptake in the brain and significantly higher dopamine and NADA levels in the brain, suggesting that dopamine synthesis could be controlled by the amount of DDC substrate. Levodopa 20-24 aromatic-L-amino-acid decarboxylase Apis mellifera 204-207 23130169-11 2012 CONCLUSIONS: Renalase metabolizes circulating epinephrine and l-3,4-dihydroxyphenylalanine, and its capacity to decrease blood pressure is directly correlated to its enzymatic activity. Levodopa 62-90 renalase, FAD dependent amine oxidase Homo sapiens 13-21 22709943-8 2012 Inhibitors of the ERK signaling pathway, which plays an important role in the development of l-DOPA-induced dyskinesia (LID), have been shown to attenuate this condition in animal models. Levodopa 93-99 mitogen-activated protein kinase 1 Homo sapiens 18-21 22117566-2 2012 ATP13A2 mutations are responsible for Kufor-Rakeb syndrome (KRS), a rare autosomal recessive juvenile parkinsonism characterized by the subacute onset of extrapyramidal, pyramidal and cognitive dysfunction with secondary nonresponsiveness to levodopa. Levodopa 242-250 ATPase cation transporting 13A2 Homo sapiens 0-7 22698780-1 2012 In vitro studies, using combined spectrophotometry and oximetry together with hplc/ms examination of the products of tyrosinase action demonstrate that hydroquinone is not a primary substrate for the enzyme but is vicariously oxidised by a redox exchange mechanism in the presence of either catechol, L-3,4-dihydroxyphenylalanine or 4-ethylphenol. Levodopa 301-329 tyrosinase Homo sapiens 117-127 22764226-0 2012 Acute administration of L-DOPA induces changes in methylation metabolites, reduced protein phosphatase 2A methylation, and hyperphosphorylation of Tau protein in mouse brain. Levodopa 24-30 protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform Mus musculus 91-105 22764226-4 2012 Here we show in human SH-SY5Y cells, in dopaminergic neurons, and in wild-type mice that l-dopa results in a reduced SAM/SAH ratio that is associated with hypomethylation of PP2A and increased phosphorylation of Tau (p-Tau) at the Alzheimer"s disease-like PHF-1 phospho-epitope. Levodopa 89-95 protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform Mus musculus 174-178 22751085-1 2012 OBJECTIVES: The aim of this study was to examine the effects of the peripheral dopamine D2-receptor antagonist, domperidone, on the plasma kinetics of levodopa in patients with Parkinson disease (PD). Levodopa 151-159 dopamine receptor D2 Homo sapiens 79-99 22764226-5 2012 The effect of L-dopa on PP2A and p-Tau was exacerbated in cells exposed to folate deficiency. Levodopa 14-20 protein phosphatase 2 phosphatase activator Homo sapiens 24-28 22764226-6 2012 In the folate-deficient mouse model, L-dopa resulted in a marked depletion of SAM and an increase in SAH in various brain regions with parallel downregulation of PP2A methylation and increased Tau phosphorylation. Levodopa 37-43 protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform Mus musculus 162-166 22764226-7 2012 L-Dopa also enhanced demethylated PP2A amounts in the liver. Levodopa 0-6 protein phosphatase 2 phosphatase activator Homo sapiens 34-38 22764226-8 2012 These findings reveal a novel mechanism involving methylation-dependent pathways in L-dopa induces PP2A hypomethylation and increases Tau phosphorylation, which may be potentially detrimental to neuronal cells. Levodopa 84-90 protein phosphatase 2 phosphatase activator Homo sapiens 99-103 22358431-15 2012 Furthermore, SDHB gene mutations could influence (18)F-DOPA PET or PET/CT diagnostic performance. Levodopa 55-59 succinate dehydrogenase complex iron sulfur subunit B Homo sapiens 13-17 22531611-12 2012 Significant predictive factors of worst disease severity and negative response to levodopa were hypertension, vascular lesions in basal ganglia/periventricular regions, and normal DAT uptake. Levodopa 82-90 solute carrier family 6 member 3 Homo sapiens 180-183 22483311-3 2012 The implication of tyrosine hydroxylase (TH), the enzyme that catalyzes the formation of L-3,4-dihydroxyphenylalanine, in the pathogenesis of PD at different levels makes it a promising candidate for developing efficient treatment based on correcting or bypassing the enzyme deficiency. Levodopa 89-117 tyrosine hydroxylase Homo sapiens 19-39 22450660-4 2012 In contrast to amino acid neurotransmitters, catecholamine neurotransmitters, L-DOPA, and curcumin prevent significant iron-mediated DNA damage (IC(50) values of 3.2 to 18 muM) and are electrochemically active. Levodopa 78-84 latexin Homo sapiens 172-175 22483311-3 2012 The implication of tyrosine hydroxylase (TH), the enzyme that catalyzes the formation of L-3,4-dihydroxyphenylalanine, in the pathogenesis of PD at different levels makes it a promising candidate for developing efficient treatment based on correcting or bypassing the enzyme deficiency. Levodopa 89-117 tyrosine hydroxylase Homo sapiens 41-43 22372951-6 2012 We found that CNTF, acting through gp130, stimulated the rate of l-3,4-dihydroxyphenylalanine production while at the same time decreasing TH enzyme levels, thereby increasing the specific activity of the enzyme. Levodopa 65-93 ciliary neurotrophic factor Homo sapiens 14-18 22583428-1 2012 Tyrosine hydroxylase (TH) is the rate limiting enzyme responsible for converting tyrosine to L-DOPA in the dopamine synthesis pathway. Levodopa 93-99 tyrosine hydroxylase Homo sapiens 0-20 22583428-1 2012 Tyrosine hydroxylase (TH) is the rate limiting enzyme responsible for converting tyrosine to L-DOPA in the dopamine synthesis pathway. Levodopa 93-99 tyrosine hydroxylase Homo sapiens 22-24 22583428-4 2012 TH activity variations during L-DOPA and new antiparkinsonian treatments have been extensively studied. Levodopa 30-36 tyrosine hydroxylase Homo sapiens 0-2 22136069-0 2012 Intestinal levodopa infusion and COMT inhibition - a promising link. Levodopa 11-19 catechol-O-methyltransferase Homo sapiens 33-37 22136163-1 2012 BACKGROUND AND PURPOSE: Catechol-O-methyltransferase inhibitors may be used to decrease levodopa requirement. Levodopa 88-96 catechol-O-methyltransferase Homo sapiens 24-52 22136163-2 2012 The objective was to investigate whether the levodopa/carbidopa intestinal gel infusion dose can be reduced by 20% without worsening of motor fluctuations and levodopa concentration stability when oral catechol-O-methyltransferase inhibitors are added. Levodopa 45-53 catechol-O-methyltransferase Homo sapiens 202-230 22136163-10 2012 CONCLUSIONS: According to this small, short-term pilot study, oral catechol-O-methyltransferase inhibitors administered in 5-h intervals may be useful in cases where levodopa/carbidopa intestinal gel dose reduction is wanted. Levodopa 166-174 catechol-O-methyltransferase Homo sapiens 67-95 22283753-4 2012 This has led to development of a selective 5-HT2A antagonist, ACP-103 (pimavanserin), which has been found to be effective as monotherapy in L-DOPA psychosis and has promise as an add-on agent for sub-effective doses of atypical APDs. Levodopa 141-147 5-hydroxytryptamine receptor 2A Homo sapiens 43-49 22372951-6 2012 We found that CNTF, acting through gp130, stimulated the rate of l-3,4-dihydroxyphenylalanine production while at the same time decreasing TH enzyme levels, thereby increasing the specific activity of the enzyme. Levodopa 65-93 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 35-40 22912975-0 2012 Rhes-mTORC1 interaction: a new possible therapeutic target in Parkinson"s disease and L-dopa-induced dyskinesia? Levodopa 86-92 RASD family member 2 Homo sapiens 0-4 22912975-0 2012 Rhes-mTORC1 interaction: a new possible therapeutic target in Parkinson"s disease and L-dopa-induced dyskinesia? Levodopa 86-92 CREB regulated transcription coactivator 1 Mus musculus 5-11 22449381-2 2012 Previous studies using animal models show that repeated administration of l-DOPA results in alterations of some signaling molecules, including DeltaFosB, phospho-DARPP32 and phosoho-GluA1 (also referred to as GluR1 or GluR-A) AMPA receptor subunits. Levodopa 74-80 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 209-214 22349357-6 2012 We discuss a possibility of RLS in these patients and suggest to take a trial of l-dopa in patients with isolated insomnia who has a positive family history of RLS or in a patient who do not show response to usual therapies for RLS. Levodopa 81-87 RLS1 Homo sapiens 160-163 22349357-6 2012 We discuss a possibility of RLS in these patients and suggest to take a trial of l-dopa in patients with isolated insomnia who has a positive family history of RLS or in a patient who do not show response to usual therapies for RLS. Levodopa 81-87 RLS1 Homo sapiens 160-163 22293035-6 2012 In addition, 50 muM sesamin exhibited a protective effect against L-DOPA (100 and 200 muM)-induced cytotoxicity via the inhibition of reactive oxygen species (ROS) production and superoxide dismutase reduction, induction of extracellular signal-regulated kinase (ERK)1/2 and BadSer112 phosphorylation and Bcl-2 expression, and inhibition of cleaved-caspase-3 formation. Levodopa 66-72 mitogen activated protein kinase 3 Rattus norvegicus 224-270 22293035-6 2012 In addition, 50 muM sesamin exhibited a protective effect against L-DOPA (100 and 200 muM)-induced cytotoxicity via the inhibition of reactive oxygen species (ROS) production and superoxide dismutase reduction, induction of extracellular signal-regulated kinase (ERK)1/2 and BadSer112 phosphorylation and Bcl-2 expression, and inhibition of cleaved-caspase-3 formation. Levodopa 66-72 BCL2, apoptosis regulator Rattus norvegicus 305-310 22293035-6 2012 In addition, 50 muM sesamin exhibited a protective effect against L-DOPA (100 and 200 muM)-induced cytotoxicity via the inhibition of reactive oxygen species (ROS) production and superoxide dismutase reduction, induction of extracellular signal-regulated kinase (ERK)1/2 and BadSer112 phosphorylation and Bcl-2 expression, and inhibition of cleaved-caspase-3 formation. Levodopa 66-72 caspase 3 Rattus norvegicus 349-358 22293035-7 2012 These results suggested that sesamin enhanced dopamine biosynthesis and L-DOPA-induced increase in dopamine levels by inducing TH activity and TH gene expression, which was mediated by cAMP-PKA-CREB systems. Levodopa 72-78 tyrosine hydroxylase Rattus norvegicus 127-129 22293035-7 2012 These results suggested that sesamin enhanced dopamine biosynthesis and L-DOPA-induced increase in dopamine levels by inducing TH activity and TH gene expression, which was mediated by cAMP-PKA-CREB systems. Levodopa 72-78 cAMP responsive element binding protein 1 Rattus norvegicus 194-198 22293035-8 2012 Sesamin also protected against L-DOPA (100-200 muM)-induced cytotoxicity through the suppression of ROS activity via the modulation of ERK1/2, BadSer112, Bcl-2, and caspase-3 pathways in PC12 cells. Levodopa 31-37 caspase 3 Rattus norvegicus 165-174 22449381-2 2012 Previous studies using animal models show that repeated administration of l-DOPA results in alterations of some signaling molecules, including DeltaFosB, phospho-DARPP32 and phosoho-GluA1 (also referred to as GluR1 or GluR-A) AMPA receptor subunits. Levodopa 74-80 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 162-169 22449381-2 2012 Previous studies using animal models show that repeated administration of l-DOPA results in alterations of some signaling molecules, including DeltaFosB, phospho-DARPP32 and phosoho-GluA1 (also referred to as GluR1 or GluR-A) AMPA receptor subunits. Levodopa 74-80 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 182-187 22449381-2 2012 Previous studies using animal models show that repeated administration of l-DOPA results in alterations of some signaling molecules, including DeltaFosB, phospho-DARPP32 and phosoho-GluA1 (also referred to as GluR1 or GluR-A) AMPA receptor subunits. Levodopa 74-80 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 218-224 22449381-8 2012 In agreement with the behavioral analysis, 7-nitroindazole reduced the l-DOPA-induced increases in DeltaFosB, phospho-DARPP32 and phospho-GluA1 AMPA receptor subunit levels in the striatum of 6-hydroxydopamine-lesioned rats. Levodopa 71-77 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 118-125 22449381-8 2012 In agreement with the behavioral analysis, 7-nitroindazole reduced the l-DOPA-induced increases in DeltaFosB, phospho-DARPP32 and phospho-GluA1 AMPA receptor subunit levels in the striatum of 6-hydroxydopamine-lesioned rats. Levodopa 71-77 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 138-143 22449381-10 2012 These findings suggest that nNOS-derived NO is involved in the development of l-DOPA-induced dyskinesia through a post-synaptic mechanism. Levodopa 78-84 nitric oxide synthase 1 Rattus norvegicus 28-32 22366535-7 2012 l-dopa had no effects on voluntary blinking but reversed the increased inter-phase pause duration seen during STN-DBS. Levodopa 0-6 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 110-113 22406356-1 2012 Large increases in regional cerebral blood flow (rCBF) have been measured in patients with Parkinson"s disease (PD) following the administration of L-DOPA, but the underlying mechanisms have remained unknown. Levodopa 148-154 CCAAT/enhancer binding protein zeta Rattus norvegicus 49-53 22406356-5 2012 Significant changes in rCBF and rCGU on the side ipsilateral to the 6-OHDA lesion relative to the non-lesioned side were seen at 60 min ("ON") but not 24h ("OFF") following L-DOPA administration. Levodopa 173-179 CCAAT/enhancer binding protein zeta Rattus norvegicus 23-27 22406356-7 2012 In the output nuclei of the basal ganglia (the entopeduncular nucleus and the substantia nigra pars reticulata) both rCBF and rCGU were elevated both in acutely L-DOPA-treated rats and chronically L-DOPA-treated rats displaying dyskinesia, but did not change significantly in chronically L-DOPA-treated non-dyskinetic cases. Levodopa 161-167 CCAAT/enhancer binding protein zeta Rattus norvegicus 117-121 22406356-7 2012 In the output nuclei of the basal ganglia (the entopeduncular nucleus and the substantia nigra pars reticulata) both rCBF and rCGU were elevated both in acutely L-DOPA-treated rats and chronically L-DOPA-treated rats displaying dyskinesia, but did not change significantly in chronically L-DOPA-treated non-dyskinetic cases. Levodopa 197-203 CCAAT/enhancer binding protein zeta Rattus norvegicus 117-121 22406356-7 2012 In the output nuclei of the basal ganglia (the entopeduncular nucleus and the substantia nigra pars reticulata) both rCBF and rCGU were elevated both in acutely L-DOPA-treated rats and chronically L-DOPA-treated rats displaying dyskinesia, but did not change significantly in chronically L-DOPA-treated non-dyskinetic cases. Levodopa 197-203 CCAAT/enhancer binding protein zeta Rattus norvegicus 117-121 22406356-10 2012 The present results are the first to show that the administration of L-DOPA is followed by transient and robust increases in rCBF in the dopamine-denervated basal ganglia. Levodopa 69-75 CCAAT/enhancer binding protein zeta Rattus norvegicus 125-129 22406356-12 2012 Increases in rCBF ON L-DOPA are not necessarily accompanied by enhanced glucose utilisation in the affected regions, pointing to altered mechanisms of neurovascular coupling. Levodopa 21-27 CCAAT/enhancer binding protein zeta Rattus norvegicus 13-17 22406356-13 2012 Finally, our results show that increases in rCBF ON L-DOPA may be accompanied by BBB hyperpermeability in the most affected regions. Levodopa 52-58 CCAAT/enhancer binding protein zeta Rattus norvegicus 44-48 22483291-0 2012 Role of catechol-O-methyltransferase (COMT)-dependent processes in Parkinson"s disease and L-DOPA treatment. Levodopa 91-97 catechol-O-methyltransferase Homo sapiens 8-36 22483291-0 2012 Role of catechol-O-methyltransferase (COMT)-dependent processes in Parkinson"s disease and L-DOPA treatment. Levodopa 91-97 catechol-O-methyltransferase Homo sapiens 38-42 22483291-3 2012 There are several mechanisms for the potential involvement of COMT-related processes in the pathophysiology of Parkinson"s disease or the consequences of L-DOPA treatment. Levodopa 154-160 catechol-O-methyltransferase Homo sapiens 62-66 22483291-4 2012 COMT-mediated metabolism of LDOPA in the periphery influences brain dopamine levels, while the product of central COMT-mediated dopamine metabolism, 3-methoxytyramine, can affect movement via interaction with Trace Amine-Associated Receptor 1 (TAAR1). Levodopa 28-33 catechol-O-methyltransferase Homo sapiens 0-4 22483291-4 2012 COMT-mediated metabolism of LDOPA in the periphery influences brain dopamine levels, while the product of central COMT-mediated dopamine metabolism, 3-methoxytyramine, can affect movement via interaction with Trace Amine-Associated Receptor 1 (TAAR1). Levodopa 28-33 trace amine associated receptor 1 Homo sapiens 244-249 21628600-1 2012 Rasagiline is an irreversible monoamine oxidase type B (MAO-B) inhibitor indicated for the treatment of the signs and symptoms of idiopathic Parkinson disease as initial monotherapy and as adjunct therapy to levodopa. Levodopa 208-216 monoamine oxidase B Homo sapiens 56-61 22443313-0 2012 Ghrelin prevents levodopa-induced inhibition of gastric emptying and increases circulating levodopa in fasted rats. Levodopa 17-25 ghrelin and obestatin prepropeptide Rattus norvegicus 0-7 22419526-10 2012 Gross abnormalities in 5-HT(1A) levels in ventral visual areas occurred in all PD patients exposed to L-dopa. Levodopa 102-108 5-hydroxytryptamine receptor 1A Homo sapiens 23-30 22443313-0 2012 Ghrelin prevents levodopa-induced inhibition of gastric emptying and increases circulating levodopa in fasted rats. Levodopa 91-99 ghrelin and obestatin prepropeptide Rattus norvegicus 0-7 22443313-20 2012 CONCLUSIONS & INFERENCES: Ghrelin counteracts L-dopa-induced delayed gastric emptying but not Fos induction in the brain and enhances circulating L-dopa levels. Levodopa 50-56 ghrelin and obestatin prepropeptide Rattus norvegicus 30-37 22443313-20 2012 CONCLUSIONS & INFERENCES: Ghrelin counteracts L-dopa-induced delayed gastric emptying but not Fos induction in the brain and enhances circulating L-dopa levels. Levodopa 150-156 ghrelin and obestatin prepropeptide Rattus norvegicus 30-37 22539851-2 2012 In the dopamine (DA)-denervated striatum, L-DOPA activates DA D1 receptor(D1R) signaling, including cAMP-dependent protein kinase A (PKA) and extracellular signal-regulated kinase (ERK), two responses associated with LID. Levodopa 42-48 mitogen-activated protein kinase 1 Mus musculus 142-179 22539851-2 2012 In the dopamine (DA)-denervated striatum, L-DOPA activates DA D1 receptor(D1R) signaling, including cAMP-dependent protein kinase A (PKA) and extracellular signal-regulated kinase (ERK), two responses associated with LID. Levodopa 42-48 mitogen-activated protein kinase 1 Mus musculus 181-184 22539851-0 2012 Galpha(olf) mutation allows parsing the role of cAMP-dependent and extracellular signal-regulated kinase-dependent signaling in L-3,4-dihydroxyphenylalanine-induced dyskinesia. Levodopa 128-156 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 0-11 22539851-5 2012 We report here that increased Galpha(olf) levels in hemiparkinsonian mice are correlated with LID after chronic L-DOPA treatment. Levodopa 112-118 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 30-41 22539851-0 2012 Galpha(olf) mutation allows parsing the role of cAMP-dependent and extracellular signal-regulated kinase-dependent signaling in L-3,4-dihydroxyphenylalanine-induced dyskinesia. Levodopa 128-156 mitogen-activated protein kinase 1 Mus musculus 67-104 22539851-8 2012 In Gnal+/- mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation of GluA1 Ser845 and DARPP-32 (32 kDa DA- and cAMP-regulated phosphoprotein) Thr34 was dramatically reduced, whereas ERK activation was preserved. Levodopa 36-42 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 3-7 22539851-8 2012 In Gnal+/- mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation of GluA1 Ser845 and DARPP-32 (32 kDa DA- and cAMP-regulated phosphoprotein) Thr34 was dramatically reduced, whereas ERK activation was preserved. Levodopa 36-42 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 95-100 22539851-8 2012 In Gnal+/- mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation of GluA1 Ser845 and DARPP-32 (32 kDa DA- and cAMP-regulated phosphoprotein) Thr34 was dramatically reduced, whereas ERK activation was preserved. Levodopa 36-42 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 112-120 22539851-8 2012 In Gnal+/- mice, the lesion-induced L-DOPA stimulation of cAMP/PKA-mediated phosphorylation of GluA1 Ser845 and DARPP-32 (32 kDa DA- and cAMP-regulated phosphoprotein) Thr34 was dramatically reduced, whereas ERK activation was preserved. Levodopa 36-42 mitogen-activated protein kinase 1 Mus musculus 208-211 22539851-10 2012 Thus, in lesioned animals, Galpha(olf) upregulation is critical for the activation by L-DOPA of D1R-stimulated cAMP/PKA but not ERK signaling. Levodopa 86-92 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 27-38 22539851-12 2012 In contrast, the persistence of L-DOPA-induced ERK activation in Gnal+/- mice supports its causal role in LID development. Levodopa 32-38 mitogen-activated protein kinase 1 Mus musculus 47-50 22539851-12 2012 In contrast, the persistence of L-DOPA-induced ERK activation in Gnal+/- mice supports its causal role in LID development. Levodopa 32-38 guanine nucleotide binding protein, alpha stimulating, olfactory type Mus musculus 65-69 22186668-3 2012 Monoamine oxidase A V(T), an index of MAO-A density, was decreased (mean: 14%+-9%) following tryptophan depletion in prefrontal cortex (P<0.031), and elevated (mean: 17%+-11%) in striatum following carbidopa-levodopa administration (P<0.007). Levodopa 208-216 monoamine oxidase A Homo sapiens 0-19 22236652-1 2012 Peripheral aromatic amino acid decarboxylase (AADC) inhibitors, such as benserazide, are routinely used to potentiate the effects of L-3,4-dihydroxyphenylalanine (L-DOPA) in Parkinson"s disease (PD) and in experimental models of PD. Levodopa 133-161 dopa decarboxylase Rattus norvegicus 46-50 22236652-1 2012 Peripheral aromatic amino acid decarboxylase (AADC) inhibitors, such as benserazide, are routinely used to potentiate the effects of L-3,4-dihydroxyphenylalanine (L-DOPA) in Parkinson"s disease (PD) and in experimental models of PD. Levodopa 163-169 dopa decarboxylase Rattus norvegicus 46-50 22236652-8 2012 When L-DOPA treatment was delayed for 1, 2, or 3 h after benserazide, the rotational response declined suggesting loss of AADC inhibition. Levodopa 5-11 dopa decarboxylase Rattus norvegicus 122-126 22325981-4 2012 Recently, we demonstrated that the dopamine agonist pramipexole improves the therapeutic effect of L-dopa in 6-pyruvoyl tetrahydropterin synthase (PTPS) deficiency, the most common disorder of BH4 metabolism. Levodopa 99-105 6-pyruvoyltetrahydropterin synthase Homo sapiens 147-151 21555194-5 2012 We describe the clinical phenotype and response to levodopa treatment in a 6 year-old girl affected with sporadic non-progressive chorea, and a de novo TITF-1 gene mutation, in order to increase understanding of this rare and misdiagnosed disorder. Levodopa 51-59 NK2 homeobox 1 Homo sapiens 152-158 22068827-2 2012 Two children presenting with frequent daily falling are reported with GCH1 gene mutations with persistent response to low-dose levodopa/carbidopa. Levodopa 127-135 GTP cyclohydrolase 1 Homo sapiens 70-74 22192465-0 2012 The cannabinoid agonist WIN55212-2 decreases L-DOPA-induced PKA activation and dyskinetic behavior in 6-OHDA-treated rats. Levodopa 45-51 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 60-63 21459482-1 2012 The type 1 cannabinoid receptor (CB1) is a crucial modulator of synaptic transmission in brain and has been proposed as a potential therapeutic target in Parkinson"s disease (PD), especially for treatment of levodopa-induced dyskinesias (LID). Levodopa 208-216 cannabinoid receptor 1 Homo sapiens 33-36 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 8-16 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 195-211 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 8-16 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 213-216 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 8-16 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 263-271 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 18-24 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 195-211 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 18-24 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 213-216 22354693-0 2012 Coenzyme Q10, hyperhomocysteinemia and MTHFR C677T polymorphism in levodopa-treated Parkinson"s disease patients. Levodopa 67-75 methylenetetrahydrofolate reductase Homo sapiens 39-44 22192465-1 2012 Chronic Levodopa (L-DOPA), the gold standard therapy for Parkinson"s disease (PD), causes disabling motor complications (dyskinesias) that are associated with changes in the activity of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32). Levodopa 18-24 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 263-271 22192465-4 2012 Striatal PKA activity was positively correlated with the severity of L-DOPA-induced axial and limb dyskinesias, suggesting a role for the cAMP/PKA signaling pathway in the expression of these motor disturbances. Levodopa 69-75 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 9-12 22192465-4 2012 Striatal PKA activity was positively correlated with the severity of L-DOPA-induced axial and limb dyskinesias, suggesting a role for the cAMP/PKA signaling pathway in the expression of these motor disturbances. Levodopa 69-75 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 143-146 22273600-1 2012 Mn(III)-loaded apoferritin is promptly reduced to Mn(II)-apoferritin by the oxidation of L-DOPA to melanin. Levodopa 89-95 ferritin heavy chain 1 Homo sapiens 15-26 22273600-1 2012 Mn(III)-loaded apoferritin is promptly reduced to Mn(II)-apoferritin by the oxidation of L-DOPA to melanin. Levodopa 89-95 ferritin heavy chain 1 Homo sapiens 57-68 22017504-1 2012 Degeneration of nigrostriatal neurons in Parkinson"s disease (PD) causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa (l-DOPA) into dopamine in the striatum. Levodopa 162-170 dopa decarboxylase Homo sapiens 93-128 22262741-1 2012 OBJECTIVE: To describe the phenotype of levodopa-induced "on" freezing of gait (FOG) in Parkinson disease (PD). Levodopa 40-48 zinc finger protein, FOG family member 1 Homo sapiens 80-83 22017504-1 2012 Degeneration of nigrostriatal neurons in Parkinson"s disease (PD) causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa (l-DOPA) into dopamine in the striatum. Levodopa 162-170 dopa decarboxylase Homo sapiens 130-134 22017504-1 2012 Degeneration of nigrostriatal neurons in Parkinson"s disease (PD) causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa (l-DOPA) into dopamine in the striatum. Levodopa 172-178 dopa decarboxylase Homo sapiens 93-128 22017504-1 2012 Degeneration of nigrostriatal neurons in Parkinson"s disease (PD) causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa (l-DOPA) into dopamine in the striatum. Levodopa 172-178 dopa decarboxylase Homo sapiens 130-134 22017504-2 2012 Because loss of this enzyme appears to be a major driver of progressive impairment of response to the mainstay drug, l-DOPA, one promising approach has been to use gene therapy to restore AADC activity in the human putamen and thereby restore normal l-DOPA response in patients with PD. Levodopa 117-123 dopa decarboxylase Homo sapiens 188-192 22238104-1 2012 Aberrant membrane localization of dopamine D(1) receptor (D1R) is associated with L-DOPA-induced dyskinesia (LID), a major complication of L-DOPA treatment in Parkinson"s disease (PD). Levodopa 82-88 dopamine receptor D1 Mus musculus 34-56 22265536-1 2012 An analytical method was researched for the simultaneous determination of reactants and products during the binding of important small molecules such as levodopa (LD) with biopolymers such as bovine serum albumin (BSA). Levodopa 153-161 albumin Homo sapiens 199-212 22088953-0 2012 The metabotropic glutamate receptor 4-positive allosteric modulator VU0364770 produces efficacy alone and in combination with L-DOPA or an adenosine 2A antagonist in preclinical rodent models of Parkinson"s disease. Levodopa 126-132 glutamate metabotropic receptor 4 Rattus norvegicus 4-37 22123108-1 2012 In the past years, it has been recognised that the levodopa therapy may be improved with therapeutic regimens including a catechol-O-methyltransferase (COMT) inhibitor. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 122-150 22123108-1 2012 In the past years, it has been recognised that the levodopa therapy may be improved with therapeutic regimens including a catechol-O-methyltransferase (COMT) inhibitor. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 152-156 22238104-1 2012 Aberrant membrane localization of dopamine D(1) receptor (D1R) is associated with L-DOPA-induced dyskinesia (LID), a major complication of L-DOPA treatment in Parkinson"s disease (PD). Levodopa 139-145 dopamine receptor D1 Mus musculus 34-56 23095782-5 2012 In comparison to controls, a trend to a slightly worse deterioration in phonemic verbal fluency was observed in the STN-DBS patients and was significantly correlated with reductions in the L-dopa-equivalent daily dose (r = 0.850, p = 0.007). Levodopa 189-195 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 116-119 23093014-3 2012 Herein, we aimed to test the possible influence of MAOB and COMT genetic polymorphisms on the effective daily dose of levodopa administered in the fifth year of treatment. Levodopa 118-126 monoamine oxidase B Homo sapiens 51-55 23093014-3 2012 Herein, we aimed to test the possible influence of MAOB and COMT genetic polymorphisms on the effective daily dose of levodopa administered in the fifth year of treatment. Levodopa 118-126 catechol-O-methyltransferase Homo sapiens 60-64 23093014-13 2012 The present data suggest that pharmacokinetic or pharmacodynamic factors other than the investigated genetic variants of the MAOB and COMT enzymes seem to determine the response to levodopa in the Iranian PD patients. Levodopa 181-189 monoamine oxidase B Homo sapiens 125-129 23093014-13 2012 The present data suggest that pharmacokinetic or pharmacodynamic factors other than the investigated genetic variants of the MAOB and COMT enzymes seem to determine the response to levodopa in the Iranian PD patients. Levodopa 181-189 catechol-O-methyltransferase Homo sapiens 134-138 22863920-1 2012 It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy. Levodopa 70-98 catechol-O-methyltransferase Homo sapiens 118-146 22863920-1 2012 It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy. Levodopa 70-98 catechol-O-methyltransferase Homo sapiens 148-152 22863920-1 2012 It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy. Levodopa 100-106 catechol-O-methyltransferase Homo sapiens 118-146 22863920-1 2012 It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy. Levodopa 100-106 catechol-O-methyltransferase Homo sapiens 148-152 21982296-1 2012 This study proposes a combination method of using 3,4-dihydorxy-l-phenylalanine (DOPA) conjugated heparin (heparin-DOPA) and a low dose of anti-CD154 monoclonal antibody (MR-1) treatment to improve the survival time of intrahepatic islet xenograft. Levodopa 81-85 major histocompatibility complex, class I-related Mus musculus 171-175 23185117-0 2012 Levodopa/benserazide microspheres reduced levodopa-induced dyskinesia by downregulating phosphorylated GluR1 expression in 6-OHDA-lesioned rats. Levodopa 0-8 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 103-108 23185117-0 2012 Levodopa/benserazide microspheres reduced levodopa-induced dyskinesia by downregulating phosphorylated GluR1 expression in 6-OHDA-lesioned rats. Levodopa 42-50 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 103-108 23185117-19 2012 CONCLUSION: These data indicated that levodopa/benserazide-loaded microspheres could be used to ameliorate the expression of LID by reducing the expression of pGluR1S831 and pGluR1S845 as well as Arc and Penk. Levodopa 38-46 proenkephalin Rattus norvegicus 204-208 24312786-2 2012 Our recent study showed that activation of 5-HT1A receptors could improve the anti-cataleptic effect of L-DOPA in parkinsonian rats. Levodopa 104-110 5-hydroxytryptamine receptor 1A Rattus norvegicus 43-49 24312786-15 2012 CONCLUSION: According to the results, it may be concluded that fluoxetine improves 6-OHDA-induced catalepsy and motor imbalance in L-DOPA- treated rats through activation of 5-HT1A. Levodopa 131-137 5-hydroxytryptamine receptor 1A Rattus norvegicus 174-180 22553754-0 2012 Influences of levodopa on expression of N-methyl-D-aspartate receptor-1-subunit in the visual cortex of monocular deprivation rats. Levodopa 14-22 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 40-79 22553754-13 2012 Levodopa may influence the expression of NMDAR1 and improve visual function, and its target may lie in the visual cortex. Levodopa 0-8 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 41-47 22031516-8 2012 The third patient had a paternally inherited ABCC8 (A1493T) mutation, and the initial [(18)F]DOPA PET scan indicated extensive uptake of DOPA in the body and tail of the pancreas. Levodopa 137-141 ATP binding cassette subfamily C member 8 Homo sapiens 45-50 22547925-6 2012 GPR143 is activated by L-DOPA (1 muM) which decreased VEGF-A secretion as opposed to the previously reported increase in PEDF secretion. Levodopa 23-29 G protein-coupled receptor 143 Homo sapiens 0-6 22547925-6 2012 GPR143 is activated by L-DOPA (1 muM) which decreased VEGF-A secretion as opposed to the previously reported increase in PEDF secretion. Levodopa 23-29 vascular endothelial growth factor A Homo sapiens 54-60 23430895-1 2012 Aromatic L-amino acid decarboxylase (AADC) decarboxylates 3,4-L-dihydroxylphenylalanine (L-dopa) to dopamine, and 5-hydroxytryptophan to serotonin. Levodopa 89-95 dopa decarboxylase Homo sapiens 0-35 23646099-0 2012 A rapid non invasive L-DOPA-13C breath test for optimally suppressing extracerebral AADC enzyme activity - toward individualizing carbidopa therapy in Parkinson"s disease. Levodopa 21-27 dopa decarboxylase Homo sapiens 84-88 23646099-1 2012 BACKGROUND: Peripheral carbidopa (CD) levels directly impact on central dopamine (DA) production in Parkinson disease (PD) through extracerebral inhibition of dopa decarboxylase (AADC) resulting in an increase in levodopa (LD) bioavailability. Levodopa 213-221 dopa decarboxylase Homo sapiens 159-177 23646099-1 2012 BACKGROUND: Peripheral carbidopa (CD) levels directly impact on central dopamine (DA) production in Parkinson disease (PD) through extracerebral inhibition of dopa decarboxylase (AADC) resulting in an increase in levodopa (LD) bioavailability. Levodopa 213-221 dopa decarboxylase Homo sapiens 179-183 22510520-0 2012 Effect of selective serotonin reuptake inhibitors via 5-HT1A receptors on L-DOPA-induced rotational behavior in a hemiparkinsonian rat model. Levodopa 74-80 5-hydroxytryptamine receptor 1A Rattus norvegicus 54-60 22510520-9 2012 Additionally, fluoxetine suppressed L-DOPA-induced ERK1/2 and histone H3 phosphorylation. Levodopa 36-42 mitogen activated protein kinase 3 Rattus norvegicus 51-57 23430895-1 2012 Aromatic L-amino acid decarboxylase (AADC) decarboxylates 3,4-L-dihydroxylphenylalanine (L-dopa) to dopamine, and 5-hydroxytryptophan to serotonin. Levodopa 89-95 dopa decarboxylase Homo sapiens 37-41 23430895-5 2012 In this study, the hypothesis that in AADC deficiency relatively high-residual renal AADC-activity combined with high substrate availability of L-dopa leads to normal or elevated levels of urinary dopamine is tested and verified using 24-h urine collection of two AADC-deficient patients.Renal dopamine is a major regulator of natriuresis and plays a crucial role in the maintenance of sodium homeostasis. Levodopa 144-150 dopa decarboxylase Homo sapiens 38-42 21876323-0 2012 An autoradiographic study on the pathogenesis of levodopa-induced dyskinesia: regulation of dopamine transporter by levodopa in a rat model of Parkinson"s disease. Levodopa 49-57 solute carrier family 6 member 3 Rattus norvegicus 92-112 22038903-7 2012 LRRK2 p.S1761R carriers developed levodopa-responsive asymmetrical parkinsonism, with variable age at onset (range: 37-72 years) suggesting age-dependent penetrance. Levodopa 34-42 leucine rich repeat kinase 2 Homo sapiens 0-5 21051107-1 2012 Serotonergic 1A (5-HT(1A)) receptor agonists reduce L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia in Parkinson"s disease (PD), though the mechanism(s) and site(s) of action remain unclear. Levodopa 52-80 5-hydroxytryptamine receptor 1A Homo sapiens 17-24 21051107-1 2012 Serotonergic 1A (5-HT(1A)) receptor agonists reduce L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia in Parkinson"s disease (PD), though the mechanism(s) and site(s) of action remain unclear. Levodopa 82-88 5-hydroxytryptamine receptor 1A Homo sapiens 17-24 21051107-5 2012 While 5-HT(1A) receptor binding is low in the matrix of the caudate nucleus in normal macaques, it increases (by 200%, p < 0.05) in MPTP-L-DOPA-chronic macaques. Levodopa 140-146 5-hydroxytryptamine receptor 1A Homo sapiens 6-23 21051107-6 2012 These data suggest that 5-HT(1A) receptors are involved in the pathophysiology of both parkinsonism and complications of L-DOPA therapy. Levodopa 121-127 5-hydroxytryptamine receptor 1A Homo sapiens 24-31 22037042-4 2012 In the current study, using the 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD, we demonstrated that the calcium-dependent proteins calpains and cdk5 of the striatum play a critical role in the behavioral and molecular changes evoked by L-DOPA therapy. Levodopa 242-248 cyclin-dependent kinase 5 Rattus norvegicus 150-154 22037042-7 2012 Notably, the calpains and cdk5 inhibitors totally reversed the striatal molecular changes attributed to L-DOPA therapy, such as ERK1/2 and dynamin phosphorylation. Levodopa 104-110 cyclin-dependent kinase 5 Rattus norvegicus 26-30 22037042-7 2012 Notably, the calpains and cdk5 inhibitors totally reversed the striatal molecular changes attributed to L-DOPA therapy, such as ERK1/2 and dynamin phosphorylation. Levodopa 104-110 mitogen activated protein kinase 3 Rattus norvegicus 128-134 20561716-0 2012 5-HT2A receptor levels increase in MPTP-lesioned macaques treated chronically with L-DOPA. Levodopa 83-89 5-hydroxytryptamine receptor 2A Homo sapiens 0-15 20561716-3 2012 Moreover, 5-HT(2A) receptor antagonists can reduce L-DOPA-induced dyskinesia (LID). Levodopa 51-57 5-hydroxytryptamine receptor 2A Homo sapiens 10-27 20561716-6 2012 5-HT(2A) receptor binding was increased in the caudate, putamen, and middle layers of the motor cortex in chronically L-DOPA-treated animals, by 50%, 50%, and 45% respectively, compared with normal macaques. Levodopa 118-124 5-hydroxytryptamine receptor 2A Homo sapiens 0-17 22001606-0 2012 A30P alpha-synuclein impairs dopaminergic fiber regeneration and interacts with L-DOPA replacement in MPTP-treated mice. Levodopa 80-86 synuclein, alpha Mus musculus 5-20 21876323-0 2012 An autoradiographic study on the pathogenesis of levodopa-induced dyskinesia: regulation of dopamine transporter by levodopa in a rat model of Parkinson"s disease. Levodopa 116-124 solute carrier family 6 member 3 Rattus norvegicus 92-112 23264832-1 2012 Dopa decarboxylase (DDC) is a pyridoxal 5"-phosphate (PLP)-dependent enzyme that by catalyzing the decarboxylation of L-Dopa and L-5-hydroxytryptophan produces the neurotransmitters dopamine and serotonin. Levodopa 118-124 dopa decarboxylase Homo sapiens 0-18 23264832-1 2012 Dopa decarboxylase (DDC) is a pyridoxal 5"-phosphate (PLP)-dependent enzyme that by catalyzing the decarboxylation of L-Dopa and L-5-hydroxytryptophan produces the neurotransmitters dopamine and serotonin. Levodopa 118-124 pyridoxal phosphatase Homo sapiens 54-57 21876323-2 2012 OBJECTIVE: To evaluate the correlation between dopamine transporter (DAT) regulated by L-DOPA and the pathogenesis of dyskinesia in PD rats. Levodopa 87-93 solute carrier family 6 member 3 Rattus norvegicus 47-67 21876323-2 2012 OBJECTIVE: To evaluate the correlation between dopamine transporter (DAT) regulated by L-DOPA and the pathogenesis of dyskinesia in PD rats. Levodopa 87-93 solute carrier family 6 member 3 Rattus norvegicus 69-72 21876323-14 2012 CONCLUSION: L-DOPA was shown to downregulate DAT in some PD model rats. Levodopa 12-18 solute carrier family 6 member 3 Rattus norvegicus 45-48 22888467-2 2012 However, there is no previous evidence of the presence of LAT transporter for L-DOPA in brain astrocytes except in culture. Levodopa 78-84 linker for activation of T cells Rattus norvegicus 58-61 23226401-8 2012 The greatest density of TH-ir striatal cells was detected in the striatum of the L-Dopa treated monkeys and particularly in its associative territory. Levodopa 81-87 tyrosine hydroxylase Homo sapiens 24-26 22166420-5 2012 Patients with the dystonia plus syndrome DYT5 display levodopa-responsive dystonia sometimes associated with tremor or parkinsonism (DYT5a, mutations in GCH1); a more severe phenotype with psychomotor involvement can be seen in recessive forms (DYT5b with TH mutations, SPR-deficiency syndrome). Levodopa 54-62 GTP cyclohydrolase 1 Homo sapiens 41-45 22166420-5 2012 Patients with the dystonia plus syndrome DYT5 display levodopa-responsive dystonia sometimes associated with tremor or parkinsonism (DYT5a, mutations in GCH1); a more severe phenotype with psychomotor involvement can be seen in recessive forms (DYT5b with TH mutations, SPR-deficiency syndrome). Levodopa 54-62 GTP cyclohydrolase 1 Homo sapiens 133-138 22166420-5 2012 Patients with the dystonia plus syndrome DYT5 display levodopa-responsive dystonia sometimes associated with tremor or parkinsonism (DYT5a, mutations in GCH1); a more severe phenotype with psychomotor involvement can be seen in recessive forms (DYT5b with TH mutations, SPR-deficiency syndrome). Levodopa 54-62 GTP cyclohydrolase 1 Homo sapiens 153-157 22166420-5 2012 Patients with the dystonia plus syndrome DYT5 display levodopa-responsive dystonia sometimes associated with tremor or parkinsonism (DYT5a, mutations in GCH1); a more severe phenotype with psychomotor involvement can be seen in recessive forms (DYT5b with TH mutations, SPR-deficiency syndrome). Levodopa 54-62 tyrosine hydroxylase Homo sapiens 245-250 23251356-1 2012 BACKGROUND: Mitochondrial DNA polymerase gamma (POLG1) mutations were associated with levodopa-responsive Parkinsonism. Levodopa 86-94 DNA polymerase gamma, catalytic subunit Homo sapiens 48-53 23209759-9 2012 Increased homocysteine by levodopa led to increased apoptosis of NPCs through the NMDA receptor-dependent the extracellular signal-regulated kinase (ERK) signaling pathways. Levodopa 26-34 mitogen-activated protein kinase 1 Homo sapiens 110-147 23209759-9 2012 Increased homocysteine by levodopa led to increased apoptosis of NPCs through the NMDA receptor-dependent the extracellular signal-regulated kinase (ERK) signaling pathways. Levodopa 26-34 mitogen-activated protein kinase 1 Homo sapiens 149-152 23209759-12 2012 Our present study demonstrated that increased homocysteine by levodopa has a detrimental effect on neurogenesis through NMDA receptor-mediated ERK signaling pathway. Levodopa 62-70 mitogen-activated protein kinase 1 Homo sapiens 143-146 22166450-2 2012 In three forms, caused by mutations in parkin (PARK2), PINK1 (PARK6), or DJ-1 (PARK7), the phenotype is usually characterized by levodopa-responsive parkinsonism without atypical features. Levodopa 129-137 parkin RBR E3 ubiquitin protein ligase Homo sapiens 47-52 22166450-2 2012 In three forms, caused by mutations in parkin (PARK2), PINK1 (PARK6), or DJ-1 (PARK7), the phenotype is usually characterized by levodopa-responsive parkinsonism without atypical features. Levodopa 129-137 PTEN induced kinase 1 Homo sapiens 55-60 22166450-2 2012 In three forms, caused by mutations in parkin (PARK2), PINK1 (PARK6), or DJ-1 (PARK7), the phenotype is usually characterized by levodopa-responsive parkinsonism without atypical features. Levodopa 129-137 PTEN induced kinase 1 Homo sapiens 62-67 22166450-2 2012 In three forms, caused by mutations in parkin (PARK2), PINK1 (PARK6), or DJ-1 (PARK7), the phenotype is usually characterized by levodopa-responsive parkinsonism without atypical features. Levodopa 129-137 Parkinsonism associated deglycase Homo sapiens 73-77 22166450-2 2012 In three forms, caused by mutations in parkin (PARK2), PINK1 (PARK6), or DJ-1 (PARK7), the phenotype is usually characterized by levodopa-responsive parkinsonism without atypical features. Levodopa 129-137 Parkinsonism associated deglycase Homo sapiens 79-84 23300642-14 2012 Increased inhibition of DA uptake by L-DOPA and its preferential inhibition of NE over DA uptake, indicates that NET-mediated DA uptake may be modulated by L-DOPA when DAT loss exceeds 70%. Levodopa 37-43 solute carrier family 6 member 3 Rattus norvegicus 168-171 23300642-14 2012 Increased inhibition of DA uptake by L-DOPA and its preferential inhibition of NE over DA uptake, indicates that NET-mediated DA uptake may be modulated by L-DOPA when DAT loss exceeds 70%. Levodopa 156-162 solute carrier family 6 member 3 Rattus norvegicus 168-171 23226401-12 2012 We conclude that chronic L-Dopa administration produced a long-lasting increase in the number of TH-ir cells, even after a washout period of 6 months. Levodopa 25-31 tyrosine hydroxylase Homo sapiens 97-99 23226401-13 2012 L-Dopa also modified the phenotype of these cells with a significant reduction of the TH/CR phenotype in favor of an increased number of TH/GAD cells that do not express CR. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 86-88 23226401-13 2012 L-Dopa also modified the phenotype of these cells with a significant reduction of the TH/CR phenotype in favor of an increased number of TH/GAD cells that do not express CR. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 137-139 23226401-14 2012 We suggest that the increased number of striatal TH-ir cells might be involved in the development of aberrant striatal circuits and the appearance of L-Dopa induced dyskinesias. Levodopa 150-156 tyrosine hydroxylase Homo sapiens 49-51 22242182-7 2012 After inhibition of aromatic acid decarboxylase, L-DOPA tissue content per recovered TH protein was greatest in NAc, matched by differences in ser31, but not ser40, phosphorylation. Levodopa 49-55 tyrosine hydroxylase Rattus norvegicus 85-87 23133663-1 2012 Recessive mutations in the F-box only protein 7 gene (FBXO7) cause PARK15, a mendelian form of early-onset, levodopa-responsive parkinsonism with severe loss of nigrostriatal dopaminergic neurons. Levodopa 108-116 F-box protein 7 Danio rerio 27-47 23133663-1 2012 Recessive mutations in the F-box only protein 7 gene (FBXO7) cause PARK15, a mendelian form of early-onset, levodopa-responsive parkinsonism with severe loss of nigrostriatal dopaminergic neurons. Levodopa 108-116 F-box protein 7 Danio rerio 54-59 22384042-3 2012 Co-administration of L-Dopa with peripheral DDC inhibitors (carbidopa or benserazide) is the most effective symptomatic treatment for PD. Levodopa 21-27 dopa decarboxylase Homo sapiens 44-47 22179112-0 2011 Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia. Levodopa 71-77 RASD family member 2 Homo sapiens 0-4 23196528-3 2012 Furthermore, levodopa-induced dyskinesias are dramatically improved because STN stimulation permits an approximately 50% reduction in antiparkinsonian treatment. Levodopa 13-21 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 76-79 22393477-6 2012 These data indicate that approaches to regulate GRK6 activity could be useful in modulating both therapeutic and side-effects of L-DOPA. Levodopa 129-135 G protein-coupled receptor kinase 6 Mus musculus 48-52 22200605-9 2012 In contrast, the administration of L-3, 4-dihydroxyphenylalanine (L-DOPA) had marginal effects on Tdg (-/-) embryonic lethality. Levodopa 35-64 thymine DNA glycosylase Mus musculus 98-101 22200605-9 2012 In contrast, the administration of L-3, 4-dihydroxyphenylalanine (L-DOPA) had marginal effects on Tdg (-/-) embryonic lethality. Levodopa 66-72 thymine DNA glycosylase Mus musculus 98-101 22027820-7 2011 Concurrently, in vivo synthesis activity of l-dihydroxyphenylalanine, the dopamine precursor, per TH protein level was augmented, suggesting up-regulation of dopamine synthesis activity in the intact nigrostriatal axons. Levodopa 44-68 tyrosine hydroxylase Mus musculus 98-100 22027820-8 2011 Collectively, our conditional Th gene targeting method demonstrates two regulatory mechanisms of TH in axon terminals for dopamine homeostasis in vivo: local regulation of TH protein amount independent of soma and trans-axonal regulation of apparent L-dihydroxyphenylalanine synthesis activity per TH protein. Levodopa 250-274 tyrosine hydroxylase Mus musculus 97-99 22179112-1 2011 L-DOPA-induced dyskinesia, the rate-limiting side effect in the therapy of Parkinson"s disease, is mediated by activation of mammalian target of rapamycin (mTOR) signaling in the striatum. Levodopa 0-6 mechanistic target of rapamycin kinase Homo sapiens 125-154 22179112-1 2011 L-DOPA-induced dyskinesia, the rate-limiting side effect in the therapy of Parkinson"s disease, is mediated by activation of mammalian target of rapamycin (mTOR) signaling in the striatum. Levodopa 0-6 mechanistic target of rapamycin kinase Homo sapiens 156-160 22179112-3 2011 Moreover, Rhes(-/-) mice showed reduced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for Rhes-binding drugs. Levodopa 127-133 RASD family, member 2 Mus musculus 10-14 21946266-2 2011 In this regard, the NMDAR channel blocker amantadine is so far the only drug available for clinical use that attenuates L-DOPA-induced dyskinesia (LID). Levodopa 120-126 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 20-25 22133327-4 2011 Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson"s disease and to reduce off-time in patients with more advanced Parkinson"s disease and motor fluctuations related to levodopa. Levodopa 269-277 monoamine oxidase B Homo sapiens 4-9 22133327-5 2011 A third MAO-B inhibitor (safinamide), which also combines additional non-dopaminergic properties of potential benefit to Parkinson"s disease, is currently under development in phase III clinical trials as adjuvant therapy to either a dopamine agonist or levodopa. Levodopa 254-262 monoamine oxidase B Homo sapiens 8-13 21946266-6 2011 Indeed, lesioned mutant mice display physiological L-DOPA-dependent enhancement of striatal D1 receptor/PKA/protein phosphatase-1 and ERK signaling. Levodopa 51-57 mitogen-activated protein kinase 1 Mus musculus 134-137 21946266-7 2011 Moreover, in line with synaptic rearrangements of NMDAR subunits occurring in dyskinetic animal models, a short L-DOPA treatment produces a dramatic and selective reduction of the NR2B subunit in the striatal post-synaptic fraction of Ddo(-/-) lesioned mutants but not in controls. Levodopa 112-118 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 50-55 21946266-7 2011 Moreover, in line with synaptic rearrangements of NMDAR subunits occurring in dyskinetic animal models, a short L-DOPA treatment produces a dramatic and selective reduction of the NR2B subunit in the striatal post-synaptic fraction of Ddo(-/-) lesioned mutants but not in controls. Levodopa 112-118 glutamate receptor, ionotropic, NMDA2B (epsilon 2) Mus musculus 180-184 21946266-7 2011 Moreover, in line with synaptic rearrangements of NMDAR subunits occurring in dyskinetic animal models, a short L-DOPA treatment produces a dramatic and selective reduction of the NR2B subunit in the striatal post-synaptic fraction of Ddo(-/-) lesioned mutants but not in controls. Levodopa 112-118 D-aspartate oxidase Mus musculus 235-238 21683736-0 2011 L-DOPA neurotoxicity is prevented by neuroprotective effects of erythropoietin. Levodopa 0-6 erythropoietin Rattus norvegicus 64-78 22093536-4 2011 Dopamine agonists, catechol-O-methyltransferase inhibitors and monoamine oxidase-B inhibitors are anti-parkinsonian (anti-PD) drugs that have been found to further improve the potency of l-dopa and prevent the onset of motor complications. Levodopa 187-193 catechol-O-methyltransferase Homo sapiens 19-47 22093536-4 2011 Dopamine agonists, catechol-O-methyltransferase inhibitors and monoamine oxidase-B inhibitors are anti-parkinsonian (anti-PD) drugs that have been found to further improve the potency of l-dopa and prevent the onset of motor complications. Levodopa 187-193 monoamine oxidase B Homo sapiens 63-82 21161716-3 2011 Different negative allosteric modulators (NAMs) of mGluR5 were repeatedly shown to be efficacious in models of L: -DOPA-induced dyskinesia (LID), anxiety, and some forms of pain. Levodopa 111-119 glutamate receptor, ionotropic, kainate 1 Mus musculus 51-57 21683736-2 2011 Considering the well known neuroprotective effects of erythropoietin (EPO), the inhibitory effects of EPO on L-DOPA neurotoxicity need to be evaluated. Levodopa 109-115 erythropoietin Rattus norvegicus 102-105 21683736-7 2011 Free radicals and hydroxyl radical levels increased by L-DOPA were decreased after combined treatment of L-DOPA and EPO. Levodopa 55-61 erythropoietin Rattus norvegicus 105-119 21683736-10 2011 Pretreatment with LY294002, a phosphatidylinositol 3-kinase inhibitor, prior to combined treatment with EPO and L-DOPA almost completely blocked the protective effects of EPO. Levodopa 112-118 erythropoietin Rattus norvegicus 171-174 21683736-11 2011 These results indicate that EPO can prevent L-DOPA neurotoxicity by activating the PI3K pathway as well as reducing oxidative stress. Levodopa 44-50 erythropoietin Rattus norvegicus 28-31 22131969-3 2011 However, abnormal Ras-ERK signaling has also been linked to a number of neuropsychiatric conditions, including mental retardation syndromes ("RASopathies"), drug addiction, and l-DOPA induced dyskinesia (LID). Levodopa 177-183 mitogen-activated protein kinase 1 Homo sapiens 22-25 22028687-0 2011 L-DOPA-Induced Dyskinesia and Abnormal Signaling in Striatal Medium Spiny Neurons: Focus on Dopamine D1 Receptor-Mediated Transmission. Levodopa 0-6 dopamine receptor D1 Homo sapiens 92-112 21752681-7 2011 In contrast to the previously published patients with a FOLR1 gene defect, our patient presented with an abnormal l-dopa metabolism in CSF and high 3-O-methyl-dopa. Levodopa 114-120 folate receptor alpha Homo sapiens 56-61 21871902-0 2011 L-Dihydroxyphenylalanine modulates the steady-state expression of mouse striatal tyrosine hydroxylase, aromatic L-amino acid decarboxylase, dopamine and its metabolites in an MPTP mouse model of Parkinson"s disease. Levodopa 0-24 dopa decarboxylase Mus musculus 103-138 21871902-2 2011 L-DOPA efficacy relies on its decarboxylation by aromatic l-amino acid decarboxylase (AAAD) to form dopamine (DA). Levodopa 0-6 dopa decarboxylase Mus musculus 49-84 21871902-2 2011 L-DOPA efficacy relies on its decarboxylation by aromatic l-amino acid decarboxylase (AAAD) to form dopamine (DA). Levodopa 0-6 dopa decarboxylase Mus musculus 86-90 21963945-0 2011 The involvement of RGS9 in l-3,4-dihydroxyphenylalanine-induced dyskinesias in unilateral 6-OHDA lesion rat model. Levodopa 27-55 regulator of G-protein signaling 9 Rattus norvegicus 19-23 21963945-10 2011 In addition, expressions of RGS9 protein or mRNA analyzed by Western blot or real-time PCR with striatal extracts increased significantly after L-DOPA/benserazide. Levodopa 144-150 regulator of G-protein signaling 9 Rattus norvegicus 28-32 21963945-11 2011 These data demonstrate that RGS9 expression can be modulated by sub-chronic L-DOPA/benserazide administration and increased RGS9 expression in striatum may be one of the reasons for the side effects such as dyskinesia induced by L-DOPA therapy. Levodopa 76-82 regulator of G-protein signaling 9 Rattus norvegicus 28-32 21963945-11 2011 These data demonstrate that RGS9 expression can be modulated by sub-chronic L-DOPA/benserazide administration and increased RGS9 expression in striatum may be one of the reasons for the side effects such as dyskinesia induced by L-DOPA therapy. Levodopa 229-235 regulator of G-protein signaling 9 Rattus norvegicus 28-32 21963945-11 2011 These data demonstrate that RGS9 expression can be modulated by sub-chronic L-DOPA/benserazide administration and increased RGS9 expression in striatum may be one of the reasons for the side effects such as dyskinesia induced by L-DOPA therapy. Levodopa 229-235 regulator of G-protein signaling 9 Rattus norvegicus 124-128 21871902-7 2011 KEY FINDINGS: In the MPTP model, L-DOPA reduced the steady-state expression and the activity of striatal AAAD by 52% and 50%, respectively, DA and metabolites were also significantly decreased. Levodopa 33-39 dopa decarboxylase Mus musculus 105-109 21871902-8 2011 SIGNIFICANCE: The outcome shows that while L-DOPA replenishes striatal DA it also down-regulates AAAD and the steady-state synthesis and metabolic capability of the dopaminergic system. Levodopa 43-49 dopa decarboxylase Mus musculus 97-101 21871902-3 2011 So exogenous L-DOPA drives the reaction and AAAD becomes the rate limiting enzyme in the supply of DA. Levodopa 13-19 dopa decarboxylase Mus musculus 44-48 21871902-4 2011 In turn, exogenous L-DOPA regulates the expression and activity of AAAD as well as the synthesis of DA and its metabolites, changes that may be linked to the efficacy and side-effects of L-DOPA. Levodopa 19-25 dopa decarboxylase Mus musculus 67-71 21871902-4 2011 In turn, exogenous L-DOPA regulates the expression and activity of AAAD as well as the synthesis of DA and its metabolites, changes that may be linked to the efficacy and side-effects of L-DOPA. Levodopa 187-193 dopa decarboxylase Mus musculus 67-71 22028687-2 2011 Accumulating evidence indicates that l-DOPA-induced dyskinesia (LID) is primarily caused by the development of sensitized dopamine D1 receptor (D1R) transmission in the medium spiny neurons (MSNs) of the striatum. Levodopa 37-43 dopamine receptor D1 Homo sapiens 122-142 21917769-1 2011 BACKGROUND: Several in vitro studies have suggested levodopa (L-dopa) to be toxic to dopaminergic neurons and that it can modulate the aggregation process of alpha-synuclein. Levodopa 52-60 synuclein alpha Homo sapiens 158-173 21815648-0 2011 Levodopa activates apoptosis signaling kinase 1 (ASK1) and promotes apoptosis in a neuronal model: implications for the treatment of Parkinson"s disease. Levodopa 0-8 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 49-53 21815648-3 2011 Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. Levodopa 15-21 glutaredoxin Homo sapiens 202-214 21815648-3 2011 Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. Levodopa 15-21 glutaredoxin Homo sapiens 216-220 21815648-3 2011 Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. Levodopa 15-21 thioredoxin Homo sapiens 226-237 21815648-3 2011 Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. Levodopa 15-21 thioredoxin Homo sapiens 239-243 21815648-5 2011 Considering this loss of both Grx1 and Trx1 activities upon L-DOPA treatment, we sought to elucidate the mechanism(s) of L-DOPA-induced apoptosis. Levodopa 60-66 glutaredoxin Homo sapiens 30-34 21815648-5 2011 Considering this loss of both Grx1 and Trx1 activities upon L-DOPA treatment, we sought to elucidate the mechanism(s) of L-DOPA-induced apoptosis. Levodopa 60-66 thioredoxin Homo sapiens 39-43 21815648-9 2011 In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Levodopa 37-43 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 13-17 21815648-9 2011 In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Levodopa 37-43 mitogen-activated protein kinase 14 Homo sapiens 146-149 21815648-9 2011 In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Levodopa 37-43 mitogen-activated protein kinase 8 Homo sapiens 154-157 21815648-10 2011 Chemical inhibition of either p38 or JNK provided protection from L-DOPA-induced apoptosis. Levodopa 66-72 mitogen-activated protein kinase 14 Homo sapiens 30-33 21815648-10 2011 Chemical inhibition of either p38 or JNK provided protection from L-DOPA-induced apoptosis. Levodopa 66-72 mitogen-activated protein kinase 8 Homo sapiens 37-40 21815648-11 2011 Moreover, direct knockdown of ASK1 protected from L-DOPA-induced neuronal cell death. Levodopa 50-56 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 30-34 21815648-12 2011 These results identify ASK1 as the main pro-apoptotic pathway activated in response to L-DOPA treatment, implicating it as a potential target for adjunct therapy in PD. Levodopa 87-93 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 23-27 22087552-7 2011 Other therapies, including dopamine agonists and monoamine oxidase type-B (MAO-B) inhibitors, may limit the rate of dyskinesia relative to levodopa-based regimens. Levodopa 139-147 monoamine oxidase B Homo sapiens 75-80 21917769-1 2011 BACKGROUND: Several in vitro studies have suggested levodopa (L-dopa) to be toxic to dopaminergic neurons and that it can modulate the aggregation process of alpha-synuclein. Levodopa 62-68 synuclein alpha Homo sapiens 158-173 22053701-5 2011 We defined the COMT-index as [baseline 3-OMD concentration] / [levodopa Cmax when 100 mg levodopa was administered alone]. Levodopa 63-71 catechol-O-methyltransferase Homo sapiens 15-19 21939547-4 2011 DISCUSSION: In multiple studies, MAO-B inhibitors, such as selegiline and rasagiline, have shown to provide mild symptomatic effects, delay the need for levodopa, and to reduce the incidence of motor fluctuations. Levodopa 153-161 monoamine oxidase B Homo sapiens 33-38 21484883-6 2011 We investigated the effects of the mGluR5 antagonist, 2-methyl-6-(phenylethynyl) pyridine (MPEP) on the striatal expression of VGlut1 and VGlut2 in levodopa-treated hemiparkinsonian rats. Levodopa 148-156 glutamate receptor, ionotropic, kainate 1 Mus musculus 35-41 21484883-6 2011 We investigated the effects of the mGluR5 antagonist, 2-methyl-6-(phenylethynyl) pyridine (MPEP) on the striatal expression of VGlut1 and VGlut2 in levodopa-treated hemiparkinsonian rats. Levodopa 148-156 solute carrier family 17 member 7 Rattus norvegicus 127-133 21484883-6 2011 We investigated the effects of the mGluR5 antagonist, 2-methyl-6-(phenylethynyl) pyridine (MPEP) on the striatal expression of VGlut1 and VGlut2 in levodopa-treated hemiparkinsonian rats. Levodopa 148-156 solute carrier family 17 member 6 Rattus norvegicus 138-144 21939547-2 2011 Due to marked advances in PD treatment during the last decades, physicians are nowadays fortunately equipped with a variety of substances that can effectively ameliorate emerging motor symptoms of the disease, among them levodopa, dopamine agonists and monoamine oxidase type B (MAO-B) inhibitors. Levodopa 221-229 monoamine oxidase B Homo sapiens 279-284 22121348-5 2011 STN-DBS allowed complete postoperative levodopa withdrawal and HAART restart, without infectious complications after 12 months of follow-up. Levodopa 39-47 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 0-3 22053701-5 2011 We defined the COMT-index as [baseline 3-OMD concentration] / [levodopa Cmax when 100 mg levodopa was administered alone]. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 15-19 21665941-0 2011 Nicotine reduces L-DOPA-induced dyskinesias by acting at beta2* nicotinic receptors. Levodopa 17-23 hemoglobin, beta adult minor chain Mus musculus 57-62 21665941-9 2011 L-DOPA-induced AIMs were approximately 40% less in the beta2(-/-) mice compared with the wild-type mice. Levodopa 0-6 hemoglobin, beta adult minor chain Mus musculus 55-60 21488084-9 2011 At 14 months of age, the alpha-Syn mice presented with significantly lower striatal tissue dopamine and tyrosine hydroxylase content relative to WT littermates, accompanied by an L-DOPA-reversible sensory motor deficit. Levodopa 179-185 synuclein, alpha Mus musculus 25-34 21542062-1 2011 Kufor-Rakeb syndrome (KRS) is a rare form of autosomal recessive juvenile or early-onset, levodopa responsive parkinsonism and has been associated with mutations in ATP13A2(also known as PARK9), a lysosomal type 5 P-type ATPase. Levodopa 90-98 ATPase cation transporting 13A2 Homo sapiens 165-172 21542062-1 2011 Kufor-Rakeb syndrome (KRS) is a rare form of autosomal recessive juvenile or early-onset, levodopa responsive parkinsonism and has been associated with mutations in ATP13A2(also known as PARK9), a lysosomal type 5 P-type ATPase. Levodopa 90-98 ATPase cation transporting 13A2 Homo sapiens 187-192 21635907-2 2011 To better characterize this possible mechanism, c-fos immunohistochemistry was first used to determine the effects of systemic administration of the full 5-HT1AR agonist +-8-OH-DPAT on L-Dopa-induced immediate early gene expression within M1 and the prefrontal cortex (PFC) of rats with unilateral medial forebrain bundle (MFB) dopamine (DA) lesions. Levodopa 185-191 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 48-53 21635907-5 2011 While no treatment effects were seen within the PFC, systemic +-8-OH-DPAT suppressed L-Dopa-induced c-fos within M1. Levodopa 85-91 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 100-105 21624436-11 2011 Thus, oxidative stress may upregulate the synthesis of NM, which may be a result of the increased TH activity observed in response to the elevated ROS in l-DOPA-treated PC12 cells. Levodopa 154-160 tyrosine hydroxylase Rattus norvegicus 98-100 21771855-0 2011 Vascular endothelial growth factor is upregulated by L-dopa in the parkinsonian brain: implications for the development of dyskinesia. Levodopa 53-59 vascular endothelial growth factor A Homo sapiens 0-34 21771855-2 2011 Using a validated rat model of l-dopa-induced dyskinesia, this study demonstrates that chronic treatment with l-dopa dose dependently induces the expression of vascular endothelial growth factor in the basal ganglia nuclei. Levodopa 31-37 vascular endothelial growth factor A Homo sapiens 160-194 21771855-2 2011 Using a validated rat model of l-dopa-induced dyskinesia, this study demonstrates that chronic treatment with l-dopa dose dependently induces the expression of vascular endothelial growth factor in the basal ganglia nuclei. Levodopa 110-116 vascular endothelial growth factor A Homo sapiens 160-194 21771855-4 2011 When co-administered with l-dopa, a small molecule inhibitor of vascular endothelial growth factor signalling significantly attenuated the development of dyskinesia and completely blocked the angiogenic response and associated increase in blood-brain barrier permeability induced by the treatment. Levodopa 26-32 vascular endothelial growth factor A Homo sapiens 64-98 21771855-6 2011 These congruent findings in the rat model and human patients indicate that vascular endothelial growth factor is implicated in the pathophysiology of l-dopa-induced dyskinesia and emphasize an involvement of the microvascular compartment in the adverse effects of l-dopa pharmacotherapy in Parkinson"s disease. Levodopa 150-156 vascular endothelial growth factor A Homo sapiens 75-109 21710366-4 2011 The results showed that L-DOPA increased the PPO activity and, further, the melanin content. Levodopa 24-30 aureusidin synthase Glycine max 45-48 21710366-8 2011 It was concluded that the reduction in the O -2 and H(2)O(2) contents and lipid peroxidation in soybean roots was due to the enhanced SOD and POD activities and thus a possible antioxidant role of L-DOPA. Levodopa 197-203 peroxidase Glycine max 142-145 21514317-8 2011 DOPAL in cell lysate significantly inhibited TH activity as measured by decreased l-DOPA production. Levodopa 82-88 tyrosine hydroxylase Homo sapiens 45-47 21808606-8 2011 Administration of L-DOPA promotes cAMP signaling and activates the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) in the D1R-expressing MSNs, which form the striatonigral, or direct pathway. Levodopa 18-24 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 67-120 21808606-8 2011 Administration of L-DOPA promotes cAMP signaling and activates the dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) in the D1R-expressing MSNs, which form the striatonigral, or direct pathway. Levodopa 18-24 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 122-130 21713068-4 2011 The primary findings of this study were that NG-nitro-l-Arginine, an inhibitor of endothelial and neuronal nitric oxide synthase, attenuated AIMs induced by chronic and acute l-DOPA. Levodopa 175-181 nitric oxide synthase 1 Rattus norvegicus 98-128 21530574-7 2011 In conclusion, increased thermal sensitivity was reversed by L-DOPA and could be caused by a reduction TH levels in the PAG. Levodopa 61-67 tyrosine hydroxylase Rattus norvegicus 103-105 21713068-6 2011 The 6-OHDA lesion and the l-DOPA treatment induced a bilateral increase (1.5 times) in the neuronal nitric oxide synthase (nNOS) protein and nNOS mRNA in the striatum and in the frontal cortex. Levodopa 26-32 nitric oxide synthase 1 Rattus norvegicus 91-121 21713068-6 2011 The 6-OHDA lesion and the l-DOPA treatment induced a bilateral increase (1.5 times) in the neuronal nitric oxide synthase (nNOS) protein and nNOS mRNA in the striatum and in the frontal cortex. Levodopa 26-32 nitric oxide synthase 1 Rattus norvegicus 123-127 21713068-6 2011 The 6-OHDA lesion and the l-DOPA treatment induced a bilateral increase (1.5 times) in the neuronal nitric oxide synthase (nNOS) protein and nNOS mRNA in the striatum and in the frontal cortex. Levodopa 26-32 nitric oxide synthase 1 Rattus norvegicus 141-145 21713068-8 2011 The exception was in the contralateral striatum and the ipsilateral frontal cortex, where chronic l-DOPA treatment induced an increase of approximately 10 times the nNOS mRNA. Levodopa 98-104 nitric oxide synthase 1 Rattus norvegicus 165-169 21461922-4 2011 The shortened response duration and increased peak turning, resembling human wearing-off fluctuations and dyskinesia, were associated with a marked increase in Ser-845 phosphorylated GluR1 (pGluR1S845) immunoreactivity in lesioned striatum in response to levodopa treatment. Levodopa 255-263 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 183-188 21352823-1 2011 Serotonin 1A receptor (5-HT(1A)R) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Levodopa 55-61 5-hydroxytryptamine receptor 1A Rattus norvegicus 0-21 21310234-5 2011 After the behavioral studies, the induction of phosphorylated extracellular signal-regulated kinases 1 and 2 (pERK1/2) by acute L-DOPA (30 mg/kg) was used as a marker of post-synaptic supersensitivity. Levodopa 128-134 mitogen-activated protein kinase 3 Mus musculus 62-108 21310234-11 2011 In all groups, the L-DOPA-induced AIM scores correlated closely with the number of cells immunoreactive for tyrosine hydroxylase or FosB/ FosB in the striatum. Levodopa 19-25 FBJ osteosarcoma oncogene B Mus musculus 132-136 21310234-11 2011 In all groups, the L-DOPA-induced AIM scores correlated closely with the number of cells immunoreactive for tyrosine hydroxylase or FosB/ FosB in the striatum. Levodopa 19-25 FBJ osteosarcoma oncogene B Mus musculus 138-142 21461922-2 2011 To investigate molecular mechanisms that underlie the persisting alterations in motor response occurring with levodopa treatment of parkinsonian patients, we evaluated the time course of these changes in relation to the phosphorylation of GluR1 in 6-hydroxydopamine (6-OHDA) lesioned animals. Levodopa 110-118 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 239-244 21461922-5 2011 The time course of changes in GluR1 phosphorylation correlated with the time course of changes in motor behavior after withdrawal of chronic levodopa therapy. Levodopa 141-149 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 30-35 21533995-0 2011 Inhibition of catechol-O-methyltransferase modifies acute homocysteine rise during repeated levodopa application in patients with Parkinson"s disease. Levodopa 92-100 catechol-O-methyltransferase Homo sapiens 14-42 21533995-2 2011 Degradation of levodopa to 3-O-methyldopa via the enzyme catechol-O-methyltransferase (COMT) is a methyl group demanding reaction. Levodopa 15-23 catechol-O-methyltransferase Homo sapiens 57-85 21606452-1 2011 OBJECTIVE: To investigate striatal adenosine A2A receptor availability in patients with Parkinson disease (PD) with and without levodopa-induced dyskinesias (LIDs). Levodopa 128-136 adenosine A2a receptor Homo sapiens 35-57 21533995-2 2011 Degradation of levodopa to 3-O-methyldopa via the enzyme catechol-O-methyltransferase (COMT) is a methyl group demanding reaction. Levodopa 15-23 catechol-O-methyltransferase Homo sapiens 87-91 21533995-10 2011 Levodopa bioavailability was higher on day 2 due to the COMT inhibition. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 56-60 21507338-0 2011 Differential expression of FosB, c-Fos, and Zif268 in forebrain regions after acute or chronic L-DOPA treatment in a rat model of Parkinson"s disease. Levodopa 95-101 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 27-31 21507338-0 2011 Differential expression of FosB, c-Fos, and Zif268 in forebrain regions after acute or chronic L-DOPA treatment in a rat model of Parkinson"s disease. Levodopa 95-101 early growth response 1 Rattus norvegicus 44-50 21507338-1 2011 A study was carried out to examine the effects of acute and chronic L-DOPA treatment on the distribution of the immediate-early gene (IEG) proteins (FosB, c-Fos, and Zif268) in forebrain regions in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease. Levodopa 68-74 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 149-153 21507338-1 2011 A study was carried out to examine the effects of acute and chronic L-DOPA treatment on the distribution of the immediate-early gene (IEG) proteins (FosB, c-Fos, and Zif268) in forebrain regions in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease. Levodopa 68-74 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 155-160 21507338-1 2011 A study was carried out to examine the effects of acute and chronic L-DOPA treatment on the distribution of the immediate-early gene (IEG) proteins (FosB, c-Fos, and Zif268) in forebrain regions in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease. Levodopa 68-74 early growth response 1 Rattus norvegicus 166-172 21507338-3 2011 Compared with the rats in the acute L-DOPA treatment group, those in the chronic treatment group had significantly more FosB-immunopositive cells in the anterior cingulate (Cg) and the dorsolateral caudate-putamen ipsilateral to the lesion and significantly fewer c-Fos-immunopositive cells in the Cg, the nucleus accumbens shell, and the basolateral nucleus of amygdala ipsilateral to the lesion. Levodopa 36-42 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 120-124 21538606-1 2011 L-Dopa, the standard therapeutic for Parkinson"s disease, is inactivated by the enzyme catechol-O-methyltransferase (COMT). Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 87-115 21538606-1 2011 L-Dopa, the standard therapeutic for Parkinson"s disease, is inactivated by the enzyme catechol-O-methyltransferase (COMT). Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 117-121 21538606-2 2011 COMT catalyzes the transfer of an activated methyl group from S-adenosylmethionine (SAM) to its catechol substrates, such as L-dopa, in the presence of magnesium ions. Levodopa 125-131 catechol-O-methyltransferase Homo sapiens 0-4 21316292-1 2011 Subthalamic nucleus deep brain stimulation (STN-DBS) is currently the treatment of choice for medication-resistant levodopa-related motor complications in patients with Parkinson"s disease (PD). Levodopa 115-123 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 44-47 21264950-11 2011 Furthermore, MT-1/-2 expression was markedly elevated specifically in reactive astrocytes in the striatum of L-DOPA-treated hemi-parkinsonian mice or METH-injected mice. Levodopa 109-115 metallothionein 1 Mus musculus 13-20 21501255-6 2011 l-Dopa treatment that induced dyskinesias increased 5-HT(2A) receptor-specific binding in the caudate nucleus and the anterior cingulate gyrus (AcgG) compared with control monkeys. Levodopa 0-6 5-hydroxytryptamine receptor 2A Homo sapiens 52-69 21284755-4 2011 The biochemical and functional characterization of the At2g20340 gene product revealed that it is an aromatic aldehyde synthase (AtAAS), which catalyzes the conversion of phenylalanine and 3,4-dihydroxy-L-phenylalanine to phenylacetaldehyde and dopaldehyde, respectively. Levodopa 189-218 Pyridoxal phosphate (PLP)-dependent transferases superfamily protein Arabidopsis thaliana 101-127 21284755-4 2011 The biochemical and functional characterization of the At2g20340 gene product revealed that it is an aromatic aldehyde synthase (AtAAS), which catalyzes the conversion of phenylalanine and 3,4-dihydroxy-L-phenylalanine to phenylacetaldehyde and dopaldehyde, respectively. Levodopa 189-218 Pyridoxal phosphate (PLP)-dependent transferases superfamily protein Arabidopsis thaliana 129-134 21493132-0 2011 Restless legs syndrome (RLS) augmentation associated with dopamine agonist and levodopa usage in a community sample. Levodopa 79-87 RLS1 Homo sapiens 24-27 21054558-3 2011 In human skin melanocytes, the cellular tyrosinase inhibition was examined by the conversion of l-tyrosine and oxidation of l-DOPA to dopaquinone. Levodopa 124-130 tyrosinase Homo sapiens 40-50 21543973-0 2011 Levodopa induces synthesis of nerve growth factor and growth hormone in patients with Parkinson disease. Levodopa 0-8 nerve growth factor Homo sapiens 30-49 21543973-0 2011 Levodopa induces synthesis of nerve growth factor and growth hormone in patients with Parkinson disease. Levodopa 0-8 growth hormone 1 Homo sapiens 54-68 21543973-4 2011 Levodopa may experimentally exert supportive effects on nerve growth factor synthesis and on growth hormone production, a hormonal compound with regenerative potential. Levodopa 0-8 growth hormone 1 Homo sapiens 93-107 21543973-5 2011 OBJECTIVE: The objective of this study was to investigate the effects of soluble 250-mg levodopa/benserazide administration on plasma occurrence of levodopa, nerve growth factor, and growth hormone in patients with Parkinson disease over an interval of 60 minutes. Levodopa 88-96 nerve growth factor Homo sapiens 158-177 21543973-5 2011 OBJECTIVE: The objective of this study was to investigate the effects of soluble 250-mg levodopa/benserazide administration on plasma occurrence of levodopa, nerve growth factor, and growth hormone in patients with Parkinson disease over an interval of 60 minutes. Levodopa 88-96 growth hormone 1 Homo sapiens 183-197 21543973-6 2011 RESULTS: Levodopa moderately increased bioavailability of nerve growth factor and growth hormone combined with the rise of levodopa. Levodopa 9-17 nerve growth factor Homo sapiens 58-77 21543973-6 2011 RESULTS: Levodopa moderately increased bioavailability of nerve growth factor and growth hormone combined with the rise of levodopa. Levodopa 9-17 growth hormone 1 Homo sapiens 82-96 21543973-8 2011 CONCLUSIONS: Axonal degeneration may not be due to levodopa itself, as levodopa supports production of nerve growth factor and of growth hormone. Levodopa 71-79 nerve growth factor Homo sapiens 103-122 21543973-8 2011 CONCLUSIONS: Axonal degeneration may not be due to levodopa itself, as levodopa supports production of nerve growth factor and of growth hormone. Levodopa 71-79 growth hormone 1 Homo sapiens 130-144 21316993-1 2011 We report a case of levodopa-responsive juvenile parkinsonism (JP) associated with a heterozygous ATP13A2 gene frameshift mutation. Levodopa 20-28 ATPase cation transporting 13A2 Homo sapiens 98-105 25205926-5 2011 Other pharmacological measures like catechol-O-methyltrasferase (COMT) inhibitors like entacopone, telcapone and monoamine oxidase B (MAO-B) inhibitors like selegiline and rasagiline are also useful, while L-dopa remains the gold standard in the treatment of PD. Levodopa 206-212 catechol-O-methyltransferase Homo sapiens 36-63 25205926-5 2011 Other pharmacological measures like catechol-O-methyltrasferase (COMT) inhibitors like entacopone, telcapone and monoamine oxidase B (MAO-B) inhibitors like selegiline and rasagiline are also useful, while L-dopa remains the gold standard in the treatment of PD. Levodopa 206-212 monoamine oxidase B Homo sapiens 113-132 21305354-6 2011 A small proportion of patients receiving L-dopa therapy were found to have a CSF PLP concentration below the appropriate reference range. Levodopa 41-47 pyridoxal phosphatase Homo sapiens 81-84 19419794-5 2011 Treatment with L-DOPA+benserazide (12 weeks) resulted in less severe dyskinesias in CB1 KO than in WT mice. Levodopa 15-21 cannabinoid receptor 1 (brain) Mus musculus 84-87 19419794-6 2011 The results revealed that the lack of cannabinoid CB1 receptors increased the severity of motor impairment and DA lesion, and reduced L-DOPA-induced dyskinesias. Levodopa 134-140 cannabinoid receptor 1 (brain) Mus musculus 50-53 19419794-7 2011 These results suggest that activation of CB1 receptors offers neuroprotection against dopaminergic lesion and the development of L-DOPA-induced dyskinesias. Levodopa 129-135 cannabinoid receptor 1 (brain) Mus musculus 41-44 21347293-1 2011 Mutations in the F-box only protein 7 gene (FBXO7) cause PARK15, an autosomal recessive neurodegenerative disease presenting with severe levodopa-responsive parkinsonism and pyramidal disturbances. Levodopa 137-145 F-box protein 7 Homo sapiens 17-37 21195062-6 2011 CSC treatment ameliorated the shortening of the rotational motor response duration, partly attenuated dyskinesia and reduced striatal expression of adenosine A(2A) receptor induced by l-DOPA. Levodopa 184-190 adenosine A2a receptor Rattus norvegicus 148-172 21381113-0 2011 Novel mutations in SPG11 cause hereditary spastic paraplegia associated with early-onset levodopa-responsive Parkinsonism. Levodopa 89-97 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 19-24 21129389-10 2011 BN82451 treatment significantly reversed the overexpression of c-Fos, FosB and Arc mRNA associated with the dyskinesiogenic action of L-dopa. Levodopa 134-140 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-68 21129389-10 2011 BN82451 treatment significantly reversed the overexpression of c-Fos, FosB and Arc mRNA associated with the dyskinesiogenic action of L-dopa. Levodopa 134-140 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 70-74 21129389-11 2011 A significant correlation between the degree of overexpression of c-Fos, FosB and Arc mRNA and the dyskinesiogenic action of L-dopa was observed. Levodopa 125-131 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 66-71 21129389-11 2011 A significant correlation between the degree of overexpression of c-Fos, FosB and Arc mRNA and the dyskinesiogenic action of L-dopa was observed. Levodopa 125-131 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 73-77 21475622-8 2011 The properly balanced administration of l-dopa in conjunction with 5-HTP, l-tyrosine, l-cysteine, and cofactors under the guidance of organic cation transporter functional status determination (herein referred to as "OCT assay interpretation") of urinary serotonin and dopamine, is at the heart of this novel treatment protocol. Levodopa 40-46 plexin A2 Homo sapiens 217-220 21475622-9 2011 RESULTS: When 5-HTP and l-dopa are administered in proper balance along with l-tyrosine, l-cysteine, and cofactors under the guidance of OCT assay interpretation, the long list of problems that can interfere with optimum administration of l-dopa becomes controllable and manageable or does not occur at all. Levodopa 239-245 plexin A2 Homo sapiens 137-140 21347293-1 2011 Mutations in the F-box only protein 7 gene (FBXO7) cause PARK15, an autosomal recessive neurodegenerative disease presenting with severe levodopa-responsive parkinsonism and pyramidal disturbances. Levodopa 137-145 F-box protein 7 Homo sapiens 44-49 21347293-1 2011 Mutations in the F-box only protein 7 gene (FBXO7) cause PARK15, an autosomal recessive neurodegenerative disease presenting with severe levodopa-responsive parkinsonism and pyramidal disturbances. Levodopa 137-145 F-box protein 7 Homo sapiens 57-63 21108621-0 2011 The role of apolipoprotein E polymorphisms in levodopa-induced dyskinesia. Levodopa 46-54 apolipoprotein E Homo sapiens 12-28 21108621-1 2011 OBJECTIVES: To determine the relationship between apolipoprotein E (APOE) polymorphisms to the time to appearance of levodopa-induced dyskinesia (LID) in patients with Parkinson"s disease. Levodopa 117-125 apolipoprotein E Homo sapiens 50-66 21108621-1 2011 OBJECTIVES: To determine the relationship between apolipoprotein E (APOE) polymorphisms to the time to appearance of levodopa-induced dyskinesia (LID) in patients with Parkinson"s disease. Levodopa 117-125 apolipoprotein E Homo sapiens 68-72 21108621-2 2011 METHODS: The APOE genotype of 155 consecutive patients treated with levodopa was determined and its effect on the time of onset of LID was examined using Cox regression model, controlling for gender, age of disease onset, time to initiation of levodopa treatment and history of smoking. Levodopa 68-76 apolipoprotein E Homo sapiens 13-17 20966038-0 2011 Fatty acid amide hydrolase (FAAH) inhibition reduces L-3,4-dihydroxyphenylalanine-induced hyperactivity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned non-human primate model of Parkinson"s disease. Levodopa 53-81 fatty-acid amide hydrolase 1 Callithrix jacchus 0-26 21091640-4 2011 In the treatment of patients with Parkinson"s disease, 5-HT(1A) agonists are expected to improve not only affective symptoms (e.g., anxiety and depression), but also the core parkinsonian symptoms as well as antiparkinsonian agents-induced side effects (e.g., L-DOPA-induced dyskinesia). Levodopa 260-266 5-hydroxytryptamine receptor 1A Homo sapiens 55-62 20809346-4 2011 SCA-3 can present with a levodopa responsive parkinsonism phenotype, and an abnormal DAT scan showing predominant impairment of presynaptic dopamine function. Levodopa 25-33 ataxin 3 Homo sapiens 0-5 20966038-3 2011 The role of fatty acid amide hydrolase (FAAH) in mediating l-3,4-dihydroxyphenylalanine (L-DOPA)-induced behaviors was explored in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned marmoset model of PD. Levodopa 59-87 fatty-acid amide hydrolase 1 Callithrix jacchus 40-44 20966038-3 2011 The role of fatty acid amide hydrolase (FAAH) in mediating l-3,4-dihydroxyphenylalanine (L-DOPA)-induced behaviors was explored in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned marmoset model of PD. Levodopa 89-95 fatty-acid amide hydrolase 1 Callithrix jacchus 12-38 20966038-3 2011 The role of fatty acid amide hydrolase (FAAH) in mediating l-3,4-dihydroxyphenylalanine (L-DOPA)-induced behaviors was explored in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned marmoset model of PD. Levodopa 89-95 fatty-acid amide hydrolase 1 Callithrix jacchus 40-44 21145586-6 2011 On the other hand, we have characterized the effects of a variety of surface treatments and coatings, and found that double coating with 3,4-dihydroxy-l-phenylalanine and an ECM markedly improves HPTC performance and results in the formation of differentiated epithelia on PSF/PVP membranes. Levodopa 137-166 insulin like growth factor binding protein 7 Homo sapiens 273-276 20966038-0 2011 Fatty acid amide hydrolase (FAAH) inhibition reduces L-3,4-dihydroxyphenylalanine-induced hyperactivity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned non-human primate model of Parkinson"s disease. Levodopa 53-81 fatty acid amide hydrolase Homo sapiens 28-32 20966038-13 2011 Inhibition of FAAH may represent a novel approach to reducing L-DOPA-induced side effects, such as ICD and DDS, while maintaining the antiparkinsonian benefits of L-DOPA treatment. Levodopa 62-68 fatty acid amide hydrolase Homo sapiens 14-18 20966038-13 2011 Inhibition of FAAH may represent a novel approach to reducing L-DOPA-induced side effects, such as ICD and DDS, while maintaining the antiparkinsonian benefits of L-DOPA treatment. Levodopa 163-169 fatty acid amide hydrolase Homo sapiens 14-18 20966038-3 2011 The role of fatty acid amide hydrolase (FAAH) in mediating l-3,4-dihydroxyphenylalanine (L-DOPA)-induced behaviors was explored in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned marmoset model of PD. Levodopa 59-87 fatty-acid amide hydrolase 1 Callithrix jacchus 12-38 20680652-1 2011 Substrates for the Organic Cation Transporter 1, encoded by the SLC22A1 gene, are metformin, amantadine, pramipexole, and, possibly, levodopa. Levodopa 133-141 solute carrier family 22 member 1 Homo sapiens 19-47 20535562-1 2011 L-Dopa decarboxylase (DDC) catalyses the decarboxylation of L-Dopa. Levodopa 0-6 dopa decarboxylase Homo sapiens 22-25 20850462-0 2011 Evaluation of the D3 dopamine receptor selective agonist/partial agonist PG01042 on L-dopa dependent animal involuntary movements in rats. Levodopa 84-90 dopamine receptor D3 Rattus norvegicus 18-38 20850462-10 2011 These studies and previously published studies suggest that both D3 dopamine receptor selective antagonists, partial agonists and agonists, as defined by an adenylyl cyclase inhibition assay and a mitogenic assay, are pharmacotherapeutic candidates for the treatment of L-dopa-associated dyskinesia in patients with Parkinson"s Disease. Levodopa 270-276 dopamine receptor D3 Homo sapiens 65-85 20853184-1 2011 Mutations in the ATP13A2 (PARK9) and FBXO7 (PARK15) genes are linked to different forms of autosomal recessive juvenile-onset neurodegenerative diseases with overlapping phenotypes, including levodopa-responsive parkinsonism, pyramidal disturbances, cognitive decline, and supranuclear gaze disturbance. Levodopa 192-200 ATPase cation transporting 13A2 Homo sapiens 17-24 20680652-1 2011 Substrates for the Organic Cation Transporter 1, encoded by the SLC22A1 gene, are metformin, amantadine, pramipexole, and, possibly, levodopa. Levodopa 133-141 solute carrier family 22 member 1 Homo sapiens 64-71 21280081-1 2011 OBJECTIVE: In Parkinson disease (PD), the selective C-O-methyltransferase (COMT) inhibitor entacapone prolongs the effect of levodopa on motor symptoms (ON time) by increasing its bioavailability. Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 52-73 21078384-3 2011 hPHS-1- and hPHS-2-expressing cells incubated with DA, L-DOPA, DOPAC, or HVA exhibited increased cytotoxicity compared to untransfected cells, and cytotoxicity was increased further by exogenous arachidonic acid (AA), which increased hPHS activity. Levodopa 55-61 pterin-4 alpha-carbinolamine dehydratase 1 Homo sapiens 0-4 21078384-3 2011 hPHS-1- and hPHS-2-expressing cells incubated with DA, L-DOPA, DOPAC, or HVA exhibited increased cytotoxicity compared to untransfected cells, and cytotoxicity was increased further by exogenous arachidonic acid (AA), which increased hPHS activity. Levodopa 55-61 pterin-4 alpha-carbinolamine dehydratase 1 Homo sapiens 12-16 21078384-3 2011 hPHS-1- and hPHS-2-expressing cells incubated with DA, L-DOPA, DOPAC, or HVA exhibited increased cytotoxicity compared to untransfected cells, and cytotoxicity was increased further by exogenous arachidonic acid (AA), which increased hPHS activity. Levodopa 55-61 pterin-4 alpha-carbinolamine dehydratase 1 Homo sapiens 12-16 21187382-4 2011 After repeated L-DOPA treatment, however, ERK activation diminishes in medium spiny neurons and increases in striatal cholinergic interneurons. Levodopa 15-21 mitogen-activated protein kinase 1 Mus musculus 42-45 21187382-6 2011 Pharmacological blockers of ERK activation inhibit L-DOPA-induced changes in ERK phosphorylation, neuronal excitability, and the behavioral manifestation of LID. Levodopa 51-57 mitogen-activated protein kinase 1 Mus musculus 28-31 21187382-6 2011 Pharmacological blockers of ERK activation inhibit L-DOPA-induced changes in ERK phosphorylation, neuronal excitability, and the behavioral manifestation of LID. Levodopa 51-57 mitogen-activated protein kinase 1 Mus musculus 77-80 20853184-1 2011 Mutations in the ATP13A2 (PARK9) and FBXO7 (PARK15) genes are linked to different forms of autosomal recessive juvenile-onset neurodegenerative diseases with overlapping phenotypes, including levodopa-responsive parkinsonism, pyramidal disturbances, cognitive decline, and supranuclear gaze disturbance. Levodopa 192-200 ATPase cation transporting 13A2 Homo sapiens 26-31 20853184-1 2011 Mutations in the ATP13A2 (PARK9) and FBXO7 (PARK15) genes are linked to different forms of autosomal recessive juvenile-onset neurodegenerative diseases with overlapping phenotypes, including levodopa-responsive parkinsonism, pyramidal disturbances, cognitive decline, and supranuclear gaze disturbance. Levodopa 192-200 F-box protein 7 Homo sapiens 37-42 20853184-1 2011 Mutations in the ATP13A2 (PARK9) and FBXO7 (PARK15) genes are linked to different forms of autosomal recessive juvenile-onset neurodegenerative diseases with overlapping phenotypes, including levodopa-responsive parkinsonism, pyramidal disturbances, cognitive decline, and supranuclear gaze disturbance. Levodopa 192-200 F-box protein 7 Homo sapiens 44-50 20854831-4 2011 We administered L-3,4-dihydroxyphenylalanine (L-DOPA) in drinking water to timed-pregnant CD1 mice from the 11th day of gestation until the day of parturition. Levodopa 16-44 CD1 antigen complex Mus musculus 90-93 20854831-4 2011 We administered L-3,4-dihydroxyphenylalanine (L-DOPA) in drinking water to timed-pregnant CD1 mice from the 11th day of gestation until the day of parturition. Levodopa 46-52 CD1 antigen complex Mus musculus 90-93 21283636-2 2011 Our data revealed that this predicted AAAD protein use L-dopa as a substrate, as does Ddc, but it catalyzes the production of 3,4-dihydroxylphenylacetaldehyde (DHPAA) directly from L-dopa and apparently has nothing to do with the production of any aromatic amine. Levodopa 55-61 Dopa decarboxylase Drosophila melanogaster 86-89 21283636-2 2011 Our data revealed that this predicted AAAD protein use L-dopa as a substrate, as does Ddc, but it catalyzes the production of 3,4-dihydroxylphenylacetaldehyde (DHPAA) directly from L-dopa and apparently has nothing to do with the production of any aromatic amine. Levodopa 181-187 Dopa decarboxylase Drosophila melanogaster 86-89 21078384-5 2011 Protein oxidation was increased in hPHS-1 and -2 cells exposed to DA or L-DOPA and further increased by AA addition. Levodopa 72-78 prostaglandin-endoperoxide synthase 1 Homo sapiens 35-48 21078384-6 2011 DNA oxidation was enhanced earlier and at lower substrate concentrations than protein oxidation in both hPHS-1 and -2 cells by DA, L-DOPA, DOPAC, and HVA and further enhanced by AA addition. Levodopa 131-137 prostaglandin-endoperoxide synthase 1 Homo sapiens 104-117 21280081-1 2011 OBJECTIVE: In Parkinson disease (PD), the selective C-O-methyltransferase (COMT) inhibitor entacapone prolongs the effect of levodopa on motor symptoms (ON time) by increasing its bioavailability. Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 75-79 21280081-8 2011 Area under the concentration over time curve of levodopa increased more after entacapone in COMT(HH) than in COMT(LL) patients (+62 +- 6% vs +34 +- 8%, p = 0.01). Levodopa 48-56 catechol-O-methyltransferase Homo sapiens 92-96 21280081-8 2011 Area under the concentration over time curve of levodopa increased more after entacapone in COMT(HH) than in COMT(LL) patients (+62 +- 6% vs +34 +- 8%, p = 0.01). Levodopa 48-56 catechol-O-methyltransferase Homo sapiens 109-113 21280081-10 2011 INTERPRETATION: The COMT(HH) genotype in PD patients enhances the effect of entacapone on the pharmacodynamics and pharmacokinetics of levodopa. Levodopa 135-143 catechol-O-methyltransferase Homo sapiens 20-24 22615679-0 2011 5-HT(1A) receptor activation improves anti-cataleptic effects of levodopa in 6-hydroxydopamine-lesioned rats. Levodopa 65-73 5-hydroxytryptamine receptor 1A Rattus norvegicus 0-7 21164341-1 2011 OBJECTIVES: Entacapone is a highly potent, reversible, peripherally acting catechol-O-methyl transferase (COMT) inhibitor that is used as an adjunct to L-dopa in the treatment of patients with Parkinson disease (PD). Levodopa 152-158 catechol-O-methyltransferase Homo sapiens 75-104 21164341-1 2011 OBJECTIVES: Entacapone is a highly potent, reversible, peripherally acting catechol-O-methyl transferase (COMT) inhibitor that is used as an adjunct to L-dopa in the treatment of patients with Parkinson disease (PD). Levodopa 152-158 catechol-O-methyltransferase Homo sapiens 106-110 22615679-2 2011 In this investigation the effect of 8-OHDAPT, as a 5-HT(1A) agonist on anti-cataleptic effect of L-DOPA in 6-hydroxydopamine (6-OHDA) lesioned male Wistar rats was investigated. Levodopa 97-103 5-hydroxytryptamine receptor 1A Rattus norvegicus 51-58 22615679-12 2011 According to the obtained results, it may be concluded that activation of 5-HT(1A) receptors by 8-OHDAPT may improve anti-cataleptic effect of L-DOPA in a 6-OHDA- induced rat model of PD. Levodopa 143-149 5-hydroxytryptamine receptor 1A Rattus norvegicus 74-81 20947659-6 2011 PD patients with GBA mutations more frequently had bradykinesia as the presenting symptom and levodopa-induced dyskinesias. Levodopa 94-102 glucosylceramidase beta Homo sapiens 17-20 20736067-0 2011 L-DOPA-induced dyskinesia in hemiparkinsonian rats is associated with up-regulation of adenylyl cyclase type V/VI and increased GABA release in the substantia nigra reticulata. Levodopa 0-6 adenylate cyclase 5 Rattus norvegicus 87-113 22035027-6 2011 Although treatment for each patient should be individualized and based on their specific symptoms, severity, and lifestyle, in general MAO-B inhibitors may be used initially to treat mild symptoms, adding a dopamine agonist in younger patients or levodopa in older patients, as symptoms become more severe. Levodopa 247-255 monoamine oxidase B Homo sapiens 135-140 20407462-1 2011 The catecholamine, dopamine (DA), is synthesized from 3,4-dihydroxy-L-phenylalanine (L-DOPA) by aromatic L-amino acid decarboxylase (AADC). Levodopa 54-83 dopa decarboxylase Rattus norvegicus 105-131 20407462-1 2011 The catecholamine, dopamine (DA), is synthesized from 3,4-dihydroxy-L-phenylalanine (L-DOPA) by aromatic L-amino acid decarboxylase (AADC). Levodopa 54-83 dopa decarboxylase Rattus norvegicus 133-137 20407462-1 2011 The catecholamine, dopamine (DA), is synthesized from 3,4-dihydroxy-L-phenylalanine (L-DOPA) by aromatic L-amino acid decarboxylase (AADC). Levodopa 85-91 dopa decarboxylase Rattus norvegicus 105-131 20407462-1 2011 The catecholamine, dopamine (DA), is synthesized from 3,4-dihydroxy-L-phenylalanine (L-DOPA) by aromatic L-amino acid decarboxylase (AADC). Levodopa 85-91 dopa decarboxylase Rattus norvegicus 133-137 23933656-1 2011 The transcription factor DeltaFosB is a mediator of maladaptive neuroplasticity in animal models of Parkinson"s disease (PD) and L-DOPA-induced dyskinesia. Levodopa 129-135 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-34 23933656-8 2011 The putaminal elevation of FosB/DeltaFosB-like immunoreactivity in patients who had been affected by L-DOPA-induced dyskinesia is consistent with results from both rat and non-human primate models of this movement disorder. Levodopa 101-107 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-31 23933656-8 2011 The putaminal elevation of FosB/DeltaFosB-like immunoreactivity in patients who had been affected by L-DOPA-induced dyskinesia is consistent with results from both rat and non-human primate models of this movement disorder. Levodopa 101-107 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 32-41 23933656-9 2011 The present findings support the hypothesis of an involvement of DeltaFosB-related transcription factors in the molecular mechanisms of L-DOPA-induced dyskinesia. Levodopa 136-142 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-74 23939262-1 2011 Tyrosine hydroxylase (TH) is a tetrahydrobiopterin (BH4) dependent enzyme that catalyses the conversion of L-tyrosine to L-dopa, the rate-limiting step in the biosynthesis of dopamine. Levodopa 121-127 tyrosine hydroxylase Homo sapiens 0-20 23939262-1 2011 Tyrosine hydroxylase (TH) is a tetrahydrobiopterin (BH4) dependent enzyme that catalyses the conversion of L-tyrosine to L-dopa, the rate-limiting step in the biosynthesis of dopamine. Levodopa 121-127 tyrosine hydroxylase Homo sapiens 22-24 23939343-2 2011 In this study, we examined a novel orthosteric agonist at the mGlu4 receptor, LSP1-2111, for its ability to affect L-DOPA-induced dyskinesia (LID), in a mouse model. Levodopa 115-121 lymphocyte specific 1 Mus musculus 78-82 23939343-3 2011 In 6-OHDA-lesioned mice treated with L-DOPA, chronic co-administration of LSP1-2111 significantly attenuated the development of abnormal involuntary movements, which are regarded as a marker of dyskinesia. Levodopa 37-43 lymphocyte specific 1 Mus musculus 74-78 23939343-6 2011 These results indicate that co-administration of LSP1-2111 may improve the efficacy of standard L-DOPA therapy by attenuating its liability for dyskinesia. Levodopa 96-102 lymphocyte specific 1 Mus musculus 49-53 20736067-7 2011 In contrast, in the animals in which l-DOPA treatment induced severe dyskinesia all the parameters, except for Galpha(olf) levels, were significantly higher in the denervated side. Levodopa 37-43 G protein subunit alpha L Rattus norvegicus 111-122 22001994-3 2011 These results demonstrate that levodopa differs from dopamine agonists in its regulation of dopamine transporter expression in peripheral blood lymphocytes. Levodopa 31-39 solute carrier family 6 member 3 Homo sapiens 92-112 21073474-2 2011 This work demonstrates that irradiation of the eye by ultraviolet-A (UVA) specifically increased DOPA-positive cells in the mucosa of the jejunum and colon of C57BL/6J mice by some HPA- and iNOS-independent mechanism. Levodopa 97-101 nitric oxide synthase 2, inducible Mus musculus 190-194 22110725-6 2011 Levodopa influenced in which task version errors grew from conditioning to deconditioning: in unmedicated patients just as controls errors only rose in the NoGo version with an increase of incorrect responses to target cues. Levodopa 0-8 reticulon 4 Homo sapiens 156-160 20858480-1 2010 Serotonin 1A receptor agonists have attracted much interest recently as potential therapeutic agents for levodopa-induced motor complications, such as dyskinesia and motor fluctuations. Levodopa 105-113 5-hydroxytryptamine receptor 1A Rattus norvegicus 0-21 21984936-4 2011 For the first time MALDI-TOF imaging mass spectrometry (IMS) was used for unbiased assessment and topographical elucidation of prodynorphin-derived peptides in the substantia nigra of a unilateral rat model of Parkinson"s disease and L-DOPA induced dyskinesia. Levodopa 234-240 prodynorphin Rattus norvegicus 127-139 21738693-1 2011 BACKGROUND: Levodopa treatment in Parkinson"s disease (PD) increases in serum homocysteine levels due to its metabolism via catechol O-methyltransferase. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 124-152 20927559-8 2010 CONCLUSION: Our findings suggest that 123I-MIBG scintigraphy in combination with levodopa-responsiveness evaluation may represent a useful tool for prediction of outcomes in patients subjected to STN stimulation. Levodopa 81-89 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 196-199 21115823-0 2010 Inhibition of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) signaling in the striatum reverts motor symptoms associated with L-dopa-induced dyskinesia. Levodopa 132-138 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 14-55 21115823-0 2010 Inhibition of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) signaling in the striatum reverts motor symptoms associated with L-dopa-induced dyskinesia. Levodopa 132-138 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 57-65 21115823-5 2010 Furthermore, in a nonhuman primate model of LID, lentiviral vectors expressing dominant negative forms of Ras-GRF1 caused a dramatic reversion of dyskinesia severity leaving intact the therapeutic effect of L-dopa. Levodopa 207-213 RAS protein-specific guanine nucleotide-releasing factor 1 Mus musculus 106-114 21112832-3 2010 L-DOPA (50-200 muM) co-treatment increased the survival of the rotenone-treated animals (LC50: 0.51 +- 0.23 muM, 1.03 +- 0.66 muM, and 0.76 +- 0.52 muM, respectively). Levodopa 0-6 latexin Homo sapiens 15-18 21112832-3 2010 L-DOPA (50-200 muM) co-treatment increased the survival of the rotenone-treated animals (LC50: 0.51 +- 0.23 muM, 1.03 +- 0.66 muM, and 0.76 +- 0.52 muM, respectively). Levodopa 0-6 latexin Homo sapiens 108-111 21112832-3 2010 L-DOPA (50-200 muM) co-treatment increased the survival of the rotenone-treated animals (LC50: 0.51 +- 0.23 muM, 1.03 +- 0.66 muM, and 0.76 +- 0.52 muM, respectively). Levodopa 0-6 latexin Homo sapiens 108-111 21112832-3 2010 L-DOPA (50-200 muM) co-treatment increased the survival of the rotenone-treated animals (LC50: 0.51 +- 0.23 muM, 1.03 +- 0.66 muM, and 0.76 +- 0.52 muM, respectively). Levodopa 0-6 latexin Homo sapiens 108-111 21112832-5 2010 Nauplii treated in 100 mM L-DOPA and rotenone together showed further increase of GST activity all across the range of rotenone concentrations. Levodopa 26-32 glutathione S-transferase kappa 1 Homo sapiens 82-85 21112832-7 2010 Biochemical measurements suggest a protective role of L-DOPA by increasing the GST activity as part of the intracellular defences during toxin-evoked oxidative stress. Levodopa 54-60 glutathione S-transferase kappa 1 Homo sapiens 79-82 21085660-0 2010 Levodopa-induced dyskinesia is associated with increased thyrotropin releasing hormone in the dorsal striatum of hemi-parkinsonian rats. Levodopa 0-8 thyrotropin releasing hormone Rattus norvegicus 57-86 21124922-4 2010 METHODOLOGY/PRINCIPAL FINDINGS: We tested the possibility that L-DOPA might interfere with DAT binding. Levodopa 63-69 solute carrier family 6 member 3 Homo sapiens 91-94 21085660-4 2010 With this technique, we determined that thyrotropin releasing hormone (TRH) was greatly increased in the dopamine-depleted striatum of hemi-parkinsonian rats that developed abnormal movements in response to L-DOPA therapy, relative to the levels measured in the contralateral non-dopamine-depleted striatum, and in the striatum of non-dyskinetic control rats. Levodopa 207-213 thyrotropin releasing hormone Rattus norvegicus 40-69 21085660-4 2010 With this technique, we determined that thyrotropin releasing hormone (TRH) was greatly increased in the dopamine-depleted striatum of hemi-parkinsonian rats that developed abnormal movements in response to L-DOPA therapy, relative to the levels measured in the contralateral non-dopamine-depleted striatum, and in the striatum of non-dyskinetic control rats. Levodopa 207-213 thyrotropin releasing hormone Rattus norvegicus 71-74 20882603-3 2010 METHODS: As an index of terminal serotonin innervation density, we measured radioligand binding to the plasma membrane serotonin transporter (SERT) in levodopa-treated dyskinetic and nondyskinetic subjects, using brain tissue from both rat and monkey models of Parkinson disease as well as parkinsonian patients. Levodopa 151-159 solute carrier family 6 member 4 Rattus norvegicus 119-140 20882603-3 2010 METHODS: As an index of terminal serotonin innervation density, we measured radioligand binding to the plasma membrane serotonin transporter (SERT) in levodopa-treated dyskinetic and nondyskinetic subjects, using brain tissue from both rat and monkey models of Parkinson disease as well as parkinsonian patients. Levodopa 151-159 solute carrier family 6 member 4 Rattus norvegicus 142-146 21048351-0 2010 N-(3,5-dihydroxybenzoyl)-6-hydroxytryptamine as a novel human tyrosinase inhibitor that inactivates the enzyme in cooperation with l-3,4-dihydroxyphenylalanine. Levodopa 131-159 tyrosinase Homo sapiens 62-72 21048351-3 2010 Furthermore, compound 2 exhibited a unique property of inactivating the human tyrosinase in the presence of low concentrations of DOPA. Levodopa 130-134 tyrosinase Homo sapiens 78-88 21048351-5 2010 Tyrosinase is the enzyme that oxidizes tyrosine to DOPA and further oxidizes DOPA to the melanin precursor dopaquinone. Levodopa 51-55 tyrosinase Homo sapiens 0-10 21048351-5 2010 Tyrosinase is the enzyme that oxidizes tyrosine to DOPA and further oxidizes DOPA to the melanin precursor dopaquinone. Levodopa 77-81 tyrosinase Homo sapiens 0-10 21048351-6 2010 A compound such as 2 that inactivates the enzyme in the presence of a small amount of DOPA is therefore attractive as a new type of tyrosinase inhibitor. Levodopa 86-90 tyrosinase Homo sapiens 132-142 20964730-5 2010 Similarly, 6-hydroxydopamine-induced chronic dopaminergic denervation induced a significant increase in expression of AT1, AT2 and p47(phox) , which decreased with L-dopa administration. Levodopa 164-170 cytochrome b-245 alpha chain Rattus norvegicus 131-140 20824733-1 2010 There is a consensus that in Parkinson"s disease, the extent of preoperative levodopa responsiveness predicts the efficacy of subthalamic nucleus deep brain stimulation (STN DBS). Levodopa 77-85 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 170-173 20656029-3 2010 Daily treatment of young MitoPark mice for eight weeks with the A(2A)R antagonist MSX-3 prevented the reduction of spontaneous locomotor activity observed in saline or L-DOPA treated animals. Levodopa 168-174 adenosine A2a receptor Mus musculus 64-70 20670675-3 2010 At the low concentration, L-DOPA was not cytotoxic and its presence increased the activities of extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, BadSer112, Bcl-2, and caspase-12. Levodopa 26-32 mitogen activated protein kinase 3 Rattus norvegicus 96-142 20670675-3 2010 At the low concentration, L-DOPA was not cytotoxic and its presence increased the activities of extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, BadSer112, Bcl-2, and caspase-12. Levodopa 26-32 mitogen activated protein kinase 14 Rattus norvegicus 144-147 20670675-3 2010 At the low concentration, L-DOPA was not cytotoxic and its presence increased the activities of extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, BadSer112, Bcl-2, and caspase-12. Levodopa 26-32 BCL2, apoptosis regulator Rattus norvegicus 165-170 20670675-3 2010 At the low concentration, L-DOPA was not cytotoxic and its presence increased the activities of extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, BadSer112, Bcl-2, and caspase-12. Levodopa 26-32 caspase 12 Rattus norvegicus 176-186 20670675-4 2010 At the high concentrations, L-DOPA was cytotoxic and stimulated the activities of ERK1/2, p38 MAPK, c-Jun N-terminal kinase (JNK)1/2, BadSer155, caspase-12 and caspase-3. Levodopa 28-34 mitogen activated protein kinase 3 Rattus norvegicus 82-88 20670675-4 2010 At the high concentrations, L-DOPA was cytotoxic and stimulated the activities of ERK1/2, p38 MAPK, c-Jun N-terminal kinase (JNK)1/2, BadSer155, caspase-12 and caspase-3. Levodopa 28-34 mitogen activated protein kinase 14 Rattus norvegicus 90-93 20670675-4 2010 At the high concentrations, L-DOPA was cytotoxic and stimulated the activities of ERK1/2, p38 MAPK, c-Jun N-terminal kinase (JNK)1/2, BadSer155, caspase-12 and caspase-3. Levodopa 28-34 mitogen-activated protein kinase 8 Rattus norvegicus 100-130 20670675-4 2010 At the high concentrations, L-DOPA was cytotoxic and stimulated the activities of ERK1/2, p38 MAPK, c-Jun N-terminal kinase (JNK)1/2, BadSer155, caspase-12 and caspase-3. Levodopa 28-34 caspase 12 Rattus norvegicus 145-155 20670675-4 2010 At the high concentrations, L-DOPA was cytotoxic and stimulated the activities of ERK1/2, p38 MAPK, c-Jun N-terminal kinase (JNK)1/2, BadSer155, caspase-12 and caspase-3. Levodopa 28-34 caspase 3 Rattus norvegicus 160-169 20938027-13 2010 PLA2G6 mutations should be considered in patients with early-onset l-dopa-responsive parkinsonism and dementia with frontotemporal lobar atrophy. Levodopa 67-73 phospholipase A2 group VI Homo sapiens 0-6 20670675-5 2010 The increased levels of ERK1/2 and BadSer155 in the presence of high concentrations of L-DOPA did not protect against L-DOPA-mediated cytotoxicity. Levodopa 87-93 mitogen activated protein kinase 3 Rattus norvegicus 24-30 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 mitogen activated protein kinase 3 Rattus norvegicus 131-137 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 BCL2, apoptosis regulator Rattus norvegicus 153-158 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 caspase 3 Rattus norvegicus 212-221 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 mitogen activated protein kinase 14 Rattus norvegicus 263-266 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 mitogen activated protein kinase 3 Rattus norvegicus 267-271 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 66-72 caspase 12 Rattus norvegicus 346-356 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 191-197 caspase 3 Rattus norvegicus 212-221 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 191-197 mitogen activated protein kinase 14 Rattus norvegicus 263-266 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 191-197 mitogen activated protein kinase 3 Rattus norvegicus 267-271 20670675-7 2010 These results suggest that, at a low and non-toxic concentration, L-DOPA may promote cell survival by increasing the activities of ERK1/2, BadSer112 and Bcl-2, while, at high concentrations, L-DOPA activates the caspase-3 cell death enzyme through the JNK1/2 and p38 MAPK signaling pathways as well as endoplasmic reticulum stress that activates caspase-12. Levodopa 191-197 caspase 12 Rattus norvegicus 346-356 20510935-5 2010 As a demonstration, a candidate peptide, TOP1, that weakly binds to the target protein, the Src homology 3 (SH3) domain of human Abelson tyrosine kinase (Abl), was fused to green fluorescent protein (GFP) and l-DOPA was site-specifically incorporated into the peptide region (TOP1-DOPA-GFP). Levodopa 209-215 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 154-157 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 23-51 NK2 homeobox 5 Gallus gallus 134-141 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 23-51 T-box 5 Gallus gallus 143-147 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 23-51 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 153-158 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 53-59 NK2 homeobox 5 Gallus gallus 134-141 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 53-59 T-box 5 Gallus gallus 143-147 20525643-9 2010 Similarly, addition of l-3,4-dihydroxyphenylalanine (l-DOPA) or dopamine induced ectopic expression of cardiac transcription factors (cNkx2.5, Tbx5) and AMHC1 as well as sarcomere formation. Levodopa 53-59 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 153-158 20929666-0 2010 [GRK6, a new therapeutic approach to alleviate L-dopa-induced dyskinesia]. Levodopa 47-53 G protein-coupled receptor kinase 6 Homo sapiens 1-5 21992878-12 2010 Levodopa could be prescribed at optimum doses following STN-DBS in patients with YOPD as abnormal movements are better controlled following STN-DBS implantation. Levodopa 0-8 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 56-59 20464572-1 2010 Peripheral metabolism of L-DOPA via enzyme catechol-O-methyltransferase (COMT) is one of the possible sources of homocysteine (HCY). Levodopa 25-31 catechol-O-methyltransferase Homo sapiens 43-71 20464572-1 2010 Peripheral metabolism of L-DOPA via enzyme catechol-O-methyltransferase (COMT) is one of the possible sources of homocysteine (HCY). Levodopa 25-31 catechol-O-methyltransferase Homo sapiens 73-77 21992878-12 2010 Levodopa could be prescribed at optimum doses following STN-DBS in patients with YOPD as abnormal movements are better controlled following STN-DBS implantation. Levodopa 0-8 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 140-143 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 phospholipase A2 group VI Homo sapiens 32-38 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 phospholipase A2 group VI Homo sapiens 40-46 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 F-box protein 7 Homo sapiens 49-54 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 F-box protein 7 Homo sapiens 56-62 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 69-78 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 214-222 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 80-85 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 phospholipase A2 group VI Homo sapiens 32-38 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 phospholipase A2 group VI Homo sapiens 40-46 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 F-box protein 7 Homo sapiens 49-54 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 F-box protein 7 Homo sapiens 56-62 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 69-78 20669327-5 2010 Mutations in three other genes, PLA2G6 (PARK14), FBXO7 (PARK15), and Spatacsin (SPG11) also produce clinical similar phenotypes in that they presented with rapidly progressive parkinsonism, initially responsive to Levodopa treatment but later, developed additional features including cognitive decline and loss of Levodopa responsiveness. Levodopa 314-322 SPG11 vesicle trafficking associated, spatacsin Homo sapiens 80-85 20856911-3 2010 Levodopa is routinely combined with a dopa-decarboxylase inhibitor (DDCI) to prevent the conversion of levodopa into dopamine in peripheral circulation. Levodopa 0-8 dopa decarboxylase Homo sapiens 38-56 20856911-3 2010 Levodopa is routinely combined with a dopa-decarboxylase inhibitor (DDCI) to prevent the conversion of levodopa into dopamine in peripheral circulation. Levodopa 103-111 dopa decarboxylase Homo sapiens 38-56 20856911-5 2010 In recent years, a new, safe, and efficacious armamentarium of treatment options has been provided by the marketing of the catechol-O-methyltransferase (COMT) inhibitor, entacapone, a peripheral blocker of dopa to 3-0-methyldopa metabolism, which increments levodopa brain availability. Levodopa 258-266 catechol-O-methyltransferase Homo sapiens 123-151 20856911-5 2010 In recent years, a new, safe, and efficacious armamentarium of treatment options has been provided by the marketing of the catechol-O-methyltransferase (COMT) inhibitor, entacapone, a peripheral blocker of dopa to 3-0-methyldopa metabolism, which increments levodopa brain availability. Levodopa 258-266 catechol-O-methyltransferase Homo sapiens 153-157 20542064-0 2010 Locomotor response to L-DOPA in reserpine-treated rats following central inhibition of aromatic L-amino acid decarboxylase: further evidence for non-dopaminergic actions of L-DOPA and its metabolites. Levodopa 22-28 dopa decarboxylase Rattus norvegicus 87-122 19819090-2 2010 We report three patients with XPA being administered low-dose levodopa (0.3-1.5 mg/kg/day) for laryngeal dystonia. Levodopa 62-70 XPA, DNA damage recognition and repair factor Homo sapiens 30-33 19819090-4 2010 Two XPA patients responded to low-dose levodopa, and paroxysmal choking and involuntary movements resolved, although one of the two patients showed incomplete resolution due to suspected vocal cord paralysis. Levodopa 39-47 XPA, DNA damage recognition and repair factor Homo sapiens 4-7 19819090-8 2010 Thus, low-dose levodopa may improve laryngeal dystonia by alleviating DA receptor supersensitivity in XPA patients. Levodopa 15-23 XPA, DNA damage recognition and repair factor Homo sapiens 102-105 19819090-9 2010 We recommend that low-dose levodopa be used for treatment of paroxysmal respiratory disturbances and/or involuntary movements in XPA patients. Levodopa 27-35 XPA, DNA damage recognition and repair factor Homo sapiens 129-132 20599976-8 2010 Thresholds for perception of axial twisting were increased when PD subjects were ON levodopa versus OFF in both the hip (p<0.01) and the trunk (p<0.05). Levodopa 84-92 hedgehog interacting protein Homo sapiens 116-119 20599976-9 2010 The magnitude of decrease in sensitivity due to being ON levodopa was significantly correlated with the increase in UPDRS motor scores (Hip: r=0.90, p<0.01 and Trunk: r=0.60, p<0.05). Levodopa 57-65 hedgehog interacting protein Homo sapiens 136-139 20815935-3 2010 We report here a design of using D-phenylglycine to guard L-dopa for better absorption in the intestine via intestinal peptide transporter I (PepT1). Levodopa 58-64 solute carrier family 15 member 1 Rattus norvegicus 142-147 20815935-13 2010 RESULTS: The BBMV uptake of D-phenylglycine-L-dopa was inhibited by Gly-Pro, Gly-Phe and cephradine, the typical PepT1 substrates, but not by amino acids Phe or L-dopa. Levodopa 44-50 solute carrier family 15 member 1 Rattus norvegicus 113-118 20815935-18 2010 CONCLUSION: The BBMV uptake studies indicated that D-phenylglycine facilitated the transport of L-dopa through the intestinal PepT1 transporter. Levodopa 96-102 solute carrier family 15 member 1 Rattus norvegicus 126-131 20452425-0 2010 A mGluR5 antagonist under clinical development improves L-DOPA-induced dyskinesia in parkinsonian rats and monkeys. Levodopa 56-62 glutamate receptor, ionotropic, kainate 1 Mus musculus 2-8 20542064-2 2010 The anti-parkinsonian and pro-dyskinetic actions of L-DOPA are widely attributed to its conversion, by the enzyme aromatic L-amino acid decarboxylase (AADC), to dopamine. Levodopa 52-58 dopa decarboxylase Rattus norvegicus 123-149 20542064-2 2010 The anti-parkinsonian and pro-dyskinetic actions of L-DOPA are widely attributed to its conversion, by the enzyme aromatic L-amino acid decarboxylase (AADC), to dopamine. Levodopa 52-58 dopa decarboxylase Rattus norvegicus 151-155 20542064-8 2010 The hyperactivity induced by L-DOPA and NSD1015 was reduced by the alpha(2C) antagonist rauwolscine (1 mg/kg) and the 5-HT(2C) agonist MK212 (5 mg/kg), but not by the D2 dopamine receptor antagonist remoxipride (3 mg/kg) or the D1 dopamine receptor antagonist SCH23390 (1 mg/kg). Levodopa 29-35 dopamine receptor D2 Rattus norvegicus 167-187 20697051-11 2010 Higher age at onset, higher baseline levodopa-equivalent doses, probable rapid eye movement (REM) sleep behavior disorder at baseline, and follow-up time were independent risk factors of incident PDP. Levodopa 37-45 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 196-199 20808799-1 2010 BACKGROUND: In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. Levodopa 66-72 dopamine receptor D1 Homo sapiens 139-159 20808799-1 2010 BACKGROUND: In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. Levodopa 66-72 mitogen-activated protein kinase 1 Homo sapiens 222-263 20808799-1 2010 BACKGROUND: In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. Levodopa 66-72 mitogen-activated protein kinase 1 Homo sapiens 265-268 20808799-3 2010 METHODOLOGY/RESULTS: We here studied, in the gold-standard non-human primate model of Parkinson"s disease, the changes in PKA-dependent phosphorylation of DARPP-32 and GluR1 AMPA receptor, as well as in ERK and ribosomal protein S6 (S6) phosphorylation, associated to acute and chronic administration of L-DOPA. Levodopa 304-310 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 155-163 20808799-4 2010 Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. Levodopa 69-75 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 29-37 20808799-4 2010 Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. Levodopa 69-75 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 42-47 20808799-5 2010 In contrast, phosphorylation of ERK and S6 was enhanced preferentially after acute L-DOPA administration and decreased during the course of chronic treatment. Levodopa 83-89 mitogen-activated protein kinase 1 Homo sapiens 32-35 20808799-6 2010 CONCLUSION: Dysregulation of cAMP signalling is maintained during the course of chronic L-DOPA administration, while abnormal ERK signalling peaks during the initial phase of L-DOPA treatment and decreases following prolonged exposure. Levodopa 175-181 mitogen-activated protein kinase 1 Homo sapiens 126-129 20682746-4 2010 Using these mice, we found that the loss of DARPP-32 in striatonigral neurons decreased basal and cocaine-induced locomotion and abolished dyskinetic behaviors in response to the Parkinson"s disease drug L-DOPA. Levodopa 204-210 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 44-52 20678653-1 2010 An analytical methodology based on differential pulse voltammetry (DPV) on a glassy carbon electrode and the partial least-squares (PLS-1) algorithm for the simultaneous determination of levodopa, carbidopa and benserazide in pharmaceutical formulations was developed and validated. Levodopa 187-195 plastin 1 Homo sapiens 132-137 20678653-6 2010 In conclusion, the methodology proposed based on DPV data processed with the PLS-1 algorithm was able to quantify simultaneously levodopa, carbidopa and benserazide in its pharmaceuticals formulations using a ternary calibration model for these drugs in presence of excipients. Levodopa 129-137 plastin 1 Homo sapiens 77-82 20700524-2 2010 Studies have shown that concomitant use of a COMT inhibitor is highly beneficial in controlling the wearing-off phenomenon by improving L-DOPA bioavailability as well as brain entry. Levodopa 136-142 catechol-O-methyltransferase Homo sapiens 45-49 20700524-5 2010 EGCG strongly inhibited human liver COMT-mediated O-methylation of L-DOPA in a concentration-dependent manner in vitro, with an average IC50 of 0.36 microM. Levodopa 67-73 catechol-O-methyltransferase Homo sapiens 36-40 20697051-12 2010 Significant concomitant features of patients with PDP during the 12-year study period were low activities of daily living function (UPDRS II), dementia, high levodopa-equivalent dose, and probable REM sleep behavior disorder. Levodopa 158-166 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 50-53 20492352-11 2010 Moreover, compound III stabilizes in vitro the human TH mutant R202H, associated to autosomal recessive L-DOPA-responsive dystonia, revealing the potential of pharmacological chaperones for the treatment of disorders associated with TH misfolding. Levodopa 104-110 tyrosine hydroxylase Homo sapiens 53-55 20673310-2 2010 High-frequency stimulation of the subthalamic nucleus (STN-HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the L-DOPA requirement. Levodopa 156-162 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 55-58 20531394-4 2010 Restoration of AADC activity restored normal response to levodopa and gene expression could be quantitated repeatedly over many years by 6-[(18)F]fluoro-meta-tyrosine (FMT)-positron emission tomography (PET) and confirm that AADC transgene expression remained unchanged at the 8-year point. Levodopa 57-65 dopa decarboxylase Homo sapiens 15-19 20531394-8 2010 The present data suggest that the improvement in the L-3,4-dihydroxyphenylalanine (L-Dopa) therapeutic window brought about by AADC gene therapy is pronounced and persistent for many years. Levodopa 53-81 dopa decarboxylase Homo sapiens 127-131 20531394-8 2010 The present data suggest that the improvement in the L-3,4-dihydroxyphenylalanine (L-Dopa) therapeutic window brought about by AADC gene therapy is pronounced and persistent for many years. Levodopa 83-89 dopa decarboxylase Homo sapiens 127-131 20340169-3 2010 The aim of this study was to investigate the in vivo effect of the commonly used antiparkinsonian drugs, levodopa (L-DOPA) and bromocriptine, on type 1 cannabinoid (CB1) receptors, using the PET radioligand [(18)F]MK-9470. Levodopa 105-113 cannabinoid receptor 1 Rattus norvegicus 165-168 20457180-8 2010 CONCLUSIONS: Our patients showed two different patterns of clinical and neuroradiological features, that is, atypical parkinsonism with normal DAT density, which is clearly differentiated from PD versus levodopa-responsive parkinsonism with reduced DAT density (classical PD). Levodopa 203-211 solute carrier family 6 member 3 Homo sapiens 143-146 20457180-8 2010 CONCLUSIONS: Our patients showed two different patterns of clinical and neuroradiological features, that is, atypical parkinsonism with normal DAT density, which is clearly differentiated from PD versus levodopa-responsive parkinsonism with reduced DAT density (classical PD). Levodopa 203-211 solute carrier family 6 member 3 Homo sapiens 249-252 20340169-3 2010 The aim of this study was to investigate the in vivo effect of the commonly used antiparkinsonian drugs, levodopa (L-DOPA) and bromocriptine, on type 1 cannabinoid (CB1) receptors, using the PET radioligand [(18)F]MK-9470. Levodopa 115-121 cannabinoid receptor 1 Rattus norvegicus 165-168 20812452-1 2010 In Stalevo tablets, used in the therapy of patients with Parkinson"s disease, levodopa is combined with decarboxylase inhibitors and COMT inhibitors to provide a more steady plasma concentration of levodopa. Levodopa 198-206 catechol-O-methyltransferase Homo sapiens 133-137 20310030-0 2010 Effect of histamine H2 receptor antagonism on levodopa-induced dyskinesia in the MPTP-macaque model of Parkinson"s disease. Levodopa 46-54 histamine receptor H2 Homo sapiens 10-31 20215052-1 2010 Under aerobic or anaerobic conditions, tyrosinase undergoes a process of irreversible inactivation induced by its physiological substrate L-dopa. Levodopa 138-144 tyrosinase Homo sapiens 39-49 20581466-3 2010 Recent evidence indicates that L-DOPA-induced dyskinesia (LID) is associated with persistent activation of the mammalian target of rapamycin complex 1 (mTORC1) in the medium spiny neurons (MSNs) of the striatum, the main component of the basal ganglia. Levodopa 31-37 CREB regulated transcription coactivator 1 Mus musculus 152-158 20581466-5 2010 Such sensitization confers to dopaminergic drugs (including L-DOPA) the ability to activate the extracellular signal-regulated protein kinases 1/2, which, in turn promote mTORC1 signaling. Levodopa 60-66 CREB regulated transcription coactivator 1 Mus musculus 171-177 20582993-2 2010 It has been hypothesized that providing more continuous delivery of L-dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L-dopa with entacapone, an inhibitor of catechol-O-methyltransferase, to extend its elimination half-life. Levodopa 183-189 catechol-O-methyltransferase Homo sapiens 223-251 20456008-9 2010 Chronic IEM 1460 treatment reversed L-DOPA-induced up-regulation of pre-proenkephalin-A, and normalised pre-proenkephalin-B mRNA expression in the lateral striatum, indicating an inhibition of both behavioural and molecular correlates of priming. Levodopa 36-42 proenkephalin Rattus norvegicus 72-87 20590807-13 2010 Rapid-onset dystonia-parkinsonism (RPD, DYT12) is a rare disorder with an abrupt onset of symptoms over minutes to days, prominent bulbar involvement and parkinsonism with a lack of response to levodopa. Levodopa 194-202 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 40-45 20303948-6 2010 But in general, commonly used dose levels of dopa decarboxylase inhibitors appeared to produce a maximal motor response to L-DOPA. Levodopa 123-129 aromatic-L-amino-acid decarboxylase Callithrix jacchus 45-63 20303948-0 2010 The timing of administration, dose dependence and efficacy of dopa decarboxylase inhibitors on the reversal of motor disability produced by L-DOPA in the MPTP-treated common marmoset. Levodopa 140-146 aromatic-L-amino-acid decarboxylase Callithrix jacchus 62-80 20368333-9 2010 The donating agents and the L-DOPA hybrids reduced the release of tumor necrosis factor-alpha, interleukin-6, and nitric oxide from stimulated microglia, astrocytes as well as the THP-1 and U373 cell lines. Levodopa 28-34 tumor necrosis factor Homo sapiens 66-93 20368333-9 2010 The donating agents and the L-DOPA hybrids reduced the release of tumor necrosis factor-alpha, interleukin-6, and nitric oxide from stimulated microglia, astrocytes as well as the THP-1 and U373 cell lines. Levodopa 28-34 interleukin 6 Homo sapiens 95-108 20368333-12 2010 The H(2)S-releasing L-DOPA hybrid molecules also inhibited MAO B activity. Levodopa 20-26 monoamine oxidase B Homo sapiens 59-64 20303948-1 2010 Dopa decarboxylase inhibitors are routinely used to potentiate the effects of L-DOPA in the treatment of Parkinson"s disease. Levodopa 78-84 aromatic-L-amino-acid decarboxylase Callithrix jacchus 0-18 20303948-9 2010 This study shows that currently, dopa decarboxylase inhibitors may be routinely employed in the MPTP-treated primate at doses which are higher than those necessary to produce a maximal potentiation of the anti-parkinsonian effect of L-DOPA. Levodopa 233-239 aromatic-L-amino-acid decarboxylase Callithrix jacchus 33-51 20303948-3 2010 We now report on the choice of dopa decarboxylase inhibitors, dose and the time of dosing relationships of carbidopa, benserazide and L-alpha-methyl dopa (L-AMD) in potentiating the effects of L-DOPA in the 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-treated common marmoset. Levodopa 193-199 aromatic-L-amino-acid decarboxylase Callithrix jacchus 31-49 20518729-6 2010 In addition, recent studies have revealed new insights into the therapeutic role of 5-HT(1A) receptors in treating various CNS disorders, including not only depressive disorders (e.g., delayed onset of action and refractory symptoms), but also schizophrenia (e.g., cognitive impairment and antipsychotic-induced extrapyramidal side effects) and Parkinson"s disease (e.g., extrapyramidal motor symptoms and L-DOPA-induced dyskinesia). Levodopa 406-412 5-hydroxytryptamine receptor 1A Homo sapiens 84-91 20504213-0 2010 Effect of cdk5 antagonist on L-dopa-induced dyskinesias in a rat model of Parkinson"s disease. Levodopa 29-35 cyclin-dependent kinase 5 Rattus norvegicus 10-14 20504213-1 2010 Increased cyclin-dependent kinase 5 (Cdk5) has associated with the development of L-dopa-induced dyskinesias (LID). Levodopa 82-88 cyclin-dependent kinase 5 Rattus norvegicus 10-35 20504213-1 2010 Increased cyclin-dependent kinase 5 (Cdk5) has associated with the development of L-dopa-induced dyskinesias (LID). Levodopa 82-88 cyclin-dependent kinase 5 Rattus norvegicus 37-41 20437561-6 2010 RESULTS: We show that the deficiency in motor skill learning in PITx3(-/-) is dramatic and can be rescued with levodopa treatment. Levodopa 111-119 paired-like homeodomain transcription factor 3 Mus musculus 64-69 20505100-0 2010 Striatal overexpression of DeltaFosB reproduces chronic levodopa-induced involuntary movements. Levodopa 56-64 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 27-36 20505100-5 2010 Transgenic DeltaFosB overexpression reproduced the entire spectrum of altered motor behaviors in response to acute levodopa tests, including different types of abnormal involuntary movements and hypersensitivity of rotational responses that are typically associated with chronic levodopa treatment. Levodopa 115-123 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 11-20 20505100-5 2010 Transgenic DeltaFosB overexpression reproduced the entire spectrum of altered motor behaviors in response to acute levodopa tests, including different types of abnormal involuntary movements and hypersensitivity of rotational responses that are typically associated with chronic levodopa treatment. Levodopa 279-287 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 11-20 20074579-7 2010 Our results showed a beneficial antidyskinetic effect of blocking mGluR5 in L-Dopa-treated MPTP monkeys. Levodopa 76-82 glutamate receptor, ionotropic, kainate 1 Mus musculus 66-72 20132464-1 2010 Behavioral investigations of selective and potent metabotropic glutamate receptor type 5 (mGluR5) antagonists in animal models suggest involvement of mGluR5 in compensatory mechanisms of the basal ganglia circuitry in Parkinson"s disease and levodopa (L-Dopa) induced motor complications. Levodopa 242-250 glutamate receptor, ionotropic, kainate 1 Mus musculus 90-96 20132464-1 2010 Behavioral investigations of selective and potent metabotropic glutamate receptor type 5 (mGluR5) antagonists in animal models suggest involvement of mGluR5 in compensatory mechanisms of the basal ganglia circuitry in Parkinson"s disease and levodopa (L-Dopa) induced motor complications. Levodopa 252-258 glutamate receptor, ionotropic, kainate 1 Mus musculus 90-96 20132464-1 2010 Behavioral investigations of selective and potent metabotropic glutamate receptor type 5 (mGluR5) antagonists in animal models suggest involvement of mGluR5 in compensatory mechanisms of the basal ganglia circuitry in Parkinson"s disease and levodopa (L-Dopa) induced motor complications. Levodopa 252-258 glutamate receptor, ionotropic, kainate 1 Mus musculus 150-156 20132464-3 2010 The effect of a chronic 1 month treatment with L-Dopa on mGluR5-specific binding and mRNA levels was investigated in MPTP monkeys killed 4 or 24 h after their last L-Dopa administration. Levodopa 47-53 glutamate receptor, ionotropic, kainate 1 Mus musculus 57-63 20132464-6 2010 In contrast, caudate nucleus and putamen mGluR5 mRNA levels were elevated only in L-Dopa-treated MPTP monkeys killed 4 h after their last L-Dopa administration. Levodopa 82-88 glutamate receptor, ionotropic, kainate 1 Mus musculus 41-47 20132464-6 2010 In contrast, caudate nucleus and putamen mGluR5 mRNA levels were elevated only in L-Dopa-treated MPTP monkeys killed 4 h after their last L-Dopa administration. Levodopa 138-144 glutamate receptor, ionotropic, kainate 1 Mus musculus 41-47 20132464-7 2010 MPTP monkeys killed 4 h after their last L-Dopa treatment showed higher caudate nucleus and putamen L-Dopa concentrations compared with those killed after 24 h. Hence, mGluR5 in the putamen are sensitive to presence of L-Dopa leading to a rapid decrease of [(3)H]ABP688-specific binding possibly involving a direct mGluR5/dopamine receptors interaction. Levodopa 41-47 glutamate receptor, ionotropic, kainate 1 Mus musculus 168-174 20132464-7 2010 MPTP monkeys killed 4 h after their last L-Dopa treatment showed higher caudate nucleus and putamen L-Dopa concentrations compared with those killed after 24 h. Hence, mGluR5 in the putamen are sensitive to presence of L-Dopa leading to a rapid decrease of [(3)H]ABP688-specific binding possibly involving a direct mGluR5/dopamine receptors interaction. Levodopa 100-106 glutamate receptor, ionotropic, kainate 1 Mus musculus 168-174 20132464-7 2010 MPTP monkeys killed 4 h after their last L-Dopa treatment showed higher caudate nucleus and putamen L-Dopa concentrations compared with those killed after 24 h. Hence, mGluR5 in the putamen are sensitive to presence of L-Dopa leading to a rapid decrease of [(3)H]ABP688-specific binding possibly involving a direct mGluR5/dopamine receptors interaction. Levodopa 100-106 glutamate receptor, ionotropic, kainate 1 Mus musculus 168-174 20437543-0 2010 Perry syndrome due to the DCTN1 G71R mutation: a distinctive levodopa responsive disorder with behavioral syndrome, vertical gaze palsy, and respiratory failure. Levodopa 61-69 dynactin subunit 1 Homo sapiens 26-31 19914604-0 2010 Dopamine receptor D4 polymorphism predicts the effect of L-DOPA on gambling behavior. Levodopa 57-63 dopamine receptor D4 Homo sapiens 0-20 20424616-1 2010 BACKGROUND: L-DOPA decarboxylase (DDC) is an enzyme that catalyses, mainly, the decarboxylation of L-DOPA to dopamine and was found to be involved in many malignancies. Levodopa 12-18 dopa decarboxylase Homo sapiens 34-37 20026151-9 2010 In conclusion, our results showed that in MPTP monkeys, loss of striatal dopamine decreased Akt/GSK3 signaling and that increased phosphorylation of Akt and GSK3beta was associated with L-Dopa-induced dyskinesias. Levodopa 186-192 AKT serine/threonine kinase 1 Homo sapiens 149-152 20026151-9 2010 In conclusion, our results showed that in MPTP monkeys, loss of striatal dopamine decreased Akt/GSK3 signaling and that increased phosphorylation of Akt and GSK3beta was associated with L-Dopa-induced dyskinesias. Levodopa 186-192 glycogen synthase kinase 3 beta Homo sapiens 157-165 20410529-0 2010 Lentiviral overexpression of GRK6 alleviates L-dopa-induced dyskinesia in experimental Parkinson"s disease. Levodopa 45-51 G protein-coupled receptor kinase 6 Homo sapiens 29-33 20410529-7 2010 GRK6 suppressed dyskinesia in monkeys without compromising the antiparkinsonian effects of l-dopa and even prolonged the antiparkinsonian effect of a lower dose of l-dopa. Levodopa 164-170 G protein-coupled receptor kinase 6 Homo sapiens 0-4 20410529-8 2010 Our finding that increased availability of GRK6 ameliorates dyskinesia and increases duration of the antiparkinsonian action of l-dopa suggests a promising approach for controlling both dyskinesia and motor fluctuations in Parkinson"s disease. Levodopa 128-134 G protein-coupled receptor kinase 6 Homo sapiens 43-47 20026151-0 2010 Striatal Akt/GSK3 signaling pathway in the development of L-Dopa-induced dyskinesias in MPTP monkeys. Levodopa 58-64 AKT serine/threonine kinase 1 Homo sapiens 9-12 20026151-2 2010 Recently, impairment of striatal Akt/GSK3 signaling was proposed to play a role in the mechanisms implicated in development of L-Dopa-induced dyskinesias in a rodent model of Parkinson"s disease. Levodopa 127-133 AKT serine/threonine kinase 1 Homo sapiens 33-36 20026151-3 2010 The present experiment investigated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys, the effects on Akt/GSK3 of chronic L-Dopa treatment inducing dyskinesias compared to L-Dopa with CI-1041 (NMDA receptor antagonist) or a low dose of cabergoline (dopamine D2 receptor agonist) preventing dyskinesias. Levodopa 135-141 AKT serine/threonine kinase 1 Homo sapiens 115-118 20026151-3 2010 The present experiment investigated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys, the effects on Akt/GSK3 of chronic L-Dopa treatment inducing dyskinesias compared to L-Dopa with CI-1041 (NMDA receptor antagonist) or a low dose of cabergoline (dopamine D2 receptor agonist) preventing dyskinesias. Levodopa 135-141 dopamine receptor D2 Homo sapiens 262-282 20026151-8 2010 Extent of phosphorylation of Akt and GSK3beta in putamen correlated positively with dyskinesias scores of MPTP monkeys; these correlations were higher with dopaminergic drugs (L-Dopa, cabergoline) suggesting implication of additional mechanisms and/or signaling molecules in the NMDA antagonist antidyskinetic effect. Levodopa 176-182 AKT serine/threonine kinase 1 Homo sapiens 29-32 19914604-5 2010 METHODS: We administered 300 mg of L-dihydroxyphenylalanine (L-DOPA) or placebo to 200 healthy male subjects who were all genotyped for their DRD4 polymorphism. Levodopa 35-59 dopamine receptor D4 Homo sapiens 142-146 19914604-8 2010 As expected, however, an individual"s DRD4 polymorphism accounted for variation in gambling behavior after the administration of L-DOPA. Levodopa 129-135 dopamine receptor D4 Homo sapiens 38-42 20429403-2 2010 Three non-ergoline dopamine agonists and levodopa/benserazide are now specifically licensed for RLS in Germany. Levodopa 41-49 RLS1 Homo sapiens 96-99 20141169-8 2010 l-DOPA treatments also led to decreased activities of thioredoxin (Trx) and thioredoxin reductase (TR), concomitant with diminution of their cellular contents. Levodopa 0-6 thioredoxin Homo sapiens 54-65 20123022-1 2010 Tyrosine hydroxylase (TH) is the rate limiting enzyme for dopamine synthesis, catalyzing transformation of l-tyrosine to l-DOPA. Levodopa 121-127 tyrosine hydroxylase Danio rerio 0-20 20123022-1 2010 Tyrosine hydroxylase (TH) is the rate limiting enzyme for dopamine synthesis, catalyzing transformation of l-tyrosine to l-DOPA. Levodopa 121-127 tyrosine hydroxylase Danio rerio 22-24 20060905-0 2010 Striatal inhibition of PKA prevents levodopa-induced behavioural and molecular changes in the hemiparkinsonian rat. Levodopa 36-44 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 23-26 20060905-3 2010 Using the 6-hydroxydopamine-lesioned rat model of PD, we showed that l-DOPA elicits profound alterations in the activity of three LID molecular markers, namely DeltaFosB, dopamine, cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), as well as in phosphorylation levels of the cytoskeletal-associated protein tau. Levodopa 69-75 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 222-230 20060905-3 2010 Using the 6-hydroxydopamine-lesioned rat model of PD, we showed that l-DOPA elicits profound alterations in the activity of three LID molecular markers, namely DeltaFosB, dopamine, cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), as well as in phosphorylation levels of the cytoskeletal-associated protein tau. Levodopa 69-75 mitogen activated protein kinase 3 Rattus norvegicus 236-282 20060905-3 2010 Using the 6-hydroxydopamine-lesioned rat model of PD, we showed that l-DOPA elicits profound alterations in the activity of three LID molecular markers, namely DeltaFosB, dopamine, cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), as well as in phosphorylation levels of the cytoskeletal-associated protein tau. Levodopa 69-75 mitogen activated protein kinase 3 Rattus norvegicus 284-290 20060905-4 2010 These modifications are triggered by protein kinase A (PKA) activation and intermittent stimulation of dopamine receptors as they are totally prevented by intrastriatal injections of Rp-cAMPS, a PKA inhibitor, or by continuous administration of l-DOPA via subcutaneous mini-pump. Levodopa 245-251 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 37-53 20060905-4 2010 These modifications are triggered by protein kinase A (PKA) activation and intermittent stimulation of dopamine receptors as they are totally prevented by intrastriatal injections of Rp-cAMPS, a PKA inhibitor, or by continuous administration of l-DOPA via subcutaneous mini-pump. Levodopa 245-251 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-58 20060905-4 2010 These modifications are triggered by protein kinase A (PKA) activation and intermittent stimulation of dopamine receptors as they are totally prevented by intrastriatal injections of Rp-cAMPS, a PKA inhibitor, or by continuous administration of l-DOPA via subcutaneous mini-pump. Levodopa 245-251 calmodulin 2, pseudogene 1 Rattus norvegicus 186-191 20060905-4 2010 These modifications are triggered by protein kinase A (PKA) activation and intermittent stimulation of dopamine receptors as they are totally prevented by intrastriatal injections of Rp-cAMPS, a PKA inhibitor, or by continuous administration of l-DOPA via subcutaneous mini-pump. Levodopa 245-251 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 195-198 20141169-8 2010 l-DOPA treatments also led to decreased activities of thioredoxin (Trx) and thioredoxin reductase (TR), concomitant with diminution of their cellular contents. Levodopa 0-6 thioredoxin Homo sapiens 67-70 20141169-8 2010 l-DOPA treatments also led to decreased activities of thioredoxin (Trx) and thioredoxin reductase (TR), concomitant with diminution of their cellular contents. Levodopa 0-6 peroxiredoxin 5 Homo sapiens 76-97 20141169-8 2010 l-DOPA treatments also led to decreased activities of thioredoxin (Trx) and thioredoxin reductase (TR), concomitant with diminution of their cellular contents. Levodopa 0-6 peroxiredoxin 5 Homo sapiens 99-101 20141169-12 2010 However, Grx was inactivated in a time- and concentration-dependent fashion indicative of irreversible adduction of dopaquinone to its nucleophilic active-site Cys-22, consistent with the intracellular loss of Grx activity but not Grx protein content after l-DOPA treatment. Levodopa 257-263 glutaredoxin Homo sapiens 9-12 20141169-13 2010 Overall l-DOPA is shown to impair the collaborative contributions of the Grx and Trx systems to neuron survival. Levodopa 8-14 glutaredoxin Homo sapiens 73-76 20141169-13 2010 Overall l-DOPA is shown to impair the collaborative contributions of the Grx and Trx systems to neuron survival. Levodopa 8-14 thioredoxin Homo sapiens 81-84 20083145-5 2010 In this study, we developed a novel technology for the production of l-DOPA, an electroenzymatic synthesis with a tyrosinase-immobilized cathode under the reduction potential of DOPAquinone, which is -530 mV. Levodopa 69-75 tyrosinase Homo sapiens 114-124 20297870-5 2010 Monoamine oxidase type B (MAO-B) inhibitors provide mild symptomatic benefit, delay the need for levodopa, are very well tolerated, and may provide long-term disease-modifying effects. Levodopa 97-105 monoamine oxidase B Homo sapiens 0-24 20297870-5 2010 Monoamine oxidase type B (MAO-B) inhibitors provide mild symptomatic benefit, delay the need for levodopa, are very well tolerated, and may provide long-term disease-modifying effects. Levodopa 97-105 monoamine oxidase B Homo sapiens 26-31 20297872-3 2010 Early treatment of PD with other agents such as dopamine agonists and monoamine oxidase type B inhibitors can provide symptomatic benefit and delay initiation of levodopa therapy. Levodopa 162-170 monoamine oxidase B Homo sapiens 70-94 20026252-1 2010 Dyskinesia eventually develops in the majority of Parkinson"s disease patients treated with l-3,4-dihydroxyphenylalanine (l-DOPA). Levodopa 122-128 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 92-95 19676096-4 2010 Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism. Levodopa 163-171 catechol-O-methyltransferase Homo sapiens 50-54 19566901-1 2010 BACKGROUND: Dopa-responsive dystonia (DRD), a movement disorder characterized by onset in early childhood and a dramatic response to low doses of levodopa, has been shown to be caused by a number of different mutations in the GCH1 gene. Levodopa 146-154 GTP cyclohydrolase 1 Homo sapiens 226-230 19756826-1 2010 The European Restless Legs Syndrome (RLS) Study Group performed the first multi-center, long-term study systematically evaluating RLS augmentation under levodopa treatment. Levodopa 153-161 RLS1 Homo sapiens 37-40 20077469-1 2010 Levodopa combined with a dopa-decarboxylase inhibitor, such as carbidopa, shifts the metabolism to the COMT pathway. Levodopa 0-8 dopa decarboxylase Homo sapiens 25-43 20077469-1 2010 Levodopa combined with a dopa-decarboxylase inhibitor, such as carbidopa, shifts the metabolism to the COMT pathway. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 103-107 20199208-4 2010 Treatment with levodopa alone did not change rCBF, whereas it increased basal ganglion DAT activity in the most affected hemisphere. Levodopa 15-23 solute carrier family 6 member 3 Homo sapiens 87-90 20199208-5 2010 Patients who received levodopa and complementary acupuncture had increased rCBF in the frontal lobe, the occipital lobe, the basal ganglion, and the cerebellum in the most affected hemisphere as compared to baseline, but there were no changes in basal ganglia DAT levels. Levodopa 22-30 CCAAT/enhancer binding protein zeta Rattus norvegicus 75-79 20199208-5 2010 Patients who received levodopa and complementary acupuncture had increased rCBF in the frontal lobe, the occipital lobe, the basal ganglion, and the cerebellum in the most affected hemisphere as compared to baseline, but there were no changes in basal ganglia DAT levels. Levodopa 22-30 solute carrier family 6 member 3 Homo sapiens 260-263 19756826-1 2010 The European Restless Legs Syndrome (RLS) Study Group performed the first multi-center, long-term study systematically evaluating RLS augmentation under levodopa treatment. Levodopa 153-161 RLS1 Homo sapiens 130-133 19811797-2 2010 Double-blind clinical trials and, above all, clinical experience have demonstrated that l-DOPA is effective in reducing FOG. Levodopa 88-94 zinc finger protein, FOG family member 1 Homo sapiens 120-123 19815246-10 2010 In the rare cases of levodopa-induced FOG, STN stimulation may be indirectly effective, as it enables reduction or arrest of the levodopa treatment. Levodopa 21-29 zinc finger protein, FOG family member 1 Homo sapiens 38-41 19815246-10 2010 In the rare cases of levodopa-induced FOG, STN stimulation may be indirectly effective, as it enables reduction or arrest of the levodopa treatment. Levodopa 129-137 zinc finger protein, FOG family member 1 Homo sapiens 38-41 19879254-12 2010 Thus, COMT inhibitors are useful for decreasing the amount of levodopa administered to Parkinson"s disease patients. Levodopa 62-70 catechol-O-methyltransferase Homo sapiens 6-10 20014115-3 2010 We compared striatal BDNF levels measured by ELISA in levodopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys having developed LIDs compared with animals where LIDs were prevented by the addition of CI-1041 (NR1A/2B NMDA receptor antagonist) or low doses of cabergoline (dopamine D2 receptor agonist). Levodopa 54-62 brain derived neurotrophic factor Homo sapiens 21-25 20014115-4 2010 We observed reduced striatal BDNF concentrations in levodopa-treated MPTP monkeys with or without LIDs, suggesting that levodopa treatment is associated with reduced striatal BDNF levels and is independent of dyskinesias. Levodopa 52-60 brain derived neurotrophic factor Homo sapiens 29-33 20014115-4 2010 We observed reduced striatal BDNF concentrations in levodopa-treated MPTP monkeys with or without LIDs, suggesting that levodopa treatment is associated with reduced striatal BDNF levels and is independent of dyskinesias. Levodopa 52-60 brain derived neurotrophic factor Homo sapiens 175-179 20014115-4 2010 We observed reduced striatal BDNF concentrations in levodopa-treated MPTP monkeys with or without LIDs, suggesting that levodopa treatment is associated with reduced striatal BDNF levels and is independent of dyskinesias. Levodopa 120-128 brain derived neurotrophic factor Homo sapiens 29-33 20014115-4 2010 We observed reduced striatal BDNF concentrations in levodopa-treated MPTP monkeys with or without LIDs, suggesting that levodopa treatment is associated with reduced striatal BDNF levels and is independent of dyskinesias. Levodopa 120-128 brain derived neurotrophic factor Homo sapiens 175-179 19595762-3 2010 Autosomal recessive mutations in PTEN-induced kinase 1 (PINK1) cause an L-DOPA responsive parkinsonian syndrome, stimulating extensive interest in the normal neuroprotective and mitoprotective functions of PINK1. Levodopa 72-78 PTEN induced kinase 1 Homo sapiens 33-54 19909787-7 2010 Our results also support the conclusion that COMT inhibitors (entacapone or tolcapone), when administered in PD patients treated with l-Dopa, may potentiate the endogenous AdoHcy-dependent COMT inhibition mechanism already operative in a variable fashion. Levodopa 134-140 catechol-O-methyltransferase Homo sapiens 45-49 19909787-7 2010 Our results also support the conclusion that COMT inhibitors (entacapone or tolcapone), when administered in PD patients treated with l-Dopa, may potentiate the endogenous AdoHcy-dependent COMT inhibition mechanism already operative in a variable fashion. Levodopa 134-140 catechol-O-methyltransferase Homo sapiens 189-193 19595762-3 2010 Autosomal recessive mutations in PTEN-induced kinase 1 (PINK1) cause an L-DOPA responsive parkinsonian syndrome, stimulating extensive interest in the normal neuroprotective and mitoprotective functions of PINK1. Levodopa 72-78 PTEN induced kinase 1 Homo sapiens 56-61 20606323-5 2010 LAT1 mRNA expression in whole brain was not affected at 1, 3 and 5 d after the treatment, but was reduced by 46.3% at 7 d. LAT1 mediates the transport of large neutral amino acids, including tyrosine, as well as the PD-therapeutic drug levodopa, across the BBB. Levodopa 236-244 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 0-4 20606323-5 2010 LAT1 mRNA expression in whole brain was not affected at 1, 3 and 5 d after the treatment, but was reduced by 46.3% at 7 d. LAT1 mediates the transport of large neutral amino acids, including tyrosine, as well as the PD-therapeutic drug levodopa, across the BBB. Levodopa 236-244 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 123-127 20606323-6 2010 Our findings indicate that decreased LAT1 expression at the BBB in PD patients may adversely affect amino acid supply from the circulating blood and levodopa distribution into the brain. Levodopa 149-157 solute carrier family 7 member 5 Homo sapiens 37-41 19585587-8 2010 L-dopa had significant main effects on the amplitude of BOLD signal in bilateral primary motor cortex and left SMA. Levodopa 0-6 survival of motor neuron 1, telomeric Homo sapiens 111-114 19585587-9 2010 In contrast, L-dopa-mediated spatial changes were apparent in bilateral cerebellar hemispheres, M1, SMA, and right prefrontal cortex. Levodopa 13-19 survival of motor neuron 1, telomeric Homo sapiens 100-103 21095464-9 2010 The most common adverse event with COMT inhibitors is dyskinesia which is usually managed by decreasing levodopa dose. Levodopa 104-112 catechol-O-methyltransferase Homo sapiens 35-39 20122661-8 2010 CONCLUSION: These results indicate that large reductions in dopamine concentrations in the rat brain can produce modest but significant changes in the binding of radioligands to VMAT2, which can be reversed by replenishment of dopamine using exogenous L-DOPA. Levodopa 252-258 solute carrier family 18 member A2 Rattus norvegicus 178-183 19771390-1 2010 Catechol-O-methyltransferase (COMT) inhibition is widely used to potentiate the effects of levodopa in Parkinson"s disease but the effects of nigral dopaminergic cell loss and levodopa treatment on COMT activity are not known. Levodopa 91-99 catechol O-methyltransferase Callithrix jacchus 0-28 19771390-1 2010 Catechol-O-methyltransferase (COMT) inhibition is widely used to potentiate the effects of levodopa in Parkinson"s disease but the effects of nigral dopaminergic cell loss and levodopa treatment on COMT activity are not known. Levodopa 91-99 catechol O-methyltransferase Callithrix jacchus 30-34 19771390-1 2010 Catechol-O-methyltransferase (COMT) inhibition is widely used to potentiate the effects of levodopa in Parkinson"s disease but the effects of nigral dopaminergic cell loss and levodopa treatment on COMT activity are not known. Levodopa 176-184 catechol O-methyltransferase Callithrix jacchus 30-34 19771390-1 2010 Catechol-O-methyltransferase (COMT) inhibition is widely used to potentiate the effects of levodopa in Parkinson"s disease but the effects of nigral dopaminergic cell loss and levodopa treatment on COMT activity are not known. Levodopa 176-184 catechol O-methyltransferase Callithrix jacchus 198-202 19576910-6 2010 An increase of PPE and PPD mRNA levels was observed in anterior caudate nucleus of L-DOPA treated MPTP monkeys compared to controls and to Saline-treated MPTP monkeys whereas PPT-A mRNA levels were unchanged. Levodopa 83-89 proenkephalin Homo sapiens 15-18 19576910-6 2010 An increase of PPE and PPD mRNA levels was observed in anterior caudate nucleus of L-DOPA treated MPTP monkeys compared to controls and to Saline-treated MPTP monkeys whereas PPT-A mRNA levels were unchanged. Levodopa 83-89 prodynorphin Homo sapiens 23-26 19576910-7 2010 Striatal PPE and PPD mRNA levels remained elevated in L-DOPA plus naltrexone-treated MPTP monkeys, while co-treatment with DHA, CI-1041 or Ro 61-8048 prevented their increase to various extents. Levodopa 54-60 proenkephalin Homo sapiens 9-12 19576910-7 2010 Striatal PPE and PPD mRNA levels remained elevated in L-DOPA plus naltrexone-treated MPTP monkeys, while co-treatment with DHA, CI-1041 or Ro 61-8048 prevented their increase to various extents. Levodopa 54-60 prodynorphin Homo sapiens 17-20 19576910-9 2010 These results show that drugs displaying a wide range of pharmacological activities can modulate L-DOPA induced dyskinesias and this activity is correlated with striatal PPD and PPE mRNA levels suggesting a convergent mechanism. Levodopa 97-103 prodynorphin Homo sapiens 170-173 19576910-9 2010 These results show that drugs displaying a wide range of pharmacological activities can modulate L-DOPA induced dyskinesias and this activity is correlated with striatal PPD and PPE mRNA levels suggesting a convergent mechanism. Levodopa 97-103 proenkephalin Homo sapiens 178-181 21095456-0 2010 Introductory remarks: Catechol-O-methyltransferase inhibition--an innovative approach to enhance L-dopa therapy in Parkinson"s disease with dual enzyme inhibition. Levodopa 97-103 catechol-O-methyltransferase Homo sapiens 22-50 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 195-203 catechol-O-methyltransferase Homo sapiens 0-28 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 195-203 catechol-O-methyltransferase Homo sapiens 30-34 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 195-203 dopa decarboxylase Homo sapiens 229-247 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 195-203 catechol-O-methyltransferase Homo sapiens 322-326 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 205-211 catechol-O-methyltransferase Homo sapiens 0-28 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 205-211 catechol-O-methyltransferase Homo sapiens 30-34 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 205-211 dopa decarboxylase Homo sapiens 229-247 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 205-211 catechol-O-methyltransferase Homo sapiens 322-326 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 222-228 catechol-O-methyltransferase Homo sapiens 0-28 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 222-228 catechol-O-methyltransferase Homo sapiens 30-34 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 222-228 dopa decarboxylase Homo sapiens 229-247 21095456-1 2010 Catechol-O-methyltransferase (COMT) enzyme and its inhibition have been closely related to the treatment of Parkinson"s disease (PD) patients with motor fluctuations needing enhancement of their levodopa (L-dopa) therapy (L-dopa/dopa decarboxylase inhibitor), this indication being so far the only clinical application of COMT inhibitors. Levodopa 222-228 catechol-O-methyltransferase Homo sapiens 322-326 21095456-3 2010 The introduction of clinically effective and safe COMT inhibitors has greatly increased the usefulness of L-dopa therapy, but how to utilize the full potential of L-dopa is still unsolved leaving a need for more potent COMT inhibitors. Levodopa 106-112 catechol-O-methyltransferase Homo sapiens 50-54 21095459-2 2010 Homocysteine decrease may therefore be a future therapeutic challenge, which may be achieved by supplementation with certain vitamins or by combination of a catechol-O-methyltransferase (COMT) inhibitor with L-dopa/DDI administration. Levodopa 208-214 catechol-O-methyltransferase Homo sapiens 187-191 21095460-1 2010 Catechol-O-methyltransferase (COMT) is an important enzyme in the metabolism of catechol structured compounds such as catecholamines, catecholestrogens, and L-dopa. Levodopa 157-163 catechol-O-methyltransferase Mus musculus 0-28 21095460-1 2010 Catechol-O-methyltransferase (COMT) is an important enzyme in the metabolism of catechol structured compounds such as catecholamines, catecholestrogens, and L-dopa. Levodopa 157-163 catechol-O-methyltransferase Mus musculus 30-34 21095460-3 2010 Bioavailability and efficacy of L-dopa treatment can be enhanced greatly by the use of COMT inhibitors. Levodopa 32-38 catechol-O-methyltransferase Mus musculus 87-91 21095461-3 2010 One approach to provide a more continuous and sustained delivery of dopamine has targeted one of the principal enzymes responsible for metabolic deactivation of L-dopa, namely catechol-O-methyltransferase (COMT). Levodopa 161-167 catechol-O-methyltransferase Homo sapiens 176-204 21095461-3 2010 One approach to provide a more continuous and sustained delivery of dopamine has targeted one of the principal enzymes responsible for metabolic deactivation of L-dopa, namely catechol-O-methyltransferase (COMT). Levodopa 161-167 catechol-O-methyltransferase Homo sapiens 206-210 21095462-1 2010 The development of catechol-O-methyltransferase (COMT) inhibitors for the adjunct treatment to levodopa and aromatic L-amino acid decarboxylase (AADC) inhibitors in Parkinson"s disease started in the late 1950s. Levodopa 95-103 catechol-O-methyltransferase Homo sapiens 19-47 21095462-1 2010 The development of catechol-O-methyltransferase (COMT) inhibitors for the adjunct treatment to levodopa and aromatic L-amino acid decarboxylase (AADC) inhibitors in Parkinson"s disease started in the late 1950s. Levodopa 95-103 catechol-O-methyltransferase Homo sapiens 49-53 21095463-4 2010 One approach to the CDS is to prolong the half-life of L-dopa inhibiting its degradation by means of the administration of catechol-O-methyltransferase (COMT) inhibitors, as entacapone, a potent, selective, and reversible peripherally acting inhibitor. Levodopa 55-61 catechol-O-methyltransferase Rattus norvegicus 123-151 21095463-4 2010 One approach to the CDS is to prolong the half-life of L-dopa inhibiting its degradation by means of the administration of catechol-O-methyltransferase (COMT) inhibitors, as entacapone, a potent, selective, and reversible peripherally acting inhibitor. Levodopa 55-61 catechol-O-methyltransferase Rattus norvegicus 153-157 19850096-9 2010 In addition, it is important that cytoplasmic accumulation of alpha-synuclein was observed in the substantia nigra of mice treated with LPS plus MA, and that L-Dopa treatment significantly attenuated behavioral changes and dopaminergic deficits induced by LPS plus MA. Levodopa 158-164 synuclein, alpha Mus musculus 62-77 20037632-2 2009 Its product, L-DOPA, is an established treatment for Parkinson"s disease (PD), suggesting that TH regulation influences locomotion. Levodopa 13-19 tyrosine hydroxylase Rattus norvegicus 95-97 20887875-6 2010 Evaluation of central pharmacokinetics of levodopa action by PET has demonstrated the role of increased synaptic dopamine turnover and downregulation of the dopamine transporter in the pathophysiology of levodopa-induced dyskinesias. Levodopa 42-50 solute carrier family 6 member 3 Homo sapiens 157-177 20887875-6 2010 Evaluation of central pharmacokinetics of levodopa action by PET has demonstrated the role of increased synaptic dopamine turnover and downregulation of the dopamine transporter in the pathophysiology of levodopa-induced dyskinesias. Levodopa 204-212 solute carrier family 6 member 3 Homo sapiens 157-177 20355321-6 2010 Kinetic analysis with HMV-II tyrosinase showed that the inhibition by hydroxyindoles 4, 5, and 6 was competitive with respect to the substrate L-DOPA. Levodopa 143-149 tyrosinase Homo sapiens 29-39 20007772-7 2009 Measurement of extracellular DOPAC, a dopamine metabolite, following l-DOPA injection supported a role for RAB3B in enhancing the dopamine storage capacity of synaptic terminals. Levodopa 69-75 RAB3B, member RAS oncogene family Rattus norvegicus 107-112 19930170-0 2009 Importance of membrane-bound catechol-O-methyltransferase in L-DOPA metabolism: a pharmacokinetic study in two types of Comt gene modified mice. Levodopa 61-67 catechol-O-methyltransferase Mus musculus 29-57 19786283-0 2009 Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson"s disease patients. Levodopa 77-85 methylenetetrahydrofolate reductase Homo sapiens 0-35 19930170-12 2009 CONCLUSIONS AND IMPLICATIONS: In S-COMT-deficient mice, MB-COMT in the liver and the duodenum is able to O-methylate about one-half of exogenous L-DOPA. Levodopa 145-151 catechol-O-methyltransferase Mus musculus 35-39 19930170-12 2009 CONCLUSIONS AND IMPLICATIONS: In S-COMT-deficient mice, MB-COMT in the liver and the duodenum is able to O-methylate about one-half of exogenous L-DOPA. Levodopa 145-151 catechol-O-methyltransferase Mus musculus 59-63 19698780-10 2009 Nevertheless, it has been shown that most monoenzymatic TH neurons and AADC neurons are capable to produce l-3,4-dihydroxyphenylalanine (L-DOPA) from l-tyrosine and DA from L-DOPA, respectively. Levodopa 107-135 dopa decarboxylase Homo sapiens 71-75 19698780-10 2009 Nevertheless, it has been shown that most monoenzymatic TH neurons and AADC neurons are capable to produce l-3,4-dihydroxyphenylalanine (L-DOPA) from l-tyrosine and DA from L-DOPA, respectively. Levodopa 137-143 dopa decarboxylase Homo sapiens 71-75 19698780-10 2009 Nevertheless, it has been shown that most monoenzymatic TH neurons and AADC neurons are capable to produce l-3,4-dihydroxyphenylalanine (L-DOPA) from l-tyrosine and DA from L-DOPA, respectively. Levodopa 173-179 dopa decarboxylase Homo sapiens 71-75 19698780-12 2009 Moreover, according to our hypothesis L-DOPA released from monoenzymatic TH neurons is captured by monoenzymatic AADC neurons for DA synthesis. Levodopa 38-44 dopa decarboxylase Homo sapiens 113-117 19815446-6 2009 This contrasts with homozygous parkin, PINK1 or DJ1 parkinsonism, characterized by young-onset (usually <40 years), and a comparatively benign course of predominantly levodopa-responsive symptoms without dementia or prominent dysautonomia. Levodopa 167-175 PTEN induced kinase 1 Homo sapiens 39-44 19815446-6 2009 This contrasts with homozygous parkin, PINK1 or DJ1 parkinsonism, characterized by young-onset (usually <40 years), and a comparatively benign course of predominantly levodopa-responsive symptoms without dementia or prominent dysautonomia. Levodopa 167-175 Parkinsonism associated deglycase Homo sapiens 48-51 20082986-3 2009 If such a factor exists, and GDNF seems a strong candidate, then one could anticipate that this treatment would be as effective as L-dopa therapy. Levodopa 131-137 glial cell derived neurotrophic factor Homo sapiens 29-33 19801645-8 2009 Our results shed light on interaction mechanisms that might be relevant for the modulation of the distribution of TH in the cytoplasm and membrane fractions and regulation of L-DOPA and dopamine synthesis. Levodopa 175-181 tyrosine hydroxylase Homo sapiens 114-116 19786063-7 2009 However, treatment of L-DOPA significantly increased expressions of cytosolic cytochrome c and cleaved caspase-3, which are death-related signaling proteins, in nPC12 cells, but combined treatment with the PI3K activator reduced those expressions. Levodopa 22-28 cytochrome c, somatic Homo sapiens 78-90 19828868-1 2009 BACKGROUND: In Parkinson disease (PD), the benefit of levodopa therapy becomes less marked over time, perhaps because degeneration of nigrostrial neurons causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa into dopamine. Levodopa 54-62 dopa decarboxylase Homo sapiens 181-216 19828868-1 2009 BACKGROUND: In Parkinson disease (PD), the benefit of levodopa therapy becomes less marked over time, perhaps because degeneration of nigrostrial neurons causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa into dopamine. Levodopa 54-62 dopa decarboxylase Homo sapiens 218-222 19828868-1 2009 BACKGROUND: In Parkinson disease (PD), the benefit of levodopa therapy becomes less marked over time, perhaps because degeneration of nigrostrial neurons causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa into dopamine. Levodopa 250-258 dopa decarboxylase Homo sapiens 181-216 19828868-1 2009 BACKGROUND: In Parkinson disease (PD), the benefit of levodopa therapy becomes less marked over time, perhaps because degeneration of nigrostrial neurons causes progressive loss of aromatic l-amino acid decarboxylase (AADC), the enzyme that converts levodopa into dopamine. Levodopa 250-258 dopa decarboxylase Homo sapiens 218-222 19828868-2 2009 In a primate model of PD, intrastriatal infusion of an adeno-associated viral type 2 vector containing the human AADC gene (AAV-hAADC) results in robust response to low-dose levodopa without the side effects associated with higher doses. Levodopa 174-182 dopa decarboxylase Homo sapiens 113-117 19864600-5 2009 As the rate limiting step for adenosine generation from pericellular ATP is the ecto-ATPase CD39, we next show that inhibition of CD39 activity using the inhibitor ARL 67156 partially overcomes T cell hyporesponsiveness in a subset of patient samples. Levodopa 164-167 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 92-96 19864600-5 2009 As the rate limiting step for adenosine generation from pericellular ATP is the ecto-ATPase CD39, we next show that inhibition of CD39 activity using the inhibitor ARL 67156 partially overcomes T cell hyporesponsiveness in a subset of patient samples. Levodopa 164-167 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 130-134 19936145-4 2009 Recent LD trials indicate that a combination of LD with carbidopa (CD) and the catechol-O-methyltransferase (COMT) inhibitor entacapone (EN) may reduce the onset of these motor complications to a certain extent. Levodopa 7-9 catechol-O-methyltransferase Homo sapiens 79-107 19660528-1 2009 The present study examined the effect of a subchronic systemic administration of the glutamate metabotropic mGluR5 receptor antagonist MPEP on l-DOPA-induced dyskinesias and striatal gene expression in adult rats with a unilateral 6-OHDA lesion of dopamine neurons. Levodopa 143-149 glutamate receptor, ionotropic, kainate 1 Mus musculus 108-114 19660528-4 2009 Subchronic l-DOPA administration was paralleled by a significant increase in mRNA levels of the two isoforms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD67 and GAD65) and preprodynorphin (PPD). Levodopa 11-17 glutamate decarboxylase 1 Rattus norvegicus 170-175 19660528-4 2009 Subchronic l-DOPA administration was paralleled by a significant increase in mRNA levels of the two isoforms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD67 and GAD65) and preprodynorphin (PPD). Levodopa 11-17 glutamate decarboxylase 2 Rattus norvegicus 180-185 19660528-4 2009 Subchronic l-DOPA administration was paralleled by a significant increase in mRNA levels of the two isoforms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD67 and GAD65) and preprodynorphin (PPD). Levodopa 11-17 prodynorphin Rattus norvegicus 191-206 19660528-5 2009 Single cell analysis on emulsion radioautographs indicated that l-DOPA-induced increases in GAD67 occurred predominantly in preproenkephalin-unlabeled striatonigral and, to a lesser extent, in preproenkephalin-labeled striatopallidal neurons. Levodopa 64-70 glutamate decarboxylase 1 Rattus norvegicus 92-97 19660528-6 2009 MPEP completely reversed the effects of l-DOPA on GAD67 and reduced the increases in GAD65 and PPD mRNA levels in striatonigral neurons. Levodopa 40-46 glutamate decarboxylase 1 Rattus norvegicus 50-55 19660528-7 2009 MPEP also reversed the small l-DOPA-induced increase in GAD67 mRNA levels in striatopallidal neurons. Levodopa 29-35 glutamate decarboxylase 1 Rattus norvegicus 56-61 19660528-8 2009 Altogether, the findings support the idea that the relative efficacy of mGluR5 receptor antagonists to oppose l-DOPA-induced abnormal involuntary movements involves an ability to oppose increases in GAD gene expression and GABA-mediated signaling in striatonigral and striatopallidal neurons. Levodopa 110-116 glutamate receptor, ionotropic, kainate 1 Mus musculus 72-78 19660528-9 2009 The results also confirm the potential usefulness of antagonists of mGluR5 receptors as adjuncts in the treatment of l-DOPA-induced dyskinesia in patients with Parkinson"s disease. Levodopa 117-123 glutamate receptor, ionotropic, kainate 1 Mus musculus 68-74 19660528-0 2009 Metabotropic glutamate mGluR5 receptor blockade opposes abnormal involuntary movements and the increases in glutamic acid decarboxylase mRNA levels induced by l-DOPA in striatal neurons of 6-hydroxydopamine-lesioned rats. Levodopa 159-165 glutamate receptor, ionotropic, kainate 1 Mus musculus 23-29 19936145-4 2009 Recent LD trials indicate that a combination of LD with carbidopa (CD) and the catechol-O-methyltransferase (COMT) inhibitor entacapone (EN) may reduce the onset of these motor complications to a certain extent. Levodopa 7-9 catechol-O-methyltransferase Homo sapiens 109-113 19765187-7 2009 Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice. Levodopa 22-28 mitogen-activated protein kinase 8 Mus musculus 103-106 19396395-1 2009 Tyrosine hydroxylase (TH) catalyzes the conversion of L: -tyrosine to L: -dopa, which is the initial and rate-limiting step in the biosynthesis of catecholamines [CA; dopamine (DA), noradrenaline, and adrenaline], and plays a central role in the neurotransmission and hormonal actions of CA. Levodopa 70-78 tyrosine hydroxylase Homo sapiens 0-20 19396395-1 2009 Tyrosine hydroxylase (TH) catalyzes the conversion of L: -tyrosine to L: -dopa, which is the initial and rate-limiting step in the biosynthesis of catecholamines [CA; dopamine (DA), noradrenaline, and adrenaline], and plays a central role in the neurotransmission and hormonal actions of CA. Levodopa 70-78 tyrosine hydroxylase Homo sapiens 22-24 19667975-6 2009 During the tests, choreic dyskinesias were associated with a central levodopa influx of 10 x 10(-3) nmol min(-1) g(-1) or greater, and foot dystonia occurred with a central levodopa influx less than 9 x 10(-3) nmol min(-1) g(-1). Levodopa 69-77 CD59 molecule (CD59 blood group) Homo sapiens 105-114 19396395-8 2009 The expression of the following three enzymes, TH, GTP cyclohydrolase I, which synthesizes the tetrahydrobiopterin cofactor of TH, and aromatic-L: -amino acid decarboxylase, which produces DA from L: -dopa, were induced in the monkey striatum using harmless adeno-associated virus vectors, resulting in a remarkable improvement in the symptoms affecting PD model monkeys Muramatsu (Hum Gene Ther 13:345-354, 2002). Levodopa 197-205 dopa decarboxylase Homo sapiens 135-172 19765187-7 2009 Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice. Levodopa 22-28 BCL2-associated X protein Mus musculus 124-127 19765187-7 2009 Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice. Levodopa 22-28 B cell leukemia/lymphoma 2 Mus musculus 175-180 19703902-0 2009 Oxidative status of DJ-1-dependent activation of dopamine synthesis through interaction of tyrosine hydroxylase and 4-dihydroxy-L-phenylalanine (L-DOPA) decarboxylase with DJ-1. Levodopa 145-151 Parkinsonism associated deglycase Homo sapiens 20-24 19606087-3 2009 Moreover, we have asked whether L-DOPA-induced angiogenesis can be blocked by co-treatment with either a D1- or a D2 receptor antagonist (SCH23390 and eticlopride, respectively), or by an inhibitor of extracellular signal-regulated kinases 1 and 2 (ERK1/2) (SL327). Levodopa 32-38 mitogen activated protein kinase 3 Rattus norvegicus 249-255 19606087-8 2009 Inhibition of ERK1/2 by SL327 attenuated L-DOPA-induced dyskinesia and completely inhibited all markers of angiogenesis. Levodopa 41-47 mitogen activated protein kinase 3 Rattus norvegicus 14-20 19606087-10 2009 L-DOPA-induced angiogenesis requires stimulation of D1 receptors and activation of ERK1/2, whereas the stimulation of D2 receptors seems to oppose this response. Levodopa 0-6 mitogen activated protein kinase 3 Rattus norvegicus 83-89 19703902-0 2009 Oxidative status of DJ-1-dependent activation of dopamine synthesis through interaction of tyrosine hydroxylase and 4-dihydroxy-L-phenylalanine (L-DOPA) decarboxylase with DJ-1. Levodopa 145-151 Parkinsonism associated deglycase Homo sapiens 172-176 19686730-3 2009 A single administration of subcutaneous TRK-820 significantly increased spontaneous ipsilateral rotational behavior of hemi-parkinsonian rats at 30 microg/kg though the efficacy was moderate and also significantly inhibited L-DOPA-induced dyskinesia at 10 and 30 microg/kg; this inhibition was reversed in the presence of nor-binaltorphimine, a kappa opioid receptor antagonist. Levodopa 224-230 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 40-43 21180628-12 2009 Using levodopa with a dopa-decarboxylase inhibitor lessens adverse effects, and further adding a catechol-O-methyl transferase inhibitor can improve symptom control. Levodopa 6-14 dopa decarboxylase Homo sapiens 22-40 19686730-4 2009 In vivo microdialysis study, TRK-820 (30 microg/kg, s.c.) significantly inhibited L-DOPA-derived extracellular dopamine content in the 6-OHDA-treated striatum in dyskinesia rats, but not in hemi-parkinsonian rats. Levodopa 82-88 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 29-32 19686730-5 2009 Moreover, the development of L-DOPA-induced dyskinesia was suppressed by the 3-week co-administration of TRK-820 (3 and 10 microg/kg, s.c.) with L-DOPA. Levodopa 29-35 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 105-108 19686730-5 2009 Moreover, the development of L-DOPA-induced dyskinesia was suppressed by the 3-week co-administration of TRK-820 (3 and 10 microg/kg, s.c.) with L-DOPA. Levodopa 145-151 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 105-108 19686730-6 2009 These results have suggested that TRK-820 ameliorates L-DOPA-induced dyskinesia with a moderate anti-parkinsonian effect by inhibiting L-DOPA-induced excessive dopamine release through kappa opioid receptors only in dyskinesia rats; therefore, TRK-820 is expected to become a useful agent for the treatment of L-DOPA-induced dyskinesia. Levodopa 54-60 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 34-37 19686730-6 2009 These results have suggested that TRK-820 ameliorates L-DOPA-induced dyskinesia with a moderate anti-parkinsonian effect by inhibiting L-DOPA-induced excessive dopamine release through kappa opioid receptors only in dyskinesia rats; therefore, TRK-820 is expected to become a useful agent for the treatment of L-DOPA-induced dyskinesia. Levodopa 135-141 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 34-37 19686730-6 2009 These results have suggested that TRK-820 ameliorates L-DOPA-induced dyskinesia with a moderate anti-parkinsonian effect by inhibiting L-DOPA-induced excessive dopamine release through kappa opioid receptors only in dyskinesia rats; therefore, TRK-820 is expected to become a useful agent for the treatment of L-DOPA-induced dyskinesia. Levodopa 135-141 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 34-37 19922897-2 2009 Coadministration of a COMT inhibitor with levodopa and a dopa-decarboxylase inhibitor (carbidopa or benserazide) increases levodopa exposure and its therapeutic effect. Levodopa 42-50 catechol-O-methyltransferase Homo sapiens 22-26 19767236-5 2009 Increase of the postexcitatory inhibition towards normal values and decrease of the P300 latency were observed (P<0.001) following the administration of Levodopa. Levodopa 153-161 E1A binding protein p300 Homo sapiens 84-88 19922897-2 2009 Coadministration of a COMT inhibitor with levodopa and a dopa-decarboxylase inhibitor (carbidopa or benserazide) increases levodopa exposure and its therapeutic effect. Levodopa 123-131 catechol-O-methyltransferase Homo sapiens 22-26 19922897-2 2009 Coadministration of a COMT inhibitor with levodopa and a dopa-decarboxylase inhibitor (carbidopa or benserazide) increases levodopa exposure and its therapeutic effect. Levodopa 123-131 dopa decarboxylase Homo sapiens 57-75 19686242-2 2009 Recombinant adeno-associated viral (rAAV) vector in particular has been utilized for continuous l-3,4 dihydroxyphenylalanine (DOPA) delivery by expressing the tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) genes which are necessary and sufficient for efficient synthesis of DOPA from dietary tyrosine. Levodopa 96-124 tyrosine hydroxylase Rattus norvegicus 159-179 19618251-5 2009 The extracts of W. coriacea (bark part of aerial root) and D. petandra (aerial root) showed tyrosinase inhibitory activity of more than 40% using L-DOPA as a substrate at 500 microg/ml. Levodopa 146-152 tyrosinase Mus musculus 92-102 19657587-0 2009 Peripheral COMT inhibition prevents levodopa associated homocysteine increase. Levodopa 36-44 catechol-O-methyltransferase Homo sapiens 11-15 19686242-2 2009 Recombinant adeno-associated viral (rAAV) vector in particular has been utilized for continuous l-3,4 dihydroxyphenylalanine (DOPA) delivery by expressing the tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) genes which are necessary and sufficient for efficient synthesis of DOPA from dietary tyrosine. Levodopa 96-124 tyrosine hydroxylase Rattus norvegicus 181-183 19686242-2 2009 Recombinant adeno-associated viral (rAAV) vector in particular has been utilized for continuous l-3,4 dihydroxyphenylalanine (DOPA) delivery by expressing the tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) genes which are necessary and sufficient for efficient synthesis of DOPA from dietary tyrosine. Levodopa 96-124 GTP cyclohydrolase 1 Rattus norvegicus 189-209 19686242-2 2009 Recombinant adeno-associated viral (rAAV) vector in particular has been utilized for continuous l-3,4 dihydroxyphenylalanine (DOPA) delivery by expressing the tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) genes which are necessary and sufficient for efficient synthesis of DOPA from dietary tyrosine. Levodopa 96-124 GTP cyclohydrolase 1 Rattus norvegicus 211-215 19615446-2 2009 Here, we provide evidence that anti-akinetic STN-HFS or dyskinesiogenic L-DOPA similarly reversed the dopamine lesion-induced increases in gene expression of cytochrome oxidase subunit I (CoI), a metabolic marker of neuronal activity, in the globus pallidus, STN and substantia nigra pars reticulata (SNr) in rats. Levodopa 72-78 cytochrome c oxidase I, mitochondrial Rattus norvegicus 158-186 19615446-2 2009 Here, we provide evidence that anti-akinetic STN-HFS or dyskinesiogenic L-DOPA similarly reversed the dopamine lesion-induced increases in gene expression of cytochrome oxidase subunit I (CoI), a metabolic marker of neuronal activity, in the globus pallidus, STN and substantia nigra pars reticulata (SNr) in rats. Levodopa 72-78 cytochrome c oxidase I, mitochondrial Rattus norvegicus 188-191 19635563-6 2009 On the other hand, denervation reduced Nur77 mRNA levels, whereas chronic L-Dopa treatment strongly induced Nur77 transcripts. Levodopa 74-80 nuclear receptor subfamily 4 group A member 1 Homo sapiens 108-113 19635563-8 2009 Interestingly, combination of L-Dopa with DHA further increases Nur77 mRNA levels in the anterior caudate-putamen, and mainly in striosomes. Levodopa 30-36 nuclear receptor subfamily 4 group A member 1 Homo sapiens 64-69 19481198-2 2009 The transcription factor DeltaFosB accumulates in the denervated striatum and dimerizes primarily with JunD upon repeated L-3,4-dihydroxyphenylalanine (L-DOPA) administration. Levodopa 122-150 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-107 19635563-10 2009 Taken together, our results show that Nur77 expression is modulated following dopamine denervation and chronic L-Dopa therapy in a non-human primate model of Parkinson"s disease, and suggest that strong modulation of Nur77 expression might be linked to a reduced risk to develop LIDs. Levodopa 111-117 nuclear receptor subfamily 4 group A member 1 Homo sapiens 38-43 19481198-2 2009 The transcription factor DeltaFosB accumulates in the denervated striatum and dimerizes primarily with JunD upon repeated L-3,4-dihydroxyphenylalanine (L-DOPA) administration. Levodopa 152-158 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-107 19520364-9 2009 D1 receptor inactivation abolished L-DOPA-induced dyskinesias and associated molecular changes. Levodopa 35-41 dopamine receptor D1 Mus musculus 0-11 19520364-11 2009 CONCLUSIONS: Our results demonstrate that the dopamine D1 receptor is critical for the development of L-DOPA-induced dyskinesias in mice and in the underlying molecular changes in the denervated striatum and that the D2 receptor has little or no involvement. Levodopa 102-108 dopamine receptor D1 Mus musculus 46-66 19520364-11 2009 CONCLUSIONS: Our results demonstrate that the dopamine D1 receptor is critical for the development of L-DOPA-induced dyskinesias in mice and in the underlying molecular changes in the denervated striatum and that the D2 receptor has little or no involvement. Levodopa 102-108 dopamine receptor D2 Mus musculus 217-228 19538218-5 2009 Levodopa efficacy and duration of effect may be enhanced by combination with a catechol-O-methyl transferase inhibitor. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 79-108 19894644-3 2009 Furthermore, entacapone, a COMT inhibitor, is known to retain greater levodopa levels in plasma during coadministration. Levodopa 70-78 catechol-O-methyltransferase Rattus norvegicus 27-31 19704083-12 2009 CONCLUSIONS: The addition of pramipexole to the treatment of 6-pyruvoyl tetrahydropterin synthase deficiency improves the results of l-3,4 dihydroxyphenylalanine therapy. Levodopa 133-161 6-pyruvoyltetrahydropterin synthase Homo sapiens 61-97 19440221-9 2009 This inhibition partially depended on whether L-dopa or L-tyrosine was the substrate, suggesting that tyrosinase may contain contains two distinct catalytic sites. Levodopa 46-52 tyrosinase Homo sapiens 102-112 19118628-0 2009 Dopamine D3 receptor stimulation underlies the development of L-DOPA-induced dyskinesia in animal models of Parkinson"s disease. Levodopa 62-68 dopamine receptor D3 Rattus norvegicus 0-20 19580779-1 2009 The pyridoxal 5"-phosphate dependent-enzyme Dopa decarboxylase, responsible for the irreversible conversion of l-Dopa to dopamine, is an attractive drug target. Levodopa 111-117 dopa decarboxylase Homo sapiens 44-62 19656174-8 2009 Hence, we investigated changes of GPR88 expression in a model of Parkinson"s disease (unilateral 6-hydroxydopamine-lesioned rats) following repeated L-DOPA treatment. Levodopa 149-155 G-protein coupled receptor 88 Rattus norvegicus 34-39 19656174-10 2009 L-DOPA treatment led to a normalization of GPR88 levels through dopamine D1 and D2 receptor-mediated mechanisms in striatopallidal and striatonigral MSNs, respectively. Levodopa 0-6 G-protein coupled receptor 88 Rattus norvegicus 43-48 19656174-12 2009 These findings provide the first evidence that GPR88 is confined to striatal MSNs and indicate that L-DOPA-mediated behavioural effects in hemiparkinsonian rats may involve normalization of striatal GPR88 levels probably through dopamine receptor-mediated mechanisms and modulations of corticostriatal pathway activity. Levodopa 100-106 G-protein coupled receptor 88 Rattus norvegicus 47-52 19656174-12 2009 These findings provide the first evidence that GPR88 is confined to striatal MSNs and indicate that L-DOPA-mediated behavioural effects in hemiparkinsonian rats may involve normalization of striatal GPR88 levels probably through dopamine receptor-mediated mechanisms and modulations of corticostriatal pathway activity. Levodopa 100-106 G-protein coupled receptor 88 Rattus norvegicus 199-204 19332422-2 2009 A classic phenotype of young-onset lower-limb dystonia, diurnal fluctuations and excellent response to levodopa has been well recognised in association with GCH1 mutations, and rare atypical presentations have been reported. Levodopa 103-111 GTP cyclohydrolase 1 Homo sapiens 157-161 19118628-6 2009 Additionally, L-DOPA-induced elevations in striatal pre-proenkephalin-A (PPE-A) (but not PPE-B, phospho[Thr(34)]DARPP-32, D1, and D2 receptor mRNA or D3 receptor levels) were reduced in S33084 treated animals. Levodopa 14-20 proenkephalin Rattus norvegicus 56-71 19283475-0 2009 Comparative effects of acute or chronic administration of levodopa to 6-OHDA-lesioned rats on the expression and phosphorylation of N-methyl-D-aspartate receptor NR1 subunits in the striatum. Levodopa 58-66 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 162-165 19283475-7 2009 Chronic treatment of lesioned rats with levodopa markedly upregulated pNR1S890, pNR1S896, and pNR1S897 in lesioned striatum with a concomitant normalization of the plasma membrane NR1 abundance. Levodopa 40-48 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 71-74 19259810-6 2009 Parkinson"s cases treated with L-DOPA and MAO-B inhibitor exhibited decreased platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone. Levodopa 31-37 monoamine oxidase B Homo sapiens 87-92 19118628-6 2009 Additionally, L-DOPA-induced elevations in striatal pre-proenkephalin-A (PPE-A) (but not PPE-B, phospho[Thr(34)]DARPP-32, D1, and D2 receptor mRNA or D3 receptor levels) were reduced in S33084 treated animals. Levodopa 14-20 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 112-120 19259810-6 2009 Parkinson"s cases treated with L-DOPA and MAO-B inhibitor exhibited decreased platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone. Levodopa 157-163 monoamine oxidase B Homo sapiens 42-47 19259810-7 2009 Interestingly, Parkinson"s cases treated with L-DOPA and amantadine also had lower platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone. Levodopa 46-52 monoamine oxidase B Homo sapiens 92-97 19283475-10 2009 Activated NMDA receptor NR1-mediated mechanisms are involved in the persistent expression of the motor response alterations that appear during chronic levodopa therapy of parkinsonian rats and continue after treatment withdrawal. Levodopa 151-159 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 24-27 19167259-8 2009 CONCLUSION: The use of COMT or MAO-B inhibitors plus levodopa is superior to levodopa alone at reducing PD symptoms in patients with advanced PD. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 23-27 19259810-8 2009 Activity of platelet MAO-B in Parkinson"s patients was increased in naive cases and those treated with L-DOPA alone or in combination with other drugs compared to controls. Levodopa 103-109 monoamine oxidase B Homo sapiens 21-26 19412946-1 2009 Controlled-release carbidopa and levodopa (CL-CR) and the combination of carbidopa, levodopa, and entacapone (CLE) are used for extending levodopa (L-dopa) effects. Levodopa 148-154 RNA transcription, translation and transport factor Homo sapiens 110-113 19622830-1 2009 In a mouse model of Parkinson"s disease, new evidence shows that l-DOPA, which is used to treat the symptoms of the disease but also causes dyskinesia, results in a persistent activation of the protein kinase mTOR (mammalian target of rapamycin) in a subset of striatal medium spiny neurons. Levodopa 65-71 mechanistic target of rapamycin kinase Mus musculus 209-213 19622830-1 2009 In a mouse model of Parkinson"s disease, new evidence shows that l-DOPA, which is used to treat the symptoms of the disease but also causes dyskinesia, results in a persistent activation of the protein kinase mTOR (mammalian target of rapamycin) in a subset of striatal medium spiny neurons. Levodopa 65-71 mechanistic target of rapamycin kinase Homo sapiens 215-244 19622830-3 2009 Thus, mTORC1 may be a viable therapeutic target for dyskinesia caused by l-DOPA treatment in patients with Parkinson"s disease. Levodopa 73-79 CREB regulated transcription coactivator 1 Mus musculus 6-12 19622833-0 2009 Inhibition of mTOR signaling in Parkinson"s disease prevents L-DOPA-induced dyskinesia. Levodopa 61-67 mechanistic target of rapamycin kinase Mus musculus 14-18 19622833-3 2009 We show that administration of l-DOPA in a mouse model of Parkinsonism led to dopamine D1 receptor-mediated activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which is implicated in several forms of synaptic plasticity. Levodopa 31-37 dopamine receptor D1 Mus musculus 78-98 19622833-3 2009 We show that administration of l-DOPA in a mouse model of Parkinsonism led to dopamine D1 receptor-mediated activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which is implicated in several forms of synaptic plasticity. Levodopa 31-37 mechanistic target of rapamycin kinase Homo sapiens 126-155 19622833-3 2009 We show that administration of l-DOPA in a mouse model of Parkinsonism led to dopamine D1 receptor-mediated activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which is implicated in several forms of synaptic plasticity. Levodopa 31-37 mechanistic target of rapamycin kinase Homo sapiens 157-161 19622833-3 2009 We show that administration of l-DOPA in a mouse model of Parkinsonism led to dopamine D1 receptor-mediated activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which is implicated in several forms of synaptic plasticity. Levodopa 31-37 CREB regulated transcription coactivator 1 Mus musculus 174-180 19622833-5 2009 The l-DOPA-mediated activation of mTORC1 persisted in mice that developed dyskinesia. Levodopa 4-10 CREB regulated transcription coactivator 1 Mus musculus 34-40 19412946-4 2009 The mean hourly fluctuation index for L-dopa concentration was 235% for CLE and 196% for CL-CR (P = 0.004). Levodopa 38-44 RNA transcription, translation and transport factor Homo sapiens 72-75 19412946-6 2009 During the PK studies, the mean time that L-dopa concentration was > or =1,000 ng/mL for CLE was 291 +/- 88 minutes and for CL-CR, 306 +/- 86 (P = 0.33). Levodopa 42-48 RNA transcription, translation and transport factor Homo sapiens 89-92 19425084-1 2009 Levodopa (L-dopa) administered with a dopadecarboxylase inhibitor (DDI) increases homocysteine plasma levels. Levodopa 0-8 dopa decarboxylase Homo sapiens 38-55 19425084-1 2009 Levodopa (L-dopa) administered with a dopadecarboxylase inhibitor (DDI) increases homocysteine plasma levels. Levodopa 10-16 dopa decarboxylase Homo sapiens 38-55 19589043-5 2009 A dopa decarboxylase inhibitor (DDCI), such as carbidopa or benserazide, is administered with levodopa to attenuate its peripheral conversion to dopamine, reduce nausea and increase central bioavailability. Levodopa 94-102 dopa decarboxylase Homo sapiens 2-20 19491146-13 2009 Patient with mutation in the PARK2 gene had Dopa-responsive dystonia with a good improvement with L-Dopa, similar to Dopa-responsive dystonia secondary to GCH1 mutations. Levodopa 98-104 parkin RBR E3 ubiquitin protein ligase Homo sapiens 29-34 19589043-6 2009 When levodopa is administered with a DDCI, its main route of peripheral metabolism is via catechol-O-methyl transferase (COMT). Levodopa 5-13 catechol-O-methyltransferase Homo sapiens 90-119 19589043-6 2009 When levodopa is administered with a DDCI, its main route of peripheral metabolism is via catechol-O-methyl transferase (COMT). Levodopa 5-13 catechol-O-methyltransferase Homo sapiens 121-125 19589043-7 2009 A COMT inhibitor can be added to the combination of levodopa and a DDCI to further extend the levodopa peripheral half-life and increase central bioavailability. Levodopa 52-60 catechol-O-methyltransferase Homo sapiens 2-6 19589043-7 2009 A COMT inhibitor can be added to the combination of levodopa and a DDCI to further extend the levodopa peripheral half-life and increase central bioavailability. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 2-6 19798454-0 2009 Genetic polymorphism of catechol O-methyltransferase and pharmacokinetics of levodopa in healthy Chinese subjects. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 24-52 19357321-6 2009 In the acute treatment studies, only MTEP and EMQMCM significantly attenuated L-DOPA-induced phospho-ERK1/2 and/or phospho-MSK-1 expression, with MTEP being the most effective (70-80% reduction). Levodopa 78-84 ribosomal protein S6 kinase A5 Rattus norvegicus 123-128 19553450-4 2009 Previously, we have shown that mice with a 95% genetic reduction in vesicular monoamine transporter expression (VMAT2-deficient, VMAT2 LO) display progressive loss of striatal dopamine, L-DOPA-responsive motor deficits, alpha-synuclein accumulation, and nigral dopaminergic cell loss. Levodopa 186-192 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 112-117 19557698-4 2009 The pharmacodynamical evidence indicates that pharmacological effects such as short-term response (SDR) and the long-term response (LDR) are an integral part of the therapeutic response to levodopa. Levodopa 189-197 caveolae associated protein 2 Homo sapiens 99-102 19503083-2 2009 We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. Levodopa 116-124 leucine-rich repeat kinase 2 Mus musculus 13-18 19553450-4 2009 Previously, we have shown that mice with a 95% genetic reduction in vesicular monoamine transporter expression (VMAT2-deficient, VMAT2 LO) display progressive loss of striatal dopamine, L-DOPA-responsive motor deficits, alpha-synuclein accumulation, and nigral dopaminergic cell loss. Levodopa 186-192 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 129-134 19553450-4 2009 Previously, we have shown that mice with a 95% genetic reduction in vesicular monoamine transporter expression (VMAT2-deficient, VMAT2 LO) display progressive loss of striatal dopamine, L-DOPA-responsive motor deficits, alpha-synuclein accumulation, and nigral dopaminergic cell loss. Levodopa 186-192 synuclein, alpha Mus musculus 220-235 19393228-1 2009 8-(3-chlorostryryl) caffeine (CSC), a selective adenosine A(2A) receptor antagonist, has been reported to inhibit the levodopa-induced motor fluctuation in Parkinson"s disease. Levodopa 118-126 adenosine A2a receptor Rattus norvegicus 48-72 19393228-7 2009 The chronic levodopa treatment upregulated the adenosine A(2A) receptor expression and modified downstream signaling pathway including decreasing the phosphorylation of DARPP-32 at Thr75 site and increasing the phosphorylation of ERK1/2 in the lesioned striatum. Levodopa 12-20 adenosine A2a receptor Rattus norvegicus 47-71 19393228-7 2009 The chronic levodopa treatment upregulated the adenosine A(2A) receptor expression and modified downstream signaling pathway including decreasing the phosphorylation of DARPP-32 at Thr75 site and increasing the phosphorylation of ERK1/2 in the lesioned striatum. Levodopa 12-20 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 169-177 19393228-7 2009 The chronic levodopa treatment upregulated the adenosine A(2A) receptor expression and modified downstream signaling pathway including decreasing the phosphorylation of DARPP-32 at Thr75 site and increasing the phosphorylation of ERK1/2 in the lesioned striatum. Levodopa 12-20 mitogen activated protein kinase 3 Rattus norvegicus 230-236 19393228-8 2009 However, the following CSC treatment attenuated the levodopa-induced adenosine A(2A) receptor upregulation and abolished the aberrant phosphorylation of DARPP-32 at Thr75 site and that of ERK1/2. Levodopa 52-60 adenosine A2a receptor Rattus norvegicus 69-93 19393228-8 2009 However, the following CSC treatment attenuated the levodopa-induced adenosine A(2A) receptor upregulation and abolished the aberrant phosphorylation of DARPP-32 at Thr75 site and that of ERK1/2. Levodopa 52-60 mitogen activated protein kinase 3 Rattus norvegicus 188-194 19393228-9 2009 Our results indicate that the inhibitory effect of CSC on levodopa-induced motor fluctuation may be associated with the inhibition of Adenosine A(2A) Receptor and downstream DARPP-32 and ERK1/2 signaling pathway. Levodopa 58-66 adenosine A2a receptor Rattus norvegicus 134-158 19393228-9 2009 Our results indicate that the inhibitory effect of CSC on levodopa-induced motor fluctuation may be associated with the inhibition of Adenosine A(2A) Receptor and downstream DARPP-32 and ERK1/2 signaling pathway. Levodopa 58-66 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 174-182 19393228-9 2009 Our results indicate that the inhibitory effect of CSC on levodopa-induced motor fluctuation may be associated with the inhibition of Adenosine A(2A) Receptor and downstream DARPP-32 and ERK1/2 signaling pathway. Levodopa 58-66 mitogen activated protein kinase 3 Rattus norvegicus 187-193 19115412-1 2009 Clinical and experimental studies implicate the use of serotonin (5-HT)1A receptor agonists for the reduction of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID). Levodopa 113-141 5-hydroxytryptamine receptor 1A Rattus norvegicus 55-82 18704766-10 2009 Hence, MPTP lesion, L-DOPA treatment and prevention of LID with CI-1041 and cabergoline, or reduction with Ro 61-8048 were associated with modulation of NR2B/NMDA glutamate receptors. Levodopa 20-26 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 153-157 19433789-5 2009 Furthermore, in vivo dopamine depletion leads to a decrease in precursor cell proliferation in the SVZ concomitant with a reduction in local EGF production, which is reversed through the administration of the dopamine precursor levodopa (L-DOPA). Levodopa 228-236 epidermal growth factor Homo sapiens 141-144 19433789-5 2009 Furthermore, in vivo dopamine depletion leads to a decrease in precursor cell proliferation in the SVZ concomitant with a reduction in local EGF production, which is reversed through the administration of the dopamine precursor levodopa (L-DOPA). Levodopa 238-244 epidermal growth factor Homo sapiens 141-144 19115412-1 2009 Clinical and experimental studies implicate the use of serotonin (5-HT)1A receptor agonists for the reduction of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID). Levodopa 143-149 5-hydroxytryptamine receptor 1A Rattus norvegicus 55-82 19115412-6 2009 To establish the effects of 5-HT1AR stimulation on L-DOPA-induced c-fos and preprodynorphin (PPD) mRNA within the dopamine-depleted striatum, immunohistochemistry and real-time reverse transcription polymerase chain reaction, respectively, were used. Levodopa 51-57 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 66-71 19115412-6 2009 To establish the effects of 5-HT1AR stimulation on L-DOPA-induced c-fos and preprodynorphin (PPD) mRNA within the dopamine-depleted striatum, immunohistochemistry and real-time reverse transcription polymerase chain reaction, respectively, were used. Levodopa 51-57 prodynorphin Rattus norvegicus 76-91 19353703-2 2009 As recent observations indicate the dopamine D(3) receptor (DRD3) to modulate both therapeutic action of levodopa and dyskinesia, we reappraised the impact of the DRD3 Ser9Gly polymorphism on development of motor complications in a large scale association study based on the gene bank of the German Competence Network on Parkinson"s disease. Levodopa 105-113 dopamine receptor D3 Homo sapiens 60-64 19115412-9 2009 Striatal c-fos immunoreactivity and PPD mRNA ipsilateral to the lesion were strongly induced by L-DOPA, while +/-8-OH-DPAT suppressed these effects. Levodopa 96-102 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 9-14 19426692-1 2009 Catechol-O-methyl transferase (COMT) methylates catechols, such as L-dopa and dopamine, and COMT deficient mice show dramatic shifts in the metabolite levels of catechols. Levodopa 67-73 catechol-O-methyltransferase Mus musculus 0-29 19426692-1 2009 Catechol-O-methyl transferase (COMT) methylates catechols, such as L-dopa and dopamine, and COMT deficient mice show dramatic shifts in the metabolite levels of catechols. Levodopa 67-73 catechol-O-methyltransferase Mus musculus 31-35 19054775-0 2009 Effect of L-dopa on interleukin-1 beta-induced suppression of luteinizing hormone secretion in intact female rats. Levodopa 10-16 interleukin 1 beta Rattus norvegicus 20-38 19183257-1 2009 Studies showed that the dopamine (DA) transporter (DAT) modulates changes in levodopa-derived synaptic dopamine levels (Delta(DA)) in Parkinson"s disease (PD). Levodopa 77-85 solute carrier family 6 member 3 Rattus norvegicus 51-54 19374330-3 2009 DA, its L-dihydroxyphenylalanine (L-DOPA), precursor, and its dihydroxyphenylacetic acid (DOPAC) metabolite were excellent PHS-1 substrates, resulting in PHS-1-dependent ROS formation that initiated oxidative DNA damage, selectively quantified as 8-oxo-2"-deoxyguanosine. Levodopa 8-32 prostaglandin-endoperoxide synthase 1 Bos taurus 123-128 19374330-3 2009 DA, its L-dihydroxyphenylalanine (L-DOPA), precursor, and its dihydroxyphenylacetic acid (DOPAC) metabolite were excellent PHS-1 substrates, resulting in PHS-1-dependent ROS formation that initiated oxidative DNA damage, selectively quantified as 8-oxo-2"-deoxyguanosine. Levodopa 8-32 prostaglandin-endoperoxide synthase 1 Bos taurus 154-159 19374330-3 2009 DA, its L-dihydroxyphenylalanine (L-DOPA), precursor, and its dihydroxyphenylacetic acid (DOPAC) metabolite were excellent PHS-1 substrates, resulting in PHS-1-dependent ROS formation that initiated oxidative DNA damage, selectively quantified as 8-oxo-2"-deoxyguanosine. Levodopa 34-40 prostaglandin-endoperoxide synthase 1 Bos taurus 123-128 19374330-3 2009 DA, its L-dihydroxyphenylalanine (L-DOPA), precursor, and its dihydroxyphenylacetic acid (DOPAC) metabolite were excellent PHS-1 substrates, resulting in PHS-1-dependent ROS formation that initiated oxidative DNA damage, selectively quantified as 8-oxo-2"-deoxyguanosine. Levodopa 34-40 prostaglandin-endoperoxide synthase 1 Bos taurus 154-159 19406006-4 2009 Also, silymarin inhibited L-DOPA oxidation activity of tyrosinase, the rate-limiting melanogenic enzyme, in cell based-systems but it did not directly affect cell-free tyrosinase activity. Levodopa 26-32 tyrosinase Mus musculus 55-65 19371585-0 2009 Evaluation of the D3 dopamine receptor selective antagonist PG01037 on L-dopa-dependent abnormal involuntary movements in rats. Levodopa 71-77 dopamine receptor D3 Rattus norvegicus 18-38 19371585-14 2009 These studies suggest that D3 dopamine receptor selective antagonists are potential pharmacotherapeutic candidates for the treatment of L-dopa-associated dyskinesia in patients with Parkinson"s Disease. Levodopa 136-142 dopamine receptor D3 Homo sapiens 27-47 19371586-0 2009 Evaluation of D2 and D3 dopamine receptor selective compounds on L-dopa-dependent abnormal involuntary movements in rats. Levodopa 65-71 dopamine receptor D2 Rattus norvegicus 14-41 19371586-1 2009 A panel of novel D2 and D3 dopamine receptor selective antagonists, partial agonists and full agonists have been evaluated for the ability to attenuate L-dopa-associated abnormal involuntary movements (AIMs) in 6-hydroxydopamine (6-OHDA) unilaterally lesioned male Sprague Dawley rats, which is an animal model of L-dopa-induced dyskinesia (LID). Levodopa 152-158 dopamine receptor D2 Rattus norvegicus 17-44 19371586-12 2009 The results of these studies suggest that substituted phenylpiperazine D3 dopamine receptor selective compounds are potential pharmacotherapeutic agents for the treatment of L-dopa-associated dyskinesia in patients with Parkinson"s Disease. Levodopa 174-180 dopamine receptor D3 Homo sapiens 71-91 19409267-5 2009 DA(cyt) was not altered by alpha-synuclein deletion, although dopaminergic neurons lacking alpha-synuclein were resistant to L-DOPA-induced cell death. Levodopa 125-131 synuclein alpha Homo sapiens 91-106 19570739-3 2009 Children in the GHD-1 subgroup (n=33) had low GH values (<10 microg/L) after clonidine and levo-dopa while those in the GHD-2 subgroup (n=32) had normal GH values after pharmacologic provocation but low 24-hour GH secretory rates compared to 187 Normal Statured (NS) children. Levodopa 94-103 growth hormone 1 Homo sapiens 46-48 19570739-3 2009 Children in the GHD-1 subgroup (n=33) had low GH values (<10 microg/L) after clonidine and levo-dopa while those in the GHD-2 subgroup (n=32) had normal GH values after pharmacologic provocation but low 24-hour GH secretory rates compared to 187 Normal Statured (NS) children. Levodopa 94-103 growth hormone 1 Homo sapiens 46-48 19270393-5 2009 Additionally, the incubation of SH in mushroom tyrosinase inhibited the oxidation of l-dopa to o-dopaquinone, which implies that SH is a potent tyrosinase inhibitor. Levodopa 85-91 tyrosinase Mus musculus 47-57 19270393-5 2009 Additionally, the incubation of SH in mushroom tyrosinase inhibited the oxidation of l-dopa to o-dopaquinone, which implies that SH is a potent tyrosinase inhibitor. Levodopa 85-91 tyrosinase Mus musculus 144-154 19085934-9 2009 Exogenous L-DOPA inhibited lymphocyte proliferation producing the cell cycle arrest in G1/0 and dramatically inhibited the production of IL-1beta, TNF-alpha, IL-6 and IL-10. Levodopa 10-16 interleukin 1 beta Homo sapiens 137-145 19085934-9 2009 Exogenous L-DOPA inhibited lymphocyte proliferation producing the cell cycle arrest in G1/0 and dramatically inhibited the production of IL-1beta, TNF-alpha, IL-6 and IL-10. Levodopa 10-16 tumor necrosis factor Homo sapiens 147-156 19085934-9 2009 Exogenous L-DOPA inhibited lymphocyte proliferation producing the cell cycle arrest in G1/0 and dramatically inhibited the production of IL-1beta, TNF-alpha, IL-6 and IL-10. Levodopa 10-16 interleukin 6 Homo sapiens 158-162 19085934-9 2009 Exogenous L-DOPA inhibited lymphocyte proliferation producing the cell cycle arrest in G1/0 and dramatically inhibited the production of IL-1beta, TNF-alpha, IL-6 and IL-10. Levodopa 10-16 interleukin 10 Homo sapiens 167-172 19054775-10 2009 IL-1 beta treatment caused failure of ovulation and this effect was also reversed by L-dopa. Levodopa 85-91 interleukin 1 beta Rattus norvegicus 0-9 19244540-9 2009 Combining sulpiride with L-dopa reestablished iPAS-induced inhibition, but did not affect ePAS-induced plasticity. Levodopa 25-31 hypoxia inducible factor 3 subunit alpha Homo sapiens 46-50 19171906-2 2009 We show here that 2 striatum-enriched regulators of the Ras/Rap/ERK MAP kinase signal transduction cascade, matrix-enriched CalDAG-GEFI and striosome-enriched CalDAG-GEFII (also known as RasGRP), are strongly and inversely dysregulated in proportion to the severity of abnormal movements induced by l-DOPA in a rat model of parkinsonism. Levodopa 299-305 LDL receptor related protein associated protein 1 Rattus norvegicus 60-63 19171906-2 2009 We show here that 2 striatum-enriched regulators of the Ras/Rap/ERK MAP kinase signal transduction cascade, matrix-enriched CalDAG-GEFI and striosome-enriched CalDAG-GEFII (also known as RasGRP), are strongly and inversely dysregulated in proportion to the severity of abnormal movements induced by l-DOPA in a rat model of parkinsonism. Levodopa 299-305 Eph receptor B1 Rattus norvegicus 64-67 19171906-3 2009 In the dopamine-depleted striatum, the l-DOPA treatments produce down-regulation of CalDAG-GEFI and up-regulation of CalDAG-GEFII mRNAs and proteins, and quantification of the mRNA levels shows that these changes are closely correlated with the severity of the dyskinesias. Levodopa 39-45 RAS guanyl releasing protein 2 Rattus norvegicus 84-95 19171906-3 2009 In the dopamine-depleted striatum, the l-DOPA treatments produce down-regulation of CalDAG-GEFI and up-regulation of CalDAG-GEFII mRNAs and proteins, and quantification of the mRNA levels shows that these changes are closely correlated with the severity of the dyskinesias. Levodopa 39-45 RAS guanyl releasing protein 1 Rattus norvegicus 117-129 19171906-4 2009 As these CalDAG-GEFs control ERK cascades, which are implicated in l-DOPA-induced dyskinesias, and have differential compartmental expression patterns in the striatum, we suggest that they may be key molecules involved in the expression of the dyskinesias. Levodopa 67-73 Eph receptor B1 Rattus norvegicus 29-32 19133653-0 2009 Responsiveness to levodopa in epsilon-sarcoglycan deletions. Levodopa 18-26 sarcoglycan epsilon Homo sapiens 30-49 19084027-0 2009 Behavioural and neurochemical response of alpha-synuclein A30P transgenic mice to the effects of L-DOPA. Levodopa 97-103 synuclein, alpha Mus musculus 42-57 19084027-2 2009 We suggested that overexpression of alpha-synuclein may change sensitivity of these mice to L-DOPA. Levodopa 92-98 synuclein, alpha Mus musculus 36-51 19449783-7 2009 In this case, L-tyrosine is transformed to L-DOPA in TH containing neurons that is followed by L-DOPA release and uptake to AADC containing neurons with a semi-specific membrane transporter of large neutral amino acids for DA synthesis. Levodopa 43-49 dopa decarboxylase Rattus norvegicus 124-128 19151015-0 2009 A new perspective on brain derived neurotrophin factor polymorphism in L-dopa induced dyskinesia. Levodopa 71-77 brain derived neurotrophic factor Homo sapiens 35-47 19028082-2 2009 Dopamine D(1) receptor agonists are potential alternative treatments to current therapies that employ L-DOPA, a dopamine precursor. Levodopa 102-108 dopamine receptor D1 Homo sapiens 0-22 19187092-0 2009 L-DOPA activates ERK signaling and phosphorylates histone H3 in the striatonigral medium spiny neurons of hemiparkinsonian mice. Levodopa 0-6 mitogen-activated protein kinase 1 Mus musculus 17-20 19187092-1 2009 In the dopamine-depleted striatum, extracellular signal-regulated kinase (ERK) signaling is implicated in the development of L-DOPA-induced dyskinesia. Levodopa 125-131 mitogen-activated protein kinase 1 Mus musculus 35-72 19187092-1 2009 In the dopamine-depleted striatum, extracellular signal-regulated kinase (ERK) signaling is implicated in the development of L-DOPA-induced dyskinesia. Levodopa 125-131 mitogen-activated protein kinase 1 Mus musculus 74-77 19187092-2 2009 To gain insights on its role in this disorder, we examined the effects of L-DOPA on the state of phosphorylation of ERK and downstream target proteins in striatopallidal and striatonigral medium spiny neurons (MSNs). Levodopa 74-80 mitogen-activated protein kinase 1 Mus musculus 116-119 19187092-4 2009 In 6-hydroxydopamine-lesioned Drd2-EGFP mice, L-DOPA increased the phosphorylation of ERK, mitogen- and stress-activated kinase 1 and histone H3, selectively in EGFP-negative MSNs. Levodopa 46-52 dopamine receptor D2 Mus musculus 30-34 19187092-4 2009 In 6-hydroxydopamine-lesioned Drd2-EGFP mice, L-DOPA increased the phosphorylation of ERK, mitogen- and stress-activated kinase 1 and histone H3, selectively in EGFP-negative MSNs. Levodopa 46-52 mitogen-activated protein kinase 1 Mus musculus 86-89 19187092-4 2009 In 6-hydroxydopamine-lesioned Drd2-EGFP mice, L-DOPA increased the phosphorylation of ERK, mitogen- and stress-activated kinase 1 and histone H3, selectively in EGFP-negative MSNs. Levodopa 46-52 H3 clustered histone 7 Mus musculus 91-144 19187092-7 2009 The same pattern of activation of ERK signaling was observed in dyskinetic mice, after repeated administration of L-DOPA. Levodopa 114-120 mitogen-activated protein kinase 1 Mus musculus 34-37 19187092-8 2009 Our results demonstrate that in the dopamine-depleted striatum, L-DOPA activates ERK signaling specifically in striatonigral MSNs. Levodopa 64-70 mitogen-activated protein kinase 1 Mus musculus 81-84 18977816-0 2009 BDNF val66met influences time to onset of levodopa induced dyskinesia in Parkinson"s disease. Levodopa 42-50 brain derived neurotrophic factor Homo sapiens 0-4 19041269-1 2009 L-DOPA decarboxylase (DDC) is a pyridoxal 5-phosphate (PLP)-dependent enzyme that catalyses the decarboxylation of L-DOPA to dopamine. Levodopa 0-6 dopa decarboxylase Homo sapiens 22-25 18977816-3 2009 METHODS: The influence of a common functional polymorphism of the BDNF gene on the risk of developing dyskinesias in a large cohort of patients with PD (n = 315), who were independently and variably treated with levodopa and/or other dopaminergic treatments, was investigated. Levodopa 212-220 brain derived neurotrophic factor Homo sapiens 66-70 18805557-3 2009 Among genetic factors, increasing evidences suggest that deletion/insertion (D/I) gene polymorphism of the angiotensin I-converting enzyme (ACE) may be involved in the pathogenesis of PD and in the occurrence of the adverse effects of chronic L-dopa therapy. Levodopa 243-249 angiotensin I converting enzyme Homo sapiens 107-138 18805557-3 2009 Among genetic factors, increasing evidences suggest that deletion/insertion (D/I) gene polymorphism of the angiotensin I-converting enzyme (ACE) may be involved in the pathogenesis of PD and in the occurrence of the adverse effects of chronic L-dopa therapy. Levodopa 243-249 angiotensin I converting enzyme Homo sapiens 140-143 19056347-3 2009 The main clinical interest in COMT results from the possibility of using COMT inhibitors as adjuncts in the therapy of Parkinson"s disease (PD) with l-DOPA. Levodopa 149-155 catechol-O-methyltransferase Homo sapiens 30-34 19056347-3 2009 The main clinical interest in COMT results from the possibility of using COMT inhibitors as adjuncts in the therapy of Parkinson"s disease (PD) with l-DOPA. Levodopa 149-155 catechol-O-methyltransferase Homo sapiens 73-77 19122286-3 2009 The kinetic studies of tyrosinase inhibition revealed that TMBC acts as a competitive inhibitor of mushroom tyrosinase with L-dopa as the substrate. Levodopa 124-130 tyrosinase Mus musculus 23-33 19122286-3 2009 The kinetic studies of tyrosinase inhibition revealed that TMBC acts as a competitive inhibitor of mushroom tyrosinase with L-dopa as the substrate. Levodopa 124-130 tyrosinase Mus musculus 108-118 19041269-6 2009 Enzymatic activity experiments revealed that DDC is active towards the decarboxylation of L-DOPA. Levodopa 90-96 dopa decarboxylase Homo sapiens 45-48 20411784-6 2009 In addition, MPTP and L-DOPA separately induced reductions of TH protein expression within the substantia nigra. Levodopa 22-28 tyrosine hydroxylase Rattus norvegicus 62-64 19660177-6 2009 When 0.5-1 x 10(6) TH- and GCH1-expressing ADSCs were intrathecally grafted in rats, elevated levels of levodopa and dopamine metabolites were found in CSF at 3 days, although at lower concentrations than expected. Levodopa 104-112 GTP cyclohydrolase 1 Rattus norvegicus 27-31 19407449-3 2009 Current strategies include concomitant treatment with inhibitors of dopa decarboxylase (DDC) and catechol-O-methyltransferase (COMT) to prolong the peripheral levodopa half-life and increase CNS bioavailability. Levodopa 159-167 dopa decarboxylase Homo sapiens 68-86 19407449-3 2009 Current strategies include concomitant treatment with inhibitors of dopa decarboxylase (DDC) and catechol-O-methyltransferase (COMT) to prolong the peripheral levodopa half-life and increase CNS bioavailability. Levodopa 159-167 catechol-O-methyltransferase Homo sapiens 97-125 19407449-3 2009 Current strategies include concomitant treatment with inhibitors of dopa decarboxylase (DDC) and catechol-O-methyltransferase (COMT) to prolong the peripheral levodopa half-life and increase CNS bioavailability. Levodopa 159-167 catechol-O-methyltransferase Homo sapiens 127-131 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 dopa decarboxylase Homo sapiens 93-119 19358813-4 2009 TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons, where they are capable of converting L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA) and L-DOPA to dopamine (DA) (or 5-hydroxy-tryptophan, 5-HTP to serotonin), respectively. Levodopa 138-167 dopa decarboxylase Homo sapiens 7-11 19358813-4 2009 TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons, where they are capable of converting L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA) and L-DOPA to dopamine (DA) (or 5-hydroxy-tryptophan, 5-HTP to serotonin), respectively. Levodopa 169-175 dopa decarboxylase Homo sapiens 7-11 19358813-4 2009 TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons, where they are capable of converting L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA) and L-DOPA to dopamine (DA) (or 5-hydroxy-tryptophan, 5-HTP to serotonin), respectively. Levodopa 181-187 dopa decarboxylase Homo sapiens 7-11 19358813-5 2009 According to our data L-DOPA synthesized in monoenzymatic TH-neurons is released and taken up by monoenzymatic AADC-neurons for DA synthesis. Levodopa 22-28 dopa decarboxylase Homo sapiens 111-115 19648757-4 2009 The L-dopa test was performed on those with IGF-I SDSs above the -1.8 cut-off level. Levodopa 4-10 insulin like growth factor 1 Homo sapiens 44-49 19110205-7 2009 When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised. Levodopa 30-38 monoamine oxidase B Homo sapiens 54-59 19110205-7 2009 When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised. Levodopa 111-119 monoamine oxidase B Homo sapiens 54-59 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 catechol-O-methyltransferase Homo sapiens 158-162 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 monoamine oxidase B Homo sapiens 168-187 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 dopa decarboxylase Homo sapiens 121-125 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 monoamine oxidase B Homo sapiens 189-194 19131039-3 2009 DA in the striatum may be produced from exogenously administered l-dopa by various AADC-containing cells, such as serotonin neurons. Levodopa 65-71 dopa decarboxylase Homo sapiens 83-87 19131039-2 2009 The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B). Levodopa 12-18 catechol-O-methyltransferase Homo sapiens 128-156 18226951-1 2009 BACKGROUND: Abnormally high CSF 3-OMD occurs frequently for RLS patients indicating either increased l-dopa synthesis, limitations in l-dopa decarboxylation or increased MAT/COMT activity, or some combination of these. Levodopa 101-107 colony stimulating factor 3 Homo sapiens 28-33 19240805-0 2009 L-DOPA neurotoxicity is mediated by up-regulation of DMT1-IRE expression. Levodopa 0-6 solute carrier family 11 member 2 Homo sapiens 53-57 19240805-2 2009 Based on recent findings, we speculated that the increased expression of divalent metal transporter 1 without iron-response element (DMT1-IRE) induced by L-DOPA might play a critical role in the development of L-DOPA neurotoxicity. Levodopa 154-160 solute carrier family 11 member 2 Homo sapiens 133-137 19240805-2 2009 Based on recent findings, we speculated that the increased expression of divalent metal transporter 1 without iron-response element (DMT1-IRE) induced by L-DOPA might play a critical role in the development of L-DOPA neurotoxicity. Levodopa 210-216 solute carrier family 11 member 2 Homo sapiens 133-137 19240805-4 2009 METHODS AND FINDINGS: We demonstrated that neurons treated with L-DOPA have a significant dose-dependent decrease in neuronal viability (MTT Assay) and increase in iron content (using a graphite furnace atomic absorption spectrophotometer), DMT1-IRE expression (Western blot analysis) and ferrous iron (55Fe(II)) uptake. Levodopa 64-70 solute carrier family 11 member 2 Homo sapiens 241-245 19240805-8 2009 CONCLUSION: The up-regulation of DMT1-IRE and the increase in DMT1-IRE-mediated iron influx play a key role in L-DOPA neurotoxicity in cortical neurons. Levodopa 111-117 solute carrier family 11 member 2 Homo sapiens 33-37 19240805-8 2009 CONCLUSION: The up-regulation of DMT1-IRE and the increase in DMT1-IRE-mediated iron influx play a key role in L-DOPA neurotoxicity in cortical neurons. Levodopa 111-117 solute carrier family 11 member 2 Homo sapiens 62-66 19556833-6 2009 Preoperative levodopa responsiveness only led to consistent UPDRS part III improvement from STN-DBS at 3 months, and this predictive value did not exist in the long term. Levodopa 13-21 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 92-95 18226951-1 2009 BACKGROUND: Abnormally high CSF 3-OMD occurs frequently for RLS patients indicating either increased l-dopa synthesis, limitations in l-dopa decarboxylation or increased MAT/COMT activity, or some combination of these. Levodopa 134-140 colony stimulating factor 3 Homo sapiens 28-33 18952677-0 2008 Combined 5-HT1A and 5-HT1B receptor agonists for the treatment of L-DOPA-induced dyskinesia. Levodopa 66-72 5-hydroxytryptamine receptor 1A Rattus norvegicus 9-15 18817742-2 2008 The logarithm of enzyme activity is linearly correlated with the diameter of the dark, l-3,4-dihydroxyphenylalanine (l-DOPA) oxidized circles produced in the gel, thereby allowing quantification of PPO. Levodopa 87-115 protoporphyrinogen oxidase Homo sapiens 198-201 18817742-2 2008 The logarithm of enzyme activity is linearly correlated with the diameter of the dark, l-3,4-dihydroxyphenylalanine (l-DOPA) oxidized circles produced in the gel, thereby allowing quantification of PPO. Levodopa 117-123 protoporphyrinogen oxidase Homo sapiens 198-201 18842830-9 2008 Insulin-induced stimulation of L-dopa uptake was also abolished by inhibition of phosphatidylinositol 3-kinase (PI3K; 100 nM wortmannin, and 25 microM LY-294002) and protein kinase C (PKC; 1 microM RO-318220). Levodopa 31-37 phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma Rattus norvegicus 81-110 18952677-5 2008 The results demonstrate the existence of a potent synergistic effect between 5-HT(1A) and 5-HT(1B) agonists in their ability to dampen l-DOPA-induced dyskinesia in the MPTP-treated macaques. Levodopa 135-141 5-hydroxytryptamine receptor 1A Rattus norvegicus 77-84 18952677-2 2008 We have recently demonstrated that dopamine released from serotonin neurons is responsible for l-DOPA-induced dyskinesia in 6-hydroxydopamine (6-OHDA)-lesioned rats, raising the possibility that blockade of serotonin neuron activity by combination of 5-HT(1A) and 5-HT(1B) agonists could reduce l-DOPA-induced dyskinesia. Levodopa 95-101 5-hydroxytryptamine receptor 1A Rattus norvegicus 251-258 18952677-7 2008 Furthermore, chronic administration of low doses of the 5-HT(1) agonists in combination was able to prevent development of dyskinesia, and reduce the up-regulation of FosB after daily treatment with l-DOPA in the rat 6-OHDA model. Levodopa 199-205 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 167-171 18952677-3 2008 In the present study, we have investigated the efficacy of 5-HT(1A) and 5-HT(1B) agonists to counteract l-DOPA-induced dyskinesia in 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP)-treated macaques, the gold standard model of Parkinson"s disease. Levodopa 104-110 5-hydroxytryptamine receptor 1A Rattus norvegicus 59-66 18952677-8 2008 Our results support the importance of a clinical investigation of the effect of 5-HT(1A) and 5-HT(1B) agonists, particularly in combination, in dyskinetic l-DOPA-treated Parkinson"s disease patients. Levodopa 155-161 5-hydroxytryptamine receptor 1A Homo sapiens 80-87 18721798-0 2008 Intermittent L-DOPA treatment differentially alters synaptotagmin 4 and 7 gene expression in the striatum of hemiparkinsonian rats. Levodopa 13-19 synaptotagmin 4 Rattus norvegicus 52-73 19014386-0 2008 The novel nociceptin/orphanin FQ receptor antagonist Trap-101 alleviates experimental parkinsonism through inhibition of the nigro-thalamic pathway: positive interaction with L-DOPA. Levodopa 175-181 prepronociceptin Rattus norvegicus 10-20 19014386-0 2008 The novel nociceptin/orphanin FQ receptor antagonist Trap-101 alleviates experimental parkinsonism through inhibition of the nigro-thalamic pathway: positive interaction with L-DOPA. Levodopa 175-181 prepronociceptin Rattus norvegicus 21-32 19014386-0 2008 The novel nociceptin/orphanin FQ receptor antagonist Trap-101 alleviates experimental parkinsonism through inhibition of the nigro-thalamic pathway: positive interaction with L-DOPA. Levodopa 175-181 tudor domain containing 7 Rattus norvegicus 53-57 19014386-7 2008 When combined with ineffective doses of l-DOPA (0.1 mg/Kg), Trap-101 evoked larger neurochemical and behavioral responses. Levodopa 40-46 tudor domain containing 7 Rattus norvegicus 60-64 18438720-8 2008 The use of adenosine A(2A) receptor antagonists in combination therapy enables the reduction of the L-DOPA doses, as well as a reduction of side effects. Levodopa 100-106 adenosine A2a receptor Homo sapiens 11-35 18937611-2 2008 As primary therapy in early disease monoamine oxidase B inhibitors reduce motor disability and delay the need for levodopa. Levodopa 114-122 monoamine oxidase B Homo sapiens 36-55 18937611-3 2008 In more advanced disease requiring levodopa, adjunctive monoamine oxidase B inhibitors reduce "off" time and may improve gait and freezing. Levodopa 35-43 monoamine oxidase B Homo sapiens 56-75 18937611-8 2008 CONCLUSION: Accumulating data support the use of monoamine oxidase B inhibitors as monotherapy for early and mild Parkinson"s disease and as adjunctive therapy for more advanced Parkinson"s disease with levodopa-associated motor fluctuations. Levodopa 203-211 monoamine oxidase B Homo sapiens 49-68 18690408-0 2008 Investigation on tolerance development to subchronic blockade of mGluR5 in models of learning, anxiety, and levodopa-induced dyskinesia in rats. Levodopa 108-116 glutamate receptor, ionotropic, kainate 1 Mus musculus 65-71 18817789-12 2008 As a current replacement therapy, oral administration of levodopa 10 mg/kg/day (group V), caused symptomatic improvement in the form of reduction of catalepsy score with restoration of striatal dopamine levels, but it did not show any significant effects on either striatal complex I activity, ATP levels or the expression of Bcl-2, pointing to the lack of its disease-modifying role. Levodopa 57-65 BCL2, apoptosis regulator Rattus norvegicus 326-331 18817789-14 2008 Moreover, administration of high dose coenzyme Q10 with L-dopa provided a significant increase in striatal complex I activity, ATP levels and Bcl-2 expression in comparison to group administered coenzyme Q10 low dose with L-dopa, in addition to the significant restoration of striatal dopamine levels and both plasma and striatal Co Q10 levels. Levodopa 56-62 BCL2, apoptosis regulator Rattus norvegicus 142-147 18721798-9 2008 On contrary, intermittent L-DOPA treatment downregulated Syt 4 mRNA and prolonged the elevation of Syt 7 mRNA in the denervated striatum. Levodopa 26-32 synaptotagmin 4 Rattus norvegicus 57-62 18721798-9 2008 On contrary, intermittent L-DOPA treatment downregulated Syt 4 mRNA and prolonged the elevation of Syt 7 mRNA in the denervated striatum. Levodopa 26-32 synaptotagmin 7 Rattus norvegicus 99-104 18721798-10 2008 We conclude that Syt 4 and Syt 7 might be specifically involved in striatal plasticity caused by repeated L-DOPA administration that accompanies sensitization. Levodopa 106-112 synaptotagmin 4 Rattus norvegicus 17-22 18721798-10 2008 We conclude that Syt 4 and Syt 7 might be specifically involved in striatal plasticity caused by repeated L-DOPA administration that accompanies sensitization. Levodopa 106-112 synaptotagmin 7 Rattus norvegicus 27-32 18721798-3 2008 We have previously reported that acute L-DOPA treatment upregulated the expression of Syt 4 and Syt 7 mRNAs in hypersensitive striatum of 6-OHDA rat model for PD. Levodopa 39-45 synaptotagmin 4 Rattus norvegicus 86-91 18721798-3 2008 We have previously reported that acute L-DOPA treatment upregulated the expression of Syt 4 and Syt 7 mRNAs in hypersensitive striatum of 6-OHDA rat model for PD. Levodopa 39-45 synaptotagmin 7 Rattus norvegicus 96-101 18721798-4 2008 Here we investigate whether intermittent L-DOPA treatment that produces behavior sensitization affects the Syt 1, Syt 2, Syt 4, Syt 7 and Syt 10 mRNAs in striatum of 6-OHDA rats killed 4 and 12 h after the last L-DOPA injection. Levodopa 41-47 synaptotagmin 1 Rattus norvegicus 107-112 18721798-4 2008 Here we investigate whether intermittent L-DOPA treatment that produces behavior sensitization affects the Syt 1, Syt 2, Syt 4, Syt 7 and Syt 10 mRNAs in striatum of 6-OHDA rats killed 4 and 12 h after the last L-DOPA injection. Levodopa 41-47 synaptotagmin 2 Rattus norvegicus 114-119 18721798-4 2008 Here we investigate whether intermittent L-DOPA treatment that produces behavior sensitization affects the Syt 1, Syt 2, Syt 4, Syt 7 and Syt 10 mRNAs in striatum of 6-OHDA rats killed 4 and 12 h after the last L-DOPA injection. Levodopa 41-47 synaptotagmin 4 Rattus norvegicus 121-126 18721798-4 2008 Here we investigate whether intermittent L-DOPA treatment that produces behavior sensitization affects the Syt 1, Syt 2, Syt 4, Syt 7 and Syt 10 mRNAs in striatum of 6-OHDA rats killed 4 and 12 h after the last L-DOPA injection. Levodopa 41-47 synaptotagmin 7 Rattus norvegicus 128-133 18721798-4 2008 Here we investigate whether intermittent L-DOPA treatment that produces behavior sensitization affects the Syt 1, Syt 2, Syt 4, Syt 7 and Syt 10 mRNAs in striatum of 6-OHDA rats killed 4 and 12 h after the last L-DOPA injection. Levodopa 41-47 synaptotagmin 10 Rattus norvegicus 138-144 18721798-7 2008 Acute l-DOPA induced an increase of Syt 4 and Syt 7 mRNAs in the denervated striatum leaving the levels of Syt 1, Syt 2 and Syt 10 mRNAs unaffected. Levodopa 6-12 synaptotagmin 4 Rattus norvegicus 36-41 18721798-7 2008 Acute l-DOPA induced an increase of Syt 4 and Syt 7 mRNAs in the denervated striatum leaving the levels of Syt 1, Syt 2 and Syt 10 mRNAs unaffected. Levodopa 6-12 synaptotagmin 7 Rattus norvegicus 46-51 18721798-7 2008 Acute l-DOPA induced an increase of Syt 4 and Syt 7 mRNAs in the denervated striatum leaving the levels of Syt 1, Syt 2 and Syt 10 mRNAs unaffected. Levodopa 6-12 synaptotagmin 1 Rattus norvegicus 107-112 18721798-7 2008 Acute l-DOPA induced an increase of Syt 4 and Syt 7 mRNAs in the denervated striatum leaving the levels of Syt 1, Syt 2 and Syt 10 mRNAs unaffected. Levodopa 6-12 synaptotagmin 2 Rattus norvegicus 114-119 18752647-0 2008 Pleiotrophin receptor RPTP-zeta/beta expression is up-regulated by L-DOPA in striatal medium spiny neurons of parkinsonian rats. Levodopa 67-73 pleiotrophin Rattus norvegicus 0-12 18759356-2 2008 In a randomized, double-blind, placebo-controlled clinical trial, we investigated the acute effects of placebo and two doses of a NR2B subunit selective NMDA glutamate antagonist, CP-101,606, on the response to 2-hour levodopa infusions in 12 PD subjects with motor fluctuations and dyskinesia. Levodopa 218-226 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 130-134 18656534-3 2008 Only a few drugs (less than 10) are substrates of LAT1 and LAT2, including L-DOPA, alpha-methyldopa, melphalan, and gabapentin. Levodopa 75-81 solute carrier family 7 member 5 Homo sapiens 50-54 18656534-3 2008 Only a few drugs (less than 10) are substrates of LAT1 and LAT2, including L-DOPA, alpha-methyldopa, melphalan, and gabapentin. Levodopa 75-81 linker for activation of T cells family member 2 Homo sapiens 59-63 18752647-0 2008 Pleiotrophin receptor RPTP-zeta/beta expression is up-regulated by L-DOPA in striatal medium spiny neurons of parkinsonian rats. Levodopa 67-73 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 22-31 18752647-3 2008 Pleiotrophin, a trophic factor that we have shown to be up-regulated in the striatum of parkinsonian rats after long-term L-DOPA treatment may play a role in these plastic changes. Levodopa 122-128 pleiotrophin Rattus norvegicus 0-12 18752647-5 2008 Both pleiotrophin and RPTP-zeta/beta expression was up-regulated in the striatum but not in the mesencephalon of lesioned rats and RPTP-zeta/beta expression was even further increased by L-DOPA. Levodopa 187-193 pleiotrophin Rattus norvegicus 5-17 18752647-5 2008 Both pleiotrophin and RPTP-zeta/beta expression was up-regulated in the striatum but not in the mesencephalon of lesioned rats and RPTP-zeta/beta expression was even further increased by L-DOPA. Levodopa 187-193 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 22-31 18752647-5 2008 Both pleiotrophin and RPTP-zeta/beta expression was up-regulated in the striatum but not in the mesencephalon of lesioned rats and RPTP-zeta/beta expression was even further increased by L-DOPA. Levodopa 187-193 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 131-140 18752647-6 2008 The levels of the RPTP-zeta/beta protein were also increased in the striatum of L-DOPA-treated lesioned rats. Levodopa 80-86 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 18-32 18752647-8 2008 RPTP-zeta/beta might therefore be implicated in the plastic changes triggered by L-DOPA treatment and might merit further study as a potential candidate for Parkinon"s disease therapy. Levodopa 81-87 protein tyrosine phosphatase, receptor type Z1 Rattus norvegicus 0-9 18828673-0 2008 L-DOPA is an endogenous ligand for OA1. Levodopa 0-6 OA1 Homo sapiens 35-38 18828673-10 2008 Further, inhibition of tyrosinase, the enzyme that makes L-DOPA, resulted in decreased PEDF secretion by RPE. Levodopa 57-63 tyrosinase Homo sapiens 23-33 18828673-7 2008 Radiolabeled ligand binding confirmed that OA1 exhibited a single, saturable binding site for L-DOPA. Levodopa 94-100 OA1 Homo sapiens 43-46 18828673-8 2008 Dopamine competed with L-DOPA for the single OA1 binding site, suggesting it could function as an OA1 antagonist. Levodopa 23-29 OA1 Homo sapiens 45-48 18828673-10 2008 Further, inhibition of tyrosinase, the enzyme that makes L-DOPA, resulted in decreased PEDF secretion by RPE. Levodopa 57-63 serpin family F member 1 Homo sapiens 87-91 18828673-8 2008 Dopamine competed with L-DOPA for the single OA1 binding site, suggesting it could function as an OA1 antagonist. Levodopa 23-29 OA1 Homo sapiens 98-101 18828673-9 2008 OA1 response to L-DOPA was defined by several common measures of G-protein coupled receptor (GPCR) activation, including influx of intracellular calcium and recruitment of beta-arrestin. Levodopa 16-22 OA1 Homo sapiens 0-3 18828673-9 2008 OA1 response to L-DOPA was defined by several common measures of G-protein coupled receptor (GPCR) activation, including influx of intracellular calcium and recruitment of beta-arrestin. Levodopa 16-22 C-X-C motif chemokine receptor 6 Homo sapiens 65-91 18828673-11 2008 Further, stimulation of OA1 in RPE with L-DOPA resulted in increased PEDF secretion. Levodopa 40-46 OA1 Homo sapiens 24-27 18828673-11 2008 Further, stimulation of OA1 in RPE with L-DOPA resulted in increased PEDF secretion. Levodopa 40-46 serpin family F member 1 Homo sapiens 69-73 18828673-12 2008 Taken together, our results illustrate an autocrine loop between OA1 and tyrosinase linked through L-DOPA, and this loop includes the secretion of at least one very potent retinal neurotrophic factor. Levodopa 99-105 OA1 Homo sapiens 65-68 18828673-12 2008 Taken together, our results illustrate an autocrine loop between OA1 and tyrosinase linked through L-DOPA, and this loop includes the secretion of at least one very potent retinal neurotrophic factor. Levodopa 99-105 tyrosinase Homo sapiens 73-83 18828673-9 2008 OA1 response to L-DOPA was defined by several common measures of G-protein coupled receptor (GPCR) activation, including influx of intracellular calcium and recruitment of beta-arrestin. Levodopa 16-22 C-X-C motif chemokine receptor 6 Homo sapiens 93-97 18602388-2 2008 l-DOPA treatment (20-200 microM) increased the levels of dopamine by 226%-504% after 3-6 h of treatment and enhanced the activities of tyrosine hydroxylase (TH) and aromatic l-amino acid decarboxylase (AADC). Levodopa 0-6 dopa decarboxylase Rattus norvegicus 202-206 18687386-9 2008 Real-time reverse-transcription polymerase chain reaction of striatal tissue implicated a role for interleukin-1 (IL-1) beta in these effects as its expression was increased on the lesioned side in rats treated with l-DOPA (within the DA-depleted striatum) and attenuated with CORT. Levodopa 216-222 interleukin 1 beta Rattus norvegicus 114-124 18687386-10 2008 In the final experiment, interleukin-1 receptor antagonist (IL-1ra) was microinjected into the striatum of l-DOPA-primed rats to assess the impact of IL-1 signaling on LID. Levodopa 107-113 interleukin 1 receptor antagonist Rattus norvegicus 25-58 18687386-10 2008 In the final experiment, interleukin-1 receptor antagonist (IL-1ra) was microinjected into the striatum of l-DOPA-primed rats to assess the impact of IL-1 signaling on LID. Levodopa 107-113 interleukin 1 receptor antagonist Rattus norvegicus 60-66 18598736-4 2008 Among the antiparkinsonian drugs tested, levodopa, bromocriptine, pergolide and pramipexole were ABCB1 substrates. Levodopa 41-49 ATP binding cassette subfamily B member 1A Rattus norvegicus 97-102 18602388-3 2008 l-DOPA (20-200 muM) treatment led to a 562%-937% increase in l-DOPA influx at 1 h, which inhibited the activity of TH, but not AADC, during the same period. Levodopa 0-6 dopa decarboxylase Rattus norvegicus 127-131 18602388-9 2008 One pathway involves l-DOPA directly entering the cells to convert dopamine through AADC activity (l-DOPA decarboxylation). Levodopa 21-27 dopa decarboxylase Rattus norvegicus 84-88 18602388-9 2008 One pathway involves l-DOPA directly entering the cells to convert dopamine through AADC activity (l-DOPA decarboxylation). Levodopa 99-105 dopa decarboxylase Rattus norvegicus 84-88 18582514-5 2008 The synthesis of dopamine from L-DOPA supplied to Muller cultures is inhibited by m-hydroxybenzylhydrazine, a DDC inhibitor. Levodopa 31-37 dopa decarboxylase Mus musculus 110-113 18729255-6 2008 However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Levodopa 82-106 tyrosinase Mus musculus 48-58 18698234-0 2008 The association of functional catechol-O-methyltransferase haplotypes with risk of Parkinson"s disease, levodopa treatment response, and complications. Levodopa 104-112 catechol-O-methyltransferase Homo sapiens 30-58 18698234-1 2008 INTRODUCTION: Differences in catechol-O-methyltransferase (COMT) activity and genotype may determine individual variations in the therapeutic response to levodopa or Parkinson"s disease (PD) susceptibility. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 29-57 18698234-1 2008 INTRODUCTION: Differences in catechol-O-methyltransferase (COMT) activity and genotype may determine individual variations in the therapeutic response to levodopa or Parkinson"s disease (PD) susceptibility. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 59-63 18698234-3 2008 OBJECTIVES: In this case-control study, we investigated the association of the most common COMT gene haplotypes (formed by single nucleotide polymorphisms (SNPs): rs6269:A>G; rs4633C>T; rs4818:C>G; and rs4680:A>G) with PD risk and the association of the COMT haplotypes with the dose and complications of levodopa therapy in PD patients. Levodopa 305-313 catechol-O-methyltransferase Homo sapiens 91-95 18698234-15 2008 The doses of levodopa treatment can be influenced by specific COMT haplotypes and this may be useful in instituting individualized therapy for PD patients. Levodopa 13-21 catechol-O-methyltransferase Homo sapiens 62-66 18509855-0 2008 Reuptake of L-DOPA-derived extracellular DA in the striatum of a rodent model of Parkinson"s disease via norepinephrine transporter. Levodopa 12-18 solute carrier family 6 member 2 Rattus norvegicus 105-131 18502672-11 2008 The known, impressive beneficial response of SR deficient patients to treatment with L-dopa, is illustrated again in our cases. Levodopa 85-91 sepiapterin reductase Homo sapiens 45-47 18509855-1 2008 To determine the role of norepinephrine transporter in reuptake of L-DOPA-derived extracellular DA in the DA-denervated Parkinsonian striatum, we examined extracellular DA levels in the striatum of 6-hydroxyDA-lesioned rats that received L-DOPA (50 mg/kg with 12.5 mg/kg of benserazide) and L-DOPA plus desipramine (25 mg/kg), a selective norepinephrine reuptake inhibitor, using in vivo microdialysis. Levodopa 67-73 solute carrier family 6 member 2 Rattus norvegicus 25-51 18509855-3 2008 This study provides evidence that L-DOPA-derived DA is taken up by the norepinephrine transporter, instead of the dopamine transporter, in the striatum with dopaminergic denervation. Levodopa 34-40 solute carrier family 6 member 2 Rattus norvegicus 71-97 18419768-2 2008 Primary inherited defects in TH have been associated with l-DOPA responsive and non-responsive dystonia and infantile parkinsonism. Levodopa 58-64 tyrosine hydroxylase Homo sapiens 29-31 18670186-3 2008 Glutathione inhibited the binding between tyrosinase and L-DOPA. Levodopa 57-63 tyrosinase Homo sapiens 42-52 18410512-4 2008 In the primate model, which closely resembles human LDID, we observed that chronic levodopa and the appearance of LDID was associated with marked deacetylation of histone H4, hyperacetylation and dephosphorylation of histone H3, and enhancement of the phosphorylation of extracellular signal-regulated kinase (ERK). Levodopa 83-91 mitogen-activated protein kinase 1 Homo sapiens 271-308 18363828-9 2008 Elevated dopamine-beta-hydroxylase activity in ID provides a tentative explanation for the increased NE response to l-DOPA. Levodopa 116-122 dopamine beta-hydroxylase Rattus norvegicus 9-34 18502641-0 2008 Two novel POLG1 mutations in a patient with progressive external ophthalmoplegia, levodopa-responsive pseudo-orthostatic tremor and parkinsonism. Levodopa 82-90 DNA polymerase gamma, catalytic subunit Homo sapiens 10-15 18510366-6 2008 Changing from mono- to bisubstrate inhibitors of catechol O-methyltransferase, a target in the L-Dopa-based treatment of Parkinson"s disease, enabled the full exploitation of a previously unexplored hydrophobic pocket. Levodopa 95-101 catechol-O-methyltransferase Homo sapiens 49-77 18423776-11 2008 Altogether, these data demonstrate a differential regulation of NKB and SP by L-DOPA in an animal model of PD and indicate a unique role of NKB in long-term effects of L-DOPA. Levodopa 78-84 trefoil factor 2 Rattus norvegicus 72-74 18410512-4 2008 In the primate model, which closely resembles human LDID, we observed that chronic levodopa and the appearance of LDID was associated with marked deacetylation of histone H4, hyperacetylation and dephosphorylation of histone H3, and enhancement of the phosphorylation of extracellular signal-regulated kinase (ERK). Levodopa 83-91 mitogen-activated protein kinase 1 Homo sapiens 310-313 18410512-5 2008 In the murine model of acutely rather than chronically induced LDID, dopamine depletion and levodopa treatment also induced deacetylation of histone H4 and phosphorylation of ERK, but histone H3 exhibited decreased trimethylation and reduced rather than enhanced acetylation. Levodopa 92-100 mitogen-activated protein kinase 1 Mus musculus 175-178 17353071-2 2008 In this study receptor binding autoradiography of [3H]MPEP, a metabotropic glutamate receptor 5 (mGluR5) selective radioligand, was used to investigate possible changes in mGluR5 in the basal ganglia of l-Dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys having developed LIDs compared to animals in which LIDs was prevented by adjunct treatments. Levodopa 203-209 glutamate metabotropic receptor 5 Homo sapiens 62-95 17353071-2 2008 In this study receptor binding autoradiography of [3H]MPEP, a metabotropic glutamate receptor 5 (mGluR5) selective radioligand, was used to investigate possible changes in mGluR5 in the basal ganglia of l-Dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys having developed LIDs compared to animals in which LIDs was prevented by adjunct treatments. Levodopa 203-209 glutamate receptor, ionotropic, kainate 1 Mus musculus 172-178 18545986-0 2008 Effects of coincident 5-HT1A receptor stimulation and NMDA receptor antagonism on L-DOPA-induced dyskinesia and rotational behaviors in the hemi-parkinsonian rat. Levodopa 82-88 5-hydroxytryptamine receptor 1A Rattus norvegicus 22-28 18545986-1 2008 RATIONALE: Serotonin 1A receptor (5-HT1AR) agonists reduce L-DOPA-induced dyskinesia and enhance motor function in experimental and clinical investigations of Parkinson"s disease (PD). Levodopa 59-65 5-hydroxytryptamine receptor 1A Rattus norvegicus 11-41 18569714-4 2008 Tyrosinase is a key enzyme, which catalyzes the conversion of L-tyrosine to L-dihydroxyalanine (L-Dopa), therefore tyrosinase inhibitors are used in various skin preparations due to its pronounced effect on anti-hyperpigment. Levodopa 96-102 tyrosinase Homo sapiens 0-10 18569714-4 2008 Tyrosinase is a key enzyme, which catalyzes the conversion of L-tyrosine to L-dihydroxyalanine (L-Dopa), therefore tyrosinase inhibitors are used in various skin preparations due to its pronounced effect on anti-hyperpigment. Levodopa 96-102 tyrosinase Homo sapiens 115-125 18423776-0 2008 Neurokinin B/NK3 receptors exert feedback inhibition on L-DOPA actions in the 6-OHDA lesion rat model of Parkinson"s disease. Levodopa 56-62 tachykinin receptor 3 Rattus norvegicus 0-26 18423776-3 2008 In contrast, both acute and chronic administrations of L-DOPA restore reduced levels of SP mRNA. Levodopa 55-61 trefoil factor 2 Rattus norvegicus 88-90 18423776-4 2008 Co-treatment with the NK(3) receptor antagonist, SB222200, and L-DOPA increased contralateral rotations compared to L-DOPA alone in L-DOPA primed rats. Levodopa 116-122 tachykinin receptor 3 Rattus norvegicus 22-36 18423776-4 2008 Co-treatment with the NK(3) receptor antagonist, SB222200, and L-DOPA increased contralateral rotations compared to L-DOPA alone in L-DOPA primed rats. Levodopa 116-122 tachykinin receptor 3 Rattus norvegicus 22-36 18423776-13 2008 The inhibitory influence of NKB/NK(3)R on dopamine transmission dominates in an animal model of PD and provides a feedback inhibition on actions mediated via L-DOPA. Levodopa 158-164 tachykinin receptor 3 Rattus norvegicus 32-38 18502641-4 2008 Here we report two novel mutations in POLG1 in a compound heterozygous patient with autosomal recessive PEO, followed by pseudo-orthostatic tremor evolving into levodopa-responsive parkinsonism. Levodopa 161-169 DNA polymerase gamma, catalytic subunit Homo sapiens 38-43 18383536-7 2008 A multivariate analysis demonstrated that a lower dose of levodopa (OR = 0.993, 95%CI for OR = 0.988, 0.997, P < 0.001) and a higher age of onset of disease (OR = 1.108, 95%CI for OR = 1.035, 1.187, P < 0.001) were associated with increased odds of PD with ET, compared to patients with PD without ET. Levodopa 58-66 major facilitator superfamily domain containing 11 Homo sapiens 257-259 18387727-6 2008 In addition, 100 microM L-DOPA treatment significantly increased the activity of GSK-3 and death signals including cytochrome c, activated caspase-3 and cleaved PARP, and decreased survival signals including heat shock transcription factor-1 in a concentration-dependent manner. Levodopa 24-30 caspase 3 Rattus norvegicus 139-148 18387727-6 2008 In addition, 100 microM L-DOPA treatment significantly increased the activity of GSK-3 and death signals including cytochrome c, activated caspase-3 and cleaved PARP, and decreased survival signals including heat shock transcription factor-1 in a concentration-dependent manner. Levodopa 24-30 heat shock transcription factor 1 Rattus norvegicus 208-241 18383536-7 2008 A multivariate analysis demonstrated that a lower dose of levodopa (OR = 0.993, 95%CI for OR = 0.988, 0.997, P < 0.001) and a higher age of onset of disease (OR = 1.108, 95%CI for OR = 1.035, 1.187, P < 0.001) were associated with increased odds of PD with ET, compared to patients with PD without ET. Levodopa 58-66 major facilitator superfamily domain containing 11 Homo sapiens 298-300 18522902-0 2008 Histamine H(3) receptor ligands modulate L-dopa-evoked behavioral responses and L-dopa derived extracellular dopamine in dopamine-denervated rat striatum. Levodopa 41-47 histamine receptor H3 Rattus norvegicus 0-23 18520980-0 2008 Catechol-O-methyltransferase inhibition improves levodopa-associated strength increase in patients with Parkinson disease. Levodopa 49-57 catechol-O-methyltransferase Homo sapiens 0-28 18522902-0 2008 Histamine H(3) receptor ligands modulate L-dopa-evoked behavioral responses and L-dopa derived extracellular dopamine in dopamine-denervated rat striatum. Levodopa 80-86 histamine receptor H3 Rattus norvegicus 0-23 18342306-12 2008 Therefore, future studies are necessary to establish the potential of selective NR2B receptor antagonists as L-Dopa-sparing agents. Levodopa 109-115 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 80-84 18307263-4 2008 Here, we report the first occurrence of compound heterozygous PINK1 mutations in a sporadic patient with a phenotype indistinguishable from idiopathic Parkinson"s disease (PD), with onset in the late seventh decade, rapid progression and good response to levodopa that waned with time. Levodopa 255-263 PTEN induced kinase 1 Homo sapiens 62-67 18164541-1 2008 OBJECTIVES: The goal of this study was to assess the effect of bilateral subthalamic deep brain stimulation (STN DBS) on levodopa-induced diphasic dyskinesia in patients with Parkinson disease (PD). Levodopa 121-129 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 109-112 18434508-0 2008 The 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor lovastatin reduces severity of L-DOPA-induced abnormal involuntary movements in experimental Parkinson"s disease. Levodopa 86-92 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 4-44 18434508-1 2008 Chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment of Parkinson"s disease (PD) often leads to debilitating involuntary movements, termed L-DOPA-induced dyskinesia (LID), about which the rodent analog, the abnormal involuntary movements (AIMs), has been associated consistently with an activation of the Ras-extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase signaling pathway. Levodopa 8-36 mitogen activated protein kinase 3 Rattus norvegicus 355-361 18434508-1 2008 Chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment of Parkinson"s disease (PD) often leads to debilitating involuntary movements, termed L-DOPA-induced dyskinesia (LID), about which the rodent analog, the abnormal involuntary movements (AIMs), has been associated consistently with an activation of the Ras-extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase signaling pathway. Levodopa 38-44 mitogen activated protein kinase 3 Rattus norvegicus 355-361 18434508-1 2008 Chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment of Parkinson"s disease (PD) often leads to debilitating involuntary movements, termed L-DOPA-induced dyskinesia (LID), about which the rodent analog, the abnormal involuntary movements (AIMs), has been associated consistently with an activation of the Ras-extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase signaling pathway. Levodopa 142-148 mitogen activated protein kinase 3 Rattus norvegicus 355-361 18428105-1 2008 INTRODUCTION: The dopamine psychosis that appears in Parkinson"s disease (PDP) is a complication that is often related with frequent intake of antiparkinsonian agents, especially levodopa and dopamine agonists. Levodopa 179-187 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 74-77 18324837-3 2008 Oxidation of the capping layer by TR/O2 yields the respective L-DOPA and dopaquinone products. Levodopa 62-68 tyrosinase Homo sapiens 34-36 18413568-5 2008 After surgery, STN stimulation reproduced the improvement induced by levodopa before surgery in all but two patients with FOG and five others unable to walk. Levodopa 69-77 zinc finger protein, FOG family member 1 Homo sapiens 122-125 18394568-4 2008 Candidate genes tested in PD patients encode 1) glutamic acid decarboxylase, which is injected into the subthalamic nucleus to catalyze biosynthesis of the inhibitory neurotransmitter gamma-aminobutyric acid and so essentially mimic deep brain stimulation of this nucleus; 2) aromatic l-amino acid decarboxylase, which converts l-dopa to dopamine; and 3) neurturin, a member of the glial cell line-derived neurotrophic factor family. Levodopa 328-334 neurturin Homo sapiens 355-364 18242749-0 2008 Specific induction of PAG608 in cranial and spinal motor neurons of L-DOPA-treated parkinsonian rats. Levodopa 68-74 zinc finger, matrin type 3 Rattus norvegicus 22-28 18241048-0 2008 Receptor-activity modifying protein 1 expression is increased in the striatum following repeated L-DOPA administration in a 6-hydroxydopamine lesioned rat model of Parkinson"s disease. Levodopa 97-103 receptor activity modifying protein 1 Rattus norvegicus 0-37 18242749-1 2008 We identified p53-activated gene 608 (PAG608) as a specifically induced gene in striatal tissue of L-DOPA (100mg/kg)-injected hemi-parkinsonian rats using differential display assay. Levodopa 99-105 zinc finger, matrin type 3 Rattus norvegicus 14-36 18242749-1 2008 We identified p53-activated gene 608 (PAG608) as a specifically induced gene in striatal tissue of L-DOPA (100mg/kg)-injected hemi-parkinsonian rats using differential display assay. Levodopa 99-105 zinc finger, matrin type 3 Rattus norvegicus 38-44 18242749-2 2008 In the present study, we further examined morphological distribution of PAG608 in the central nervous system of L-DOPA-treated hemi-parkinsonian rats. Levodopa 112-118 zinc finger, matrin type 3 Rattus norvegicus 72-78 18242749-3 2008 PAG608 expression was markedly induced in fibers and neuronal cells of the lateral globus pallidus and reticular thalamic nucleus adjacent to internal capsule, specifically in the parkinsonian side of L-DOPA-treated models. Levodopa 201-207 zinc finger, matrin type 3 Rattus norvegicus 0-6 18242749-5 2008 Furthermore, L-DOPA-induced PAG608 expression on motor neurons in the contralateral side of the ventral horn of the spinal cord and the lateral corticospinal tract without cell loss. Levodopa 13-19 zinc finger, matrin type 3 Rattus norvegicus 28-34 18242749-6 2008 The specific induction of PAG608 6-48h after L-DOPA injection in the extrapyramidal tracts, pyramidal tracts and corresponding lower motor neurons of the spinal cords suggests its involvement in molecular events in stimulated motor neurons. Levodopa 45-51 zinc finger, matrin type 3 Rattus norvegicus 26-32 18241048-4 2008 In the present study, expression of RAMP1 mRNA is increased in the striatum (68-77%), following repeated L-DOPA administration, in the 6-hydroxydopamine-lesioned rat. Levodopa 105-111 receptor activity modifying protein 1 Rattus norvegicus 36-41 18286173-2 2008 The MAO-B inhibitor deprenyl, a long-standing antiparkinsonian therapy, is currently used clinically in concert with the dopamine precursor L-DOPA. Levodopa 140-146 monoamine oxidase B Mus musculus 4-9 18290846-1 2008 Catechol-O-methyl transferase (COMT) inhibition by entacapone enhances levodopa absorption and reduces "off" time in Parkinson"s disease (PD). Levodopa 71-79 catechol-O-methyltransferase Homo sapiens 0-29 18290846-1 2008 Catechol-O-methyl transferase (COMT) inhibition by entacapone enhances levodopa absorption and reduces "off" time in Parkinson"s disease (PD). Levodopa 71-79 catechol-O-methyltransferase Homo sapiens 31-35 18255227-5 2008 Exogenous l-DOPA induced DA immuno-reactivity in the striatum, which was independently detected from GFAP immuno-positive astroglial cells or Iba1 immuno-positive microglial cells in the intact side as well as in the lesioned side. Levodopa 10-16 glial fibrillary acidic protein Rattus norvegicus 101-105 18255227-5 2008 Exogenous l-DOPA induced DA immuno-reactivity in the striatum, which was independently detected from GFAP immuno-positive astroglial cells or Iba1 immuno-positive microglial cells in the intact side as well as in the lesioned side. Levodopa 10-16 allograft inflammatory factor 1 Rattus norvegicus 142-146 17996024-10 2008 In rCPu, GRK2 protein was increased in most subcellular fractions by l-DOPA but not by DA depletion alone. Levodopa 69-75 G protein-coupled receptor kinase 2 Rattus norvegicus 9-13 17996024-12 2008 GRK5 was down-regulated by l-DOPA in cCPu in the light membrane fraction, where this isoform is the most abundant. Levodopa 27-33 G protein-coupled receptor kinase 5 Rattus norvegicus 0-4 17896794-2 2008 The rate-limiting step in the biosynthesis of dopamine, noradrenalin, and adrenalin is catalyzed by tyrosine 3-monooxygenase (=tyrosine hydroxylase), which catalyzes the formation of L-DOPA. Levodopa 183-189 tyrosine hydroxylase Homo sapiens 100-124 18258746-7 2008 Treatment with l-DOPA improved mutant LRRK2-induced locomotor impairment but did not prevent the loss of tyrosine hydroxylase-positive neurons. Levodopa 15-21 leucine rich repeat kinase 2 Homo sapiens 38-43 18279311-10 2008 Finally, striatal TH-ir neurones are functionally active, expressing the neuronal activation marker FosB in response to L-DOPA treatment. Levodopa 120-126 FBJ osteosarcoma oncogene B Mus musculus 100-104 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 13-21 catechol-O-methyltransferase Homo sapiens 121-149 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 13-21 catechol-O-methyltransferase Homo sapiens 151-155 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 23-29 catechol-O-methyltransferase Homo sapiens 121-149 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 23-29 catechol-O-methyltransferase Homo sapiens 151-155 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 99-105 catechol-O-methyltransferase Homo sapiens 121-149 18289028-6 2008 Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Levodopa 99-105 catechol-O-methyltransferase Homo sapiens 151-155 18256188-0 2008 Evidence for a role of the 5-HT1B receptor and its adaptor protein, p11, in L-DOPA treatment of an animal model of Parkinsonism. Levodopa 76-82 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 27-42 18256188-0 2008 Evidence for a role of the 5-HT1B receptor and its adaptor protein, p11, in L-DOPA treatment of an animal model of Parkinsonism. Levodopa 76-82 S100 calcium binding protein A10 (calpactin) Mus musculus 68-71 18256188-5 2008 Here, we demonstrate that chronic L-DOPA administration to 6-OHDA-lesioned rodents increases, via D1 receptors, the levels of the 5-HT1B receptor and its adaptor protein, p11, in dopamine-denervated striatonigral neurons. Levodopa 34-40 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 130-145 18256188-5 2008 Here, we demonstrate that chronic L-DOPA administration to 6-OHDA-lesioned rodents increases, via D1 receptors, the levels of the 5-HT1B receptor and its adaptor protein, p11, in dopamine-denervated striatonigral neurons. Levodopa 34-40 S100 calcium binding protein A10 (calpactin) Mus musculus 171-174 18256188-6 2008 Using unilaterally 6-OHDA-lesioned p11 WT and KO mice, it was found that administration of a selective 5-HT1B receptor agonist, CP94253, inhibited L-DOPA-induced rotational behavior and abnormal involuntary movements in a p11-dependent manner. Levodopa 147-153 S100 calcium binding protein A10 (calpactin) Mus musculus 35-38 18256188-6 2008 Using unilaterally 6-OHDA-lesioned p11 WT and KO mice, it was found that administration of a selective 5-HT1B receptor agonist, CP94253, inhibited L-DOPA-induced rotational behavior and abnormal involuntary movements in a p11-dependent manner. Levodopa 147-153 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 103-118 18256188-6 2008 Using unilaterally 6-OHDA-lesioned p11 WT and KO mice, it was found that administration of a selective 5-HT1B receptor agonist, CP94253, inhibited L-DOPA-induced rotational behavior and abnormal involuntary movements in a p11-dependent manner. Levodopa 147-153 S100 calcium binding protein A10 (calpactin) Mus musculus 222-225 18506224-6 2008 The K(m) values of the PPO for caffeic acid, chlorogenic acid, pyrocatechol, 4-methyl catechol and l-DOPA as substrates were 0.077, 0.198, 1.176, 1.667 and 4.545 mM. Levodopa 99-105 polyphenol oxidase I, chloroplastic Triticum aestivum 23-26 17893915-0 2008 L-DOPA-induced activation of striatal p38MAPK and CREB in neonatal dopaminergic denervated rat: relevance to self-injurious behavior. Levodopa 0-6 cAMP responsive element binding protein 1 Rattus norvegicus 50-54 17893915-3 2008 Here, we examined whether L-DOPA-induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Levodopa 26-32 mitogen activated protein kinase 3 Rattus norvegicus 72-76 17893915-3 2008 Here, we examined whether L-DOPA-induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Levodopa 26-32 mitogen activated protein kinase 3 Rattus norvegicus 97-103 17893915-3 2008 Here, we examined whether L-DOPA-induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Levodopa 26-32 mitogen-activated protein kinase 8 Rattus norvegicus 109-112 17893915-3 2008 Here, we examined whether L-DOPA-induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Levodopa 26-32 cAMP responsive element binding protein 1 Rattus norvegicus 140-144 17893915-10 2008 The results indicate an induction of striatal p38MAPK and an activation of its nuclear target, CREB, as additional mechanisms in the genesis of L-DOPA-induced SIB. Levodopa 144-150 cAMP responsive element binding protein 1 Rattus norvegicus 95-99 17898029-8 2008 We conclude that GCH1 deletion analysis should be incorporated into the routine molecular diagnosis of all patients with DRD with a sustained response to L-Dopa. Levodopa 154-160 GTP cyclohydrolase 1 Homo sapiens 17-21 17920284-4 2008 Intrastriatal inhibition of the enzyme aromatic amino acid decarboxylase (AADC) by benserazide prevented the appearance of l-DOPA-induced dyskinetic movements at the lesioned side. Levodopa 123-129 dopa decarboxylase Rattus norvegicus 74-78 18728767-1 2008 Levodopa is the most effective treatment in Parkinson"s disease and the association with COMT inhibitors widens its plasma bioavailability and effectiveness. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 89-93 17590551-8 2008 On the other hand, even in this relatively small dosing range, the serum prolactin level showed significant negative correlation with the dosage of L-Dopa/carbidopa (R=0.645, p=0.023). Levodopa 148-154 prolactin Homo sapiens 73-82 17590551-10 2008 From these results, we suggest that the serum prolactin level may be a more sensitive marker than the CSF HVA level to guide the dose adjustment of L-Dopa/carbidopa in the management of patients with PTPS deficiency. Levodopa 148-154 prolactin Homo sapiens 46-55 17590551-0 2008 A case of 6-pyruvoyl-tetrahydropterin synthase deficiency demonstrates a more significant correlation of L-Dopa dosage with serum prolactin levels than CSF homovanillic acid levels. Levodopa 105-111 prolactin Homo sapiens 130-139 18250952-3 2008 Acute L-dopa administration normalised PPE-A mRNA and elevated PPT mRNA while PPE-B mRNA expression remained unchanged. Levodopa 6-12 tachykinin, precursor 1 Rattus norvegicus 63-66 17590551-4 2008 Here, we present a case of PTPS deficiency which showed a more significant correlation of dosage of L-Dopa/carbidopa with serum prolactin levels than with CSF HVA levels. Levodopa 100-106 prolactin Homo sapiens 128-137 17590551-5 2008 Combined treatment of BH4, L-Dopa/carbidopa, and 5HTP was started as the CSF neopterin/biopterin ratio (N/B ratio 7.54, control 0.46-1.59) and serum prolactin level (36.79 ng/ml, control <15) were elevated. Levodopa 27-33 colony stimulating factor 2 Homo sapiens 73-76 19040557-6 2008 Enhancement of AAAD activity is functional, as the formation of dopamine from exogenous L-DOPA mirrors activity. Levodopa 88-94 dopa decarboxylase Homo sapiens 15-19 19040557-7 2008 Following a lesion of nigrostriatal dopaminergic neurons, AAAD in striatum responds more robustly to pharmacological manipulations, and this is true for the decarboxylation of exogenous L-DOPA as well. Levodopa 186-192 dopa decarboxylase Homo sapiens 58-62 19040557-8 2008 We review the evidence for parallel modulation of AAAD activity and L-DOPA decarboxylation and propose that this knowledge can be exploited to optimize the formation of dopamine from exogenous L-DOPA. Levodopa 193-199 dopa decarboxylase Homo sapiens 50-54 19040557-0 2008 Enhancing aromatic L-amino acid decarboxylase activity: implications for L-DOPA treatment in Parkinson"s disease. Levodopa 73-79 dopa decarboxylase Homo sapiens 10-45 18989992-13 2008 CONCLUSION: Following concomitant administration with levodopa/carbidopa CR 200 mg/50 mg, single doses of nebicapone 50 mg, 100 mg and 200 mg significantly and dose-dependently inhibited S-COMT activity, increased systemic exposure to levodopa, and reduced 3-OMD formation. Levodopa 54-62 catechol-O-methyltransferase Homo sapiens 189-193 18250952-5 2008 Following chronic treatment with L-dopa, PPE-A mRNA expression in the lesioned striatum continued to be normalised and PPT mRNA was increased compared to the intact side. Levodopa 33-39 tachykinin, precursor 1 Rattus norvegicus 119-122 18668617-1 2008 The majority of patients with Parkinson"s disease suffer from freezing of gait (FOG), which responds more or less to levodopa. Levodopa 117-125 zinc finger protein, FOG family member 1 Homo sapiens 80-83 17960796-10 2008 For PD patients who develop an ICD in the context of DA treatment, discontinuing or significantly decreasing DA exposure, even when offset by an increase in levodopa treatment, is associated with remission of or significant reduction in ICD behaviors without worsening in motor symptoms. Levodopa 157-165 N-acetylglucosamine-1-phosphate transferase subunits alpha and beta Homo sapiens 31-34 18270468-3 2008 Inhibition kinetics studies revealed that imperanene is a competitive inhibitor of tyrosinase when L-3,4-dihydroxyphenylalanine is used as the substrate. Levodopa 99-127 tyrosinase Homo sapiens 83-93 18668617-7 2008 In the few cases of levodopa-induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Levodopa 127-135 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 42-45 18668620-2 2008 Recent studies have clearly demonstrated that the Off-related FOG is improved by levodopa (L-dopa) or entacapone treatment. Levodopa 81-89 zinc finger protein, FOG family member 1 Homo sapiens 62-65 18668620-2 2008 Recent studies have clearly demonstrated that the Off-related FOG is improved by levodopa (L-dopa) or entacapone treatment. Levodopa 91-97 zinc finger protein, FOG family member 1 Homo sapiens 62-65 18668620-3 2008 L-dopa can decrease duration of each FOG episode as well as its frequency. Levodopa 0-6 zinc finger protein, FOG family member 1 Homo sapiens 37-40 18668617-4 2008 STN stimulation was reported to improve levodopa-responsive FOG. Levodopa 40-48 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 0-3 18668617-4 2008 STN stimulation was reported to improve levodopa-responsive FOG. Levodopa 40-48 zinc finger protein, FOG family member 1 Homo sapiens 60-63 18668617-7 2008 In the few cases of levodopa-induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Levodopa 20-28 zinc finger protein, FOG family member 1 Homo sapiens 37-40 18668617-7 2008 In the few cases of levodopa-induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Levodopa 20-28 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 42-45 18668617-7 2008 In the few cases of levodopa-induced FOG, STN stimulation can indirectly be effective, thanks to a great decrease or arrest of levodopa. Levodopa 127-135 zinc finger protein, FOG family member 1 Homo sapiens 37-40 18322402-1 2008 BACKGROUND: A significant percentage of patients with Parkinson"s disease (PD) continue to experience motor fluctuations and dyskinesias despite the association of dopamine agonists and levodopa with COMT or MAO-B inhibitors. Levodopa 186-194 catechol-O-methyltransferase Homo sapiens 200-204 17933546-0 2008 Systemic administration of an mGluR5 antagonist, but not unilateral subthalamic lesion, counteracts l-DOPA-induced dyskinesias in a rodent model of Parkinson"s disease. Levodopa 100-106 glutamate receptor, ionotropic, kainate 1 Mus musculus 30-36 18322402-1 2008 BACKGROUND: A significant percentage of patients with Parkinson"s disease (PD) continue to experience motor fluctuations and dyskinesias despite the association of dopamine agonists and levodopa with COMT or MAO-B inhibitors. Levodopa 186-194 monoamine oxidase B Homo sapiens 208-213 17933546-6 2008 Our data confirm the role of glutamatergic neurotransmission in the pathogenesis of dyskinesias and the potential of mGluR5 antagonists in the treatment of l-DOPA-induced dyskinesias. Levodopa 156-162 glutamate receptor, ionotropic, kainate 1 Mus musculus 117-123 18316232-4 2008 L-Dopa with a dopa decarboxylase inhibitor was the most frequently prescribed APD, although the use of both ergot and non-ergot derivative DAs has increased, particularly, in the elderly. Levodopa 0-6 dopa decarboxylase Homo sapiens 14-32 18583175-5 2008 Zif-268 mRNA levels were decreased in both striatonigral and striatopallidal neurons by ropinirole, in contrast to hyper-expression of zif-268 mRNA selectively induced by L-dopa in striatonigral neurons. Levodopa 171-177 early growth response 1 Rattus norvegicus 135-142 18055246-0 2008 Folate and vitamin B12 levels in levodopa-treated Parkinson"s disease patients: their relationship to clinical manifestations, mood and cognition. Levodopa 33-41 NADH:ubiquinone oxidoreductase subunit B3 Homo sapiens 19-22 18055246-1 2008 We tested the hypothesis that mood, clinical manifestations and cognitive impairment of levodopa-treated Parkinson"s disease (PD) patients are associated with vitamin B12 and folate deficiency. Levodopa 88-96 NADH:ubiquinone oxidoreductase subunit B3 Homo sapiens 167-170 18055246-3 2008 Levodopa-treated PD patients showed significantly lower serum levels of folate and vitamin B12 than neurological controls, while depressed patients had significantly lower serum folate levels as compared to non-depressed. Levodopa 0-8 NADH:ubiquinone oxidoreductase subunit B3 Homo sapiens 91-94 18221241-3 2008 In fact, recent development efforts have been primarily directed at stabilizing the side effects (wearing off, drug-induced dyskinesias, motor fluctuations) that accompany prolonged levodopa therapy, such as catechol O-methyltransferase inhibiton to combat the side effects of levodopa therapy. Levodopa 182-190 catechol-O-methyltransferase Homo sapiens 208-236 18221241-3 2008 In fact, recent development efforts have been primarily directed at stabilizing the side effects (wearing off, drug-induced dyskinesias, motor fluctuations) that accompany prolonged levodopa therapy, such as catechol O-methyltransferase inhibiton to combat the side effects of levodopa therapy. Levodopa 277-285 catechol-O-methyltransferase Homo sapiens 208-236 18833115-2 2008 The results of the study revealed that the drug substantially reduced motor deficit, increased the "on"-period, decreased the duration and severity of the "off" period, improved the daily activity and quality of life of patients compared to standard therapy with an additional dosage of levodopa/DDC inhibitor. Levodopa 287-295 dopa decarboxylase Homo sapiens 296-299 17935716-1 2007 More continuous delivery of l-3,4-dihydroxyphenylalanine (l-dopa) achieved by combination with the catechol-O-methyl transfer (COMT) inhibitor entacapone reduces the onset of dyskinesia in MPTP-treated common marmosets compared with pulsatile l-dopa regimens. Levodopa 28-56 catechol O-methyltransferase Callithrix jacchus 99-125 18160641-0 2007 RGS9-2 negatively modulates L-3,4-dihydroxyphenylalanine-induced dyskinesia in experimental Parkinson"s disease. Levodopa 28-56 regulator of G-protein signaling 9 Mus musculus 0-6 18160641-5 2007 In MPTP monkeys with LID, striatal RGS9-2 overexpression--achieved by viral vector injection into the striatum--diminishes the involuntary movement intensity without lessening the anti-parkinsonian effects of the D1/D2 receptor agonist L-dopa. Levodopa 236-242 regulator of G-protein signaling 9 Mus musculus 35-41 18160641-7 2007 In unilaterally 6-OHDA-lesioned rats with LID, we show that the time course of viral vector-mediated striatal RGS9-2 overexpression parallels the time course of improvement of L-dopa-induced involuntary movements. Levodopa 176-182 regulator of G-protein signaling 9 Mus musculus 110-116 18160641-8 2007 We also find that unilateral 6-OHDA-lesioned RGS9-/- mice are more susceptible to L-dopa-induced involuntary movements than unilateral 6-OHDA-lesioned RGS9+/+ mice, albeit the rotational behavior--taken as an index of the anti-parkinsonian response--is similar between the two groups of mice. Levodopa 82-88 regulator of G-protein signaling 9 Mus musculus 45-49 18160641-10 2007 However, the findings also suggest that increasing RGS9-2 expression and/or function in PD patients may only be a suitable therapeutic strategy to control involuntary movements induced by nonselective DA agonist such as L-dopa. Levodopa 220-226 regulator of G-protein signaling 9 Mus musculus 51-57 18308560-3 2007 These symptoms are greatly improved by pharmacological DA replacement with L-3,4-dihydroxy-phenylalanine (L-DOPA), which however causes excessive involuntary movements in a majority of patients. Levodopa 106-112 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 75-78 17935716-1 2007 More continuous delivery of l-3,4-dihydroxyphenylalanine (l-dopa) achieved by combination with the catechol-O-methyl transfer (COMT) inhibitor entacapone reduces the onset of dyskinesia in MPTP-treated common marmosets compared with pulsatile l-dopa regimens. Levodopa 28-56 catechol O-methyltransferase Callithrix jacchus 127-131 17935716-1 2007 More continuous delivery of l-3,4-dihydroxyphenylalanine (l-dopa) achieved by combination with the catechol-O-methyl transfer (COMT) inhibitor entacapone reduces the onset of dyskinesia in MPTP-treated common marmosets compared with pulsatile l-dopa regimens. Levodopa 58-64 catechol O-methyltransferase Callithrix jacchus 99-125 17935716-1 2007 More continuous delivery of l-3,4-dihydroxyphenylalanine (l-dopa) achieved by combination with the catechol-O-methyl transfer (COMT) inhibitor entacapone reduces the onset of dyskinesia in MPTP-treated common marmosets compared with pulsatile l-dopa regimens. Levodopa 243-249 catechol O-methyltransferase Callithrix jacchus 127-131 17935716-6 2007 The addition of l-dopa BID or QID without entacapone produced only a minor further reversal of motor deficits, but significantly increased the intensity of dyskinesia. Levodopa 16-22 BH3-interacting domain death agonist Callithrix jacchus 23-26 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 29-35 BH3-interacting domain death agonist Callithrix jacchus 36-39 18052761-3 2007 Catechol-O-methyltransferase (COMT) is a selective and widely distributed enzyme involved in the catabolism of levodopa. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 0-28 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 29-35 BH3-interacting domain death agonist Callithrix jacchus 166-169 18052761-3 2007 Catechol-O-methyltransferase (COMT) is a selective and widely distributed enzyme involved in the catabolism of levodopa. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 30-34 18052761-4 2007 Tolcapone and entacapone are selective and potent COMT inhibitors that slow the metabolism of levodopa, thus prolonging its effects. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 50-54 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 159-165 BH3-interacting domain death agonist Callithrix jacchus 36-39 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 159-165 BH3-interacting domain death agonist Callithrix jacchus 166-169 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 159-165 BH3-interacting domain death agonist Callithrix jacchus 36-39 17935716-7 2007 In contrast, the addition of l-dopa BID or QID with entacapone also produced some further improvement in motor function with the combination of entacapone and l-dopa BID significantly improving motor disability compared to l-dopa alone, but no further increase in dyskinesia intensity was observed compared with ropinirole alone treatment. Levodopa 159-165 BH3-interacting domain death agonist Callithrix jacchus 166-169 17573159-11 2007 These changes in glial and perivascular catechol-O-methyltransferase activity may have clinical relevance for Parkinson"s disease drug treatment due to increased metabolism of levodopa in the brain. Levodopa 176-184 catechol-O-methyltransferase Homo sapiens 40-68 17936857-5 2007 Strategies that may improve the bioavailability of levodopa, the most efficacious medication for Parkinson"s disease, include coadministering levodopa with carbidopa, a decarboxylase inhibitor, or with a catechol-O-methyltransferase inhibitor or using an alternative route of administration. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 204-232 17900568-5 2007 Administration of the cannabinoid agonist WIN 55,212-2 attenuated levodopa-induced axial, limb and oral AIMs dose-dependently via a CB(1)-mediated mechanism, whereas it had no effect on locomotive AIMs. Levodopa 66-74 cannabinoid receptor 1 Rattus norvegicus 132-137 17900568-9 2007 Our data indicate that pharmacological blockade of TRPV1 receptors unmasks the anti-dyskinetic effects of FAAH inhibitors and that CB(1) and TRPV1 receptors play opposite roles in levodopa-induced dyskinesias. Levodopa 180-188 cannabinoid receptor 1 Rattus norvegicus 131-136 17900568-9 2007 Our data indicate that pharmacological blockade of TRPV1 receptors unmasks the anti-dyskinetic effects of FAAH inhibitors and that CB(1) and TRPV1 receptors play opposite roles in levodopa-induced dyskinesias. Levodopa 180-188 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 141-146 17712844-6 2007 The percentage improvement of mFOG and UPDRS motor scores by STN DBS during levodopa off period was calculated. Levodopa 76-84 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 61-64 17712844-8 2007 During levodopa off period, STN DBS improved the UPDRS motor scores by 32.3% and the mFOG scores by 56.6%. Levodopa 7-15 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 28-31 17943771-3 2007 OBJECTIVES: To assess the efficacy and safety of bromocriptine (BR) monotherapy for delaying the onset of motor complications associated with levodopa (LD) therapy in patients with PD. Levodopa 142-150 chromosome 12 open reading frame 73 Homo sapiens 64-66 17966631-3 2007 Postoperatively, he had transient episodes of severe Parkinson symptoms, which were controled by levodopa drugs. Levodopa 97-105 3-hydroxyanthranilate 3,4-dioxygenase Homo sapiens 20-23 17884291-0 2007 Changes in the prodynorphin gene and DARPP-32 state in 6-OHDA-lesioned rats following long-term treatment with l-dopa. Levodopa 111-117 prodynorphin Rattus norvegicus 15-27 17884291-0 2007 Changes in the prodynorphin gene and DARPP-32 state in 6-OHDA-lesioned rats following long-term treatment with l-dopa. Levodopa 111-117 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 37-45 17884291-3 2007 Our data demonstrated significantly increased levels of PDyn mRNA and phospho-Thr-34 DARPP-32 and significantly decreased phospho-Thr-75 DARPP-32 in LID rats compared with control and l-dopa treated groups. Levodopa 184-190 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 137-145 17654694-4 2007 Levodopa was administered with a dopa-decarboxylase inhibitor (carbidopa 25 mg, n=8 or benserazide 25 mg, n=8). Levodopa 0-8 dopa decarboxylase Homo sapiens 33-51 17662258-0 2007 Spatiotemporal pattern of striatal ERK1/2 phosphorylation in a rat model of L-DOPA-induced dyskinesia and the role of dopamine D1 receptors. Levodopa 76-82 mitogen activated protein kinase 3 Rattus norvegicus 35-41 17662258-1 2007 BACKGROUND: We examined the activation pattern of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and its dependence on D1 versus D2 dopamine receptors in hemiparkinsonian rats treated with 3,4-dihydroxyphenyl-L-alanine (L-DOPA). Levodopa 197-226 mitogen activated protein kinase 3 Rattus norvegicus 50-95 17662258-1 2007 BACKGROUND: We examined the activation pattern of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and its dependence on D1 versus D2 dopamine receptors in hemiparkinsonian rats treated with 3,4-dihydroxyphenyl-L-alanine (L-DOPA). Levodopa 197-226 mitogen activated protein kinase 3 Rattus norvegicus 97-103 17662258-1 2007 BACKGROUND: We examined the activation pattern of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and its dependence on D1 versus D2 dopamine receptors in hemiparkinsonian rats treated with 3,4-dihydroxyphenyl-L-alanine (L-DOPA). Levodopa 228-234 mitogen activated protein kinase 3 Rattus norvegicus 50-95 17662258-1 2007 BACKGROUND: We examined the activation pattern of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and its dependence on D1 versus D2 dopamine receptors in hemiparkinsonian rats treated with 3,4-dihydroxyphenyl-L-alanine (L-DOPA). Levodopa 228-234 mitogen activated protein kinase 3 Rattus norvegicus 97-103 17662258-5 2007 RESULTS: L-DOPA treatment caused phosphorylation of ERK1/2 in the dopamine-denervated striatum after acute and chronic administration. Levodopa 9-15 mitogen activated protein kinase 3 Rattus norvegicus 52-58 17662258-10 2007 CONCLUSIONS: L-DOPA produces pronounced activation of ERK1/2 signaling in the dopamine-denervated striatum through a D1-receptor-dependent mechanism. Levodopa 13-19 mitogen activated protein kinase 3 Rattus norvegicus 54-60 17662258-12 2007 Phosphorylated ERK1/2 is localized to both dynorphinergic and enkephalinergic striatal neurons, suggesting a general role of ERK1/2 as a plasticity molecule during L-DOPA treatment. Levodopa 164-170 mitogen activated protein kinase 3 Rattus norvegicus 15-21 17662258-12 2007 Phosphorylated ERK1/2 is localized to both dynorphinergic and enkephalinergic striatal neurons, suggesting a general role of ERK1/2 as a plasticity molecule during L-DOPA treatment. Levodopa 164-170 mitogen activated protein kinase 3 Rattus norvegicus 125-131 17894650-4 2007 The last decade showed that the use of catechol-O-methyltransferase inhibitors as adjuvants to the levodopa/AADC inhibitor therapy, significantly improves the clinical benefits of this therapy. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 39-67 17894650-4 2007 The last decade showed that the use of catechol-O-methyltransferase inhibitors as adjuvants to the levodopa/AADC inhibitor therapy, significantly improves the clinical benefits of this therapy. Levodopa 99-107 dopa decarboxylase Homo sapiens 108-112 17894650-5 2007 The purpose of this article is to review the current knowledge on the enzyme catechol-O-methyltransferase (COMT) and the role of COMT inhibitors in PD as a new therapeutic approach to PD involving conversion of levodopa to dopamine at the target region in the brain and facilitation of the continuous action of this amine at the receptor sites. Levodopa 211-219 catechol-O-methyltransferase Homo sapiens 77-105 17894650-5 2007 The purpose of this article is to review the current knowledge on the enzyme catechol-O-methyltransferase (COMT) and the role of COMT inhibitors in PD as a new therapeutic approach to PD involving conversion of levodopa to dopamine at the target region in the brain and facilitation of the continuous action of this amine at the receptor sites. Levodopa 211-219 catechol-O-methyltransferase Homo sapiens 107-111 17894650-5 2007 The purpose of this article is to review the current knowledge on the enzyme catechol-O-methyltransferase (COMT) and the role of COMT inhibitors in PD as a new therapeutic approach to PD involving conversion of levodopa to dopamine at the target region in the brain and facilitation of the continuous action of this amine at the receptor sites. Levodopa 211-219 catechol-O-methyltransferase Homo sapiens 129-133 17630359-0 2007 Blockade of cannabinoid type 1 receptors augments the antiparkinsonian action of levodopa without affecting dyskinesias in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated rhesus monkeys. Levodopa 81-89 cannabinoid receptor 1 Macaca mulatta 12-40 17692830-4 2007 Intense dopamine immunoreactivity became visible in a large number of cells and axons (possibly containing AADC) with wide distribution in the brain following administration of L-DOPA with Pargyline. Levodopa 177-183 dopa decarboxylase Homo sapiens 107-111 18064905-6 2007 In this case, L-tyrosine is transformed to L-DOPA in TH containing neurons that is followed by L-DOPA release and uptake from the intercellular space to AADC containing neurons for DA synthesis. Levodopa 43-49 tyrosine hydroxylase Homo sapiens 53-55 18064905-6 2007 In this case, L-tyrosine is transformed to L-DOPA in TH containing neurons that is followed by L-DOPA release and uptake from the intercellular space to AADC containing neurons for DA synthesis. Levodopa 43-49 dopa decarboxylase Homo sapiens 153-157 18064905-6 2007 In this case, L-tyrosine is transformed to L-DOPA in TH containing neurons that is followed by L-DOPA release and uptake from the intercellular space to AADC containing neurons for DA synthesis. Levodopa 95-101 tyrosine hydroxylase Homo sapiens 53-55 17692830-5 2007 AADC is most likely active in cells and axons that take up L-DOPA, where it decarboxylates the L-DOPA to dopamine. Levodopa 59-65 dopa decarboxylase Homo sapiens 0-4 17692830-5 2007 AADC is most likely active in cells and axons that take up L-DOPA, where it decarboxylates the L-DOPA to dopamine. Levodopa 95-101 dopa decarboxylase Homo sapiens 0-4 17510732-2 2007 Analyses of more than 100 recorded clinical items revealed several specifics: I) 50% of patients with probable MSA had asymmetry of symptoms at disease onset and tremor at rest was present in 25%; II) a positive response to levodopa was recorded in 51% of patients identified initially with severe autonomic failure and cerebellar ataxia; III) a positive family history was recorded in 11% (n = 23), two of these patients were identified with spinocerebellar ataxia type 3 (SCA3). Levodopa 224-232 ataxin 3 Homo sapiens 443-472 17932860-8 2007 Rim area, rim volume, and retinal nerve fiber layer were significantly greater in the group treated with levodopa while it was the thinnest in the group receiving dopamine agonists. Levodopa 105-113 regulating synaptic membrane exocytosis 1 Homo sapiens 0-3 17932860-8 2007 Rim area, rim volume, and retinal nerve fiber layer were significantly greater in the group treated with levodopa while it was the thinnest in the group receiving dopamine agonists. Levodopa 105-113 regulating synaptic membrane exocytosis 1 Homo sapiens 10-13 17510732-2 2007 Analyses of more than 100 recorded clinical items revealed several specifics: I) 50% of patients with probable MSA had asymmetry of symptoms at disease onset and tremor at rest was present in 25%; II) a positive response to levodopa was recorded in 51% of patients identified initially with severe autonomic failure and cerebellar ataxia; III) a positive family history was recorded in 11% (n = 23), two of these patients were identified with spinocerebellar ataxia type 3 (SCA3). Levodopa 224-232 ataxin 3 Homo sapiens 474-478 17630981-0 2007 Dopamine depletion and subsequent treatment with L-DOPA, but not the long-lived dopamine agonist pergolide, enhances activity of the Akt pathway in the rat striatum. Levodopa 49-55 AKT serine/threonine kinase 1 Rattus norvegicus 133-136 17492760-0 2007 New founder germline mutations of CDKN2A in melanoma-prone families and multiple primary melanoma development in a patient receiving levodopa treatment. Levodopa 133-141 cyclin dependent kinase inhibitor 2A Homo sapiens 34-40 17492760-7 2007 Furthermore, we observed that a carrier of the founder CDKN2A [p.Leu113Leu;p.Pro114Ser] mutation as well as two MC1R moderate-risk variants, [p.Arg151Cys(+)p.Arg163Gln] developed 22 primary melanomas in the three years that followed initiation of levodopa therapy for Parkinson"s disease. Levodopa 247-255 melanocortin 1 receptor Homo sapiens 112-116 17702778-6 2007 Clinically, all 16 patients carrying a GBA mutation presented with a typical parkinsonian phenotype and experienced a good or excellent response to levodopa. Levodopa 148-156 glucosylceramidase beta Homo sapiens 39-42 18033638-2 2007 The aims of the study were: 1) to determine the genotype of NAT2 in patients with sporadic PD with dementia and in patients with sporadic AD; 2) to evaluate the relationship between the genotype of NAT2 and the age at the onset of the disease, the extent of dementia, and the dose and side effects of L-dopa (in PD patients only); 3) to evaluate the predispositions to PD and AD. Levodopa 301-307 N-acetyltransferase 2 Homo sapiens 198-202 17630981-6 2007 Pergolide was as effective as l-DOPA in reversing the lesion-induced elevation of ERK2 phosphorylation in response to acute apomorphine administration (0.05 mg/kg, s.c.). Levodopa 30-36 mitogen activated protein kinase 1 Rattus norvegicus 82-86 17630981-7 2007 Chronic l-DOPA significantly elevated the level of Akt phosphorylation at both Thr(308) and Ser(473) and concentration of phosphorylated GSK3alpha, whereas pergolide suppressed the lesion- and/or challenge-induced supersensitive Akt responses. Levodopa 8-14 AKT serine/threonine kinase 1 Rattus norvegicus 51-54 17630981-7 2007 Chronic l-DOPA significantly elevated the level of Akt phosphorylation at both Thr(308) and Ser(473) and concentration of phosphorylated GSK3alpha, whereas pergolide suppressed the lesion- and/or challenge-induced supersensitive Akt responses. Levodopa 8-14 glycogen synthase kinase 3 alpha Rattus norvegicus 137-146 17630981-7 2007 Chronic l-DOPA significantly elevated the level of Akt phosphorylation at both Thr(308) and Ser(473) and concentration of phosphorylated GSK3alpha, whereas pergolide suppressed the lesion- and/or challenge-induced supersensitive Akt responses. Levodopa 8-14 AKT serine/threonine kinase 1 Rattus norvegicus 229-232 17630981-8 2007 The data indicate that l-DOPA, unlike pergolide, exacerbates imbalances in the Akt pathway caused by the loss of DA. Levodopa 23-29 AKT serine/threonine kinase 1 Rattus norvegicus 79-82 17630981-9 2007 The results support the hypothesis that the Akt pathway is involved in long-term actions of l-DOPA and may be linked to l-DOPA-induced dyskinesia. Levodopa 92-98 AKT serine/threonine kinase 1 Rattus norvegicus 44-47 17630981-9 2007 The results support the hypothesis that the Akt pathway is involved in long-term actions of l-DOPA and may be linked to l-DOPA-induced dyskinesia. Levodopa 120-126 AKT serine/threonine kinase 1 Rattus norvegicus 44-47 17588764-0 2007 In vivo evidence of D3 dopamine receptor sensitization in parkinsonian primates and rodents with l-DOPA-induced dyskinesias. Levodopa 97-103 dopamine receptor D3 Homo sapiens 20-40 17553556-0 2007 The partial 5-HT(1A) agonist buspirone reduces the expression and development of l-DOPA-induced dyskinesia in rats and improves l-DOPA efficacy. Levodopa 81-87 5-hydroxytryptamine receptor 1A Rattus norvegicus 12-19 17553556-0 2007 The partial 5-HT(1A) agonist buspirone reduces the expression and development of l-DOPA-induced dyskinesia in rats and improves l-DOPA efficacy. Levodopa 128-134 5-hydroxytryptamine receptor 1A Rattus norvegicus 12-19 17553556-9 2007 In l-DOPA-primed rats, buspirone dose-dependently reduced LID and improved l-DOPA-related motor performance due to action at the 5-HT(1A) receptor. Levodopa 75-81 5-hydroxytryptamine receptor 1A Rattus norvegicus 129-136 17553556-9 2007 In l-DOPA-primed rats, buspirone dose-dependently reduced LID and improved l-DOPA-related motor performance due to action at the 5-HT(1A) receptor. Levodopa 3-9 5-hydroxytryptamine receptor 1A Rattus norvegicus 129-136 17553470-11 2007 The present findings indicate that 5-HT(1A)R stimulation reduces AIMs induced by D1R, D2R and l-DOPA administration while its effects on DA agonist-induced rotations were receptor-dependent, suggesting that direct 5-HT(1A)R and DA receptor interactions may contribute to the unique profile of 5-HT(1A)R agonists for the improvement of PD treatment. Levodopa 94-100 5-hydroxytryptamine receptor 1A Homo sapiens 35-42 17476684-2 2007 Those studies demonstrated the ability of adenosine A(2A) receptor antagonists to potentiate l-dopa-mediated motor improvement, whereas very little is known about counteraction of specific motor deficits and on the effects of these compounds when administered alone. Levodopa 93-99 adenosine A2a receptor Rattus norvegicus 42-66 17652604-6 2007 Thus, VMAT2 LO animals display nigrostriatal degeneration that begins in the terminal fields and progresses to eventual loss of the cell bodies, alpha-synuclein accumulation, and an L-DOPA responsive behavioral deficit, replicating many of the key aspects of Parkinson"s disease. Levodopa 182-188 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 6-11 17534955-2 2007 In the CALM-PD trial, subjects were initially randomized to levodopa or pramipexole and could later add levodopa if needed. Levodopa 60-68 synaptosome associated protein 91 Homo sapiens 7-11 17534955-2 2007 In the CALM-PD trial, subjects were initially randomized to levodopa or pramipexole and could later add levodopa if needed. Levodopa 104-112 synaptosome associated protein 91 Homo sapiens 7-11 17452372-3 2007 Removal of the serotonin afferents, or dampening of serotonin neuron activity by 5-HT1A and 5-HT1B agonist drugs, resulted in a near-complete block of the L-DOPA-induced dyskinesias, suggesting that dysregulated dopamine release from serotonin terminals is the prime trigger of dyskinesia in the rat Parkinson"s disease model. Levodopa 155-161 5-hydroxytryptamine receptor 1A Rattus norvegicus 81-87 17590511-0 2007 Endurance exercise modulates levodopa induced growth hormone release in patients with Parkinson"s disease. Levodopa 29-37 growth hormone 1 Homo sapiens 46-60 17590511-1 2007 Acute levodopa (LD) application and exercise release human growth hormone (GH). Levodopa 6-14 growth hormone 1 Homo sapiens 59-73 17590511-1 2007 Acute levodopa (LD) application and exercise release human growth hormone (GH). Levodopa 16-18 growth hormone 1 Homo sapiens 59-73 17614947-1 2007 The level of leucine-rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription-polymerase chain reaction in anterior striatum from normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated common marmosets (Callithrix jacchus) that had L-3,4-dihydroxyphenylalanine methyl ester (L-DOPA)-induced dyskinesia. Levodopa 317-323 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 13-41 18256746-5 2007 L-Dopa changed specific activity of enzymes: tyrosine hydroxylase activity in the sensorimotor cortex decreased by 25%, while monoamine oxidase B activity in the caudate nucleus increased by 33%. Levodopa 0-6 monoamine oxidase B Rattus norvegicus 126-145 17614947-1 2007 The level of leucine-rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription-polymerase chain reaction in anterior striatum from normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated common marmosets (Callithrix jacchus) that had L-3,4-dihydroxyphenylalanine methyl ester (L-DOPA)-induced dyskinesia. Levodopa 317-323 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 43-48 17614947-2 2007 The level of striatal Lrrk2 mRNA was increased in MPTP-treated common marmosets that had L-DOPA-induced dyskinesia compared with normal animals that did not receive l-DOPA. Levodopa 89-95 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 22-27 17614947-2 2007 The level of striatal Lrrk2 mRNA was increased in MPTP-treated common marmosets that had L-DOPA-induced dyskinesia compared with normal animals that did not receive l-DOPA. Levodopa 165-171 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 22-27 17614947-7 2007 The correlation between striatal Lrrk2 mRNA levels in MPTP-treated common marmoset striatum and L-DOPA-induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause L-DOPA-induced dyskinesia. Levodopa 96-102 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 33-38 17614947-7 2007 The correlation between striatal Lrrk2 mRNA levels in MPTP-treated common marmoset striatum and L-DOPA-induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause L-DOPA-induced dyskinesia. Levodopa 96-102 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 137-142 17614947-7 2007 The correlation between striatal Lrrk2 mRNA levels in MPTP-treated common marmoset striatum and L-DOPA-induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause L-DOPA-induced dyskinesia. Levodopa 199-205 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 33-38 17614947-7 2007 The correlation between striatal Lrrk2 mRNA levels in MPTP-treated common marmoset striatum and L-DOPA-induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause L-DOPA-induced dyskinesia. Levodopa 199-205 leucine-rich repeat serine/threonine-protein kinase 2 Callithrix jacchus 137-142 18040154-6 2007 As for the initial step of clinical application, AAV vector-mediated AADC (aromatic L-amino acid decarboxylase; the enzyme converting L-DOPA to DA) gene transfer in combination with oral administration of L-DOPA would be appropriate, since DA production can be regulated by adjusting the dose of L-DOPA. Levodopa 134-140 dopa decarboxylase Homo sapiens 69-73 17596448-0 2007 Critical involvement of cAMP/DARPP-32 and extracellular signal-regulated protein kinase signaling in L-DOPA-induced dyskinesia. Levodopa 101-107 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 29-37 17286588-4 2007 The striatal TH-positive neurons increase markedly in number in animal models of Parkinson"s disease (PD), where striatal DA concentrations are low, but this increase is abolished by L-dopa treatment. Levodopa 183-189 tyrosine hydroxylase Homo sapiens 13-15 17596448-7 2007 Thus, pharmacological inactivation of ERK1/2 achieved using SL327 (alpha-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile), an inhibitor of the mitogen-activated kinase/ERK kinase, MEK, during chronic L-DOPA treatment counteracts the induction dyskinesia. Levodopa 229-235 mitogen-activated protein kinase 3 Mus musculus 38-44 17596448-7 2007 Thus, pharmacological inactivation of ERK1/2 achieved using SL327 (alpha-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile), an inhibitor of the mitogen-activated kinase/ERK kinase, MEK, during chronic L-DOPA treatment counteracts the induction dyskinesia. Levodopa 229-235 mitogen-activated protein kinase 1 Mus musculus 38-41 17596448-8 2007 Together, these results indicate that a significant proportion of the abnormal involuntary movements developed in response to chronic L-DOPA are attributable to hyperactivation in striatal medium spiny neurons of a signaling pathway including sequential phosphorylation of DARPP-32, ERK1/2, MSK-1, and histone H3. Levodopa 134-140 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 273-281 17596448-8 2007 Together, these results indicate that a significant proportion of the abnormal involuntary movements developed in response to chronic L-DOPA are attributable to hyperactivation in striatal medium spiny neurons of a signaling pathway including sequential phosphorylation of DARPP-32, ERK1/2, MSK-1, and histone H3. Levodopa 134-140 mitogen-activated protein kinase 3 Mus musculus 283-289 17596448-8 2007 Together, these results indicate that a significant proportion of the abnormal involuntary movements developed in response to chronic L-DOPA are attributable to hyperactivation in striatal medium spiny neurons of a signaling pathway including sequential phosphorylation of DARPP-32, ERK1/2, MSK-1, and histone H3. Levodopa 134-140 ribosomal protein S6 kinase, polypeptide 5 Mus musculus 291-296 17596451-6 2007 The application of L-3,4-dihydroxyphenylalanine (L-DOPA) increased the IPSC in Lep(ob/ob) mice significantly more than in wild-type animals and fully restored the responses to both forskolin and cocaine. Levodopa 19-47 leptin Mus musculus 79-82 17596451-6 2007 The application of L-3,4-dihydroxyphenylalanine (L-DOPA) increased the IPSC in Lep(ob/ob) mice significantly more than in wild-type animals and fully restored the responses to both forskolin and cocaine. Levodopa 49-55 leptin Mus musculus 79-82 17440947-1 2007 Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa-responsive Parkinson"s disease (PD) in familial cases, several of which were ethnic Chinese. Levodopa 137-145 ataxin 2 Homo sapiens 91-95 17440947-1 2007 Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa-responsive Parkinson"s disease (PD) in familial cases, several of which were ethnic Chinese. Levodopa 137-145 ataxin 3 Homo sapiens 100-104 18040154-6 2007 As for the initial step of clinical application, AAV vector-mediated AADC (aromatic L-amino acid decarboxylase; the enzyme converting L-DOPA to DA) gene transfer in combination with oral administration of L-DOPA would be appropriate, since DA production can be regulated by adjusting the dose of L-DOPA. Levodopa 134-140 dopa decarboxylase Homo sapiens 75-110 17443692-4 2007 Levodopa response significantly decreased postoperatively by 31.1% at 3 years and 32.3% at 5 years, possibly related to the reduction in medication requirement, direct STN stimulation effect or PD progression. Levodopa 0-8 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 168-171 17427936-6 2007 The aim of the present study was to analyze whether high dose levodopa delivery in the transgenic MSA model is associated with neurotoxicity exacerbated by the presence of oligodendroglial alpha-synuclein inclusion pathology. Levodopa 62-70 synuclein, alpha Mus musculus 189-204 17427941-5 2007 Clinically, patients with LRRK2 mutations had typical levodopa responsive Parkinsonism with tremor being the commonest presenting feature. Levodopa 54-62 leucine rich repeat kinase 2 Homo sapiens 26-31 17264310-10 2007 Differences in urinary dopamine and tubular uptake of L-DOPA between WKY and SHR during HS intake, namely in 12-wk-old animals, may result from increases in the ASCT2 and B(0)AT1 mRNA levels and less pronounced decreases in LAT2 expression. Levodopa 54-60 solute carrier family 1 member 5 Rattus norvegicus 161-166 17264310-10 2007 Differences in urinary dopamine and tubular uptake of L-DOPA between WKY and SHR during HS intake, namely in 12-wk-old animals, may result from increases in the ASCT2 and B(0)AT1 mRNA levels and less pronounced decreases in LAT2 expression. Levodopa 54-60 solute carrier family 6 member 19 Rattus norvegicus 171-178 17264310-10 2007 Differences in urinary dopamine and tubular uptake of L-DOPA between WKY and SHR during HS intake, namely in 12-wk-old animals, may result from increases in the ASCT2 and B(0)AT1 mRNA levels and less pronounced decreases in LAT2 expression. Levodopa 54-60 linker for activation of T cells family, member 2 Rattus norvegicus 224-228 17241115-8 2007 Interestingly, Hsp70 induction, iNOS up-regulation and nitrotyrosine formation have been confirmed also in SN and striatum of rats treated with LD and carbidopa, this latter being an inhibitor of the peripheral DOPA decarboxylase. Levodopa 144-146 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 15-20 17335811-0 2007 The selective kappa-opioid receptor agonist U50,488 reduces L-dopa-induced dyskinesias but worsens parkinsonism in MPTP-treated primates. Levodopa 60-66 opioid receptor kappa 1 Homo sapiens 14-35 17241115-5 2007 In the present study, LD administration to rats resulted in a significant dose-dependent increase in Hsp70 synthesis which was specific for the SN. Levodopa 22-24 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 101-106 17241115-8 2007 Interestingly, Hsp70 induction, iNOS up-regulation and nitrotyrosine formation have been confirmed also in SN and striatum of rats treated with LD and carbidopa, this latter being an inhibitor of the peripheral DOPA decarboxylase. Levodopa 144-146 nitric oxide synthase 2 Rattus norvegicus 32-36 17241115-8 2007 Interestingly, Hsp70 induction, iNOS up-regulation and nitrotyrosine formation have been confirmed also in SN and striatum of rats treated with LD and carbidopa, this latter being an inhibitor of the peripheral DOPA decarboxylase. Levodopa 144-146 dopa decarboxylase Rattus norvegicus 211-229 17359492-2 2007 In this study, we addressed the role of mGluR5 in l-DOPA-induced dyskinesia, a movement disorder that is due to abnormal activation of both dopamine and glutamate receptors in the basal ganglia. Levodopa 50-56 glutamate receptor, ionotropic, kainate 1 Mus musculus 40-46 17350277-2 2007 While we recently demonstrated that levodopa-induced dyskinesia results from increased dopamine D(1) receptor-mediated transmission, we also questioned the possible role of subcellular localization of D(1) and D(2) receptors in mediating these effects as we previously showed that D(1) receptors undergo differential trafficking in striatal neurons of non-dyskinetic PD patients. Levodopa 36-44 dopamine receptor D1 Homo sapiens 87-109 17379358-0 2007 The effect of subchronic, intermittent L-DOPA treatment on neuronal nitric oxide synthase and soluble guanylyl cyclase expression and activity in the striatum and midbrain of normal and MPTP-treated mice. Levodopa 39-45 nitric oxide synthase 1, neuronal Mus musculus 59-89 17379358-1 2007 We have investigated the effects of low (10 mg/kg) and high (100 mg/kg) doses of L-DOPA on the expression and activity of neuronal nitric oxide synthase (nNOS) and guanylyl cyclase (GC) in the striatum and midbrain of mice. Levodopa 81-87 nitric oxide synthase 1, neuronal Mus musculus 122-152 17379358-1 2007 We have investigated the effects of low (10 mg/kg) and high (100 mg/kg) doses of L-DOPA on the expression and activity of neuronal nitric oxide synthase (nNOS) and guanylyl cyclase (GC) in the striatum and midbrain of mice. Levodopa 81-87 nitric oxide synthase 1, neuronal Mus musculus 154-158 17379358-7 2007 In normal mice, L-DOPA upregulates the expression and activity of nNOS and GC to levels found in MPTP-injected mice. Levodopa 16-22 nitric oxide synthase 1, neuronal Mus musculus 66-70 17379358-8 2007 Due to upregulation of nNOS and GC, cGMP levels in the mouse striatum and midbrain are also elevated, however, significantly lower in mice administrated with low dose of L-DOPA. Levodopa 170-176 nitric oxide synthase 1, neuronal Mus musculus 23-27 17379358-10 2007 The enhancement of nNOS mRNA and GCbeta1 mRNA levels were generated by both doses of L-DOPA, given in a time-dependent fashion. Levodopa 85-91 nitric oxide synthase 1, neuronal Mus musculus 19-23 17379358-10 2007 The enhancement of nNOS mRNA and GCbeta1 mRNA levels were generated by both doses of L-DOPA, given in a time-dependent fashion. Levodopa 85-91 guanylate cyclase 1, soluble, beta 1 Mus musculus 33-40 17303072-2 2007 It also has been suggested that D-DOPA, the stereoisomer of L-DOPA, is oxidized by DAO and then converted to dopamine via an alternative biosynthetic pathway. Levodopa 60-66 D-amino acid oxidase Homo sapiens 83-86 16950226-0 2007 Enhanced preproenkephalin-B-derived opioid transmission in striatum and subthalamic nucleus converges upon globus pallidus internalis in L-3,4-dihydroxyphenylalanine-induced dyskinesia. Levodopa 137-165 prodynorphin Homo sapiens 9-27 16950226-6 2007 CONCLUSIONS: Abnormal transmission of preproenkephalin-B-derived opioid coming from the striatum and the subthalamic nucleus converges upon GPi at the peak of dose to induce levodopa-induced dyskinesia. Levodopa 174-182 prodynorphin Homo sapiens 38-56 17447529-4 2007 One trial involves gene transfer of aromatic L-amino acid decarboxylase (AADC), an enzyme that converts L-dopa to dopamine, to restore therapeutic windows of orally administered L-dopa in advanced idiopathic PD. Levodopa 104-110 dopa decarboxylase Homo sapiens 36-71 17447529-4 2007 One trial involves gene transfer of aromatic L-amino acid decarboxylase (AADC), an enzyme that converts L-dopa to dopamine, to restore therapeutic windows of orally administered L-dopa in advanced idiopathic PD. Levodopa 104-110 dopa decarboxylase Homo sapiens 73-77 17447529-4 2007 One trial involves gene transfer of aromatic L-amino acid decarboxylase (AADC), an enzyme that converts L-dopa to dopamine, to restore therapeutic windows of orally administered L-dopa in advanced idiopathic PD. Levodopa 178-184 dopa decarboxylase Homo sapiens 36-71 17447529-4 2007 One trial involves gene transfer of aromatic L-amino acid decarboxylase (AADC), an enzyme that converts L-dopa to dopamine, to restore therapeutic windows of orally administered L-dopa in advanced idiopathic PD. Levodopa 178-184 dopa decarboxylase Homo sapiens 73-77 17447529-5 2007 After AADC transduction, the daily required dose of L-dopa can be reduced and the duration of the ON period is prolonged. Levodopa 52-58 dopa decarboxylase Homo sapiens 6-10 17388990-6 2007 All patients carrying the LRRK2 G2019S exhibited typical levodopa-responsive parkinsonism, and severe levodopa-induced dyskinesia was observed in the patient carrying the LRRK2 and parkin mutations. Levodopa 57-65 leucine rich repeat kinase 2 Homo sapiens 26-31 17388990-6 2007 All patients carrying the LRRK2 G2019S exhibited typical levodopa-responsive parkinsonism, and severe levodopa-induced dyskinesia was observed in the patient carrying the LRRK2 and parkin mutations. Levodopa 102-110 leucine rich repeat kinase 2 Homo sapiens 171-176 17495756-6 2007 In addition, preclinical studies suggest that adjunctive use of the catechol-O-methyltransferase (COMT) inhibitor entacapone when levodopa is first introduced may be associated with fewer motor complications than treatment with levodopa alone. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 68-96 17495756-6 2007 In addition, preclinical studies suggest that adjunctive use of the catechol-O-methyltransferase (COMT) inhibitor entacapone when levodopa is first introduced may be associated with fewer motor complications than treatment with levodopa alone. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 98-102 17495756-6 2007 In addition, preclinical studies suggest that adjunctive use of the catechol-O-methyltransferase (COMT) inhibitor entacapone when levodopa is first introduced may be associated with fewer motor complications than treatment with levodopa alone. Levodopa 228-236 catechol-O-methyltransferase Homo sapiens 68-96 17495756-7 2007 CONCLUSION: Treatment of early PD with an MAO-B inhibitor, dopamine agonist, or amantadine, may provide useful alternatives to treatment with levodopa. Levodopa 142-150 monoamine oxidase B Homo sapiens 42-47 17292477-6 2007 In the embryonic avian retina, before the tissue is capable of synthesizing its own dopamine via TH, dopamine synthesis is observed from L-DOPA supplied to the neuroretina from retina pigmented epithelium which results in dopaminergic communication in the embryonic tissue before TH expression. Levodopa 137-143 tyrosine hydroxylase Homo sapiens 280-282 17430130-7 2007 The DOPA delivery strategy, based on the co-transduction of tyrosine hydroxylase (TH), and GTP cyclohydrolase 1 (GCH1) genes, has been shown to be a powerful approach providing a robust behavioral recovery and reversal of side effects of the pulsatile administration of L-DOPA medication. Levodopa 270-276 tyrosine hydroxylase Homo sapiens 60-80 17430130-7 2007 The DOPA delivery strategy, based on the co-transduction of tyrosine hydroxylase (TH), and GTP cyclohydrolase 1 (GCH1) genes, has been shown to be a powerful approach providing a robust behavioral recovery and reversal of side effects of the pulsatile administration of L-DOPA medication. Levodopa 270-276 tyrosine hydroxylase Homo sapiens 82-84 17430130-7 2007 The DOPA delivery strategy, based on the co-transduction of tyrosine hydroxylase (TH), and GTP cyclohydrolase 1 (GCH1) genes, has been shown to be a powerful approach providing a robust behavioral recovery and reversal of side effects of the pulsatile administration of L-DOPA medication. Levodopa 270-276 GTP cyclohydrolase 1 Homo sapiens 113-117 17430130-9 2007 Finally, transduction of AADC alone has been proposed as a means to improve the conversion of peripherally administered L-DOPA. Levodopa 120-126 dopa decarboxylase Homo sapiens 25-29 17359492-8 2007 These data demonstrate that mGluR5 antagonism produces strong anti-dyskinetic effects in an animal model of Parkinson"s disease through central inhibition of the molecular and neurochemical underpinnings of l-DOPA-induced dyskinesia. Levodopa 207-213 glutamate receptor, ionotropic, kainate 1 Mus musculus 28-34 17578016-5 2007 AADC is enzymatically active in all studied monoenzymatic neurons converting extracellular L-dihydroxyphenylalanine (L-DOPA) or 5-hydroxytryptophan captured from the extracellular space, to DA or serotonin, respectively. Levodopa 91-115 dopa decarboxylase Homo sapiens 0-4 17240182-4 2007 METHODS: We describe assays for plasma AADC enzyme activity using both of its substrates, 5-hydroxytryptophan (5-HTP) and 3,4-dihydroxyphenylalanine (L-dopa). Levodopa 150-156 dopa decarboxylase Homo sapiens 39-43 17240182-6 2007 RESULTS: AADC enzyme activity in control plasma on average is a factor 8-12 higher with L-dopa as substrate than with 5-HTP. Levodopa 88-94 dopa decarboxylase Homo sapiens 9-13 17240182-8 2007 In AADC deficient patients, the enzyme activity towards both substrates, L-dopa and 5-HTP, are equally decreased, as are the CSF concentrations of HVA, 5-HIAA and MHPG, whereas heterozygotes have intermediate AADC activity levels. Levodopa 73-79 dopa decarboxylase Homo sapiens 3-7 17240182-10 2007 Since AADC enzyme activity is much higher with L-dopa as a substrate, this method is to be preferred over activity measurement with 5-HTP as a substrate for diagnostic purposes. Levodopa 47-53 dopa decarboxylase Homo sapiens 6-10 17578016-5 2007 AADC is enzymatically active in all studied monoenzymatic neurons converting extracellular L-dihydroxyphenylalanine (L-DOPA) or 5-hydroxytryptophan captured from the extracellular space, to DA or serotonin, respectively. Levodopa 117-123 dopa decarboxylase Homo sapiens 0-4 17451064-2 2007 The rate-limiting step of DA biosynthesis is catalyzed by the phosphorylated, therefore activated, tyrosine hydroxylase (TH) that produces L-3,4-dihydroxy-phenylalanine from tyrosine. Levodopa 139-168 tyrosine hydroxylase Rattus norvegicus 99-119 17451064-2 2007 The rate-limiting step of DA biosynthesis is catalyzed by the phosphorylated, therefore activated, tyrosine hydroxylase (TH) that produces L-3,4-dihydroxy-phenylalanine from tyrosine. Levodopa 139-168 tyrosine hydroxylase Rattus norvegicus 121-123 17218060-0 2007 Unilateral 6-hydroxydopamine lesion of dopamine neurons and subchronic L-DOPA administration in the adult rat alters the expression of the vesicular GABA transporter in different subsets of striatal neurons and in the substantia nigra, pars reticulata. Levodopa 71-77 solute carrier family 6 member 12 Rattus norvegicus 139-165 17218060-8 2007 On the other hand, the subchronic systemic administration of L-DOPA increased vGAT mRNA levels in preproenkephalin-negative neurons on the side ipsilateral and, to a lesser extent, the side contralateral to the 6-hydroxydopamine lesion. Levodopa 61-67 solute carrier family 6 member 12 Rattus norvegicus 78-82 17218060-9 2007 Systemic L-DOPA also increased vGAT protein levels in the ipsi- and contralateral SNr. Levodopa 9-15 solute carrier family 6 member 12 Rattus norvegicus 31-35 17055656-0 2007 Expression pattern of JunD after acute or chronic L-DOPA treatment: comparison with deltaFosB. Levodopa 50-56 JunD proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 22-26 17454565-5 2007 humilis (leaves and stems), Broussonetia papyrifera (leaves and bark), Cornus officinalis (fruit), Rhus javanica (gallnut), and Pinus densiflora (leaves) inhibited both tyrosinase activity and L-DOPA oxidation in a concentration-dependent manner. Levodopa 193-199 tyrosinase Mus musculus 169-179 17287504-0 2007 The nociceptin/orphanin FQ receptor antagonist J-113397 and L-DOPA additively attenuate experimental parkinsonism through overinhibition of the nigrothalamic pathway. Levodopa 60-66 prepronociceptin Rattus norvegicus 4-14 17287504-0 2007 The nociceptin/orphanin FQ receptor antagonist J-113397 and L-DOPA additively attenuate experimental parkinsonism through overinhibition of the nigrothalamic pathway. Levodopa 60-66 opioid related nociceptin receptor 1 Rattus norvegicus 15-35 17195115-7 2007 In general, the length, fresh weight, and dry weight of the roots decreased, whereas PAL and POD activities and phenolic compound and lignin content increased after L-DOPA treatments. Levodopa 165-171 peroxidase Glycine max 93-96 16932993-7 2007 The synergistic effects of co-administration of clinidine (1 mg/kg) with a subthreshold dose of L-Dopa (5 mg/kg) in elevating the motor activity of MPTP mice were reduced markedly by postnatal iron administration, as well as by pretreatment with DSP4. Levodopa 96-102 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 148-152 17259019-6 2007 We found here that repeated administration of levodopa, added with the peripheral DOPA decarboxylase inhibitor carbidopa, increased dopamine turnover rate after lesioning the striatum with 6-hydroxydopamine. Levodopa 46-54 dopa decarboxylase Rattus norvegicus 82-100 17260336-1 2007 Autosomal-recessive early-onset Parkinsonism (AREP) due to PINK1 mutations is characterized by an early-onset, slowly progressive disease, with a good response to levodopa. Levodopa 163-171 PTEN induced kinase 1 Homo sapiens 59-64 17530572-2 2007 The aims of the study were: 1) to determine the genotypes of CYP2D6 cytochrome (CYP2D6) in patients with AD and sporadic PD with dementia; 2) to evaluate the relationship between the CYP2D6 genotype and the age of onset of the disease, the extent of dementia in AD and PD, the dose and side effects of L-dopa in PD; 3) to evaluate the usefulness of CYP2D6 genotyping in predicting predispositions to PD and AD. Levodopa 302-308 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 61-67 17530572-2 2007 The aims of the study were: 1) to determine the genotypes of CYP2D6 cytochrome (CYP2D6) in patients with AD and sporadic PD with dementia; 2) to evaluate the relationship between the CYP2D6 genotype and the age of onset of the disease, the extent of dementia in AD and PD, the dose and side effects of L-dopa in PD; 3) to evaluate the usefulness of CYP2D6 genotyping in predicting predispositions to PD and AD. Levodopa 302-308 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 80-86 17530572-2 2007 The aims of the study were: 1) to determine the genotypes of CYP2D6 cytochrome (CYP2D6) in patients with AD and sporadic PD with dementia; 2) to evaluate the relationship between the CYP2D6 genotype and the age of onset of the disease, the extent of dementia in AD and PD, the dose and side effects of L-dopa in PD; 3) to evaluate the usefulness of CYP2D6 genotyping in predicting predispositions to PD and AD. Levodopa 302-308 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 80-86 17530572-2 2007 The aims of the study were: 1) to determine the genotypes of CYP2D6 cytochrome (CYP2D6) in patients with AD and sporadic PD with dementia; 2) to evaluate the relationship between the CYP2D6 genotype and the age of onset of the disease, the extent of dementia in AD and PD, the dose and side effects of L-dopa in PD; 3) to evaluate the usefulness of CYP2D6 genotyping in predicting predispositions to PD and AD. Levodopa 302-308 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 80-86 17329435-3 2007 L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. Levodopa 0-6 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 31-35 17329435-3 2007 L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. Levodopa 0-6 prodynorphin Rattus norvegicus 204-219 17329435-3 2007 L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. Levodopa 0-6 solute carrier family 1 member 2 Rattus norvegicus 259-263 17329435-6 2007 After 5 d of L-DOPA withdrawal, the only persisting drug-induced responses were an elevation in preprodynorphin mRNA levels and in the number of FosB/deltaFosB-immunoreactive neurons. Levodopa 13-19 prodynorphin Rattus norvegicus 96-111 17329435-6 2007 After 5 d of L-DOPA withdrawal, the only persisting drug-induced responses were an elevation in preprodynorphin mRNA levels and in the number of FosB/deltaFosB-immunoreactive neurons. Levodopa 13-19 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 145-149 16580727-2 2007 Cellular contents of DA were significantly increased in a time- and l-DOPA-concentration-dependent manner, suggesting the uptake of l-DOPA by MAEC and indicating the presence of aromatic l-amino acid decarboxylase (AADC). Levodopa 68-74 dopa decarboxylase Homo sapiens 215-219 17196621-4 2007 This study was designed to assess whether genetic polymorphism of the ACE could be a predictor of L-dopa-induced adverse effects in PD. Levodopa 98-104 angiotensin I converting enzyme Homo sapiens 70-73 17196621-7 2007 The frequency of the homozygote ACE-II genotype of the ACE in PD patients with L-dopa-induced psychosis was significantly higher than that in PD patients without the adverse effect (63.3% vs 43.0%; chi(2)=6.347, OR=1.435, 95%CI=1.105-1.864, p=0.012). Levodopa 79-85 angiotensin I converting enzyme Homo sapiens 32-35 17196621-7 2007 The frequency of the homozygote ACE-II genotype of the ACE in PD patients with L-dopa-induced psychosis was significantly higher than that in PD patients without the adverse effect (63.3% vs 43.0%; chi(2)=6.347, OR=1.435, 95%CI=1.105-1.864, p=0.012). Levodopa 79-85 angiotensin I converting enzyme Homo sapiens 55-58 17196621-9 2007 Furthermore, a logistic regression analysis confirmed that the ACE-II genotype was an independent risk factor for L-dopa-induced psychosis in PD patients (OR=2.542, p=0.012). Levodopa 114-120 angiotensin I converting enzyme Homo sapiens 63-66 17196621-10 2007 In conclusion, results of the study showed that ACE-II genotype might confer a primary predictor for the occurrence of psychosis in L-dopa-treated PD. Levodopa 132-138 angiotensin I converting enzyme Homo sapiens 48-51 17113046-0 2007 Cellular and behavioral effects of 5-HT1A receptor agonist 8-OH-DPAT in a rat model of levodopa-induced motor complications. Levodopa 87-95 5-hydroxytryptamine receptor 1A Rattus norvegicus 35-41 17113046-1 2007 5-HT1A autoreceptor stimulation can act to attenuate supraphysiological swings in extracellular dopamine levels following long-term levodopa treatment and may be useful in the treatment and prevention of the motor complications. Levodopa 132-140 5-hydroxytryptamine receptor 1A Rattus norvegicus 0-6 17113046-2 2007 The purpose of this study was to investigate cellular and behavioral effects of 5-HT1A receptor agonist 8-OH-DPAT in a rat model of levodopa-induced motor complications. Levodopa 132-140 5-hydroxytryptamine receptor 1A Rattus norvegicus 80-86 17113046-15 2007 Moreover, 8-OH-DPAT plus levodopa significantly reduced hyperphosphorylation of GluR1 at serine 845, which was closely associated with levodopa-induced motor complications. Levodopa 25-33 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 80-85 17113046-15 2007 Moreover, 8-OH-DPAT plus levodopa significantly reduced hyperphosphorylation of GluR1 at serine 845, which was closely associated with levodopa-induced motor complications. Levodopa 135-143 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 80-85 17055656-1 2007 In this study, we have used 6-hydroxydopamine-lesioned rats to examine changes in striatal junD and fosB/deltafosB expression induced by acute and chronic treatment with L-DOPA (5 and 15 days). Levodopa 170-176 JunD proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 91-95 17055656-1 2007 In this study, we have used 6-hydroxydopamine-lesioned rats to examine changes in striatal junD and fosB/deltafosB expression induced by acute and chronic treatment with L-DOPA (5 and 15 days). Levodopa 170-176 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 100-104 17055656-5 2007 By contrast, junD and deltafosB mRNA were both upregulated significantly above control levels after an acute injection of L-DOPA. Levodopa 122-128 JunD proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-17 17055656-6 2007 In conclusion, this study suggests a differential expression pattern of junD and deltafosB in a rat model of L-DOPA-induced dyskinesia. Levodopa 109-115 JunD proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 72-76 17924443-3 2007 It has also been suggested that 3,4-dihydroxy-D-phenylalanine (D-DOPA), the stereoisomer of 3,4-dihydroxy-L-phenylalanine (L-DOPA), is oxidized by DAO and converted to dopamine via an alternative biosynthetic pathway. Levodopa 92-121 D-amino acid oxidase Homo sapiens 147-150 17953080-9 2007 Drug treatment of the RLS comprises levodopa, dopaminergic drugs, opioids, and antiepileptic drugs; however, drug treatment is only necessary in about a third of the affected. Levodopa 36-44 RLS1 Homo sapiens 22-25 17027115-5 2007 Despite no signs of PD, neuro-imaging (DAT-Scan) showed an L-Dopa transducer decrease in putamens. Levodopa 59-65 solute carrier family 6 member 3 Homo sapiens 39-42 17503735-10 2007 L-DOPA treatment was associated with a significantly higher level of AADC and VMAT2 immunoreactivity in the caudate nucleus compared to placebo. Levodopa 0-6 dopa decarboxylase Homo sapiens 69-73 17503735-10 2007 L-DOPA treatment was associated with a significantly higher level of AADC and VMAT2 immunoreactivity in the caudate nucleus compared to placebo. Levodopa 0-6 solute carrier family 18 member A2 Homo sapiens 78-83 17924443-3 2007 It has also been suggested that 3,4-dihydroxy-D-phenylalanine (D-DOPA), the stereoisomer of 3,4-dihydroxy-L-phenylalanine (L-DOPA), is oxidized by DAO and converted to dopamine via an alternative biosynthetic pathway. Levodopa 123-129 D-amino acid oxidase Homo sapiens 147-150 24790350-8 2007 PRL response to TRH was normal and levodopa suppressed the increased basal PRL level. Levodopa 35-43 prolactin Homo sapiens 75-78 17963454-3 2007 The mechanism underlying L-Dopa-related HHcy is the O-methylation of the drug catalyzed by the enzyme catechol-O-methyltransferase (COMT). Levodopa 25-31 catechol-O-methyltransferase Homo sapiens 102-130 17963454-3 2007 The mechanism underlying L-Dopa-related HHcy is the O-methylation of the drug catalyzed by the enzyme catechol-O-methyltransferase (COMT). Levodopa 25-31 catechol-O-methyltransferase Homo sapiens 132-136 17963454-6 2007 This review summarizes data available in the literature concerning the two main therapeutic approaches to L-Dopa-related HHcy (use of COMT inhibitors or B vitamins diet supplementation). Levodopa 106-112 catechol-O-methyltransferase Homo sapiens 134-138 17702535-7 2007 Catechol-O-methyltransferase inhibitors may be used to augment levodopa in the setting of "wearing off" (i.e. motor fluctuations). Levodopa 63-71 catechol-O-methyltransferase Homo sapiens 0-28 17630819-10 2007 Selegiline ODT is also absorbed more efficiently and shows less pharmacokinetic variability than conventional oral selegiline.COMT mediates peripheral catabolism of levodopa. Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 126-130 17630819-11 2007 Therefore, agents that block COMT, such as tolcapone and entacapone, increase the elimination half-life of levodopa. Levodopa 107-115 catechol-O-methyltransferase Homo sapiens 29-33 17630819-12 2007 Given adjunctively with levodopa, COMT inhibitors can decrease "off" time and increase "on" time, as well as lower the daily levodopa dose. Levodopa 24-32 catechol-O-methyltransferase Homo sapiens 34-38 17630819-12 2007 Given adjunctively with levodopa, COMT inhibitors can decrease "off" time and increase "on" time, as well as lower the daily levodopa dose. Levodopa 125-133 catechol-O-methyltransferase Homo sapiens 34-38 17241287-9 2007 Levodopa reversed the lesion-induced increase in the expression of cytochrome oxidase mRNA in the subthalamic nucleus and glutamate decarboxylase mRNA in the pars reticulata of the substantia nigra. Levodopa 0-8 glutamate-ammonia ligase Rattus norvegicus 122-145 17241287-10 2007 After 7 days of levodopa washout, the molecular markers show a decline in the basal ganglia evolving towards the parkinsonian state, being statistically significant for the striatal PDyn mRNA. Levodopa 16-24 prodynorphin Rattus norvegicus 182-186 17241287-8 2007 After 3 days of washout, levodopa treatment maintained elevated striatal preproenkephalin mRNA expression, also inducing an increase in preprodynorphin (PDyn) and dopamine D-3 receptor mRNAs, but without any modification of the adenosine A(2A) mRNA expression induced by 6-OHDA. Levodopa 25-33 prodynorphin Rattus norvegicus 136-151 17241287-8 2007 After 3 days of washout, levodopa treatment maintained elevated striatal preproenkephalin mRNA expression, also inducing an increase in preprodynorphin (PDyn) and dopamine D-3 receptor mRNAs, but without any modification of the adenosine A(2A) mRNA expression induced by 6-OHDA. Levodopa 25-33 prodynorphin Rattus norvegicus 153-157 17027275-1 2007 We recently proposed the involvement of diffusible modulators in signalling astrocytes to increase glial cell line-derived neurotrophic factor (GDNF) expression after selective dopaminergic injury by H2O2 or L-DOPA. Levodopa 208-214 glial cell derived neurotrophic factor Homo sapiens 99-142 17241287-8 2007 After 3 days of washout, levodopa treatment maintained elevated striatal preproenkephalin mRNA expression, also inducing an increase in preprodynorphin (PDyn) and dopamine D-3 receptor mRNAs, but without any modification of the adenosine A(2A) mRNA expression induced by 6-OHDA. Levodopa 25-33 dopamine receptor D3 Rattus norvegicus 163-184 17417741-1 2007 Dopamine behaves mainly as a MAO-A substrate in rodent brain, but selective inhibition of MAO-B results in an increased turning activity following L-DOPA administration in hemi-Parkinsonian rodents. Levodopa 147-153 monoamine oxidase B Homo sapiens 90-95 17516455-2 2007 Extensive data are available for levodopa, pramipexole, and ropinirole, which have approval for the indication RLS, and to a smaller extent for cabergoline, pergolide, and rotigotine. Levodopa 33-41 RLS1 Homo sapiens 111-114 17566122-1 2007 The impressive relief from restless legs syndrome (RLS) symptoms provided by levodopa treatment indicates RLS is caused by a dopaminergic abnormality. Levodopa 77-85 RLS1 Homo sapiens 51-54 17566122-1 2007 The impressive relief from restless legs syndrome (RLS) symptoms provided by levodopa treatment indicates RLS is caused by a dopaminergic abnormality. Levodopa 77-85 RLS1 Homo sapiens 106-109 17417741-4 2007 MAO-B as well as MAO-A may contribute to deamination of dopamine produced from L-DOPA. Levodopa 79-85 monoamine oxidase B Homo sapiens 0-5 17417741-4 2007 MAO-B as well as MAO-A may contribute to deamination of dopamine produced from L-DOPA. Levodopa 79-85 monoamine oxidase A Homo sapiens 17-22 17263675-8 2007 All growth hormone (GH) parameters measured and calculated were significantly (p < 0.05) lower in TBI group than in controls after L-DOPA stimulation. Levodopa 134-140 growth hormone 1 Homo sapiens 4-18 17263675-8 2007 All growth hormone (GH) parameters measured and calculated were significantly (p < 0.05) lower in TBI group than in controls after L-DOPA stimulation. Levodopa 134-140 growth hormone 1 Homo sapiens 20-22 17027275-1 2007 We recently proposed the involvement of diffusible modulators in signalling astrocytes to increase glial cell line-derived neurotrophic factor (GDNF) expression after selective dopaminergic injury by H2O2 or L-DOPA. Levodopa 208-214 glial cell derived neurotrophic factor Homo sapiens 144-148 17192438-2 2006 Initial clinical trials of A2A antagonists targeted PD patients who had already developed treatment complications known as L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in an effort to improve symptoms while reducing existing LID. Levodopa 153-159 skull morphology 4 Mus musculus 123-126 17914182-0 2007 Effect of MTHFR polymorphisms on hyperhomocysteinemia in levodopa-treated Parkinsonian patients. Levodopa 57-65 methylenetetrahydrofolate reductase Homo sapiens 10-15 17914182-2 2007 In this study, we investigated the effects of C677T and A1298C MTHFR polymorphisms, in association with L-DOPA daily dose and vitamin status, on hyperhomocysteinemia development in PD patients. Levodopa 104-110 methylenetetrahydrofolate reductase Homo sapiens 63-68 17235434-5 2007 Augmentation, i.e., worsening of RLS symptoms not due to progression of the disease, however, represents a worrisome side effect of dopaminergic drugs, especially levodopa. Levodopa 163-171 RLS1 Homo sapiens 33-36 18379513-4 2007 The clinical picture of all patients with the LRRK2-G2019S mutation was typical for levodopa-responsive parkinsonism and age of disease onset varied widely (from 39 to 71 years). Levodopa 84-92 leucine rich repeat kinase 2 Homo sapiens 46-51 17131995-3 2006 The tyrosine units were reacted with tyrosinase/O2 to yield the respective l-DOPA and quinone derivatives. Levodopa 75-81 tyrosinase Homo sapiens 37-47 17186710-6 2006 After levodopa-related motor complications develop in advanced Parkinson"s disease, it is beneficial to initiate adjuvant therapy with dopamine agonists, catechol O-methyltransferase inhibitors, or monoamine oxidase-B inhibitors. Levodopa 6-14 monoamine oxidase B Homo sapiens 198-217 17055481-2 2006 The gradual induction of dopamine D(1) receptor supersensitivity is known as a priming phenomenon, and this process is thought to underlie not only the appearance of vacuous chewing movements in humans with tardive dyskinesia, but also the onset of motor dyskinesias in L-dihydroxyphenylalanine (L-DOPA)-treated Parkinson"s disease patients. Levodopa 270-294 dopamine receptor D1 Homo sapiens 25-47 17055481-2 2006 The gradual induction of dopamine D(1) receptor supersensitivity is known as a priming phenomenon, and this process is thought to underlie not only the appearance of vacuous chewing movements in humans with tardive dyskinesia, but also the onset of motor dyskinesias in L-dihydroxyphenylalanine (L-DOPA)-treated Parkinson"s disease patients. Levodopa 296-302 dopamine receptor D1 Homo sapiens 25-47 17156382-5 2006 These findings show that functional gender-related differences in the central nervous system involve the human subthalamic area (STN) and its response to levodopa in Parkinson"s disease. Levodopa 154-162 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 129-132 20408626-4 2006 Using a variety of surface analytical techniques, the authors show that a four-armed poly(ethylene glycol) polymer functionalized with a single DOPA residue at the terminus of each arm (PEG-(DOPA)(4)) adsorbed strongly to surface immobilized mucin. Levodopa 144-148 LOC100508689 Homo sapiens 242-247 20408626-4 2006 Using a variety of surface analytical techniques, the authors show that a four-armed poly(ethylene glycol) polymer functionalized with a single DOPA residue at the terminus of each arm (PEG-(DOPA)(4)) adsorbed strongly to surface immobilized mucin. Levodopa 191-195 LOC100508689 Homo sapiens 242-247 20408626-6 2006 This conclusion was confirmed with single molecule atomic force microscopy experiments that revealed a surprisingly strong interaction force of 371+/-93 pN between DOPA and adsorbed mucin. Levodopa 164-168 LOC100508689 Homo sapiens 182-187 20641732-15 2004 Like endogenous l-DOPA, [(18)F]FDOPA is converted by the enzyme aromatic l-amino acid decarboxylase (AAAD) to the dopamine analog fluorodopamine. Levodopa 16-22 dopa decarboxylase Homo sapiens 64-99 17105517-2 2006 The medications used most commonly to treat RLS include dopaminergic drugs (levodopa, dopamine agonists), benzodiazepines, and narcotic analgesics. Levodopa 76-84 RLS1 Homo sapiens 44-47 17094783-6 2006 On treatment with excess pyridoxal-5"-phosphate (PLP), the L-DOPA-inactivated enzymes recovered over 80% of their original activities, thereby attributing the inactivation to a loss of the cofactor through Pictet-Spengler condensation with L-DOPA. Levodopa 59-65 proteolipid protein 1 Homo sapiens 49-52 17094783-6 2006 On treatment with excess pyridoxal-5"-phosphate (PLP), the L-DOPA-inactivated enzymes recovered over 80% of their original activities, thereby attributing the inactivation to a loss of the cofactor through Pictet-Spengler condensation with L-DOPA. Levodopa 240-246 proteolipid protein 1 Homo sapiens 49-52 16919455-3 2006 A kinetic study revealed that 7 was a reversible and non-competitive inhibitor of mushroom tyrosinase with l-dopa as the substrate. Levodopa 107-113 tyrosinase Homo sapiens 91-101 16950829-9 2006 Identification of the enzymes as tyrosinases was confirmed by the ability of lichen thalli or leachates derived by shaking lichens in distilled water to metabolize substrates such as L-dihydroxyphenylalanine (DOPA), tyrosine and epinephrine readily in the absence of hydrogen peroxide, the sensitivity of the enzymes to the inhibitors cyanide, azide and hexylresorcinol, activation by SDS and having typical tyrosinase molecular masses of approx. Levodopa 183-207 tyrosinase Homo sapiens 33-43 16950829-9 2006 Identification of the enzymes as tyrosinases was confirmed by the ability of lichen thalli or leachates derived by shaking lichens in distilled water to metabolize substrates such as L-dihydroxyphenylalanine (DOPA), tyrosine and epinephrine readily in the absence of hydrogen peroxide, the sensitivity of the enzymes to the inhibitors cyanide, azide and hexylresorcinol, activation by SDS and having typical tyrosinase molecular masses of approx. Levodopa 209-213 tyrosinase Homo sapiens 33-43 16934409-6 2006 l-DOPA had a paradoxical effect and worsened the deficits in Thy1-aSyn mice compared with controls, whereas the high dose of apomorphine only produced few deficits above those already present in Thy1-aSyn. Levodopa 0-6 thymus cell antigen 1, theta Mus musculus 61-65 17016505-1 2006 BACKGROUND AND PURPOSE: Postural hypotension is a common side-effect of L-DOPA treatment of Parkinson"s disease, and may be potentiated when L-DOPA is combined with selegiline, a selective inhibitor of monoamine oxidase B (MAO-B). Levodopa 141-147 monoamine oxidase B Rattus norvegicus 223-228 17016505-1 2006 BACKGROUND AND PURPOSE: Postural hypotension is a common side-effect of L-DOPA treatment of Parkinson"s disease, and may be potentiated when L-DOPA is combined with selegiline, a selective inhibitor of monoamine oxidase B (MAO-B). Levodopa 141-147 monoamine oxidase B Rattus norvegicus 202-221 16814282-3 2006 Attenuation of levodopa-induced dyskinesia by normalizing dopamine D(3) receptor function. Levodopa 15-23 dopamine receptor D3 Rattus norvegicus 58-80 17042912-0 2006 D-dopa is unidirectionally converted to L-dopa by D-amino acid oxidase, followed by dopa transaminase. Levodopa 40-46 D-amino acid oxidase Mus musculus 50-70 17042912-9 2006 The role of DAAO in the chiral inversion of D-dopa to L-dopa was further investigated by using purified DAAO and mutant ddY/DAAO- mouse kidney lacking DAAO activity. Levodopa 54-60 D-amino acid oxidase Mus musculus 12-16 17042912-12 2006 Sodium benzoate, a selective inhibitor of DAAO, blocked L-dopa generation in a concentration-dependant manner. Levodopa 56-62 D-amino acid oxidase Mus musculus 42-46 17042912-16 2006 These results prove the proposal that d-dopa undergoes unidirectional chiral inversion and further suggest that D-dopa is first oxidatively deaminated by DAAO to its alpha-keto acid and then transaminated by dopa transaminase to L-dopa. Levodopa 229-235 D-amino acid oxidase Mus musculus 154-158 16814282-8 2006 Effect of the D(3) dopamine receptor partial agonist BP897 [N-[4-(4-(2-methoxyphenyl)piperazinyl)butyl]-2-naphthamide] on l-3,4-dihydroxyphenylalanine-induced dyskinesias and parkinsonism in squirrel monkeys. Levodopa 122-150 dopamine receptor D3 Rattus norvegicus 14-36 16765381-8 2006 L-dopa induced dyskinesias could be caused by changes in the balance of A2A/D2 heteromers vs A2A homomers expressed at the surface membrane, where A2A homomers dominate with abnormal increases in A2A signaling. Levodopa 0-6 immunoglobulin kappa variable 2D-29 Homo sapiens 72-78 17059382-2 2006 Tolcapone is a catechol-O-methyltransferase inhibitor that extends the action of levodopa. Levodopa 81-89 catechol-O-methyltransferase Homo sapiens 15-43 16841367-3 2006 Tyrosinase catalyses three different reactions in the biosynthetic pathway of melanin in melanocytes: the hydroxylation of tyrosine to l-DOPA and the oxidation of l-DOPA to dopaquinone; furthermore, in humans, dopaquinone is converted by a series of complex reactions to melanin. Levodopa 135-141 tyrosinase Homo sapiens 0-10 16841367-3 2006 Tyrosinase catalyses three different reactions in the biosynthetic pathway of melanin in melanocytes: the hydroxylation of tyrosine to l-DOPA and the oxidation of l-DOPA to dopaquinone; furthermore, in humans, dopaquinone is converted by a series of complex reactions to melanin. Levodopa 163-169 tyrosinase Homo sapiens 0-10 16981894-4 2006 TH, the rate-limiting enzyme in dopamine synthesis, converts tyrosine to l-dihydroxyphenylalanine (L-DOPA), which is then converted to dopamine by the enzyme, aromatic amino acid decarboxylase (AADC). Levodopa 73-97 dopa decarboxylase Mus musculus 194-198 16981894-4 2006 TH, the rate-limiting enzyme in dopamine synthesis, converts tyrosine to l-dihydroxyphenylalanine (L-DOPA), which is then converted to dopamine by the enzyme, aromatic amino acid decarboxylase (AADC). Levodopa 99-105 dopa decarboxylase Mus musculus 194-198 17053970-0 2006 Changes in subcellular distribution and phosphorylation of GluR1 in lesioned striatum of 6-hydroxydopamine-lesioned and l-dopa-treated rats. Levodopa 120-126 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 59-64 17053970-3 2006 To determine whether serine phosphorylation of GluR1 subunit by activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) contributes to the process, we examined the effects of unilateral nigrostriatal depletion with 6-hydroxydopamine and subsequent L: -dopa treatment on motor responses and phosphorylation states. Levodopa 261-269 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 47-52 17053970-6 2006 Chronic treatment of lesioned rats with L: -dopa markedly upregulated the phosphorylation of GluR1 in lesioned striatum with a concomitant normalization of the plasma membrane GluR1 abundance, which lasted at least 1 day after withdrawal of chronic L: -dopa treatment. Levodopa 40-48 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 93-98 17053970-6 2006 Chronic treatment of lesioned rats with L: -dopa markedly upregulated the phosphorylation of GluR1 in lesioned striatum with a concomitant normalization of the plasma membrane GluR1 abundance, which lasted at least 1 day after withdrawal of chronic L: -dopa treatment. Levodopa 40-48 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 176-181 17053970-6 2006 Chronic treatment of lesioned rats with L: -dopa markedly upregulated the phosphorylation of GluR1 in lesioned striatum with a concomitant normalization of the plasma membrane GluR1 abundance, which lasted at least 1 day after withdrawal of chronic L: -dopa treatment. Levodopa 249-257 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 93-98 17141847-1 2006 Previously we reported on L-DOPA"s antinociceptive effect on substance P-induced nociceptive behaviors in mice [Shimizu T, Iwata S, Morioka H, Masuyama T, Fukuda T, Nomoto M. Antinociceptive mechanism of L-DOPA. Levodopa 26-32 tachykinin 1 Mus musculus 61-72 16774768-9 2006 In conclusion, MTHFR C677T genotype is a significant factor for hyperhomocysteinemia in patients with PD, levodopa-untreated and probably even more in levodopa-treated PD patients. Levodopa 106-114 methylenetetrahydrofolate reductase Homo sapiens 15-20 16774768-9 2006 In conclusion, MTHFR C677T genotype is a significant factor for hyperhomocysteinemia in patients with PD, levodopa-untreated and probably even more in levodopa-treated PD patients. Levodopa 151-159 methylenetetrahydrofolate reductase Homo sapiens 15-20 17072193-0 2006 [CDKN2A gene mutation and loss of p16 protein activity in a patient on levodopa presenting sporadic multiple primary melanoma]. Levodopa 71-79 cyclin dependent kinase inhibitor 2A Homo sapiens 1-7 17072193-0 2006 [CDKN2A gene mutation and loss of p16 protein activity in a patient on levodopa presenting sporadic multiple primary melanoma]. Levodopa 71-79 cyclin dependent kinase inhibitor 2A Homo sapiens 34-37 16930379-2 2006 l-dopa has been shown to reduce RLS symptoms, but subsequent augmentation of symptoms occurs in up to 73% of patients during continued treatment. Levodopa 0-6 RLS1 Homo sapiens 32-35 16781894-8 2006 We conclude that little behavioral improvement can be seen until AADC activity reaches a level that is no longer rate limiting for conversion of clinical doses of L-Dopa into dopamine or for trapping of the PET tracer FMT. Levodopa 163-169 dopa decarboxylase Homo sapiens 65-69 16867213-1 2006 Antagonism of the A2A adenosine function has proved beneficial in the treatment of Parkinson"s disease, in that it increases L-dopa therapeutical effects without concomitant worsening of its side-effects. Levodopa 125-131 immunoglobulin kappa variable 2D-29 Homo sapiens 18-21 16604302-1 2006 Addition of the catechol-O-methyltransferase (COMT) inhibitor entacapone (EN) prolongs plasma metabolism of levodopa (LD). Levodopa 108-116 catechol-O-methyltransferase Homo sapiens 16-44 16604302-1 2006 Addition of the catechol-O-methyltransferase (COMT) inhibitor entacapone (EN) prolongs plasma metabolism of levodopa (LD). Levodopa 108-116 catechol-O-methyltransferase Homo sapiens 46-50 16788774-8 2006 RESULTS: HFS-STN resulted in significant improvement of motor function (62.8%) in off-medication state and levodopa-equivalent dose reduction of 68.7% (p < 0.05). Levodopa 107-115 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 13-16 16773618-4 2006 We studied the efficacy of LPP on postprandial off periods, in PD patients on levodopa therapy. Levodopa 78-86 LIM domain containing preferred translocation partner in lipoma Homo sapiens 27-30 17948614-8 2006 Catechol-O-methyltransferase (COMT)inhibitors extend the half-life of levodopa and result in significant reductions in off times in patients with motor fluctuations. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 0-28 16925991-0 2006 The novel adenosine A2a receptor antagonist ST1535 potentiates the effects of a threshold dose of L-DOPA in MPTP treated common marmosets. Levodopa 98-104 LOW QUALITY PROTEIN: adenosine receptor A2a Callithrix jacchus 10-32 16957086-4 2006 Likewise, catechol concentrations were higher in L-DOPA-treated PC12 cells overexpressing A30P or A53T compared with those expressing WT alpha-synuclein, although the ability of cells to maintain a low cytosolic dopamine level after L-DOPA challenge was markedly inhibited by either protein. Levodopa 49-55 synuclein alpha Rattus norvegicus 137-152 16829205-4 2006 AAV-hAADC restores the ability of the striatum to convert l-Dopa into dopamine efficiently. Levodopa 58-64 dopa decarboxylase Homo sapiens 4-9 16989543-7 2006 Catechol O-methyltransferase (COMT) inhibitors prolong the levodopa serum half-life and allow more levodopa to be delivered to the brain over a longer time, thereby smoothing dopaminergic stimulation. Levodopa 59-67 catechol-O-methyltransferase Homo sapiens 0-28 16989543-7 2006 Catechol O-methyltransferase (COMT) inhibitors prolong the levodopa serum half-life and allow more levodopa to be delivered to the brain over a longer time, thereby smoothing dopaminergic stimulation. Levodopa 59-67 catechol-O-methyltransferase Homo sapiens 30-34 16989543-7 2006 Catechol O-methyltransferase (COMT) inhibitors prolong the levodopa serum half-life and allow more levodopa to be delivered to the brain over a longer time, thereby smoothing dopaminergic stimulation. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 0-28 16989543-7 2006 Catechol O-methyltransferase (COMT) inhibitors prolong the levodopa serum half-life and allow more levodopa to be delivered to the brain over a longer time, thereby smoothing dopaminergic stimulation. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 30-34 17948613-7 2006 Catechol-O-methyltransferase (COMT)inhibitors, which increase dopamine levels by inhibiting the metabolism of levodopa and dopamine, recently have become available, including a tablet containing carbidopa, levodopa,and entacapone. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 0-28 17948613-7 2006 Catechol-O-methyltransferase (COMT)inhibitors, which increase dopamine levels by inhibiting the metabolism of levodopa and dopamine, recently have become available, including a tablet containing carbidopa, levodopa,and entacapone. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 30-34 17948613-7 2006 Catechol-O-methyltransferase (COMT)inhibitors, which increase dopamine levels by inhibiting the metabolism of levodopa and dopamine, recently have become available, including a tablet containing carbidopa, levodopa,and entacapone. Levodopa 206-214 catechol-O-methyltransferase Homo sapiens 0-28 17948614-8 2006 Catechol-O-methyltransferase (COMT)inhibitors extend the half-life of levodopa and result in significant reductions in off times in patients with motor fluctuations. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 30-34 17948613-7 2006 Catechol-O-methyltransferase (COMT)inhibitors, which increase dopamine levels by inhibiting the metabolism of levodopa and dopamine, recently have become available, including a tablet containing carbidopa, levodopa,and entacapone. Levodopa 206-214 catechol-O-methyltransferase Homo sapiens 30-34 16650784-10 2006 The rapid and favourable response on treatment with L-DOPA warrants the classification of SR deficiency as another autosomal recessive type of DOPA-responsive dystonia (DRD). Levodopa 52-58 sepiapterin reductase Homo sapiens 90-92 16766196-2 2006 H(2)O(2), mimicking increased oxidative stress, or l-DOPA, the main symptomatic treatment for Parkinson"s disease, increased GDNF mRNA and protein levels in a time-dependent mode in neuron-glia mixed cultures. Levodopa 51-57 glial cell derived neurotrophic factor Homo sapiens 125-129 16816791-7 2006 The mainstay of RLS therapy are dopamine agonists or levodopa. Levodopa 53-61 RLS1 Homo sapiens 16-19 16806299-11 2006 These data suggest that activation of the TRPV1 system can suppress spontaneous locomotion in normal animals and modulates several L-DOPA-induced behaviours in reserpine-treated rats. Levodopa 131-137 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 42-47 16687213-1 2006 Recent reports of SCA2 and SCA3 patients who presented with levodopa responsive parkinsonism have generated considerable interest as they have implications for genetic testing. Levodopa 60-68 ataxin 2 Homo sapiens 18-22 16687213-1 2006 Recent reports of SCA2 and SCA3 patients who presented with levodopa responsive parkinsonism have generated considerable interest as they have implications for genetic testing. Levodopa 60-68 ataxin 3 Homo sapiens 27-31 16930409-0 2006 Impaired behavioural and molecular adaptations to dopamine denervation and repeated L-DOPA treatment in Nur77-knockout mice. Levodopa 84-90 nuclear receptor subfamily 4, group A, member 1 Mus musculus 104-109 16930409-1 2006 We have previously shown that dopamine (DA) denervation and repeated L-DOPA treatment modulate the pattern of Nur77 mRNA expression in the striatum. Levodopa 69-75 nuclear receptor subfamily 4, group A, member 1 Mus musculus 110-115 16930409-5 2006 Despite similar extents of nigrostriatal denervation, L-DOPA-induced rotational response was exacerbated in Nur77-/- mice compared to Nur77+/+ ones. Levodopa 54-60 nuclear receptor subfamily 4, group A, member 1 Mus musculus 108-113 16930409-5 2006 Despite similar extents of nigrostriatal denervation, L-DOPA-induced rotational response was exacerbated in Nur77-/- mice compared to Nur77+/+ ones. Levodopa 54-60 nuclear receptor subfamily 4, group A, member 1 Mus musculus 134-139 16930409-10 2006 The present results suggest that Nur77 is involved in setting the threshold level for L-DOPA-induced rotational behaviour, rather than controlling the development of behavioural sensitization. Levodopa 86-92 nuclear receptor subfamily 4, group A, member 1 Mus musculus 33-38 16731528-5 2006 Inactivation of DJ-1 by small interference RNA (siRNA) results in decreased TH expression and l-DOPA production in human dopaminergic cell lines. Levodopa 94-100 Parkinsonism associated deglycase Homo sapiens 16-20 16758261-3 2006 A further therapeutic alternative is inhibition of catechol-O-methyltransfrase (COMT) on a regular basis, when levodopa/DDI treatment is performed. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 51-78 16725125-0 2006 Repeated l-DOPA treatment increases c-fos and BDNF mRNAs in the subthalamic nucleus in the 6-OHDA rat model of Parkinson"s disease. Levodopa 9-15 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 36-41 16725125-0 2006 Repeated l-DOPA treatment increases c-fos and BDNF mRNAs in the subthalamic nucleus in the 6-OHDA rat model of Parkinson"s disease. Levodopa 9-15 brain-derived neurotrophic factor Rattus norvegicus 46-50 16725125-2 2006 This study used the unilateral 6-OHDA rat model of Parkinson"s disease to examine effects of l-DOPA on the expression of c-fos and BDNF mRNAs in these nuclei. Levodopa 93-99 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 121-126 16725125-2 2006 This study used the unilateral 6-OHDA rat model of Parkinson"s disease to examine effects of l-DOPA on the expression of c-fos and BDNF mRNAs in these nuclei. Levodopa 93-99 brain-derived neurotrophic factor Rattus norvegicus 131-135 16725125-4 2006 Both a single and repeated injections of l-DOPA induced c-fos, but not BDNF, in the dopamine-depleted striatum. Levodopa 41-47 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 56-61 16725125-5 2006 However, repeated l-DOPA treatment increased c-fos and BDNF in the dopamine-depleted subthalamic nucleus. Levodopa 18-24 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 45-50 16725125-5 2006 However, repeated l-DOPA treatment increased c-fos and BDNF in the dopamine-depleted subthalamic nucleus. Levodopa 18-24 brain-derived neurotrophic factor Rattus norvegicus 55-59 16758261-3 2006 A further therapeutic alternative is inhibition of catechol-O-methyltransfrase (COMT) on a regular basis, when levodopa/DDI treatment is performed. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 80-84 16529858-0 2006 L-DOPA treatment of parkinsonian rats changes the expression of Src, Lyn and PKC kinases. Levodopa 0-6 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 64-67 16532454-0 2006 Histamine H3 receptor agonists reduce L-dopa-induced chorea, but not dystonia, in the MPTP-lesioned nonhuman primate model of Parkinson"s disease. Levodopa 38-44 histamine H3 receptor Callithrix jacchus 0-21 16529858-5 2006 In particular, acute (3 days) and chronic (21 days) L-DOPA treatment were differentially able to rescue the effects of DA lesion, since only the acute treatment with L-DOPA corrected the decrease in Src, Lyn and PKC kinase expression induced by 6-OHDA lesion. Levodopa 52-58 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 199-202 16504219-0 2006 L-3,4-dihydroxyphenylalanine-induced c-Fos expression in the CNS under inhibition of central aromatic L-amino acid decarboxylase. Levodopa 0-28 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 37-42 16504219-0 2006 L-3,4-dihydroxyphenylalanine-induced c-Fos expression in the CNS under inhibition of central aromatic L-amino acid decarboxylase. Levodopa 0-28 dopa decarboxylase Rattus norvegicus 93-128 16504219-2 2006 To map the DOPAergic system functionally, DOPA-induced c-Fos expression was detected under inhibition of central aromatic L-amino acid decarboxylase (AADC). Levodopa 11-15 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 55-60 16504219-2 2006 To map the DOPAergic system functionally, DOPA-induced c-Fos expression was detected under inhibition of central aromatic L-amino acid decarboxylase (AADC). Levodopa 11-15 dopa decarboxylase Rattus norvegicus 122-148 16504219-2 2006 To map the DOPAergic system functionally, DOPA-induced c-Fos expression was detected under inhibition of central aromatic L-amino acid decarboxylase (AADC). Levodopa 11-15 dopa decarboxylase Rattus norvegicus 150-154 16504219-3 2006 In rats treated with a central AADC inhibitor, DOPA significantly increased the number of c-Fos-positive nuclei in the paraventricular nuclei (PVN) and the nucleus tractus solitarii (NTS), and showed a tendency to increase in the supraoptic nuclei (SON), but not in the striatum. Levodopa 47-51 dopa decarboxylase Rattus norvegicus 31-35 16504219-3 2006 In rats treated with a central AADC inhibitor, DOPA significantly increased the number of c-Fos-positive nuclei in the paraventricular nuclei (PVN) and the nucleus tractus solitarii (NTS), and showed a tendency to increase in the supraoptic nuclei (SON), but not in the striatum. Levodopa 47-51 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 90-95 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 19-23 dopa decarboxylase Rattus norvegicus 42-46 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 19-23 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 79-84 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 19-23 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 158-163 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 138-142 dopa decarboxylase Rattus norvegicus 42-46 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 138-142 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 79-84 16504219-4 2006 On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. Levodopa 138-142 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 158-163 16504219-5 2006 In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC. Levodopa 99-103 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-131 16504219-5 2006 In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC. Levodopa 99-103 dopa decarboxylase Rattus norvegicus 198-202 16498608-0 2006 Reversion of levodopa-induced motor fluctuations by the A2A antagonist CSC is associated with an increase in striatal preprodynorphin mRNA expression in 6-OHDA-lesioned rats. Levodopa 13-21 spectrin, alpha, non-erythrocytic 1 Rattus norvegicus 56-59 16498608-0 2006 Reversion of levodopa-induced motor fluctuations by the A2A antagonist CSC is associated with an increase in striatal preprodynorphin mRNA expression in 6-OHDA-lesioned rats. Levodopa 13-21 prodynorphin Rattus norvegicus 118-133 16498608-1 2006 The molecular mechanisms involved in the reversion of levodopa-induced motor fluctuations by the adenosine A2A antagonist 8-(3-chlorostryryl) caffeine (CSC) were investigated in rats with a 6-hydroxydopamine (6-OHDA)-induced lesion and compared with the ones achieved by the kappa-opioid agonist, U50,488. Levodopa 54-62 spectrin, alpha, non-erythrocytic 1 Rattus norvegicus 107-110 16498608-3 2006 The reversion of the decrease in the duration of levodopa-induced rotations by CSC, but not by U50,488, was maintained until the end of the treatment and was associated with a further increase in levodopa-induced preprodynorphin mRNA in the lesioned striatum, being higher in the ventromedial striatum. Levodopa 196-204 prodynorphin Rattus norvegicus 213-228 16498608-4 2006 The increase in striatal preprodynorphin expression, particularly in the ventromedial striatum, may be related to the reversion of levodopa-induced motor fluctuations in the CSC-treated animals, suggesting a role of the direct striatal output pathway activity in the ventromedial striatum in the pathophysiology of motor fluctuations. Levodopa 131-139 prodynorphin Rattus norvegicus 25-40 16529858-5 2006 In particular, acute (3 days) and chronic (21 days) L-DOPA treatment were differentially able to rescue the effects of DA lesion, since only the acute treatment with L-DOPA corrected the decrease in Src, Lyn and PKC kinase expression induced by 6-OHDA lesion. Levodopa 52-58 LYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 204-207 16529858-5 2006 In particular, acute (3 days) and chronic (21 days) L-DOPA treatment were differentially able to rescue the effects of DA lesion, since only the acute treatment with L-DOPA corrected the decrease in Src, Lyn and PKC kinase expression induced by 6-OHDA lesion. Levodopa 166-172 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 199-202 16529858-5 2006 In particular, acute (3 days) and chronic (21 days) L-DOPA treatment were differentially able to rescue the effects of DA lesion, since only the acute treatment with L-DOPA corrected the decrease in Src, Lyn and PKC kinase expression induced by 6-OHDA lesion. Levodopa 166-172 LYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 204-207 16529858-0 2006 L-DOPA treatment of parkinsonian rats changes the expression of Src, Lyn and PKC kinases. Levodopa 0-6 LYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 69-72 16529858-4 2006 We found that administration of L-DOPA in rats with unilateral DA denervation resulted in a progressive increase of contraversive circling behavior and modulated the expression of Src, Lyn and PKC kinases. Levodopa 32-38 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 180-183 16529858-4 2006 We found that administration of L-DOPA in rats with unilateral DA denervation resulted in a progressive increase of contraversive circling behavior and modulated the expression of Src, Lyn and PKC kinases. Levodopa 32-38 LYN proto-oncogene, Src family tyrosine kinase Rattus norvegicus 185-188 16817869-0 2006 MDMA and fenfluramine reduce L-DOPA-induced dyskinesia via indirect 5-HT1A receptor stimulation. Levodopa 29-35 5-hydroxytryptamine receptor 1A Rattus norvegicus 68-74 16772808-1 2006 Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 123-151 16772808-1 2006 Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 153-157 16772808-1 2006 Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 123-151 16772808-1 2006 Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 153-157 16772808-2 2006 Although inhibition of COMT should theoretically prevent or reduce levodopa-induced HHcy, results from several prospective studies are conflicting. Levodopa 67-75 catechol-O-methyltransferase Homo sapiens 23-27 16772808-3 2006 Our review of these studies suggests that the ability of COMT inhibition to reduce or prevent levodopa-induced HHcy in Parkinson disease patients may be attributed to differences in the vitamin status of the study participants. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 57-61 16706847-0 2006 L-DOPA-induced dyskinesia in adult rats with a unilateral 6-OHDA lesion of dopamine neurons is paralleled by increased c-fos gene expression in the subthalamic nucleus. Levodopa 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 16706847-6 2006 The objective of this work was to study the effects of acute or chronic systemic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of dopamine neurons on c-fos expression in the STN and test the hypothesis that these effects correlate with L-DOPA-induced dyskinesias. Levodopa 99-105 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 195-200 16706847-8 2006 Our results confirm earlier evidence that the chronic administration of L-DOPA to rats with a unilateral 6-OHDA lesion increases c-fos expression in the STN. Levodopa 72-78 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 129-134 16706847-9 2006 We also report that c-fos expression can be increased following an acute injection of L-DOPA to 6-OHDA-lesioned rats but not following a chronic injection of L-DOPA to sham-operated, unlesioned rats. Levodopa 86-92 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-25 16437585-4 2006 Inhibition of the enzyme catechol-O-methyl transferase (COMT) by entacapone extends the half-life of levodopa and minimizes variability in plasma levodopa levels. Levodopa 101-109 catechol-O-methyltransferase Rattus norvegicus 25-54 16437585-4 2006 Inhibition of the enzyme catechol-O-methyl transferase (COMT) by entacapone extends the half-life of levodopa and minimizes variability in plasma levodopa levels. Levodopa 101-109 catechol-O-methyltransferase Rattus norvegicus 56-60 16437585-4 2006 Inhibition of the enzyme catechol-O-methyl transferase (COMT) by entacapone extends the half-life of levodopa and minimizes variability in plasma levodopa levels. Levodopa 146-154 catechol-O-methyltransferase Rattus norvegicus 25-54 16437585-4 2006 Inhibition of the enzyme catechol-O-methyl transferase (COMT) by entacapone extends the half-life of levodopa and minimizes variability in plasma levodopa levels. Levodopa 146-154 catechol-O-methyltransferase Rattus norvegicus 56-60 16540568-0 2006 A critical interaction between NR2B and MAGUK in L-DOPA induced dyskinesia. Levodopa 49-55 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 31-35 16564428-9 2006 However, mGluR5 antagonists may prove useful for the symptomatic treatment of L-DOPA-induced dyskinesia. Levodopa 78-84 glutamate receptor, ionotropic, kainate 1 Mus musculus 9-15 16564215-10 2006 The increased 3OMD concentration in the absence of concurrent exogenous levodopa (l-dopa) suggests changes in synthesis or metabolism of l-dopa in RLS. Levodopa 82-88 RLS1 Homo sapiens 147-150 16564215-10 2006 The increased 3OMD concentration in the absence of concurrent exogenous levodopa (l-dopa) suggests changes in synthesis or metabolism of l-dopa in RLS. Levodopa 137-143 RLS1 Homo sapiens 147-150 16325337-0 2006 Modulation of torsinA expression in the globus pallidus internus is associated with levodopa-induced dyskinesia in hemiparkinsonian rats. Levodopa 84-92 torsin family 1, member A Rattus norvegicus 14-21 16325337-2 2006 In this study, the distribution of torsinA was investigated in the basal ganglia of hemiparkinsonian rats with or without levodopa-induced dyskinesia (LID). Levodopa 122-130 torsin family 1, member A Rattus norvegicus 35-42 16540568-6 2006 These data indicate abnormal NR2B redistribution between synaptic and extrasynaptic membranes as an important molecular disturbance of the glutamatergic synapse involved in L-DOPA-induced dyskinesia. Levodopa 173-179 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 29-33 16618334-8 2006 The most consistent factor associated with SA was the duration of levodopa therapy and the predictive value of an abnormal ESS score was rather poor (40.7%). Levodopa 66-74 acyl-CoA synthetase medium chain family member 3 Homo sapiens 43-45 16211593-0 2006 Inhibition of catechol-O-methyltransferase contributes to more stable levodopa plasma levels. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 14-42 16317110-0 2006 Increased divalent metal transporter 1 expression might be associated with the neurotoxicity of L-DOPA. Levodopa 96-102 solute carrier family 11 member 2 Homo sapiens 10-38 16403819-0 2006 Congenital hyperinsulinism: pancreatic [18F]fluoro-L-dihydroxyphenylalanine (DOPA) positron emission tomography and immunohistochemistry study of DOPA decarboxylase and insulin secretion. Levodopa 77-81 insulin Homo sapiens 16-23 16403819-4 2006 OBJECTIVE: Positron emission tomography (PET) after injection of [18F]fluoro-L-DOPA (L-dihydroxyphenylalanine) has been evaluated for the preoperative differentiation between focal and diffuse HI, by imaging uptake of radiotracer and the conversion of [18F]fluoro-L-dopa into dopamine by DOPA decarboxylase. Levodopa 85-109 dopa decarboxylase Homo sapiens 288-306 16445854-2 2006 Tyrosinase, the primary enzyme in melanin synthesis commonly mutated in albinism, oxidizes l-tyrosine to l-dopaquinone using l-3,4-dihydroxyphenylalanine (L-DOPA) as an intermediate product. Levodopa 125-153 tyrosinase Homo sapiens 0-10 16317110-6 2006 The levels of DMT1(-IRE) mRNA and protein peaked in the cells treated with 10 microM L-DOPA and then decreased progressively with increasing concentrations of L-DOPA. Levodopa 159-165 solute carrier family 11 member 2 Homo sapiens 14-18 16317110-8 2006 The findings suggested that the increased DMT1(-IRE) expression might be partly associated with the neurotoxicity of L-DOPA. Levodopa 117-123 solute carrier family 11 member 2 Homo sapiens 42-46 15959853-4 2006 In contrast, selegiline failed to increase CAT and SOD activities in three brain regions of 8-week-old rats, whereas L: -dopa significantly increased SOD1 activity in the striatum. Levodopa 117-125 superoxide dismutase 1 Rattus norvegicus 150-154 15959854-1 2006 Hereditary Progressive Dystonia with marked diurnal fluctuation (HPD) is an autosomally dominantly inherited dystonia which is characterized by marked diurnal fluctuation of symptoms and by marked and sustained response to levodopa associated with mutations in guanosine triphosphate cyclohydrolase (GCH-1) deficiency gene. Levodopa 223-231 GTP cyclohydrolase 1 Homo sapiens 300-305 16317110-4 2006 However, a significant increase in the expression of DMT1(-IRE) mRNA and protein was found in cells treated, respectively, with 10 and 30 microM L-DOPA (mRNA) and 1, 5, 10 and 30 microM L-DOPA (protein). Levodopa 145-151 solute carrier family 11 member 2 Homo sapiens 53-57 16317110-4 2006 However, a significant increase in the expression of DMT1(-IRE) mRNA and protein was found in cells treated, respectively, with 10 and 30 microM L-DOPA (mRNA) and 1, 5, 10 and 30 microM L-DOPA (protein). Levodopa 186-192 solute carrier family 11 member 2 Homo sapiens 53-57 16317110-6 2006 The levels of DMT1(-IRE) mRNA and protein peaked in the cells treated with 10 microM L-DOPA and then decreased progressively with increasing concentrations of L-DOPA. Levodopa 85-91 solute carrier family 11 member 2 Homo sapiens 14-18 16365282-6 2006 Short-term L-DOPA administration improved akinesia and restored the synaptic abundance of D1R, NR1-C2 and NR2B. Levodopa 11-17 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 106-110 16309808-2 2006 For example, the symptoms of RLS can be dramatically improved by levodopa and dopamine agonists, whereas central dopamine D2 receptor antagonists can induce or aggravate RLS symptoms. Levodopa 65-73 RLS1 Homo sapiens 29-32 16445854-4 2006 Here, we have mimicked L-DOPA production by ectopically expressing tyrosine hydroxylase in mouse albino retinal pigment epithelium cells. Levodopa 23-29 tyrosine hydroxylase Mus musculus 67-87 16445854-5 2006 Tyrosine hydroxylase can only oxidize l-tyrosine to L-DOPA without further progression towards melanin. Levodopa 52-58 tyrosine hydroxylase Homo sapiens 0-20 16445854-2 2006 Tyrosinase, the primary enzyme in melanin synthesis commonly mutated in albinism, oxidizes l-tyrosine to l-dopaquinone using l-3,4-dihydroxyphenylalanine (L-DOPA) as an intermediate product. Levodopa 155-161 tyrosinase Homo sapiens 0-10 16392817-3 2006 Several aurones bearing hydroxyl groups on A-ring and different substituents on B-ring were synthesized and evaluated as inhibitors of human melanocyte-tyrosinase by an assay which measures tyrosinase-catalyzed l-Dopa oxidation. Levodopa 211-217 tyrosinase Homo sapiens 190-200 16386717-3 2006 In the present experiment, an immunohistochemical analysis of the immediate early protein c-Fos was performed as a marker for cellular activity in the brains of suspended rat pups treated with l-DOPA at P15 and P25. Levodopa 193-199 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 90-95 16386717-5 2006 Only P15 rat pups injected with L-DOPA engaged in air stepping and expressed the highest levels of c-Fos reactivity in output nuclei of the basal ganglia, as well as the pedunculopontine (PPN) and cuneiform (Cnf) nuclei. Levodopa 32-38 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-104 16364672-4 2006 STUDY DESIGN: We reviewed the characteristics of 10 PTPS-deficient patients whose treatment onset with tetrahydrobiopterin, L-DOPA, and hydroxytryptophan had been delayed. Levodopa 124-130 6-pyruvoyltetrahydropterin synthase Homo sapiens 52-56 18046910-3 2006 COMT inhibitors slow down the rapid metabolism of levodopa, resulting in a more-sustained response to dopaminergic therapy. Levodopa 50-58 catechol-O-methyltransferase Homo sapiens 0-4 16139809-0 2006 ERK phosphorylation and FosB expression are associated with L-DOPA-induced dyskinesia in hemiparkinsonian mice. Levodopa 60-66 mitogen-activated protein kinase 1 Mus musculus 0-3 16139809-0 2006 ERK phosphorylation and FosB expression are associated with L-DOPA-induced dyskinesia in hemiparkinsonian mice. Levodopa 60-66 FBJ osteosarcoma oncogene B Mus musculus 24-28 16139809-7 2006 L-DOPA also induces activation of ERK1/2 in the dopamine-depleted striatum. Levodopa 0-6 mitogen-activated protein kinase 3 Mus musculus 34-40 16139809-9 2006 Following acute L-DOPA treatment, FosB expression occurs in direct striatal output neurons, whereas chronic L-DOPA also induces FosB expression in nitric oxide synthase-positive striatal interneurons. Levodopa 16-22 FBJ osteosarcoma oncogene B Mus musculus 34-38 16139809-9 2006 Following acute L-DOPA treatment, FosB expression occurs in direct striatal output neurons, whereas chronic L-DOPA also induces FosB expression in nitric oxide synthase-positive striatal interneurons. Levodopa 108-114 FBJ osteosarcoma oncogene B Mus musculus 128-132 16269145-0 2006 Vesicular monoamine transporter-2 and aromatic L-amino acid decarboxylase gene therapy prevents development of motor complications in parkinsonian rats after chronic intermittent L-3,4-dihydroxyphenylalanine administration. Levodopa 179-207 solute carrier family 18 member A2 Rattus norvegicus 0-33 16269145-0 2006 Vesicular monoamine transporter-2 and aromatic L-amino acid decarboxylase gene therapy prevents development of motor complications in parkinsonian rats after chronic intermittent L-3,4-dihydroxyphenylalanine administration. Levodopa 179-207 dopa decarboxylase Rattus norvegicus 38-73 16269145-5 2006 In this study, we further evaluate the effect of achieving sustained level of dopamine within the striata by VMAT-2 gene on behavioral response of parkinsonian rats after chronic intermittent L-DOPA administration. Levodopa 192-198 solute carrier family 18 member A2 Rattus norvegicus 109-115 16269145-9 2006 The duration of FAS response to L-DOPA was sustained for a longer duration in rats grafted with PFVMAA cells than in those grafted with either control cells or cells with AADC alone. Levodopa 32-38 dopa decarboxylase Rattus norvegicus 171-175 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 94-122 dopa decarboxylase Rattus norvegicus 21-56 17219962-0 2006 Effect of antisense FosB and CREB on the expression of prodynorphin gene in rats with levodopa-induced dyskinesias. Levodopa 86-94 cAMP responsive element binding protein 1 Rattus norvegicus 29-33 17219962-0 2006 Effect of antisense FosB and CREB on the expression of prodynorphin gene in rats with levodopa-induced dyskinesias. Levodopa 86-94 prodynorphin Rattus norvegicus 55-67 17219962-1 2006 The effects of antisense FosB and CREB intra-striatum injection on the expression of prodynorphin (PDyn) gene in striatal neurons of Levodopa-induced dyskinesias (LID) rats with Parkinson disease (PD) were explored. Levodopa 133-141 cAMP responsive element binding protein 1 Rattus norvegicus 34-38 17219962-1 2006 The effects of antisense FosB and CREB intra-striatum injection on the expression of prodynorphin (PDyn) gene in striatal neurons of Levodopa-induced dyskinesias (LID) rats with Parkinson disease (PD) were explored. Levodopa 133-141 prodynorphin Rattus norvegicus 85-97 17219962-1 2006 The effects of antisense FosB and CREB intra-striatum injection on the expression of prodynorphin (PDyn) gene in striatal neurons of Levodopa-induced dyskinesias (LID) rats with Parkinson disease (PD) were explored. Levodopa 133-141 prodynorphin Rattus norvegicus 99-103 16108012-4 2006 Combined with published pedigrees of SCA2 manifesting as levodopa-responsive parkinsonism, this finding suggests that modifier genes could influence the clinical phenotype of SCA2. Levodopa 57-65 ataxin 2 Homo sapiens 37-41 16108012-4 2006 Combined with published pedigrees of SCA2 manifesting as levodopa-responsive parkinsonism, this finding suggests that modifier genes could influence the clinical phenotype of SCA2. Levodopa 57-65 ataxin 2 Homo sapiens 175-179 16126007-5 2006 Rapamycin-induced increases in expression of hAADC repeatedly produced robust rotational behavior in response to low doses of L-dopa. Levodopa 126-132 dopa decarboxylase Homo sapiens 45-50 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 94-122 dopa decarboxylase Rattus norvegicus 58-62 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 94-122 dopa decarboxylase Rattus norvegicus 149-153 16126007-3 2006 Expression of hAADC, the enzyme that converts L-dopa to dopamine, was dependent on reconstitution of a functional transcription factor (TF) by the dimerizer rapamycin. Levodopa 46-52 dopa decarboxylase Homo sapiens 14-19 16127720-0 2006 Prevention of levodopa-induced dyskinesias by a selective NR1A/2B N-methyl-D-aspartate receptor antagonist in parkinsonian monkeys: implication of preproenkephalin. Levodopa 14-22 thyroid hormone receptor beta Homo sapiens 58-64 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 94-122 tyrosine hydroxylase Rattus norvegicus 275-277 16127720-2 2006 The present study investigated the effect of chronic treatment with a selective NR1A/2B N-methyl-D-aspartate (NMDA) receptor antagonist, CI-1041, on the expression of preproenkephalin-A (PPE-A) in brains of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) -treated monkeys in relation to the development of LD-induced dyskinesias. Levodopa 310-312 proenkephalin Homo sapiens 167-183 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 124-130 dopa decarboxylase Rattus norvegicus 21-56 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 124-130 dopa decarboxylase Rattus norvegicus 58-62 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 124-130 dopa decarboxylase Rattus norvegicus 149-153 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 124-130 tyrosine hydroxylase Rattus norvegicus 275-277 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 233-239 dopa decarboxylase Rattus norvegicus 21-56 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 233-239 dopa decarboxylase Rattus norvegicus 58-62 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 233-239 dopa decarboxylase Rattus norvegicus 149-153 16182609-5 2006 Using this strategy, aromatic L-amino acid decarboxylase (AADC) activity was retained so that l-3,4-dihydroxyphenylalanine (L-dopa), a substrate for AADC, could be converted to dopamine in the striatum and the therapeutic effects of L-dopa preserved, even after reduction of TH expression in the case of dopamine overproduction. Levodopa 233-239 tyrosine hydroxylase Rattus norvegicus 275-277 16237129-8 2005 There is limited evidence about specific interventions but available data suggest only a partial response of motor symptoms to levodopa: severe sensitivity to typical and atypical antipsychotics in approximately 50%, and improvements in attention, visual hallucinations, and sleep disorders with cholinesterase inhibitors. Levodopa 127-135 butyrylcholinesterase Homo sapiens 296-310 16388913-10 2006 The reversal of dopamine D1-receptor activation of extracellular signal-regulated kinase in dopamine-deficient mice following chronic L-DOPA treatment shows that the lack of dopamine, rather than absence of other factors secreted from dopaminergic neurons, is responsible for dopamine supersensitivity. Levodopa 134-140 dopamine receptor D1 Mus musculus 16-36 16905880-1 2006 We examined the direct effect of deep brain stimulation of the subthalamic nucleus (STN-DBS) on levodopa-induced peak-dose dyskinesia in 45 patients with Parkinson"s disease (PD) without reducing the levodopa dosage during the early period after surgery. Levodopa 96-104 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 84-87 16298686-4 2005 In neuron-glia cultures, we found that H2O2, a product of dopamine metabolism, or l-3,4-dihydroxyphenylalanine (L-DOPA), the dopamine precursor used in the therapy of PD, induced a fast up-regulation of HO-1 mRNA and protein levels, followed by a secondary down-regulation. Levodopa 82-110 heme oxygenase 1 Homo sapiens 203-207 16298686-4 2005 In neuron-glia cultures, we found that H2O2, a product of dopamine metabolism, or l-3,4-dihydroxyphenylalanine (L-DOPA), the dopamine precursor used in the therapy of PD, induced a fast up-regulation of HO-1 mRNA and protein levels, followed by a secondary down-regulation. Levodopa 112-118 heme oxygenase 1 Homo sapiens 203-207 16298686-5 2005 H2O2 and L-DOPA also increased HO-1 expression in astrocyte cultures, but with a delayed time course in H2O2-treated cultures. Levodopa 9-15 heme oxygenase 1 Homo sapiens 31-35 16298686-7 2005 Because exogenously applied GDNF prevented HO-1 up-regulation in cultures treated with H2O2 or l-DOPA, and antibody neutralization of GDNF prevented the secondary HO-1 down-regulation observed in neuron-glia cultures, we propose that GDNF negatively modulates HO-1 expression induced by oxidative stress. Levodopa 95-101 glial cell derived neurotrophic factor Homo sapiens 28-32 16298686-7 2005 Because exogenously applied GDNF prevented HO-1 up-regulation in cultures treated with H2O2 or l-DOPA, and antibody neutralization of GDNF prevented the secondary HO-1 down-regulation observed in neuron-glia cultures, we propose that GDNF negatively modulates HO-1 expression induced by oxidative stress. Levodopa 95-101 heme oxygenase 1 Homo sapiens 43-47 16226715-1 2005 PTEN-induced kinase 1 (PINK1) is a recently identified gene, mutations of which cause levodopa-responsive parkinsonism. Levodopa 86-94 PTEN induced kinase 1 Homo sapiens 0-21 16226715-1 2005 PTEN-induced kinase 1 (PINK1) is a recently identified gene, mutations of which cause levodopa-responsive parkinsonism. Levodopa 86-94 PTEN induced kinase 1 Homo sapiens 23-28 16280010-6 2005 Kinetic data suggest that all four compounds act as competitive inhibitors of tyrosinase, most likely competing with L-3,4-dihydroxyphenylalanine (L-DOPA) for binding to the DOPA-binding site of the enzyme. Levodopa 117-145 tyrosinase Homo sapiens 78-88 16151764-0 2005 The effect of levodopa therapy on dopamine transporter SPECT imaging with( 123)I-FP-CIT in patients with Parkinson"s disease. Levodopa 14-22 solute carrier family 6 member 3 Homo sapiens 34-54 16151764-1 2005 PURPOSE: The aim of this study was to evaluate, by means of (123)I-FP-CIT SPECT, the effect of chronic treatment with levodopa on striatal dopamine transporter (DAT) in patients with Parkinson"s disease. Levodopa 118-126 solute carrier family 6 member 3 Homo sapiens 139-159 16151764-1 2005 PURPOSE: The aim of this study was to evaluate, by means of (123)I-FP-CIT SPECT, the effect of chronic treatment with levodopa on striatal dopamine transporter (DAT) in patients with Parkinson"s disease. Levodopa 118-126 solute carrier family 6 member 3 Homo sapiens 161-164 16339749-1 2005 Levodopa reportedly inhibits insulin action in skeletal muscle. Levodopa 0-8 insulin Homo sapiens 29-36 16339749-2 2005 Here we show that C2C12 myotubes produce levodopa and that insulin-stimulated glucose transport is enhanced when endogenous levodopa is depleted. Levodopa 124-132 insulin Homo sapiens 59-66 16339749-3 2005 Exogenous levodopa prevented the stimulation of glucose transport by insulin (P < 0.05) and increased cAMP concentrations (P < 0.05). Levodopa 10-18 insulin Homo sapiens 69-76 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Levodopa 63-71 insulin Homo sapiens 16-23 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Levodopa 63-71 dopa decarboxylase Homo sapiens 182-200 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Levodopa 63-71 dopa decarboxylase Homo sapiens 202-205 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Levodopa 216-224 insulin Homo sapiens 16-23 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Levodopa 216-224 dopa decarboxylase Homo sapiens 182-200 16172858-1 2005 Leucine-rich repeat kinase 2 (LRRK2) mutations have been implicated in autosomal dominant parkinsonism, consistent with typical levodopa-responsive Parkinson"s disease. Levodopa 128-136 leucine rich repeat kinase 2 Homo sapiens 0-28 16172858-1 2005 Leucine-rich repeat kinase 2 (LRRK2) mutations have been implicated in autosomal dominant parkinsonism, consistent with typical levodopa-responsive Parkinson"s disease. Levodopa 128-136 leucine rich repeat kinase 2 Homo sapiens 30-35 16280010-6 2005 Kinetic data suggest that all four compounds act as competitive inhibitors of tyrosinase, most likely competing with L-3,4-dihydroxyphenylalanine (L-DOPA) for binding to the DOPA-binding site of the enzyme. Levodopa 147-153 tyrosinase Homo sapiens 78-88 16340389-1 2005 Restless legs syndrome (RLS) is a common disorder for which agents that enhance dopaminergic activity, including dopamine agonists and levodopa, are the treatment of choice. Levodopa 135-143 RLS1 Homo sapiens 24-27 16136276-1 2005 The present study aimed to examine the presence and define the role of 4F2hc, a glycoprotein associated with the LAT2 amino acid transporter, in L-DOPA handling by LLC-PK1 cells. Levodopa 145-151 linker for activation of T cells family member 2 Sus scrofa 113-117 16136276-8 2005 It is likely that the Na+-independent and pH-sensitive uptake of L-DOPA include the hetero amino acid exchanger LAT2/4F2hc, which facilitates the trans-stimulation of L-DOPA and its outward transfer at both the apical and basal cell sides. Levodopa 65-71 linker for activation of T cells family member 2 Sus scrofa 112-116 16136276-8 2005 It is likely that the Na+-independent and pH-sensitive uptake of L-DOPA include the hetero amino acid exchanger LAT2/4F2hc, which facilitates the trans-stimulation of L-DOPA and its outward transfer at both the apical and basal cell sides. Levodopa 167-173 linker for activation of T cells family member 2 Sus scrofa 112-116 16340382-1 2005 Metabolism of levodopa via the enzyme catechol-O-methyltransferase requires S-adenosylmethionine (SAM) as a methyl donor. Levodopa 14-22 catechol-O-methyltransferase Homo sapiens 38-66 16293777-9 2005 Furthermore, we show intra-melanosomal l-dopa formation from dopachrome by 7BH(4) in a concentration range up to 134 x 10(-6) M. Based on these results, we propose a new receptor-independent mechanism in the control of tyrosinase/melanogenesis by beta-MSH and the pterin 7BH(4). Levodopa 39-45 tyrosinase Homo sapiens 219-229 16340382-4 2005 SAM levels were significantly reduced in levodopa-treated PD patients, but they showed increased enzyme methionine adenosyl transferase (MAT) activity, which induces SAM synthesis from methionine (MET). Levodopa 41-49 methionine adenosyltransferase 1A Homo sapiens 104-135 16340382-4 2005 SAM levels were significantly reduced in levodopa-treated PD patients, but they showed increased enzyme methionine adenosyl transferase (MAT) activity, which induces SAM synthesis from methionine (MET). Levodopa 41-49 methionine adenosyltransferase 1A Homo sapiens 137-140 16340382-4 2005 SAM levels were significantly reduced in levodopa-treated PD patients, but they showed increased enzyme methionine adenosyl transferase (MAT) activity, which induces SAM synthesis from methionine (MET). Levodopa 41-49 SAFB like transcription modulator Homo sapiens 197-200 16293777-9 2005 Furthermore, we show intra-melanosomal l-dopa formation from dopachrome by 7BH(4) in a concentration range up to 134 x 10(-6) M. Based on these results, we propose a new receptor-independent mechanism in the control of tyrosinase/melanogenesis by beta-MSH and the pterin 7BH(4). Levodopa 39-45 proopiomelanocortin Homo sapiens 247-255 15918034-4 2005 Quantitative trait loci (QTLs) analysis utilising a skeleton map enabled us to identify a major QTL controlling PPO activity based on L-DOPA and L-tyrosine on the long arm of chromosome 2A. Levodopa 134-140 polyphenol oxidase I, chloroplastic Triticum aestivum 112-115 15882945-1 2005 This study investigated the consequences of levodopa treatment on the expression of the 65- and 67-kDa isoforms of glutamate decarboxylase (GAD65 and GAD67) immunoreactivity in the basal ganglia and cortex of monkeys rendered Parkinsonian by systemic MPTP administration. Levodopa 44-52 glutamate decarboxylase 2 Homo sapiens 140-145 15882945-1 2005 This study investigated the consequences of levodopa treatment on the expression of the 65- and 67-kDa isoforms of glutamate decarboxylase (GAD65 and GAD67) immunoreactivity in the basal ganglia and cortex of monkeys rendered Parkinsonian by systemic MPTP administration. Levodopa 44-52 glutamate decarboxylase 1 Homo sapiens 150-155 15896973-6 2005 In this specific territory, the number of Nur77-positive cells was decreased, in response to L-DOPA, when compared to the medial part of the lesioned striatum. Levodopa 93-99 nuclear receptor subfamily 4 group A member 1 Homo sapiens 42-47 15896973-7 2005 L-DOPA treatment increased dopamine D3 receptor and glutamate transporter 1 (GLT1) mRNA expression in the lesioned striatum and that, specifically in an area overlapping one of Nur77 decrease and of NT/DYN induction. Levodopa 0-6 solute carrier family 1 member 2 Homo sapiens 52-75 15896973-7 2005 L-DOPA treatment increased dopamine D3 receptor and glutamate transporter 1 (GLT1) mRNA expression in the lesioned striatum and that, specifically in an area overlapping one of Nur77 decrease and of NT/DYN induction. Levodopa 0-6 solute carrier family 1 member 2 Homo sapiens 77-81 15896973-7 2005 L-DOPA treatment increased dopamine D3 receptor and glutamate transporter 1 (GLT1) mRNA expression in the lesioned striatum and that, specifically in an area overlapping one of Nur77 decrease and of NT/DYN induction. Levodopa 0-6 nuclear receptor subfamily 4 group A member 1 Homo sapiens 177-182 16447758-6 2005 A clinical trial to evaluate the safety and efficacy of AAV vector-mediated gene transfer of aromatic L-amino acid decarboxylase, an enzyme that converts L-dopa to dopamine, is underway. Levodopa 154-160 dopa decarboxylase Homo sapiens 93-128 16086033-0 2005 The neurochemical and behavioral effects of the novel cholinesterase-monoamine oxidase inhibitor, ladostigil, in response to L-dopa and L-tryptophan, in rats. Levodopa 125-131 butyrylcholinesterase Rattus norvegicus 54-68 16190867-7 2005 Pharmacological manipulation of dopaminergic tone with L-DOPA and selegiline showed that the reduction in CREB expression was due to reduced levels of dopamine. Levodopa 55-61 cAMP responsive element binding protein 1 Homo sapiens 106-110 16222436-20 2005 However, the beta-CIT SPECT substudy indicates the opposite effect, namely that levodopa causes a more rapid decline in the integrity of the dopamine transporter located in the nigrostriatal nerve terminals in the striatum. Levodopa 80-88 solute carrier family 6 member 3 Homo sapiens 141-161 16239764-0 2005 Impact of levodopa on reduced nerve growth factor levels in patients with Parkinson disease. Levodopa 10-18 nerve growth factor Homo sapiens 30-49 16222437-5 2005 It can, therefore, be suggested that the onset of dyskinesia may be prolonged if levodopa is administered in a more continuous manner by administering it as a combination of levodopa/DDCI and COMT inhibitor. Levodopa 81-89 catechol-O-methyltransferase Homo sapiens 192-196 16321246-17 2005 CONCLUSION: Pre-treatment with lower dose L-dopa before the paraquat administration is neuroprotective by preventing paraquat from access into central nervous system through a blood-brain barrier competitive uptake mechanism, while higher dose L-dopa shows neurotoxicity through disaggregating alpha-synuclein deposits in Parkinsonian mice. Levodopa 42-48 synuclein, alpha Mus musculus 294-309 16321246-17 2005 CONCLUSION: Pre-treatment with lower dose L-dopa before the paraquat administration is neuroprotective by preventing paraquat from access into central nervous system through a blood-brain barrier competitive uptake mechanism, while higher dose L-dopa shows neurotoxicity through disaggregating alpha-synuclein deposits in Parkinsonian mice. Levodopa 244-250 synuclein, alpha Mus musculus 294-309 16239764-2 2005 A significant positive correlation between levodopa and NGF plasma levels appeared after acute levodopa/benserazide administration. Levodopa 43-51 nerve growth factor Homo sapiens 56-59 16239764-3 2005 The data suggest that acute levodopa administration may contribute to an increase of NGF plasma concentrations, which are reduced in treated PD patients due to the ongoing disease process itself or chronic antiparkinsonian drug treatment. Levodopa 28-36 nerve growth factor Homo sapiens 85-88 16102547-6 2005 RESULTS: A low dose of L-dopa (3 mg/kg) combined with benserazide, an inhibitor of peripheral DOPA decarboxylase, significantly enhanced the antipsychotic-like effect of raclopride without any associated catalepsy. Levodopa 23-29 dopa decarboxylase Homo sapiens 94-112 15614425-0 2005 The COMT inhibitor, entacapone, reduces levodopa-induced elevations in plasma homocysteine in healthy adult rats. Levodopa 40-48 catechol-O-methyltransferase Rattus norvegicus 4-8 15614425-2 2005 Levodopa is metabolised via O-methylation by catechol-O-methyltransferase (COMT) using S-adenosyl-L-methionine (SAM) as the methyl donor, this leading to the subsequent formation of homocysteine. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 45-73 15614425-2 2005 Levodopa is metabolised via O-methylation by catechol-O-methyltransferase (COMT) using S-adenosyl-L-methionine (SAM) as the methyl donor, this leading to the subsequent formation of homocysteine. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 75-79 15614425-3 2005 In this study, the effects of the COMT inhibitor, entacapone, on levodopa-induced hyperhomocysteinaemia were studied in rats. Levodopa 65-73 catechol-O-methyltransferase Rattus norvegicus 34-38 16034956-15 2005 There was a marked levodopa-sparing effect with MAO-B inhibitors which was associated with a significant reduction in motor fluctuations (OR 0.75; 95% CI 0.59 to 0.94) but not dyskinesia (OR 0.97; 95% CI 0.76 to 1.25). Levodopa 19-27 monoamine oxidase B Homo sapiens 48-53 15791634-7 2005 Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD. Levodopa 93-101 5-hydroxytryptamine receptor 1A Homo sapiens 62-68 16000163-8 2005 l-DOPA (400 microm for 24 h) reduced the number of TH-immunoreactive cells to 50% of baseline and increased twofold the percentage of apoptotic cells in cultures of wild-type (WT) animals. Levodopa 0-6 tyrosine hydroxylase Mus musculus 51-53 16000163-9 2005 The PK-KO mice, however, are not only resistant to the l-DOPA-induced pro-apoptotic effects but they have an increased number of TH-immunoreactive neurones after treatment with l-DOPA, suggesting that l-DOPA is toxic for neurones of WT mice but not those of parkin null mice. Levodopa 177-183 tyrosine hydroxylase Mus musculus 129-131 16000163-9 2005 The PK-KO mice, however, are not only resistant to the l-DOPA-induced pro-apoptotic effects but they have an increased number of TH-immunoreactive neurones after treatment with l-DOPA, suggesting that l-DOPA is toxic for neurones of WT mice but not those of parkin null mice. Levodopa 177-183 tyrosine hydroxylase Mus musculus 129-131 16000163-14 2005 This study opens new avenues for understanding the mechanisms of action of l-DOPA on DA neurones in patients with Park-2 mutations. Levodopa 75-81 parkin RBR E3 ubiquitin protein ligase Homo sapiens 114-120 15791634-7 2005 Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD. Levodopa 93-101 5-hydroxytryptamine receptor 1A Homo sapiens 62-77 15927700-8 2005 The enhancement of the NPY induced increase in DOPA accumulation observed by BIBO3304 was attenuated when examined in the presence of the Y2 antagonist BIIE0246. Levodopa 47-51 neuropeptide Y Rattus norvegicus 23-26 16002472-4 2005 The behavioral defect of parkin mutant flies was partially restored by administering L-DOPA, and the dopamine level in the brains of parkin mutant flies was highly decreased. Levodopa 85-91 parkin Drosophila melanogaster 25-31 15779086-5 2005 tHcy export from astrocytes was also induced by the COMT substrates levodopa (L-DOPA), dopamine and quercetin, and it was blocked by the COMT inhibitors tropolone and entacapone. Levodopa 68-76 catechol-O-methyltransferase Homo sapiens 52-56 16029214-7 2005 Levodopa administration reversed the increased phosphorylation of both CaMKIIalpha and DARPP-32. Levodopa 0-8 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 87-95 15779086-5 2005 tHcy export from astrocytes was also induced by the COMT substrates levodopa (L-DOPA), dopamine and quercetin, and it was blocked by the COMT inhibitors tropolone and entacapone. Levodopa 78-84 catechol-O-methyltransferase Homo sapiens 52-56 15778083-1 2005 The tyrosinase/oxygen enzymatic system catalyses the orthohydroxylation of L-tyrosine to L-dopa and the oxidation of this to dopaquinone, which evolves non-enzymatically towards to form melanins. Levodopa 89-95 tyrosinase Homo sapiens 4-14 15936832-6 2005 In addition to stimulating D1- and D2-like dopamine receptors, dopamine might also activate adrenoceptors, novel dopamine sites, the dopamine transporter and trace amine receptors, all of which might contribute to the superior effect of L-dopa in Parkinson"s disease. Levodopa 237-243 solute carrier family 6 member 3 Homo sapiens 133-153 16544004-6 2005 After treatment with carbidopa/L-dopa, basal TSH (1.6 microU/mL) and Prl (34 ng/mL) decreased and the response to TRH was partially blocked (10.3 microU/mL and 61 ng/mL, respectively). Levodopa 31-37 prolactin Homo sapiens 69-72 15778090-3 2005 The data indicate that a rapid intracellular degradation of L-3,4-dihydroxyphenylalanine and tyramine (at 100 and 200 microM concentrations) is accompanied by 25-40% decrease in glucose production from pyruvate, alanine + glycerol + octanoate and dihydroxyacetone due to augmented generation of hydrogen peroxide via monoamine oxidase B, resulting in a decline of glutathione redox state by 40%. Levodopa 60-88 amine oxidase [flavin-containing] B Oryctolagus cuniculus 317-336 15778090-4 2005 Moreover, following inhibition of monoamine oxidase B by deprenyl or substitution of pyruvate by aspartate + glycerol + octanoate both L-3,4-dihydroxyphenylalanine and tyramine affect neither the rate of gluconeogenesis nor glutathione redox state. Levodopa 135-163 amine oxidase [flavin-containing] B Oryctolagus cuniculus 34-53 15911147-4 2005 l-Dopa-responsive parkinsonism with minimal cerebellar deficits has been described in SCA2 and SCA3. Levodopa 0-6 ataxin 2 Homo sapiens 86-90 15911147-4 2005 l-Dopa-responsive parkinsonism with minimal cerebellar deficits has been described in SCA2 and SCA3. Levodopa 0-6 ataxin 3 Homo sapiens 95-99 15955952-0 2005 A novel TITF-1 mutation causes benign hereditary chorea with response to levodopa. Levodopa 73-81 NK2 homeobox 1 Homo sapiens 8-14 16179113-5 2005 The clinical features in patients with PINK1 mutations included early onset, slow disease progression, hyperreflexia, diurnal fluctuations with sleep benefit, and good response to levodopa. Levodopa 180-188 PTEN induced kinase 1 Homo sapiens 39-44 15950665-1 2005 Women of normal weight with polycystic ovary syndrome (PCOS) and hyperinsulinemia presented high growth hormone (GH) levels in response to the l-dopa test, suggesting that the action of GH and insulin-like growth factor-1 (IGF-1) might be responsible for the elevation in LH and the consequent hyperandrogenic anovulation observed in normal weight women with PCOS. Levodopa 143-149 growth hormone 1 Homo sapiens 97-111 15950665-1 2005 Women of normal weight with polycystic ovary syndrome (PCOS) and hyperinsulinemia presented high growth hormone (GH) levels in response to the l-dopa test, suggesting that the action of GH and insulin-like growth factor-1 (IGF-1) might be responsible for the elevation in LH and the consequent hyperandrogenic anovulation observed in normal weight women with PCOS. Levodopa 143-149 growth hormone 1 Homo sapiens 113-115 15950665-1 2005 Women of normal weight with polycystic ovary syndrome (PCOS) and hyperinsulinemia presented high growth hormone (GH) levels in response to the l-dopa test, suggesting that the action of GH and insulin-like growth factor-1 (IGF-1) might be responsible for the elevation in LH and the consequent hyperandrogenic anovulation observed in normal weight women with PCOS. Levodopa 143-149 growth hormone 1 Homo sapiens 186-188 15747353-0 2005 Levodopa-responsive infantile parkinsonism due to a novel mutation in the tyrosine hydroxylase gene and exacerbation by viral infections. Levodopa 0-8 tyrosine hydroxylase Homo sapiens 74-94 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 0-28 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 30-34 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 0-28 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 30-34 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 0-28 15907741-2 2005 Catechol-O-methyltransferase (COMT) inhibitors delay the breakdown of levodopa, which leads to an increase in levodopa bioavailability and more stable concentrations of plasma levodopa. Levodopa 110-118 catechol-O-methyltransferase Homo sapiens 30-34 15907741-3 2005 The addition of a COMT inhibitor therefore combines the rapid onset of levodopa with prolonged efficacy, and theoretically provides a more continuous stimulation of dopamine receptors with reduced risk of motor complications. Levodopa 71-79 catechol-O-methyltransferase Homo sapiens 18-22 15907741-4 2005 Randomised, controlled trials have shown that in patients with PD who have motor fluctuations, the addition of the COMT-inhibitor entacapone results in an improvement in motor fluctuations, particularly of the "wearing-off" type, with about 1.0-1.7 h more on-time and less off-time per day, reduced required levodopa dose, modest improvement in motor and disability scores (mean total unified PD rating scale [UPDRS] scores of about 4.5), and in some but not all studies improvement of health-related quality of life [HRQOL] scores. Levodopa 308-316 catechol-O-methyltransferase Homo sapiens 115-119 15907741-5 2005 RECENT DEVELOPMENTS: Patients with stable PD, without motor fluctuations, also have improved HRQOL scores on treatment with entacapone in addition to levodopa with a dopa-decarboxylase inhibitor. Levodopa 150-158 dopa decarboxylase Homo sapiens 166-184 15747357-1 2005 We explored the potential effect of catechol-O-methyltransferase (COMT) genetic polymorphism on the pharmacokinetics and pharmacodynamics of a standard oral dose of levodopa in patients with Parkinson"s disease (PD). Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 66-70 15747357-1 2005 We explored the potential effect of catechol-O-methyltransferase (COMT) genetic polymorphism on the pharmacokinetics and pharmacodynamics of a standard oral dose of levodopa in patients with Parkinson"s disease (PD). Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 36-64 15893579-0 2005 A serotonin 5-HT1A receptor agonist prevents behavioral sensitization to L-DOPA in a rodent model of Parkinson"s disease. Levodopa 73-79 5-hydroxytryptamine receptor 1A Homo sapiens 12-27 15893579-5 2005 These results suggest that pharmaceutical products that stimulate 5-HT1A receptors could prove useful in prevention of the development of L-DOPA-induced motor complications in patients with Parkinson"s disease. Levodopa 138-144 5-hydroxytryptamine receptor 1A Homo sapiens 66-72 15703272-0 2005 Subcellular redistribution of the synapse-associated proteins PSD-95 and SAP97 in animal models of Parkinson"s disease and L-DOPA-induced dyskinesia. Levodopa 123-129 discs large MAGUK scaffold protein 4 Rattus norvegicus 62-68 15836622-0 2005 Adeno-associated virus-mediated gene transfer of human aromatic L-amino acid decarboxylase protects mixed striatal primary cultures from L-DOPA toxicity. Levodopa 137-143 dopa decarboxylase Homo sapiens 55-90 15836622-4 2005 Infusion of this vector into the striatum of parkinsonian rats and monkeys improves L-DOPA responsiveness by improving AADC-mediated conversion of L-DOPA to dopamine. Levodopa 84-90 dopa decarboxylase Rattus norvegicus 119-123 15836622-4 2005 Infusion of this vector into the striatum of parkinsonian rats and monkeys improves L-DOPA responsiveness by improving AADC-mediated conversion of L-DOPA to dopamine. Levodopa 147-153 dopa decarboxylase Rattus norvegicus 119-123 15836622-8 2005 Exposure of cultures to high concentrations of L-DOPA induced the following changes: cell death in nigral and striatal neurons, aggregation of neurofilaments and focal axonal swellings, abnormal expression of DARPP-32, and activation of astroglia and microglial cells. Levodopa 47-53 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 209-217 15836622-9 2005 Transduction of cultures with AAV-hAADC resulted in efficient and sustained neuronal expression of the AADC protein and prevented all the L-DOPA-induced toxicities. Levodopa 138-144 dopa decarboxylase Homo sapiens 34-39 15836622-9 2005 Transduction of cultures with AAV-hAADC resulted in efficient and sustained neuronal expression of the AADC protein and prevented all the L-DOPA-induced toxicities. Levodopa 138-144 dopa decarboxylase Homo sapiens 35-39 15836622-10 2005 The protective effects were due primarily to AADC-dependent conversion of L-DOPA to dopamine and an increase in induction of vesicular monoamine transporter resulting in dopamine storage in cultured cells. Levodopa 74-80 dopa decarboxylase Homo sapiens 45-49 15836622-11 2005 These results suggest a neuroprotective role for AADC gene transfer against L-DOPA toxicity. Levodopa 76-82 dopa decarboxylase Homo sapiens 49-53 15613619-6 2005 In rats fed a control diet, the dopamine precursor l-dihydroxyphenylalanine (l-DOPA) or the DA1 receptor agonist SKF-81297 suppressed cortical COX-2 expression. Levodopa 51-75 prostaglandin-endoperoxide synthase 2 Homo sapiens 143-148 15613619-6 2005 In rats fed a control diet, the dopamine precursor l-dihydroxyphenylalanine (l-DOPA) or the DA1 receptor agonist SKF-81297 suppressed cortical COX-2 expression. Levodopa 77-83 prostaglandin-endoperoxide synthase 2 Homo sapiens 143-148 15613619-8 2005 In contrast, l-DOPA or the dopamine-metabolizing enzyme inhibitor entacapone suppressed low-salt-induced cortical COX-2 expression. Levodopa 13-19 prostaglandin-endoperoxide synthase 2 Homo sapiens 114-119 15703272-7 2005 Post L-DOPA treatment, PSD-95 and SAP97 levels increased (367.4 +/- 43.2% and 159.9 +/- 9.5% from control values, respectively), with both being redistributed toward synaptic membranes from vesicular compartments. Levodopa 5-11 discs large MAGUK scaffold protein 4 Rattus norvegicus 23-29 15703272-7 2005 Post L-DOPA treatment, PSD-95 and SAP97 levels increased (367.4 +/- 43.2% and 159.9 +/- 9.5% from control values, respectively), with both being redistributed toward synaptic membranes from vesicular compartments. Levodopa 5-11 discs large MAGUK scaffold protein 1 Rattus norvegicus 34-39 15878587-3 2005 Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. Levodopa 98-106 catechol-O-methyltransferase Homo sapiens 39-67 15878587-3 2005 Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. Levodopa 98-106 catechol-O-methyltransferase Homo sapiens 69-73 15878587-3 2005 Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. Levodopa 189-197 catechol-O-methyltransferase Homo sapiens 39-67 15878587-3 2005 Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. Levodopa 189-197 catechol-O-methyltransferase Homo sapiens 69-73 15878587-9 2005 We suggest that the COMT inhibition may play a promising role in successfully controlling levodopa-induced hyperhomocysteinemia and in reducing the risk of pathologies probably linked to it. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 20-24 15885624-0 2005 Pathogenesis of levodopa-induced dyskinesia: focus on D1 and D3 dopamine receptors. Levodopa 16-24 dopamine receptor D3 Homo sapiens 54-82 16009007-4 2005 RESULTS: Onset age of 2 Chinese AR-JP patients is young, periods of disease is long, clinical manifestation include: resting tremor, rigidity, bradykinesias, disability, a good response to levodopa, but early levodopa induced symptom fluctuation; but no hyperactive tendon reflexes, sleep benefit, and foot dystonia. Levodopa 189-197 parkin RBR E3 ubiquitin protein ligase Homo sapiens 32-37 16009007-4 2005 RESULTS: Onset age of 2 Chinese AR-JP patients is young, periods of disease is long, clinical manifestation include: resting tremor, rigidity, bradykinesias, disability, a good response to levodopa, but early levodopa induced symptom fluctuation; but no hyperactive tendon reflexes, sleep benefit, and foot dystonia. Levodopa 209-217 parkin RBR E3 ubiquitin protein ligase Homo sapiens 32-37 15703272-0 2005 Subcellular redistribution of the synapse-associated proteins PSD-95 and SAP97 in animal models of Parkinson"s disease and L-DOPA-induced dyskinesia. Levodopa 123-129 discs large MAGUK scaffold protein 1 Rattus norvegicus 73-78 15703272-3 2005 Here, we show that expression and subcellular distribution of PSD-95 and SAP97 are altered in the striatum of unilateral 6-OHDA-lesioned rats following repeated vehicle (a model of PD) or L-DOPA administration (a model of L-DOPA-induced dyskinesia). Levodopa 188-194 discs large MAGUK scaffold protein 4 Rattus norvegicus 62-68 15703272-3 2005 Here, we show that expression and subcellular distribution of PSD-95 and SAP97 are altered in the striatum of unilateral 6-OHDA-lesioned rats following repeated vehicle (a model of PD) or L-DOPA administration (a model of L-DOPA-induced dyskinesia). Levodopa 188-194 discs large MAGUK scaffold protein 1 Rattus norvegicus 73-78 15703272-3 2005 Here, we show that expression and subcellular distribution of PSD-95 and SAP97 are altered in the striatum of unilateral 6-OHDA-lesioned rats following repeated vehicle (a model of PD) or L-DOPA administration (a model of L-DOPA-induced dyskinesia). Levodopa 222-228 discs large MAGUK scaffold protein 4 Rattus norvegicus 62-68 15703272-3 2005 Here, we show that expression and subcellular distribution of PSD-95 and SAP97 are altered in the striatum of unilateral 6-OHDA-lesioned rats following repeated vehicle (a model of PD) or L-DOPA administration (a model of L-DOPA-induced dyskinesia). Levodopa 222-228 discs large MAGUK scaffold protein 1 Rattus norvegicus 73-78 15813929-2 2005 The effects of acute and subchronic L-DOPA administration on zif-268 mRNA expression were compared in 6-hydroxydopamine-lesioned rats. Levodopa 36-42 early growth response 1 Rattus norvegicus 61-68 15659429-3 2005 In this study we used 33 rats with severe nigrostriatal dopamine depletion and showed that in vivo gene transfer of the DA-synthetic enzymes tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) using recombinant adeno-associated virus vectors can provide a constant source of DOPA production locally in the striatum, at a level that is effective in reducing L-DOPA-induced dyskinesias by >85%, and reverse lesion-induced motor impairments. Levodopa 363-369 GTP cyclohydrolase 1 Rattus norvegicus 171-191 15659429-3 2005 In this study we used 33 rats with severe nigrostriatal dopamine depletion and showed that in vivo gene transfer of the DA-synthetic enzymes tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1) using recombinant adeno-associated virus vectors can provide a constant source of DOPA production locally in the striatum, at a level that is effective in reducing L-DOPA-induced dyskinesias by >85%, and reverse lesion-induced motor impairments. Levodopa 363-369 GTP cyclohydrolase 1 Rattus norvegicus 193-197 15698633-2 2005 Catechol-O-methyltransferase (COMT) inhibitors increase the half-life and bioavailability of levodopa, providing more continuous dopamine receptor stimulation. Levodopa 93-101 catechol-O-methyltransferase Rattus norvegicus 0-28 15698633-2 2005 Catechol-O-methyltransferase (COMT) inhibitors increase the half-life and bioavailability of levodopa, providing more continuous dopamine receptor stimulation. Levodopa 93-101 catechol-O-methyltransferase Rattus norvegicus 30-34 15813929-4 2005 Three days after interruption of subchronic treatment, zif-268 mRNA was evaluated after an L-DOPA challenge. Levodopa 91-97 early growth response 1 Rattus norvegicus 55-62 15813929-5 2005 Zif-268 mRNA levels increased in the lesioned dorsolateral striatum after either acute or subchronic L-DOPA administration. Levodopa 101-107 early growth response 1 Rattus norvegicus 0-7 15813929-7 2005 Single acute L-DOPA significantly increased zif-268 in all striatal neurons reflecting a hyperresponsiveness of dopamine-depleted striatum. Levodopa 13-19 early growth response 1 Rattus norvegicus 44-51 15813929-8 2005 After subchronic L-DOPA, zif-268 mRNA labelling was still increased in the striatonigral pathway, limited to dynorphin(+) neurons, whereas in all other neurons it was similar to the control value. Levodopa 17-23 early growth response 1 Rattus norvegicus 25-32 15686961-0 2005 L-DOPA reverses the MPTP-induced elevation of the arrestin2 and GRK6 expression and enhanced ERK activation in monkey brain. Levodopa 0-6 arrestin beta 1 Homo sapiens 50-59 15686961-0 2005 L-DOPA reverses the MPTP-induced elevation of the arrestin2 and GRK6 expression and enhanced ERK activation in monkey brain. Levodopa 0-6 G protein-coupled receptor kinase 6 Homo sapiens 64-68 15686961-0 2005 L-DOPA reverses the MPTP-induced elevation of the arrestin2 and GRK6 expression and enhanced ERK activation in monkey brain. Levodopa 0-6 mitogen-activated protein kinase 1 Homo sapiens 93-96 15686961-3 2005 Using quantitative Western blotting, we detected profound differences in the expression of arrestin2 and GRKs among four experimental groups of nonhuman primates: (1) normal, (2) parkinsonian, (3) parkinsonian treated with levodopa without or (4) with dyskinesia. Levodopa 223-231 arrestin beta 1 Homo sapiens 91-100 15755478-6 2005 Levodopa treatment eliciting dyskinesia normalized NR1 and NR2B and increased NR2A subunits to 150 +/- 12% of unlesioned levels. Levodopa 0-8 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 51-54 15686961-3 2005 Using quantitative Western blotting, we detected profound differences in the expression of arrestin2 and GRKs among four experimental groups of nonhuman primates: (1) normal, (2) parkinsonian, (3) parkinsonian treated with levodopa without or (4) with dyskinesia. Levodopa 223-231 G protein-coupled receptor kinase 6 Homo sapiens 105-109 15755478-6 2005 Levodopa treatment eliciting dyskinesia normalized NR1 and NR2B and increased NR2A subunits to 150 +/- 12% of unlesioned levels. Levodopa 0-8 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 59-63 15755478-6 2005 Levodopa treatment eliciting dyskinesia normalized NR1 and NR2B and increased NR2A subunits to 150 +/- 12% of unlesioned levels. Levodopa 0-8 glutamate ionotropic receptor NMDA type subunit 2A Homo sapiens 78-82 15686961-7 2005 Changes in arrestin and GRK expression in the MPTP group were accompanied by enhanced ERK activation and elevated total ERK expression, which were also reversed by L-DOPA. Levodopa 164-170 mitogen-activated protein kinase 1 Homo sapiens 86-89 15686961-7 2005 Changes in arrestin and GRK expression in the MPTP group were accompanied by enhanced ERK activation and elevated total ERK expression, which were also reversed by L-DOPA. Levodopa 164-170 mitogen-activated protein kinase 1 Homo sapiens 120-123 15728856-1 2005 Regulator of G-protein signaling 9-2 (RGS9-2), a member of the RGS family of G GTPase accelerating proteins, is expressed specifically in the striatum, which participates in antipsychotic-induced tardive dyskinesia and in levodopa-induced dyskinesia. Levodopa 222-230 regulator of G-protein signaling 9 Mus musculus 0-36 15716217-3 2005 Previous studies have suggested that dopaminergic drugs such as L-dopa and dopamine agonists, as well as benzodiazepines and opioids, can treat RLS successfully. Levodopa 64-70 RLS1 Homo sapiens 144-147 15728856-1 2005 Regulator of G-protein signaling 9-2 (RGS9-2), a member of the RGS family of G GTPase accelerating proteins, is expressed specifically in the striatum, which participates in antipsychotic-induced tardive dyskinesia and in levodopa-induced dyskinesia. Levodopa 222-230 regulator of G-protein signaling 9 Mus musculus 38-44 15503197-4 2005 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone extend the plasma half-life of levodopa and reduce "off" time. Levodopa 97-105 catechol-O-methyltransferase Homo sapiens 0-28 15503197-4 2005 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone extend the plasma half-life of levodopa and reduce "off" time. Levodopa 97-105 catechol-O-methyltransferase Homo sapiens 30-34 16156677-7 2005 Selective monoamine oxidase type B (MAO-B) inhibitors, used as monotherapy, delay the need for the introduction of levodopa by about 9 months. Levodopa 115-123 monoamine oxidase B Homo sapiens 10-34 15514976-6 2005 Our data suggest that levodopa-induced dyskinesia results from increased dopamine D(1) receptor-mediated transmission at the level of the direct pathway. Levodopa 22-30 dopamine receptor D1 Homo sapiens 73-95 15642853-14 2005 Patients with PRKN mutations were younger at onset than those without mutations, and they required a lower dose of levodopa despite longer disease duration. Levodopa 115-123 parkin RBR E3 ubiquitin protein ligase Homo sapiens 14-18 15929554-4 2005 The level of L-DOPA released by C17.2-THGC cells, as determined by HPLC assay, was 3793 pmol/10(6) cells, which is 760-fold higher than that produced by C17.2-TH cells, indicating that GTPCH1 expression is important for L-DOPA production by transduced C17.2 cells. Levodopa 13-19 GTP cyclohydrolase 1 Mus musculus 185-191 16156677-7 2005 Selective monoamine oxidase type B (MAO-B) inhibitors, used as monotherapy, delay the need for the introduction of levodopa by about 9 months. Levodopa 115-123 monoamine oxidase B Homo sapiens 36-41 16696314-6 2005 Treatment With L-dopa or PD I plus L-dopa, up-regulation of DR1 mRNA and down-regulation of DR2 mRNA were observed in the ipsilateral striatum which were more obvious than that treated with PD I or vehicle (P < 0.05). Levodopa 15-21 down-regulator of transcription 1 Rattus norvegicus 60-63 15709899-2 2005 To minimise this problem, selective catechol-O-methyltransferase (COMT) inhibitors were developed in order to improve the poor pharmacokinetic profile of levodopa. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 36-64 15709899-2 2005 To minimise this problem, selective catechol-O-methyltransferase (COMT) inhibitors were developed in order to improve the poor pharmacokinetic profile of levodopa. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 66-70 15981741-7 2005 Exacerbation of the rate of protein nitration reactions specifically in the lungs of TNF mice was revealed by the high ratio of 3-nitrotyrosine to L-DOPA after exposure to the air pollutants (Genotype x Exposure factor interaction, p = .014). Levodopa 147-153 tumor necrosis factor Mus musculus 85-88 15689633-2 2005 The first method is based on coupling of 4-aminoantipyrine (4-AAP) with one of the dopamine derivatives (LD, CD) to give a new ligand that reacts with copper tetramine complex to give intensely colored chelates. Levodopa 105-107 serpin family F member 2 Homo sapiens 62-65 16696314-6 2005 Treatment With L-dopa or PD I plus L-dopa, up-regulation of DR1 mRNA and down-regulation of DR2 mRNA were observed in the ipsilateral striatum which were more obvious than that treated with PD I or vehicle (P < 0.05). Levodopa 15-21 prolyl 4-hydroxylase subunit beta Rattus norvegicus 190-194 16696314-6 2005 Treatment With L-dopa or PD I plus L-dopa, up-regulation of DR1 mRNA and down-regulation of DR2 mRNA were observed in the ipsilateral striatum which were more obvious than that treated with PD I or vehicle (P < 0.05). Levodopa 35-41 prolyl 4-hydroxylase subunit beta Rattus norvegicus 190-194 16198485-8 2005 There was a decrease in the relative density of immunolabeling within the dorsolateral striatum for the glutamate transporter, GLT-1, following acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment in the groups administered either vehicle or l-dopa. Levodopa 250-256 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 127-132 16280597-0 2005 Increased vulnerability to L-DOPA toxicity in dopaminergic neurons From VMAT2 heterozygote knockout mice. Levodopa 27-33 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 72-77 16280597-5 2005 We showed that dopaminergic neurons from VMAT2 heterozygous knockout mice were more vulnerable to the toxic effect of L-3, 4-dihydroxyphenylalanine (L-DOPA, a DA precursor) than those from wild-type mice. Levodopa 118-147 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 41-46 16280597-5 2005 We showed that dopaminergic neurons from VMAT2 heterozygous knockout mice were more vulnerable to the toxic effect of L-3, 4-dihydroxyphenylalanine (L-DOPA, a DA precursor) than those from wild-type mice. Levodopa 149-155 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 41-46 16280597-6 2005 Our results suggest that reduction of VMAT2 activity might attenuate the efficacy of L-DOPA therapy for patients with PD. Levodopa 85-91 solute carrier family 18 member A2 Homo sapiens 38-43 16111820-10 2005 The L-DOPA treatment does not reverse the changes in Syt II and Syt X gene expression, but recruits additional, D1 receptor-mediated changes in Syt IV and Syt VII gene expression. Levodopa 4-10 synaptotagmin 4 Rattus norvegicus 144-150 16111820-10 2005 The L-DOPA treatment does not reverse the changes in Syt II and Syt X gene expression, but recruits additional, D1 receptor-mediated changes in Syt IV and Syt VII gene expression. Levodopa 4-10 synaptotagmin 7 Rattus norvegicus 155-162 15390046-3 2005 The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. Levodopa 60-68 catechol-O-methyltransferase Homo sapiens 82-110 15390046-3 2005 The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. Levodopa 60-68 catechol-O-methyltransferase Homo sapiens 112-116 15596235-5 2005 Furthermore, a high dose of levodopa/carbidopa (50/12.5 mg/kg) enhanced LPO and caspase-3, -8, and -9 activities in 6-OHDA-lesioned mouse brain. Levodopa 28-36 caspase 3 Mus musculus 80-101 15596235-6 2005 However, when levodopa/carbidopa (50/12.5 mg/kg) was combined with cabergoline (0.25 mg/kg), the effect reduced levodopa"s enhancement of caspase-3, -8, and -9 activities in the 6-OHDA-lesioned mouse brain. Levodopa 14-22 caspase 3 Mus musculus 138-159 15596235-6 2005 However, when levodopa/carbidopa (50/12.5 mg/kg) was combined with cabergoline (0.25 mg/kg), the effect reduced levodopa"s enhancement of caspase-3, -8, and -9 activities in the 6-OHDA-lesioned mouse brain. Levodopa 112-120 caspase 3 Mus musculus 138-159 16198485-10 2005 The results demonstrate that the reversal in the extracellular level of striatal glutamate following l-dopa treatment in both the acute and subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated groups is not due to changes in either striatal dopamine nerve terminals or in the density of the glutamate transporter, GLT-1. Levodopa 101-107 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 325-330 15258132-0 2004 Levodopa with carbidopa diminishes glycogen concentration, glycogen synthase activity, and insulin-stimulated glucose transport in rat skeletal muscle. Levodopa 0-8 insulin Homo sapiens 91-98 15258132-1 2004 We hypothesized that levodopa with carbidopa, a common therapy for patients with Parkinson"s disease, might contribute to the high prevalence of insulin resistance reported in patients with Parkinson"s disease. Levodopa 21-29 insulin Homo sapiens 145-152 15258132-5 2004 Levodopa-carbidopa also inhibited the insulin-stimulated increase in glycogen synthase activity, whereas propranolol attenuated this effect. Levodopa 0-8 insulin Homo sapiens 38-45 15258132-6 2004 Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS)-1 was reduced by levodopa-carbidopa, although Akt phosphorylation was unaffected by levodopa-carbidopa. Levodopa 97-105 insulin Homo sapiens 0-7 15258132-6 2004 Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS)-1 was reduced by levodopa-carbidopa, although Akt phosphorylation was unaffected by levodopa-carbidopa. Levodopa 97-105 insulin receptor substrate 1 Rattus norvegicus 47-81 15258132-7 2004 A single in vivo dose of levodopa-carbidopa increased skeletal muscle cAMP concentrations, diminished glycogen synthase activity, and reduced tyrosine phosphorylation of IRS-1. Levodopa 25-33 insulin receptor substrate 1 Rattus norvegicus 170-175 15258132-11 2004 The data demonstrate beta-adrenergic-dependent inhibition of insulin action by levodopa-carbidopa and suggest that unrecognized insulin resistance may exist in chronically treated patients with Parkinson"s disease. Levodopa 79-87 insulin Homo sapiens 61-68 15516923-7 2004 We propose that retinal pigment epithelium (which normally expresses tyrosinase) secretes a modulatory factor, possibly L-DOPA, which regulates light adaptation in the retinal circuitry. Levodopa 120-126 tyrosinase Danio rerio 69-79 15390056-2 2004 We present a case of an individual with juvenile parkinsonism caused by homozygous deletion of exon 3 in the parkin gene with disabling long-term side-effects from levodopa who underwent bilateral STN neuromodulation. Levodopa 164-172 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 197-200 15390056-4 2004 Because levodopa responsiveness is a predictor of STN-DBS efficacy, we argued that this kind of surgical approach might be efficacious in hereditary parkin-linked juvenile parkinsonism. Levodopa 8-16 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 50-53 15385622-4 2004 We found that catecholamines (l-3,4-hydroxyphenylalanine [l-dopa], dopamine, adrenaline, and noradrenaline) elevate FUS1 and RLM1 transcription. Levodopa 58-64 Fus1p Saccharomyces cerevisiae S288C 116-120 15385622-4 2004 We found that catecholamines (l-3,4-hydroxyphenylalanine [l-dopa], dopamine, adrenaline, and noradrenaline) elevate FUS1 and RLM1 transcription. Levodopa 58-64 Rlm1p Saccharomyces cerevisiae S288C 125-129 15385622-7 2004 Further genetic analysis combined with immunoblotting revealed that Kss1, one of the mating mitogen-activated protein kinases (MAPKs), and Mpk1, an MAPK of the cell integrity pathway, participated in l-dopa-induced stimulation of FUS1 and RLM1 transcription. Levodopa 200-206 mitogen-activated serine/threonine-protein kinase KSS1 Saccharomyces cerevisiae S288C 68-72 15385622-7 2004 Further genetic analysis combined with immunoblotting revealed that Kss1, one of the mating mitogen-activated protein kinases (MAPKs), and Mpk1, an MAPK of the cell integrity pathway, participated in l-dopa-induced stimulation of FUS1 and RLM1 transcription. Levodopa 200-206 mitogen-activated serine/threonine-protein kinase SLT2 Saccharomyces cerevisiae S288C 139-143 15385622-7 2004 Further genetic analysis combined with immunoblotting revealed that Kss1, one of the mating mitogen-activated protein kinases (MAPKs), and Mpk1, an MAPK of the cell integrity pathway, participated in l-dopa-induced stimulation of FUS1 and RLM1 transcription. Levodopa 200-206 Fus1p Saccharomyces cerevisiae S288C 230-234 15385622-7 2004 Further genetic analysis combined with immunoblotting revealed that Kss1, one of the mating mitogen-activated protein kinases (MAPKs), and Mpk1, an MAPK of the cell integrity pathway, participated in l-dopa-induced stimulation of FUS1 and RLM1 transcription. Levodopa 200-206 Rlm1p Saccharomyces cerevisiae S288C 239-243 15226382-0 2004 Effect of the D3 dopamine receptor partial agonist BP897 [N-[4-(4-(2-methoxyphenyl)piperazinyl)butyl]-2-naphthamide] on L-3,4-dihydroxyphenylalanine-induced dyskinesias and parkinsonism in squirrel monkeys. Levodopa 120-148 dopamine receptor D3 Homo sapiens 14-34 15672541-9 2004 Elevated p53, Bax, cytochrome c, caspase-3 and active fragments of caspase-3 protein were observed in the cells exposed to levodopa. Levodopa 123-131 transformation related protein 53, pseudogene Mus musculus 9-12 15672541-9 2004 Elevated p53, Bax, cytochrome c, caspase-3 and active fragments of caspase-3 protein were observed in the cells exposed to levodopa. Levodopa 123-131 BCL2-associated X protein Mus musculus 14-17 15672541-9 2004 Elevated p53, Bax, cytochrome c, caspase-3 and active fragments of caspase-3 protein were observed in the cells exposed to levodopa. Levodopa 123-131 caspase 3 Mus musculus 33-42 15672541-9 2004 Elevated p53, Bax, cytochrome c, caspase-3 and active fragments of caspase-3 protein were observed in the cells exposed to levodopa. Levodopa 123-131 caspase 3 Mus musculus 67-76 15672541-12 2004 Activation of the mitochondria-dependent pathway and caspase-3 protease may contribute to the mechanism by which levodopa induces apoptosis. Levodopa 113-121 caspase 3 Mus musculus 53-62 15378681-3 2004 Although it is not possible to confirm if this patient has a de novo mutation of the SCA2 gene, this genetic defect seems to be contributing to his parkinsonian features and further supports the concept that apparently sporadic, late-onset, levodopa-responsive Parkinson"s disease may have multiple causes. Levodopa 241-249 ataxin 2 Homo sapiens 85-89 15365141-4 2004 It has been suggested that breakdown of L-dopa by catechol-O-methyltransferase results in increased homocysteine formation. Levodopa 40-46 catechol-O-methyltransferase Homo sapiens 50-78 15502970-2 2004 This study was aimed at investigating the effect of adding the catechol- O-methyltransferase (COMT) inhibitor entacapone to chronic treatment with l-DOPA/benserazide. Levodopa 147-153 catechol-O-methyltransferase Rattus norvegicus 94-98 15502970-10 2004 From a clinical point of view, this finding suggests that administration of a COMT inhibitor should allow the frequency of l-DOPA administration to decrease and to smooth the brain delivery of the l-DOPA, which in the end should facilitate a reduction in the risk of dyskinesia induction. Levodopa 123-129 catechol-O-methyltransferase Rattus norvegicus 78-82 15502970-10 2004 From a clinical point of view, this finding suggests that administration of a COMT inhibitor should allow the frequency of l-DOPA administration to decrease and to smooth the brain delivery of the l-DOPA, which in the end should facilitate a reduction in the risk of dyskinesia induction. Levodopa 197-203 catechol-O-methyltransferase Rattus norvegicus 78-82 15355491-3 2004 The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Levodopa 113-121 monoamine oxidase B Homo sapiens 51-55 15355491-3 2004 The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Levodopa 113-121 catechol-O-methyltransferase Homo sapiens 60-64 15355491-9 2004 However, the frequency of COMT(L/L) homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. Levodopa 98-106 catechol-O-methyltransferase Homo sapiens 26-30 15355491-10 2004 MAOB and COMT AG-HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG-LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Levodopa 100-108 monoamine oxidase B Homo sapiens 0-4 15355491-10 2004 MAOB and COMT AG-HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG-LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Levodopa 100-108 catechol-O-methyltransferase Homo sapiens 9-13 15355491-11 2004 CONCLUSION: The results of the study suggest that patients with COMT(L/L) genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 64-68 15355491-11 2004 CONCLUSION: The results of the study suggest that patients with COMT(L/L) genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy. Levodopa 154-162 monoamine oxidase B Homo sapiens 96-100 15340869-1 2004 Two catechol- O-methyltransferase (COMT) inhibitors, entacapone and tolcapone, were developed during the 1990"s to be used as adjuncts to levodopa (LD) - dopa decarboxylase (DDC) inhibitors in the treatment of Parkinson"s disease (PD). Levodopa 138-146 catechol-O-methyltransferase Homo sapiens 4-33 15340869-1 2004 Two catechol- O-methyltransferase (COMT) inhibitors, entacapone and tolcapone, were developed during the 1990"s to be used as adjuncts to levodopa (LD) - dopa decarboxylase (DDC) inhibitors in the treatment of Parkinson"s disease (PD). Levodopa 138-146 catechol-O-methyltransferase Homo sapiens 35-39 15389992-0 2004 Amantadine for levodopa-induced choreic dyskinesia in compound heterozygotes for GCH1 mutations. Levodopa 15-23 GTP cyclohydrolase 1 Homo sapiens 81-85 15389992-1 2004 Amantadine suppressed severe levodopa-induced choreic dyskinesia, which developed at initiation of levodopa therapy, in two siblings manifesting dystonia with motor delay phenotype of GTP cyclohydrolase I deficiency caused by compound heterozygous GCH1 mutations. Levodopa 29-37 GTP cyclohydrolase 1 Homo sapiens 248-252 15351512-11 2004 Additional in-vitro studies using human LAT1 reveal a much lower affinity of FDOPA compared to OMFD or L-DOPA. Levodopa 103-109 solute carrier family 7 member 5 Homo sapiens 40-44 15495118-0 2004 Catechol-O-methyltransferase inhibitors versus active comparators for levodopa-induced complications in Parkinson"s disease. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 0-28 15495118-2 2004 The principle aim of COMT inhibitor therapy is to increase the duration of effect of the levodopa dose and thus reduce the time patients spend in the relatively immobile "off" phase. Levodopa 89-97 catechol-O-methyltransferase Homo sapiens 21-25 15495118-7 2004 SELECTION CRITERIA: Randomised controlled trials of adjuvant COMT inhibitor therapy versus an active comparator in patients with a clinical diagnosis of idiopathic Parkinson"s disease and long-term complications of levodopa therapy. Levodopa 215-223 catechol-O-methyltransferase Homo sapiens 61-65 15495119-0 2004 Catechol-O-methyltransferase inhibitors for levodopa-induced complications in Parkinson"s disease. Levodopa 44-52 catechol-O-methyltransferase Homo sapiens 0-28 15495119-2 2004 The principle aim of COMT inhibitor therapy is to increase the duration of effect of each levodopa dose and thus reduce the time patients spend in the relatively immobile "off" phase. Levodopa 90-98 catechol-O-methyltransferase Homo sapiens 21-25 15495119-3 2004 OBJECTIVES: To compare the efficacy and safety of adjuvant COMT inhibitor therapy versus placebo in patients with Parkinson"s disease, already established on levodopa and suffering from motor complications. Levodopa 158-166 catechol-O-methyltransferase Homo sapiens 59-63 15495119-7 2004 SELECTION CRITERIA: Randomised controlled trials of adjuvant COMT inhibitor therapy versus a placebo in patients with a clinical diagnosis of idiopathic Parkinson"s disease and long-term complications of levodopa therapy. Levodopa 204-212 catechol-O-methyltransferase Homo sapiens 61-65 15477510-1 2004 BACKGROUND: The catechol O-methyltransferase inhibitor entacapone acts by extending the elimination half-life of levodopa and is currently approved as an adjunct to levodopa for the treatment of patients with Parkinson disease (PD) with motor fluctuations. Levodopa 113-121 catechol-O-methyltransferase Homo sapiens 16-44 15477510-1 2004 BACKGROUND: The catechol O-methyltransferase inhibitor entacapone acts by extending the elimination half-life of levodopa and is currently approved as an adjunct to levodopa for the treatment of patients with Parkinson disease (PD) with motor fluctuations. Levodopa 165-173 catechol-O-methyltransferase Homo sapiens 16-44 15466357-1 2004 Organ-specific overexpression of type 2 L-amino acid transporter (LAT2) in the kidney of the spontaneous hypertensive rat (SHR), accompanied by an enhanced ability to take up L-DOPA, may constitute the basis for the enhanced renal production of dopamine in the SHR in an attempt overcome the deficient dopamine-mediated natriuresis. Levodopa 175-181 linker for activation of T cells family, member 2 Rattus norvegicus 66-70 15466357-2 2004 To understand the physiological role of LAT2-mediated L-DOPA handling, we used 21-nucleotide small interfering RNA duplexes (siRNA) to specifically suppress LAT2 expression in LLC-PK1 cells, a cell line that retains several properties of proximal tubular epithelial cells and takes up L-DOPA largely through Na+-independent transporters. Levodopa 54-60 linker for activation of T cells family member 2 Sus scrofa 40-44 15466357-5 2004 The LAT2 siRNA but not the mismatch LAT2 siRNA, reduced by 85% [14C]-L-DOPA accumulation, a time- and concentration-dependent effect. Levodopa 69-75 linker for activation of T cells family member 2 Sus scrofa 4-8 15380638-1 2004 Parkinson"s disease is a neurodegenerative disease and its symptoms are relieved by administration of L-dopa (LD), which is converted by neuronal aromatic L-aminoacid decarboxylase (AADC), restoring dopamine (DA) levels in surviving neurons. Levodopa 102-108 dopa decarboxylase Rattus norvegicus 155-180 15380638-1 2004 Parkinson"s disease is a neurodegenerative disease and its symptoms are relieved by administration of L-dopa (LD), which is converted by neuronal aromatic L-aminoacid decarboxylase (AADC), restoring dopamine (DA) levels in surviving neurons. Levodopa 102-108 dopa decarboxylase Rattus norvegicus 182-186 15380638-1 2004 Parkinson"s disease is a neurodegenerative disease and its symptoms are relieved by administration of L-dopa (LD), which is converted by neuronal aromatic L-aminoacid decarboxylase (AADC), restoring dopamine (DA) levels in surviving neurons. Levodopa 110-112 dopa decarboxylase Rattus norvegicus 155-180 15380638-1 2004 Parkinson"s disease is a neurodegenerative disease and its symptoms are relieved by administration of L-dopa (LD), which is converted by neuronal aromatic L-aminoacid decarboxylase (AADC), restoring dopamine (DA) levels in surviving neurons. Levodopa 110-112 dopa decarboxylase Rattus norvegicus 182-186 15285777-1 2004 OBJECTIVES: Levodopa is the immediate precursor of dopamine and the substrate for DOPA decarboxylase, an enzyme subject to regulation in living brain. Levodopa 12-20 dopa decarboxylase Homo sapiens 82-100 15285777-6 2004 Compartmental analysis was used to probe the physiological basis of the activation of K: levodopa treatment increased by 15% the apparent distribution volume of [(18)F]fluorodopa in cerebellum (, ml/g) of both patients and control subjects, without significantly altering the unidirectional blood-brain clearance (, ml/g/min) or the relative activity of DOPA decarboxylase (, min(-1)) in putamen. Levodopa 89-97 dopa decarboxylase Homo sapiens 354-372 15285777-6 2004 Compartmental analysis was used to probe the physiological basis of the activation of K: levodopa treatment increased by 15% the apparent distribution volume of [(18)F]fluorodopa in cerebellum (, ml/g) of both patients and control subjects, without significantly altering the unidirectional blood-brain clearance (, ml/g/min) or the relative activity of DOPA decarboxylase (, min(-1)) in putamen. Levodopa 89-97 CD59 molecule (CD59 blood group) Homo sapiens 376-383 15341597-0 2004 Chronic L-DOPA treatment increases extracellular glutamate levels and GLT1 expression in the basal ganglia in a rat model of Parkinson"s disease. Levodopa 8-14 solute carrier family 1 member 2 Rattus norvegicus 70-74 15341597-8 2004 The L-DOPA-induced overexpression of GLT1 may represent a compensatory mechanism involving astrocytes to limit glutamate overactivity and subsequent toxic processes. Levodopa 4-10 solute carrier family 1 member 2 Rattus norvegicus 37-41 15358983-7 2004 Although both L-dopa and bromocriptine reduced P50 amplitude, they did so in an equal ratio for both the response to the conditioning (C) and the testing (T) stimuli, therefore not resulting in a reduction of the P50 suppression ratio (T/C). Levodopa 14-20 nuclear factor kappa B subunit 1 Homo sapiens 47-50 15341519-4 2004 We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats. Levodopa 244-252 myelin basic protein Rattus norvegicus 160-180 15341519-4 2004 We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats. Levodopa 244-252 calmodulin 1 Rattus norvegicus 185-195 15379738-1 2004 BACKGROUND: Entacapone is a COMT inhibitor used in Parkinson"s disease (PD) patients, as an adjunctive therapy to L-dopa in order to prolong its bioavailability and thus its clinical effect. Levodopa 114-120 catechol-O-methyltransferase Homo sapiens 28-32 15254790-5 2004 Patients treated with L-Dopa and dopamine agonists showed the lowest values of Bcl-2, coupled with the highest density of PBRs, while increased levels of Cu/Zn SOD were found in the group under monotherapy with L-Dopa. Levodopa 22-28 BCL2 apoptosis regulator Homo sapiens 79-84 15240551-6 2004 Compound Sox2(beta-geo/DeltaENH) heterozygotes show important cerebral malformations, with parenchymal loss and ventricle enlargement, and L-dopa-rescuable circling behaviour and epilepsy. Levodopa 139-145 SRY (sex determining region Y)-box 2 Mus musculus 9-13 15271688-0 2004 High- and low-affinity transport of L-leucine and L-DOPA by the hetero amino acid exchangers LAT1 and LAT2 in LLC-PK1 renal cells. Levodopa 50-56 L-type amino acid transporter 1 Sus scrofa 93-97 15271688-0 2004 High- and low-affinity transport of L-leucine and L-DOPA by the hetero amino acid exchangers LAT1 and LAT2 in LLC-PK1 renal cells. Levodopa 50-56 linker for activation of T cells family member 2 Sus scrofa 102-106 15180956-8 2004 L-dopa in the culture medium was increased by PTN. Levodopa 0-6 pleiotrophin Mus musculus 46-49 15254790-5 2004 Patients treated with L-Dopa and dopamine agonists showed the lowest values of Bcl-2, coupled with the highest density of PBRs, while increased levels of Cu/Zn SOD were found in the group under monotherapy with L-Dopa. Levodopa 211-217 BCL2 apoptosis regulator Homo sapiens 79-84 15180924-0 2004 The dopamine precursor L-dihydroxyphenylalanine is transported by the amino acid transporters rBAT and LAT2 in renal cortex. Levodopa 23-47 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 94-98 15039453-5 2004 In a rat model of Parkinson"s disease (unilateral 6-hydroxydopamine lesion), the pulmonary formulation of L-dopa (0.5-2.0 mg) yielded more rapid and robust elevations in striatal L-dopa, dopamine, and dihydroxyphenylacetic acid levels, as well as 2.5 to 3.7 times as many c-fos-expressing striatal neurons. Levodopa 106-112 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 272-277 15223297-0 2004 NR2B selective NMDA receptor antagonist CP-101,606 prevents levodopa-induced motor response alterations in hemi-parkinsonian rats. Levodopa 60-68 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 0-4 15223297-8 2004 These results suggest that activation of NR2B subunit containing NMDA receptors contributes to both the development and maintenance of levodopa-induced motor response alterations, through a mechanism that involves an increase in GluR1 phosphorylation in striatal spiny neurons. Levodopa 135-143 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 41-45 15223297-8 2004 These results suggest that activation of NR2B subunit containing NMDA receptors contributes to both the development and maintenance of levodopa-induced motor response alterations, through a mechanism that involves an increase in GluR1 phosphorylation in striatal spiny neurons. Levodopa 135-143 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 229-234 15249627-0 2004 L-dopa-induced dyskinesia improvement after STN-DBS depends upon medication reduction. Levodopa 0-6 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 44-47 15180924-0 2004 The dopamine precursor L-dihydroxyphenylalanine is transported by the amino acid transporters rBAT and LAT2 in renal cortex. Levodopa 23-47 solute carrier family 7 member 8 S homeolog Xenopus laevis 103-107 15180924-5 2004 Complementary RNA from two amino acid transporters yielded l-DOPA uptake significantly above water-injected controls the rBAT/b(0,+)AT dimer (rBAT) and the LAT2/4F2 dimer (LAT2). Levodopa 59-65 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 121-125 15180924-5 2004 Complementary RNA from two amino acid transporters yielded l-DOPA uptake significantly above water-injected controls the rBAT/b(0,+)AT dimer (rBAT) and the LAT2/4F2 dimer (LAT2). Levodopa 59-65 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 142-146 15180924-5 2004 Complementary RNA from two amino acid transporters yielded l-DOPA uptake significantly above water-injected controls the rBAT/b(0,+)AT dimer (rBAT) and the LAT2/4F2 dimer (LAT2). Levodopa 59-65 solute carrier family 7 member 8 S homeolog Xenopus laevis 156-164 15180924-5 2004 Complementary RNA from two amino acid transporters yielded l-DOPA uptake significantly above water-injected controls the rBAT/b(0,+)AT dimer (rBAT) and the LAT2/4F2 dimer (LAT2). Levodopa 59-65 solute carrier family 7 member 8 S homeolog Xenopus laevis 156-160 15180924-6 2004 In contradistinction to renal cortical poly-A(+), l-DOPA kinetics of rBAT and LAT2 showed classic Michaelis-Menton kinetics with K(m)s in the micromolar and millimolar range, respectively. Levodopa 50-56 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 69-73 15180924-6 2004 In contradistinction to renal cortical poly-A(+), l-DOPA kinetics of rBAT and LAT2 showed classic Michaelis-Menton kinetics with K(m)s in the micromolar and millimolar range, respectively. Levodopa 50-56 solute carrier family 7 member 8 S homeolog Xenopus laevis 78-82 15180924-7 2004 Sequence-specific antisense oligonucleotides to rBAT or LAT2 (AS) caused inhibition of rBAT and LAT2 cRNA-induced l-DOPA transport and cortical poly-A(+)-induced arginine and phenylalanine transport. Levodopa 114-120 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 48-52 15180924-7 2004 Sequence-specific antisense oligonucleotides to rBAT or LAT2 (AS) caused inhibition of rBAT and LAT2 cRNA-induced l-DOPA transport and cortical poly-A(+)-induced arginine and phenylalanine transport. Levodopa 114-120 solute carrier family 7 member 8 S homeolog Xenopus laevis 56-60 15180924-7 2004 Sequence-specific antisense oligonucleotides to rBAT or LAT2 (AS) caused inhibition of rBAT and LAT2 cRNA-induced l-DOPA transport and cortical poly-A(+)-induced arginine and phenylalanine transport. Levodopa 114-120 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 87-91 15180924-7 2004 Sequence-specific antisense oligonucleotides to rBAT or LAT2 (AS) caused inhibition of rBAT and LAT2 cRNA-induced l-DOPA transport and cortical poly-A(+)-induced arginine and phenylalanine transport. Levodopa 114-120 solute carrier family 7 member 8 S homeolog Xenopus laevis 96-100 15180924-9 2004 In cultured kidney cells, silencing inhibitory RNA (siRNA) to rBAT significantly inhibited l-DOPA uptake. Levodopa 91-97 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 62-66 15180924-10 2004 We conclude that rBAT and LAT2 can mediate apical and basolateral l-DOPA uptake into the proximal tubule, respectively. Levodopa 66-72 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 17-21 15180924-10 2004 We conclude that rBAT and LAT2 can mediate apical and basolateral l-DOPA uptake into the proximal tubule, respectively. Levodopa 66-72 solute carrier family 7 member 8 S homeolog Xenopus laevis 26-30 15283001-10 2004 Following only the nighttime administration of L-dopa, RLS patients manifested a more pronounced inhibition of prolactin release and an increase in growth hormone secretion. Levodopa 47-53 growth hormone 1 Homo sapiens 148-162 15200428-2 2004 LAT2 promotes L-DOPA renal uptake, and this may determine the rate of dopamine synthesis. Levodopa 14-20 linker for activation of T cells family, member 2 Rattus norvegicus 0-4 15200428-7 2004 RESULTS: LAT2 in WKY cells contributed almost exclusively for [(14)C]-L-DOPA uptake. Levodopa 70-76 linker for activation of T cells family, member 2 Rattus norvegicus 9-13 15200428-8 2004 In SHR cells [(14)C]-L-DOPA uptake was 25% through system B(0), 25% through LAT2 (resulting from inhibition by 1 mmol/L glycine, L-alanine, L-serine, and L-threonine), and the remaining 50% through LAT1. Levodopa 21-27 linker for activation of T cells family, member 2 Rattus norvegicus 76-80 15200428-11 2004 CONCLUSION: Differences in L-DOPA handling between SHR and WKY cells may result from over-expression of LAT1 and LAT2 transporters in the former. Levodopa 27-33 linker for activation of T cells family, member 2 Rattus norvegicus 113-117 15165835-11 2004 Chronic, selective inhibition of MAO-B by rasagiline potentiated L-DOPA-induced turning in this rodent model. Levodopa 65-71 amine oxidase [flavin-containing] B Cavia porcellus 33-38 15275774-7 2004 ), a DOPA decarboxylase inhibitor, abolished the antinociceptive effect of L-DOPA. Levodopa 75-81 dopa decarboxylase Mus musculus 5-23 15384706-6 2004 Administration of levodopa/DCI (100 mg/day) improved not only her left-sided rigidity but also the rCBF in the right corpus striatum. Levodopa 18-26 CCAAT/enhancer binding protein zeta Rattus norvegicus 99-103 15462205-8 2004 This is, probably, due to an L-tyrosine-induced competitive inhibition of the L-DOPA transport to monoenzymatic AADC neurons after its release from the monoenzymatic TH neurons. Levodopa 78-84 dopa decarboxylase Rattus norvegicus 112-116 21706729-1 2004 Tyrosinase (EC 1.14.18.1) catalyzes the oxidation of L-3,4-dihydroxyphenylalanine (L-DOPA) to 2,3,5,6-tetrahydro-5,6-dioxo-1H-indole-2-carboxylate (dopachrome), according to the classical Michaelis-Menten kinetic mechanism. Levodopa 53-81 tyrosinase Homo sapiens 0-10 21706729-1 2004 Tyrosinase (EC 1.14.18.1) catalyzes the oxidation of L-3,4-dihydroxyphenylalanine (L-DOPA) to 2,3,5,6-tetrahydro-5,6-dioxo-1H-indole-2-carboxylate (dopachrome), according to the classical Michaelis-Menten kinetic mechanism. Levodopa 83-89 tyrosinase Homo sapiens 0-10 15196506-0 2004 DARPP-32 and modulation of cAMP signaling: involvement in motor control and levodopa-induced dyskinesia. Levodopa 76-84 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 0-8 15196509-3 2004 Recent experiments in levodopa-treated MPTP animals, co-administered either a threshold dose of cabergoline or a glutamate NMDA NR2B-selective antagonist (CI-1041), have afforded protection against dyskinesia, perhaps through presynaptic inhibition of glutamate release and blockade of supersensitive postsynaptic NMDA receptors in the striatum, respectively. Levodopa 22-30 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 128-132 15462107-2 2004 Our aim was to find the efficacy of gabapentin in the treatment of RLS in HD patients by comparing a largely used drug, levodopa. Levodopa 120-128 RLS1 Homo sapiens 67-70 15462107-8 2004 CONCLUSION: To our knowledge this was the first study comparing gabapentin and levodopa efficacy for the treatment of RLS in HD patients. Levodopa 79-87 RLS1 Homo sapiens 118-121 15207281-1 2004 In parkinsonian patients as well as in primate models with levodopa-induced dyskinesias (LID), an increase in the expression of preproenkephalin in the striatal output pathways has been demonstrated. Levodopa 59-67 proenkephalin Homo sapiens 128-144 15214892-7 2004 Cell cycles were determined by flow cytometry, and the activity of tyrosinase was evaluated by L-DOPA reaction. Levodopa 95-101 tyrosinase Homo sapiens 67-77 15059976-3 2004 Here we show that L-dopa, dopamine, and other catecholamines dissolve fibrils of alpha-synuclein and Abeta peptide generated in vitro. Levodopa 18-24 synuclein, alpha Mus musculus 81-96 15059976-5 2004 In addition, intraneuronal alpha-synuclein deposits formed in a mouse model were dissolved by incubation of tissue slices with L-dopa. Levodopa 127-133 synuclein, alpha Mus musculus 27-42 15221622-1 2004 Entacapone is a specific, peripherally acting catechol- O-methyltransferase (COMT) inhibitor that prevents peripheral degradation of L-dopa, thus improving its bioavailability. Levodopa 133-139 catechol-O-methyltransferase Homo sapiens 46-75 15221622-1 2004 Entacapone is a specific, peripherally acting catechol- O-methyltransferase (COMT) inhibitor that prevents peripheral degradation of L-dopa, thus improving its bioavailability. Levodopa 133-139 catechol-O-methyltransferase Homo sapiens 77-81 15065221-0 2004 Upregulation of striatal adenosine A2A receptor mRNA in 6-hydroxydopamine-lesioned rats intermittently treated with L-DOPA. Levodopa 116-122 adenosine A2a receptor Rattus norvegicus 25-47 15192175-0 2004 Dramatic levodopa responsiveness of dystonia in a sporadic case of spinocerebellar ataxia type 3. Levodopa 9-17 ataxin 3 Homo sapiens 67-96 15192175-3 2004 A trial of levodopa for dystonia in SCA 3 may be of therapeutic benefit, at least in the initial stage of the disease. Levodopa 11-19 ataxin 3 Homo sapiens 36-41 15065221-1 2004 To determine whether the adenosine A2A receptor might play a role in L-DOPA-induced dyskinesia in Parkinson"s disease, we analyzed changes in the expression of A2A receptor mRNA in response to intermittent treatment with L-DOPA in rats with dopaminergic denervation by 6-hydroxydopamine (OHDA) infusion into the medial forebrain bundle. Levodopa 69-75 adenosine A2a receptor Rattus norvegicus 25-47 15030379-6 2004 Exposure of Caco-2 cells, a human intestinal epithelial cell line, to human IFN-gamma resulted in a concentration-dependent and long-lasting inhibition of L-DOPA uptake, which most likely explains the decrease in dopamine levels in the inflamed mucosa. Levodopa 155-161 interferon gamma Homo sapiens 76-85 15133829-0 2004 SCA2 presenting as levodopa-responsive parkinsonism in a young patient from the United Kingdom: a case report. Levodopa 19-27 ataxin 2 Homo sapiens 0-4 15109582-3 2004 alpha-Synuclein positive, neuritic pathology, in the putamen of DLB and Parkinson"s disease dementia (PDD), may contribute to postural-instability gait difficulty, parkinsonism, diminished levodopa responsiveness and increased neuroleptic sensitivity. Levodopa 189-197 synuclein alpha Homo sapiens 0-15 15018791-1 2004 A simple and rapid assay is described for the simultaneous analysis of levodopa (l-DOPA) and 3-O-methyldopa (3-OMD) in human plasma samples, applying an ion-pair reversed-phase liquid chromatographic method with electrochemical detection, designed for clinical trials performed to study the effect of peripheral catechol-O-methyltransferase inhibitors on the metabolism of l-DOPA. Levodopa 81-87 catechol-O-methyltransferase Homo sapiens 312-340 15148140-1 2004 BACKGROUND: Levodopa metabolism via catechol O-methyltransferase increases levels of the neurotoxin homocysteine, which induces an axonal-accentuated degeneration in sensory peripheral nerves in vitro. Levodopa 12-20 catechol-O-methyltransferase Homo sapiens 36-64 15030379-0 2004 Decreased availability of intestinal dopamine in transmural colitis may relate to inhibitory effects of interferon-gamma upon L-DOPA uptake. Levodopa 126-132 interferon gamma Homo sapiens 104-120 15030379-8 2004 In this model of experimental colitis, the decrease in dopamine levels is most likely explained by the inhibitory effect of IFN-gamma on L-DOPA uptake by intestinal epithelial cells. Levodopa 137-143 interferon gamma Homo sapiens 124-133 14985260-6 2004 Acute single-dose dopaminergic treatment with 100 mg levodopa + 25 mg benserazide, 90 min prior to the evening measurements, largely resolved patients" RLS symptoms, but had no effect on pin-prick pain. Levodopa 53-61 RLS1 Homo sapiens 152-155 15057519-1 2004 Patients with Parkinson"s disease (PD) and levodopa-induced motor complications experience a short-duration response (SDR) to levodopa which can be considered the basis of motor fluctuations. Levodopa 43-51 caveolae associated protein 2 Homo sapiens 118-121 22900342-4 2004 It is suggested that the changes in the oscillator strengths of different 4f-4f bands and Judd-Ofelt intensity (Tlamda) parameters can be used to predict in vivo intracellular complexation of DOPA with Ca(II) through Nd (III)-DOPA absorption spectral studies in-vitro as both Nd (III) and Ca(II) have unique similarity in their coordination behaviour. Levodopa 192-196 carbonic anhydrase 2 Homo sapiens 202-208 22900342-4 2004 It is suggested that the changes in the oscillator strengths of different 4f-4f bands and Judd-Ofelt intensity (Tlamda) parameters can be used to predict in vivo intracellular complexation of DOPA with Ca(II) through Nd (III)-DOPA absorption spectral studies in-vitro as both Nd (III) and Ca(II) have unique similarity in their coordination behaviour. Levodopa 192-196 carbonic anhydrase 2 Homo sapiens 289-295 22900342-4 2004 It is suggested that the changes in the oscillator strengths of different 4f-4f bands and Judd-Ofelt intensity (Tlamda) parameters can be used to predict in vivo intracellular complexation of DOPA with Ca(II) through Nd (III)-DOPA absorption spectral studies in-vitro as both Nd (III) and Ca(II) have unique similarity in their coordination behaviour. Levodopa 226-230 carbonic anhydrase 2 Homo sapiens 202-208 15057519-1 2004 Patients with Parkinson"s disease (PD) and levodopa-induced motor complications experience a short-duration response (SDR) to levodopa which can be considered the basis of motor fluctuations. Levodopa 126-134 caveolae associated protein 2 Homo sapiens 118-121 14701706-3 2004 Alveolar Type II cells express the enzyme aromatic-L-amino acid decarboxylase (AADC) and, when incubated with the dopamine precursor, 3-hydroxy-L-tyrosine (L-dopa), produce dopamine. Levodopa 156-162 dopa decarboxylase Rattus norvegicus 42-77 15198291-6 2004 GH levels were measured in patients with SCD with and without growth failure using arginine and L-Dopa as provocative stimulation tests. Levodopa 96-102 growth hormone 1 Homo sapiens 0-2 15056471-6 2004 Striatal FosB/Delta FosB up-regulation in SND and PD rats correlated with the severity of L-DOPA-induced dyskinesias. Levodopa 90-96 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 9-13 15056471-6 2004 Striatal FosB/Delta FosB up-regulation in SND and PD rats correlated with the severity of L-DOPA-induced dyskinesias. Levodopa 90-96 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-24 14701706-4 2004 Rats fed TSD, a precursor of L-dopa and dopamine, had increased urinary dopamine levels, which were inhibited by benserazide, an inhibitor of AADC. Levodopa 29-35 dopa decarboxylase Rattus norvegicus 142-146 14751427-0 2004 Effects of antidepressant treatment on thyrotropin-releasing hormone stimulation, growth hormone response to L-DOPA, and dexamethasone suppression tests in major depressive patients. Levodopa 109-115 growth hormone 1 Homo sapiens 82-96 15003008-4 2004 On the other hand, the polycondensates inhibited the tyrosine hydroxylation and L-DOPA oxidation by chelation to the active site of tyrosinase. Levodopa 80-86 tyrosinase Homo sapiens 132-142 14975680-1 2004 Tolcapone and entacapone are catechol-O-methyltransferase (COMT) inhibitors used as adjuncts to levodopa in the treatment of Parkinson"s disease (PD). Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 29-57 14975680-1 2004 Tolcapone and entacapone are catechol-O-methyltransferase (COMT) inhibitors used as adjuncts to levodopa in the treatment of Parkinson"s disease (PD). Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 59-63 14751427-2 2004 TSH responses to TRH showed a tendency to increase from pre- to posttreatment period, while TRH-induced PRL and L-DOPA-induced GH responses did not change with treatment in depressed patients who responded to the treatment. Levodopa 112-118 growth hormone 1 Homo sapiens 127-129 14751427-4 2004 No interconnections were found among the responses in DST, TRH stimulation test and L-DOPA-induced GH test in the patients. Levodopa 84-90 growth hormone 1 Homo sapiens 99-101 14978667-2 2004 Many reported cases that had a good response to levodopa have proved to have autosomal recessive juvenile parkinsonism (AR-JP) due to mutations in the parkin gene. Levodopa 48-56 parkin RBR E3 ubiquitin protein ligase Homo sapiens 120-125 14767720-1 2004 The aim of this trial was to evaluate the effects of the COMT inhibitor entacapone on both the pharmacokinetic profile and clinical efficacy of controlled release levodopa in Parkinson"s disease (PD) patients. Levodopa 163-171 catechol-O-methyltransferase Homo sapiens 57-61 15031547-1 2004 Catechol O-methyltransferase (COMT) inactivates catecholamines and catechol-containing drugs such as L-DOPA. Levodopa 101-107 catechol-O-methyltransferase Canis lupus familiaris 0-28 15031547-1 2004 Catechol O-methyltransferase (COMT) inactivates catecholamines and catechol-containing drugs such as L-DOPA. Levodopa 101-107 catechol-O-methyltransferase Canis lupus familiaris 30-34 14751592-0 2004 Effect of the adenosine A2A receptor antagonist 8-(3-chlorostyryl)caffeine on L-DOPA biotransformation in rat striatum. Levodopa 78-84 adenosine A2a receptor Rattus norvegicus 14-36 14751592-1 2004 In the present study, we investigated effects of the new selective adenosine A2A receptor antagonist 8-(3-chlorostyryl)caffeine (CSC) on L-DOPA-induced dopamine (DA) release in the striatum of intact and reserpine-treated rats. Levodopa 137-143 adenosine A2a receptor Rattus norvegicus 67-89 14743456-2 2004 In this study, male Sprague-Dawley rats were treated with levodopa (L-dopa)-benserazide, which increases DOPAL production by MAO, and disulfiram, an irreversible inhibitor of ALDH, which reduces the formation of DOPAC from DOPAL. Levodopa 58-66 monoamine oxidase A Rattus norvegicus 125-128 14743456-2 2004 In this study, male Sprague-Dawley rats were treated with levodopa (L-dopa)-benserazide, which increases DOPAL production by MAO, and disulfiram, an irreversible inhibitor of ALDH, which reduces the formation of DOPAC from DOPAL. Levodopa 68-74 monoamine oxidase A Rattus norvegicus 125-128 14718683-0 2004 COMT inhibitors in Parkinson"s disease: can they prevent and/or reverse levodopa-induced motor complications? Levodopa 72-80 catechol-O-methyltransferase Homo sapiens 0-4 14574438-5 2004 Further, when COMT knockout mice were challenged with l-dopa or a dopamine transporter (DAT) inhibitor, an accumulation of dopamine occurred and the neurochemical and locomotor effects of l-dopa and GBR 12909 were modified accordingly. Levodopa 188-194 catechol-O-methyltransferase Mus musculus 14-18 14574438-5 2004 Further, when COMT knockout mice were challenged with l-dopa or a dopamine transporter (DAT) inhibitor, an accumulation of dopamine occurred and the neurochemical and locomotor effects of l-dopa and GBR 12909 were modified accordingly. Levodopa 188-194 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 66-86 14574438-5 2004 Further, when COMT knockout mice were challenged with l-dopa or a dopamine transporter (DAT) inhibitor, an accumulation of dopamine occurred and the neurochemical and locomotor effects of l-dopa and GBR 12909 were modified accordingly. Levodopa 54-60 catechol-O-methyltransferase Mus musculus 14-18 14574438-5 2004 Further, when COMT knockout mice were challenged with l-dopa or a dopamine transporter (DAT) inhibitor, an accumulation of dopamine occurred and the neurochemical and locomotor effects of l-dopa and GBR 12909 were modified accordingly. Levodopa 54-60 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 66-86 14705122-1 2004 The dopamine D(1) receptor is considered to participate in levodopa"s antiparkinsonian action and levodopa-induced dyskinesias. Levodopa 59-67 dopamine receptor D1 Homo sapiens 4-26 14705122-1 2004 The dopamine D(1) receptor is considered to participate in levodopa"s antiparkinsonian action and levodopa-induced dyskinesias. Levodopa 98-106 dopamine receptor D1 Homo sapiens 4-26 14705123-2 2004 The two probands having homozygous SCA2 mutations presenting with early-onset dopa-responsive parkinsonism without ataxia develop dyskinesias within a year of starting levodopa. Levodopa 168-176 ataxin 2 Homo sapiens 35-39 14732617-1 2004 BACKGROUND: We recently reported that spinocerebellar ataxia type 2 (SCA2) caused familial parkinsonism in 2 brothers with predominant symptoms of resting tremor, rigidity, and bradykinesia that responded to levodopa. Levodopa 208-216 ataxin 2 Homo sapiens 38-67 14732617-1 2004 BACKGROUND: We recently reported that spinocerebellar ataxia type 2 (SCA2) caused familial parkinsonism in 2 brothers with predominant symptoms of resting tremor, rigidity, and bradykinesia that responded to levodopa. Levodopa 208-216 ataxin 2 Homo sapiens 69-73 14732617-11 2004 Parkinsonian SCA2 responded well to levodopa. Levodopa 36-44 ataxin 2 Homo sapiens 13-17 15354385-0 2004 MTHFR C677T polymorphism, folic acid and hyperhomocysteinemia in levodopa treated patients with Parkinson"s disease. Levodopa 65-73 methylenetetrahydrofolate reductase Homo sapiens 0-5 15090932-0 2004 Pharmacokinetic-pharmacodynamic interaction between BIA 3-202, a novel COMT inhibitor, and levodopa/carbidopa. Levodopa 91-99 catechol-O-methyltransferase Homo sapiens 71-75 15090932-15 2004 In conclusion, the novel COMT inhibitor BIA 3-202 increased the bioavailability of levodopa and reduced the formation of 3-OMD when administered with standard levodopa/carbidopa. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 25-29 15090932-15 2004 In conclusion, the novel COMT inhibitor BIA 3-202 increased the bioavailability of levodopa and reduced the formation of 3-OMD when administered with standard levodopa/carbidopa. Levodopa 159-167 catechol-O-methyltransferase Homo sapiens 25-29 14697317-10 2004 These data and previous studies suggest the involvement of enhanced opioid transmission in L-DOPA-induced dyskinesia and that part of the reason why D2/D3 dopamine receptor agonists have a reduced propensity to elicit dyskinesia may reside in their reduced ability to elevate opioid transmission. Levodopa 91-97 dopamine receptor D3 Rattus norvegicus 152-172 15221500-5 2004 GH stimulation tests were performed after the ingestion of 500 mg of L-dopa. Levodopa 69-75 growth hormone 1 Homo sapiens 0-2 15552590-3 2004 The next step in the biosynthetic pathway, the removal of the carboxyl group on the molecule by the enzyme L-aromatic acid decarboxylase (AADC), happens rapidly after L-DOPA is taken up into neurons. Levodopa 167-173 dopa decarboxylase Mus musculus 107-136 15552590-3 2004 The next step in the biosynthetic pathway, the removal of the carboxyl group on the molecule by the enzyme L-aromatic acid decarboxylase (AADC), happens rapidly after L-DOPA is taken up into neurons. Levodopa 167-173 dopa decarboxylase Mus musculus 138-142 15354384-1 2004 Levodopa and dopamine are metabolized to 3-O-methyldopa and 3-methoxytyramine, respectively, by the enzyme catechol-O-methyltransferase (COMT) leading to the production of the demethylated cofactor S-adenosylhomo-cysteine (SAH) and subsequently homocysteine (HC). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 107-135 15354384-1 2004 Levodopa and dopamine are metabolized to 3-O-methyldopa and 3-methoxytyramine, respectively, by the enzyme catechol-O-methyltransferase (COMT) leading to the production of the demethylated cofactor S-adenosylhomo-cysteine (SAH) and subsequently homocysteine (HC). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 137-141 14980733-1 2004 This study was aimed to test our hypothesis about dopamine (DA) synthesis by non-DAergic neurons expressing individual complementary enzymes of the DA synthetic pathway in cooperation, i.e. L-dihydroxyphenylalanine (L-DOPA) synthesized in tyrosine hydroxylase (TH)-expressing neurons is transported to aromatic L-amino acid decarboxylase (AADC)-expressing neurons for conversion to DA. Levodopa 190-214 dopa decarboxylase Rattus norvegicus 311-337 14667439-0 2004 Normalization of glutamate decarboxylase gene expression in the entopeduncular nucleus of rats with a unilateral 6-hydroxydopamine lesion correlates with increased GABAergic input following intermittent but not continuous levodopa. Levodopa 222-230 glutamate-ammonia ligase Rattus norvegicus 17-40 14667439-2 2004 Our results provide original evidence that continuous or intermittent levodopa administration is equally effective at reversing the lesion-induced increase in GAD67 mRNA expression in the EP when compared with vehicle controls. Levodopa 70-78 glutamate decarboxylase 1 Rattus norvegicus 159-164 14667439-4 2004 Levels of GAD67 mRNA labeling were significantly increased by intermittent, but not continuous levodopa. Levodopa 95-103 glutamate decarboxylase 1 Rattus norvegicus 10-15 14667439-6 2004 Saturation analyses of (3)H-flunitrazepam binding to GABA(A) receptors in the EP showed that the increase in GAD67 mRNA in preproenkephalin-unlabeled neurons by intermittent levodopa paralleled a significant decrease in number of GABA(A) receptors (Bmax) in the EP ipsilateral to the lesion. Levodopa 174-182 glutamate decarboxylase 1 Rattus norvegicus 109-114 14980733-1 2004 This study was aimed to test our hypothesis about dopamine (DA) synthesis by non-DAergic neurons expressing individual complementary enzymes of the DA synthetic pathway in cooperation, i.e. L-dihydroxyphenylalanine (L-DOPA) synthesized in tyrosine hydroxylase (TH)-expressing neurons is transported to aromatic L-amino acid decarboxylase (AADC)-expressing neurons for conversion to DA. Levodopa 190-214 dopa decarboxylase Rattus norvegicus 339-343 14980733-1 2004 This study was aimed to test our hypothesis about dopamine (DA) synthesis by non-DAergic neurons expressing individual complementary enzymes of the DA synthetic pathway in cooperation, i.e. L-dihydroxyphenylalanine (L-DOPA) synthesized in tyrosine hydroxylase (TH)-expressing neurons is transported to aromatic L-amino acid decarboxylase (AADC)-expressing neurons for conversion to DA. Levodopa 216-222 dopa decarboxylase Rattus norvegicus 311-337 14980733-1 2004 This study was aimed to test our hypothesis about dopamine (DA) synthesis by non-DAergic neurons expressing individual complementary enzymes of the DA synthetic pathway in cooperation, i.e. L-dihydroxyphenylalanine (L-DOPA) synthesized in tyrosine hydroxylase (TH)-expressing neurons is transported to aromatic L-amino acid decarboxylase (AADC)-expressing neurons for conversion to DA. Levodopa 216-222 dopa decarboxylase Rattus norvegicus 339-343 14980733-8 2004 This contradiction is most probably explained by the L-tyrosine-induced competitive inhibition of the L-DOPA transport to the monoenzymatic AADC-neurons after its release from the monoenzymatic TH neurons. Levodopa 102-108 dopa decarboxylase Rattus norvegicus 140-144 15033810-2 2003 All PD groups showed increased activity of caspase-3, compared to controls, particularly those under treatment only with l-Dopa. Levodopa 121-127 caspase 3 Homo sapiens 43-52 14663007-4 2003 The A2A antagonists are effective in rodent models of PD, reversing motor deficits in haloperidol-treated, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated, or reserpinized mice, and potentiating L-dopa-induced rotation in 6-hydroxydopamine-lesioned rats without inducing dyskinesia. Levodopa 207-213 spectrin, alpha, non-erythrocytic 1 Rattus norvegicus 4-7 14663007-7 2003 The data available suggest that A2A antagonists, such as KW6002, may be effective as monotherapy for the management of PD and that they will also produce additional benefit when administered in combination with L-dopa or dopamine agonist therapy. Levodopa 211-217 spectrin, alpha, non-erythrocytic 1 Rattus norvegicus 32-35 15111234-10 2004 Thus, DT-diaphorase is an enzyme to be taken into account when L-DOPA is used to treat Parkinson"s disease, or when an MAO-inhibitor is used to treat depression. Levodopa 63-69 NAD(P)H quinone dehydrogenase 1 Rattus norvegicus 6-19 15822631-8 2004 The most important pharmacologic treatment used in RLS includes L-DOPA, dopamine agonists, opiates, anticonvulsants and benzodiazepines. Levodopa 64-70 RLS1 Homo sapiens 51-54 14663008-4 2003 The expression of dynorphin and, to a lesser extent, enkephalin mRNAs was increased in the lesioned striatum of rats that received long-term L-dopa treatment but not in rats that received long-term SCH 58261 + L-dopa treatment. Levodopa 141-147 proenkephalin Rattus norvegicus 53-63 14663008-5 2003 Similarly, GAD67 mRNA was increased in the striatum and globus pallidus by long-term L-dopa administration but not by long-term SCH 58261 + L-dopa administration. Levodopa 85-91 glutamate decarboxylase 1 Rattus norvegicus 11-16 14663008-6 2003 GAD67 mRNA was strongly reduced in the lesioned substantia nigra after long-term L-dopa treatment, whereas the reduction of GAD67 mRNA was less marked after SCH 58261 + L-dopa treatment. Levodopa 81-87 glutamate decarboxylase 1 Rattus norvegicus 0-5 14663008-6 2003 GAD67 mRNA was strongly reduced in the lesioned substantia nigra after long-term L-dopa treatment, whereas the reduction of GAD67 mRNA was less marked after SCH 58261 + L-dopa treatment. Levodopa 169-175 glutamate decarboxylase 1 Rattus norvegicus 124-129 14663022-5 2003 In hemiparkinsonian rats, KW6002 reversed the intermittent L-dopa treatment-induced, protein kinase A-mediated hyperphosphorylation of striatal alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptor GluR1 S845 residues and the concomitant shortening in motor response duration. Levodopa 59-65 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 212-217 15033810-4 2003 In addition, patients taking l-Dopa + dopamine agonists showed marked decrease in Bcl-2 levels and increased PBR expression, which seems in keeping with the hypothesis that PBR may be functionally related to Bcl-2. Levodopa 29-35 BCL2 apoptosis regulator Homo sapiens 82-87 15033810-4 2003 In addition, patients taking l-Dopa + dopamine agonists showed marked decrease in Bcl-2 levels and increased PBR expression, which seems in keeping with the hypothesis that PBR may be functionally related to Bcl-2. Levodopa 29-35 translocator protein Homo sapiens 109-112 15033810-4 2003 In addition, patients taking l-Dopa + dopamine agonists showed marked decrease in Bcl-2 levels and increased PBR expression, which seems in keeping with the hypothesis that PBR may be functionally related to Bcl-2. Levodopa 29-35 translocator protein Homo sapiens 173-176 15033810-4 2003 In addition, patients taking l-Dopa + dopamine agonists showed marked decrease in Bcl-2 levels and increased PBR expression, which seems in keeping with the hypothesis that PBR may be functionally related to Bcl-2. Levodopa 29-35 BCL2 apoptosis regulator Homo sapiens 208-213 14654758-10 2003 At baseline, 24-h urinary excretion of levodopa (L-DOPA), dopamine and noradrenaline was increased by 145, 85 and 74%, respectively, in COMT (-/-) mice compared with wild-type controls. Levodopa 39-47 catechol-O-methyltransferase Mus musculus 136-140 14769359-0 2003 Blockade of A2A receptors plus l-DOPA after nigrostriatal lesion results in GAD67 mRNA changes different from l-DOPA alone in the rat globus pallidus and substantia nigra reticulata. Levodopa 31-37 glutamate decarboxylase 1 Rattus norvegicus 76-81 14769359-5 2003 Chronic l-DOPA (6 mg/kg), in contrast to SCH58261 plus l-DOPA (3 mg/kg), produced a sensitized contralateral turning indicative of dyskinetic potential and further increased GAD67 mRNA in the GP. Levodopa 8-14 glutamate decarboxylase 1 Rattus norvegicus 174-179 14769359-7 2003 However, while l-DOPA (6 mg/kg) decreased SNr GAD67 mRNA below the intact side, SCH58261 plus l-DOPA (3 mg/kg) brought GAD67 mRNA to the same level of the intact SNr. Levodopa 15-21 glutamate decarboxylase 1 Rattus norvegicus 46-51 14769359-7 2003 However, while l-DOPA (6 mg/kg) decreased SNr GAD67 mRNA below the intact side, SCH58261 plus l-DOPA (3 mg/kg) brought GAD67 mRNA to the same level of the intact SNr. Levodopa 94-100 glutamate decarboxylase 1 Rattus norvegicus 119-124 14769359-9 2003 Results suggest that an increase in GAD67 mRNA in GP and a decrease in SNr might underlie dyskinetic movements induced by chronic l-DOPA. Levodopa 130-136 glutamate decarboxylase 1 Rattus norvegicus 36-41 14654758-10 2003 At baseline, 24-h urinary excretion of levodopa (L-DOPA), dopamine and noradrenaline was increased by 145, 85 and 74%, respectively, in COMT (-/-) mice compared with wild-type controls. Levodopa 49-55 catechol-O-methyltransferase Mus musculus 136-140 14654758-12 2003 The absolute amounts of urinary L-DOPA and dopamine remained 60 and 20% greater in COMT (-/-) mice. Levodopa 32-38 catechol-O-methyltransferase Mus musculus 83-87 14683704-3 2003 However, subtle changes in prefrontal cortex (PFC) activity are seen following L-Dopa withdrawal in PD during working memory tasks, suggesting that this may be a further site of action for dopamine D2 receptor antagonists. Levodopa 79-85 dopamine receptor D2 Homo sapiens 189-209 14666410-0 2003 Increased striatal neuropeptide Y immunoreactivity and its modulation by deprenyl, clonidine and L-dopa in MPTP-treated mice. Levodopa 97-103 neuropeptide Y Mus musculus 19-33 14646622-2 2003 We have already shown that the serum L-dopa/L-tyrosine ratio (an index of tyrosinase functional activity) correlates with the tumour burden and in some cases predicted disease progression in metastatic melanoma patients. Levodopa 37-43 tyrosinase Homo sapiens 74-84 14666410-6 2003 L-dopa/carbidopa protected NPY neurons against MPTP but slightly enhanced MPTP-induced decrease in the levels of dopamine and its metabolites. Levodopa 0-6 neuropeptide Y Mus musculus 27-30 14573393-1 2003 Catechol-O-methyltransferase (COMT) is a crucial enzyme in dopamine and levodopa metabolism. Levodopa 72-80 catechol-O-methyltransferase Homo sapiens 0-28 14622157-7 2003 L-DOPA produced a high and similar increase in GAD67 mRNA in enkephalin (-) and (+) neurons. Levodopa 0-6 glutamate decarboxylase 1 Rattus norvegicus 47-52 14573393-1 2003 Catechol-O-methyltransferase (COMT) is a crucial enzyme in dopamine and levodopa metabolism. Levodopa 72-80 catechol-O-methyltransferase Homo sapiens 30-34 14623353-4 2003 Moreover, BDNF triggers behavioral sensitization to levodopa in hemiparkinsonian rats. Levodopa 52-60 brain-derived neurotrophic factor Rattus norvegicus 10-14 14623353-6 2003 Administration of a dopamine D3 receptor-selective partial agonist strongly attenuated levodopa-induced dyskinesia, while leaving unaffected the therapeutic effect of levodopa. Levodopa 87-95 dopamine receptor D3 Rattus norvegicus 20-40 14623353-7 2003 These results suggest that the dopamine D3 receptor participates in both dyskinesia and the therapeutic action of levodopa and that partial agonists may normalize dopamine D3 receptor function and correct side-effects of levodopa therapy in PD patients. Levodopa 114-122 dopamine receptor D3 Rattus norvegicus 31-51 14623353-7 2003 These results suggest that the dopamine D3 receptor participates in both dyskinesia and the therapeutic action of levodopa and that partial agonists may normalize dopamine D3 receptor function and correct side-effects of levodopa therapy in PD patients. Levodopa 221-229 dopamine receptor D3 Rattus norvegicus 31-51 14517707-0 2003 Pharmacokinetic-pharmacodynamic interaction between BIA 3-202, a novel COMT inhibitor, and levodopa/benserazide. Levodopa 91-99 catechol-O-methyltransferase Homo sapiens 71-75 14517707-1 2003 BIA 3-202 is a novel catechol-O-methyltransferase (COMT) inhibitor being developed for use as a levodopa-sparing agent in Parkinson"s disease. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 21-49 14517707-1 2003 BIA 3-202 is a novel catechol-O-methyltransferase (COMT) inhibitor being developed for use as a levodopa-sparing agent in Parkinson"s disease. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 51-55 14517707-12 2003 In conclusion, the novel COMT inhibitor BIA 3-202 was well tolerated and significantly increased the bioavailability of levodopa and reduced the formation of 3-OMD when administered with standard release levodopa/benserazide. Levodopa 120-128 catechol-O-methyltransferase Homo sapiens 25-29 14517707-12 2003 In conclusion, the novel COMT inhibitor BIA 3-202 was well tolerated and significantly increased the bioavailability of levodopa and reduced the formation of 3-OMD when administered with standard release levodopa/benserazide. Levodopa 204-212 catechol-O-methyltransferase Homo sapiens 25-29 14644812-10 2003 Many women with polycystic ovary syndrome (PCOS) have an impaired GH response to stimulation with Levo-Dopa and GH releasing hormone (GHRH). Levodopa 98-107 growth hormone 1 Homo sapiens 66-68 14637099-3 2003 In rats, KW-6002 reversed the shortened motor response produced by chronic levodopa treatment while reducing levodopa-induced hyperphosphorylation at S845 residues on AMPA receptor GluR1 subunits. Levodopa 109-117 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 181-186 14622157-7 2003 L-DOPA produced a high and similar increase in GAD67 mRNA in enkephalin (-) and (+) neurons. Levodopa 0-6 proenkephalin Rattus norvegicus 61-71 14708619-4 2003 This decrease in BRN2 accompanied a positive L-dihydroxyphenylalanine reaction and induction of melanosome maturation consistent with melanoblast differentiation seen during development. Levodopa 45-69 POU class 3 homeobox 2 Homo sapiens 17-21 15152479-6 2003 As for the initial step of clinical application, AADC (aromatic L-amino acid decarboxylase; the enzyme converting L-DOPA to DA) gene transfer in combination with oral administration of L-DOPA would be appropriate, since DA production can be regulated by the dose of L-DOPA. Levodopa 114-120 dopa decarboxylase Homo sapiens 49-53 15152479-6 2003 As for the initial step of clinical application, AADC (aromatic L-amino acid decarboxylase; the enzyme converting L-DOPA to DA) gene transfer in combination with oral administration of L-DOPA would be appropriate, since DA production can be regulated by the dose of L-DOPA. Levodopa 114-120 dopa decarboxylase Homo sapiens 55-90 12760744-4 2003 The half-life of the GE enzyme at 40 degrees C was less than 2 h, whereas the FEAGE enzyme retained about 75% of its initial activity after 2 h. Taken together our data demonstrate clearly that the technique of immobilizing tyrosinase via adsorption followed by entrapment appears promising and is hence recommended for tyrosinase immobilization for commercial production of L-DOPA (3,4-dihydroxyphenylalanine). Levodopa 375-381 tyrosinase Homo sapiens 224-234 12938190-8 2003 We explore here the hypothesis that gene transfer of aromatic acid decarboxylase (AADC), a key enzyme in the pathway, will make neuronal cells more efficiently convert L-dopa into dopamine. Levodopa 168-174 dopa decarboxylase Homo sapiens 82-86 14521483-5 2003 Dopaminergic agents including levodopa and dopamine agonists such as pergolide, pramipexole, cabergoline and ropinirole are regarded as the treatment of choice for idiopathic RLS, however, the development of augmentation of symptoms, especially under levodopa therapy, may be a major problem. Levodopa 30-38 RLS1 Homo sapiens 175-178 12975385-2 2003 L-3,4-Dihydroxyphenylalanine (L-DOPA) uptake in renal epithelial cells is promoted through the type 2 L-type amino acid transporter (LAT2), and this might rate-limit the synthesis of renal dopamine. Levodopa 0-28 linker for activation of T cells family, member 2 Rattus norvegicus 133-137 12975385-2 2003 L-3,4-Dihydroxyphenylalanine (L-DOPA) uptake in renal epithelial cells is promoted through the type 2 L-type amino acid transporter (LAT2), and this might rate-limit the synthesis of renal dopamine. Levodopa 30-36 linker for activation of T cells family, member 2 Rattus norvegicus 133-137 12975385-13 2003 We conclude that overexpression of LAT2 in the SHR kidney might contribute to the enhanced L-DOPA uptake, which is organ specific and precedes the onset of hypertension. Levodopa 91-97 linker for activation of T cells family, member 2 Rattus norvegicus 35-39 14565778-0 2003 The parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) mediates release of l-3,4-dihydroxyphenylalanine (l-DOPA) and inhibition of l-DOPA decarboxylase in the rat striatum: a microdialysis study. Levodopa 115-121 dopa decarboxylase Rattus norvegicus 141-161 14565778-6 2003 However, MPP(+) induced a transient, concentration-dependent rise of extracellular l-3,4-dihydroxyphenylalanine (l-DOPA), identified on the basis of dialysate analysis using several HPLC methods and its conversion to DA by purified l-DOPA decarboxylase (DDC). Levodopa 83-111 dopa decarboxylase Rattus norvegicus 232-252 14565778-6 2003 However, MPP(+) induced a transient, concentration-dependent rise of extracellular l-3,4-dihydroxyphenylalanine (l-DOPA), identified on the basis of dialysate analysis using several HPLC methods and its conversion to DA by purified l-DOPA decarboxylase (DDC). Levodopa 113-119 dopa decarboxylase Rattus norvegicus 232-252 12938190-13 2003 Gene transfer of AADC gene in neuronal cells imparted the ability on the transduced cells to efficiently convert L-dopa into dopamine. Levodopa 113-119 dopa decarboxylase Homo sapiens 17-21 13678671-0 2003 Denervation and repeated L-DOPA induce a coordinate expression of the transcription factor NGFI-B in striatal projection pathways in hemi-parkinsonian rats. Levodopa 25-31 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 91-97 13678671-2 2003 In this study, we have investigated the effects of denervation and repeated L-DOPA administration on the expression of the nuclear receptor nerve growth factor inducible-B (NGFI-B) in striatal output pathways of unilaterally 6-OHDA-lesioned rats. Levodopa 76-82 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 173-179 13678671-5 2003 Repeated L-DOPA treatment increased the striatal level of DYN mRNA but it further reduced the percentage of NGFI-B/DYN double-labeled cells. Levodopa 9-15 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 108-114 14598064-5 2003 In patients, we observed a negative correlation between Cu/Zn SOD levels and daily intake of L-dopa, which also tended to be negatively correlated with caspase-3 activity, but not with Bcl- 2. Levodopa 93-99 caspase 3 Homo sapiens 152-161 13678671-6 2003 On the intact side, repeated L-DOPA treatment increased NGFI-B expression in both striatal subpopulations. Levodopa 29-35 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 56-62 13678671-9 2003 These results demonstrate that the denervation process causes a differential regulation of NGFI-B in the two striatal output pathways which is further exacerbated by L-DOPA treatment. Levodopa 166-172 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 91-97 12878190-1 2003 Synthesis of melanin starts from the conversion of L-tyrosine to 3,4-dihydroxyphenylalanine (L-dopa) and then the oxidation of L-dopa yields dopaquinone by tyrosinase. Levodopa 127-133 tyrosinase Mus musculus 156-166 12950442-1 2003 Inactivation of the subthalamic nucleus (STN) or the internal segment of the pallidum (GPi)/entopeduncular nucleus (EP) by deep brain stimulation or lesioning alleviates clinical manifestations of Parkinson"s disease (PD) as well as reducing the side-effects of levodopa treatment. Levodopa 262-270 glucose-6-phosphate isomerase Rattus norvegicus 87-90 12920198-4 2003 Because the dopamine precursor l-DOPA is the most commonly used therapeutic agent for Parkinson"s disease, we investigated the effects of l-DOPA treatment on striatal nAChR expression in unlesioned and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned monkeys. Levodopa 138-144 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 167-172 12920198-9 2003 In summary, these data show that l-DOPA treatment decreases nAChR expression, in contrast with the well established up-regulation of these sites by chronic nicotine exposure. Levodopa 33-39 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 60-65 12907313-2 2003 Application of L-DOPA (30 microM) to vas deferens increased basal NA efflux but not electrical field stimulation-evoked release of NA when the tissue was pretreated with an inhibitor of MAO-B (clorgyline 1 microM) or an inhibitor of MAO-A and MOA-B (AGN-1133 1 microM). Levodopa 15-21 monoamine oxidase B Rattus norvegicus 186-191 12907313-2 2003 Application of L-DOPA (30 microM) to vas deferens increased basal NA efflux but not electrical field stimulation-evoked release of NA when the tissue was pretreated with an inhibitor of MAO-B (clorgyline 1 microM) or an inhibitor of MAO-A and MOA-B (AGN-1133 1 microM). Levodopa 15-21 monoamine oxidase A Rattus norvegicus 233-238 14577637-2 2003 It inhibited the oxidation of L-3,4-dihydroxyphenylalanine (L-DOPA) catalyzed by tyrosinase with an IC50 of 0.60 mM. Levodopa 30-58 tyrosinase Homo sapiens 81-91 14577637-2 2003 It inhibited the oxidation of L-3,4-dihydroxyphenylalanine (L-DOPA) catalyzed by tyrosinase with an IC50 of 0.60 mM. Levodopa 60-66 tyrosinase Homo sapiens 81-91 12913187-1 2003 OBJECTIVE: To evaluate the safety and efficacy of the adenosine A(2A) receptor antagonist istradefylline (KW-6002) in patients with levodopa-treated Parkinson"s disease (PD) with both motor fluctuations and peak-dose dyskinesias. Levodopa 132-140 adenosine A2a receptor Homo sapiens 54-78 12873751-2 2003 We describe a Chinese patient with a mutation at the SCA 3 locus with clinical features of levodopa-responsive dystonia. Levodopa 91-99 ataxin 3 Homo sapiens 53-58 12873751-6 2003 This expands the wide and varied phenotypic manifestations of SCA 3, and highlights the observation that features suggestive of levodopa-responsive dystonia (DRD) such as focal dystonia, gait difficulty with diurnal fluctuation of symptoms, and a marked response to low doses of levodopa can be presenting features of SCA 3. Levodopa 128-136 ataxin 3 Homo sapiens 318-323 12827644-5 2003 Our results provide original evidence that continuous L-DOPA normalizes the 6-OHDA-lesion-induced increase in mRNA levels encoding for the 67 kDa isoform of glutamate decarboxylase in neurons of the globus pallidus and cytochrome oxidase subunit I mRNA levels in the subthalamic nucleus. Levodopa 54-60 glutamate-ammonia ligase Rattus norvegicus 157-180 12827644-7 2003 In addition, intermittent L-DOPA induced an increase in the mRNA levels encoding for the 65 kDa isoform of glutamate decarboxylase in globus pallidus neurons ipsilateral to the lesion and a bilateral increase in c-fos mRNA expression in the subthalamic nucleus. Levodopa 26-32 glutamate-ammonia ligase Rattus norvegicus 107-130 12827644-7 2003 In addition, intermittent L-DOPA induced an increase in the mRNA levels encoding for the 65 kDa isoform of glutamate decarboxylase in globus pallidus neurons ipsilateral to the lesion and a bilateral increase in c-fos mRNA expression in the subthalamic nucleus. Levodopa 26-32 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 212-217 12948464-7 2003 Levodopa significantly decreased FOG frequency (p<0.001). Levodopa 0-8 zinc finger protein, FOG family member 1 Homo sapiens 33-36 12948464-9 2003 CONCLUSION: Levodopa decreases FOG in PD. Levodopa 12-20 zinc finger protein, FOG family member 1 Homo sapiens 31-34 12874410-1 2003 A 59-year-old woman with levodopa-responsive parkinsonism complicated by motor fluctuations and generalized levodopa dyskinesia underwent bilateral subthalamic deep brain stimulation (STN DBS) 7 years after symptom onset. Levodopa 25-33 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 184-187 12898345-0 2003 L-DOPA biotransformation: correlations of dosage, erythrocyte catechol O-methyltransferase and platelet SULT1A3 activities with metabolic pathways in Parkinsonian patients. Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 62-90 12898345-0 2003 L-DOPA biotransformation: correlations of dosage, erythrocyte catechol O-methyltransferase and platelet SULT1A3 activities with metabolic pathways in Parkinsonian patients. Levodopa 0-6 sulfotransferase family 1A member 3 Homo sapiens 104-111 12898345-3 2003 Levels of activity for erythrocyte COMT were also reflected in individual variation in the metabolism of L-DOPA. Levodopa 105-111 catechol-O-methyltransferase Homo sapiens 35-39 14514477-0 2003 Effect of levodopa on interleukin-15 and RANTES circulating levels in patients affected by Parkinson"s disease. Levodopa 10-18 interleukin 15 Homo sapiens 22-36 14514477-0 2003 Effect of levodopa on interleukin-15 and RANTES circulating levels in patients affected by Parkinson"s disease. Levodopa 10-18 C-C motif chemokine ligand 5 Homo sapiens 41-47 14514477-5 2003 Levodopa-treated patients showed significantly higher IL-15 and RANTES circulating levels with respect to healthy controls and higher, although not significantly, levels with respect to untreated patients. Levodopa 0-8 interleukin 15 Homo sapiens 54-59 14514477-5 2003 Levodopa-treated patients showed significantly higher IL-15 and RANTES circulating levels with respect to healthy controls and higher, although not significantly, levels with respect to untreated patients. Levodopa 0-8 C-C motif chemokine ligand 5 Homo sapiens 64-70 12899667-0 2003 The CB1 cannabinoid receptor agonist, HU-210, reduces levodopa-induced rotations in 6-hydroxydopamine-lesioned rats. Levodopa 54-62 cannabinoid receptor 1 Rattus norvegicus 4-7 12832289-1 2003 L-3,4-dihydroxyphenylalanine, the immediate precursor of dopamine, can be formed by two enzymes: tyrosine hydroxylase (TH) in catecholamine-producing neurons and chromaffin cells and tyrosinase in melanocytes. Levodopa 0-28 tyrosine hydroxylase Mus musculus 97-117 12897636-2 2003 Drugs with 5HT-(1A) agonistic activity, such as buspirone and tandospirone, have been reported to be effective in reducing l-dopa-induced dyskinesias. Levodopa 123-129 5-hydroxytryptamine receptor 1A Homo sapiens 11-18 12897642-1 2003 Animal studies indicate that beta(2)-adrenergic receptor agonists enhance transport of levodopa across the blood-brain barrier. Levodopa 87-95 adrenoceptor beta 2 Homo sapiens 29-56 12823491-11 2003 Levodopa significantly decreased FOG frequency (P < 0.0001) and the number of episodes with akinesia (P < 0.001). Levodopa 0-8 zinc finger protein, FOG family member 1 Homo sapiens 33-36 12832289-1 2003 L-3,4-dihydroxyphenylalanine, the immediate precursor of dopamine, can be formed by two enzymes: tyrosine hydroxylase (TH) in catecholamine-producing neurons and chromaffin cells and tyrosinase in melanocytes. Levodopa 0-28 tyrosine hydroxylase Mus musculus 119-121 12832289-1 2003 L-3,4-dihydroxyphenylalanine, the immediate precursor of dopamine, can be formed by two enzymes: tyrosine hydroxylase (TH) in catecholamine-producing neurons and chromaffin cells and tyrosinase in melanocytes. Levodopa 0-28 tyrosinase Mus musculus 183-193 12788472-5 2003 Protective effects of bcl-2 expression against L-DOPA neurotoxicity decreased with increasing amounts of bcl-2. Levodopa 47-53 BCL2, apoptosis regulator Rattus norvegicus 22-27 12807423-3 2003 The dopamine (DA) content of E9/10 and E15/16 retinas, pre-incubated with l-DOPA for 1 h, increased 250- and 600-fold, respectively, showing that DDC is active since early in development. Levodopa 74-80 dopa decarboxylase Gallus gallus 146-149 12788472-5 2003 Protective effects of bcl-2 expression against L-DOPA neurotoxicity decreased with increasing amounts of bcl-2. Levodopa 47-53 BCL2, apoptosis regulator Rattus norvegicus 105-110 12711835-18 2003 Quercetin through its COMT and MAO enzyme-inhibiting properties might potentiate the anticatatonic effect of L-dopa plus carbidopa treatment. Levodopa 109-115 monoamine oxidase A Rattus norvegicus 31-34 12774317-2 2003 To elucidate molecular mechanisms that underlie the persisting alterations in motor response occurring with levodopa (L-dopa) treatment of parkinsonian patients, we evaluated the time course of these changes in relation to the activation of striatal CREB in 6-hydroxydopamine (6-OHDA) lesioned animals. Levodopa 108-116 cAMP responsive element binding protein 1 Homo sapiens 250-254 12774317-2 2003 To elucidate molecular mechanisms that underlie the persisting alterations in motor response occurring with levodopa (L-dopa) treatment of parkinsonian patients, we evaluated the time course of these changes in relation to the activation of striatal CREB in 6-hydroxydopamine (6-OHDA) lesioned animals. Levodopa 118-124 cAMP responsive element binding protein 1 Homo sapiens 250-254 12774317-6 2003 The time course of changes in CREB phosphorylation correlated with the time course of changes in motor behavior after cessation of chronic L-dopa therapy. Levodopa 139-145 cAMP responsive element binding protein 1 Rattus norvegicus 30-34 12796525-0 2003 L -dopa-induced adverse effects in PD and dopamine transporter gene polymorphism. Levodopa 0-7 solute carrier family 6 member 3 Homo sapiens 42-62 12718431-1 2003 L-Dopa decarboxylase (DDC) is a pyridoxal 5-phosphate (PLP)-dependent enzyme that catalyses the decarboxylation of L-Dopa to dopamine. Levodopa 0-6 dopa decarboxylase Homo sapiens 22-25 12781600-1 2003 Autosomal recessive juvenile parkinsonism (ARJP/PARK2) is a distinct clinical and genetic entity characterized by early-onset levodopa-responsive parkinsonism, foot dystonia, sleep benefit, and hyperactive tendon reflexes. Levodopa 126-134 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-47 12781600-1 2003 Autosomal recessive juvenile parkinsonism (ARJP/PARK2) is a distinct clinical and genetic entity characterized by early-onset levodopa-responsive parkinsonism, foot dystonia, sleep benefit, and hyperactive tendon reflexes. Levodopa 126-134 parkin RBR E3 ubiquitin protein ligase Homo sapiens 48-53 12787259-1 2003 The present study evaluated the relationship between the degree of catechol-O-methyltransferase (COMT) inhibition in erythrocytes and liver by BIA 3-202 (1-[3,4-dihydroxy-5-nitrophenyl]-2-phenyl-ethanone) and determined its effects upon the O-methylation of L-DOPA in rats orally treated with L-DOPA plus benserazide. Levodopa 258-264 catechol-O-methyltransferase Rattus norvegicus 67-95 12787259-1 2003 The present study evaluated the relationship between the degree of catechol-O-methyltransferase (COMT) inhibition in erythrocytes and liver by BIA 3-202 (1-[3,4-dihydroxy-5-nitrophenyl]-2-phenyl-ethanone) and determined its effects upon the O-methylation of L-DOPA in rats orally treated with L-DOPA plus benserazide. Levodopa 258-264 catechol-O-methyltransferase Rattus norvegicus 97-101 12796525-1 2003 OBJECTIVE: To assess whether polymorphisms in the dopamine receptor genes and in the dopamine transporter gene (DAT ) are predictors of adverse effects of L -dopa. Levodopa 155-162 solute carrier family 6 member 3 Homo sapiens 85-105 12796525-1 2003 OBJECTIVE: To assess whether polymorphisms in the dopamine receptor genes and in the dopamine transporter gene (DAT ) are predictors of adverse effects of L -dopa. Levodopa 155-162 solute carrier family 6 member 3 Homo sapiens 112-115 12796525-4 2003 The entire coding and promoter regions of the DRD2 gene of 48 patients with early and severe appearance of adverse effects from L -dopa treatment and of eight never-afflicted patients were sequenced. Levodopa 128-135 dopamine receptor D2 Homo sapiens 46-50 12796525-9 2003 However, the nine copy allele 40-bp VNTR of the DAT is a predictor for the occurrence of psychosis or dyskinesia in L -dopa-treated patients. Levodopa 116-123 solute carrier family 6 member 3 Homo sapiens 48-51 12768357-5 2003 Acute L-dopa/benserazide significantly (p < 0.001) and markedly (75%) decreased the target variable PLM/h of sleep as well as all other RLS/PLM variables, but failed to improve objective sleep efficiency and subjective sleep quality in comparison to placebo. Levodopa 6-12 FXYD domain containing ion transport regulator 1 Homo sapiens 103-106 12768357-5 2003 Acute L-dopa/benserazide significantly (p < 0.001) and markedly (75%) decreased the target variable PLM/h of sleep as well as all other RLS/PLM variables, but failed to improve objective sleep efficiency and subjective sleep quality in comparison to placebo. Levodopa 6-12 FXYD domain containing ion transport regulator 1 Homo sapiens 143-146 12711835-18 2003 Quercetin through its COMT and MAO enzyme-inhibiting properties might potentiate the anticatatonic effect of L-dopa plus carbidopa treatment. Levodopa 109-115 catechol-O-methyltransferase Rattus norvegicus 22-26 12787259-7 2003 The novel COMT inhibitor BIA 3-202 is a potent COMT inhibitor that enhances the availability of L-DOPA to the brain by reducing its O-methylation, which may prove beneficial in patients with Parkinson"s disease treated with L-DOPA. Levodopa 96-102 catechol-O-methyltransferase Homo sapiens 10-14 12787259-7 2003 The novel COMT inhibitor BIA 3-202 is a potent COMT inhibitor that enhances the availability of L-DOPA to the brain by reducing its O-methylation, which may prove beneficial in patients with Parkinson"s disease treated with L-DOPA. Levodopa 96-102 catechol-O-methyltransferase Homo sapiens 47-51 12787259-7 2003 The novel COMT inhibitor BIA 3-202 is a potent COMT inhibitor that enhances the availability of L-DOPA to the brain by reducing its O-methylation, which may prove beneficial in patients with Parkinson"s disease treated with L-DOPA. Levodopa 224-230 catechol-O-methyltransferase Homo sapiens 10-14 12787259-7 2003 The novel COMT inhibitor BIA 3-202 is a potent COMT inhibitor that enhances the availability of L-DOPA to the brain by reducing its O-methylation, which may prove beneficial in patients with Parkinson"s disease treated with L-DOPA. Levodopa 224-230 catechol-O-methyltransferase Homo sapiens 47-51 12704806-9 2003 The present neo(r)-positive TH hypomorphic mice show that nigrostriatal innervation develops independently of TH and should find use as a model for conditions of reduced catecholamine synthesis, as seen in, for example, L-dihydroxyphenylalanine-responsive dystonia/infantile parkinsonism. Levodopa 220-244 tyrosine hydroxylase Mus musculus 28-30 12787259-1 2003 The present study evaluated the relationship between the degree of catechol-O-methyltransferase (COMT) inhibition in erythrocytes and liver by BIA 3-202 (1-[3,4-dihydroxy-5-nitrophenyl]-2-phenyl-ethanone) and determined its effects upon the O-methylation of L-DOPA in rats orally treated with L-DOPA plus benserazide. Levodopa 293-299 catechol-O-methyltransferase Rattus norvegicus 67-95 12787259-1 2003 The present study evaluated the relationship between the degree of catechol-O-methyltransferase (COMT) inhibition in erythrocytes and liver by BIA 3-202 (1-[3,4-dihydroxy-5-nitrophenyl]-2-phenyl-ethanone) and determined its effects upon the O-methylation of L-DOPA in rats orally treated with L-DOPA plus benserazide. Levodopa 293-299 catechol-O-methyltransferase Rattus norvegicus 97-101 14593758-3 2003 Dopaminergic agents (i.e. L-dopa and dopamine agonists), currently regarded as the best therapeutic option in the treatment of RLS, are discussed in detail. Levodopa 26-32 RLS1 Homo sapiens 127-130 12904105-1 2003 Entacapone and tolcapone are selective catechol-O-methyltransferase (COMT) inhibitors developed recently as adjuncts to levodopa for the treatment of Parkinson"s disease (PD). Levodopa 120-128 catechol-O-methyltransferase Homo sapiens 39-67 12904105-1 2003 Entacapone and tolcapone are selective catechol-O-methyltransferase (COMT) inhibitors developed recently as adjuncts to levodopa for the treatment of Parkinson"s disease (PD). Levodopa 120-128 catechol-O-methyltransferase Homo sapiens 69-73 12716433-8 2003 Taken together, these data show that anomalies in the endocannabinoid system induced by experimental parkinsonism are restricted to the striatum and can be reversed by chronic levodopa treatment, and suggest that inhibition of FAAH might represent a possible target to decrease the abnormal cortical glutamatergic drive in Parkinson"s disease. Levodopa 176-184 fatty-acid amide hydrolase-like Rattus norvegicus 227-231 12722172-3 2003 We carried out urodynamic studies before and about 1 hour after the patients had taken 100 mg of L-dopa with dopa-decarboxylase inhibitor (DCI). Levodopa 97-103 dopa decarboxylase Homo sapiens 109-127 12722172-3 2003 We carried out urodynamic studies before and about 1 hour after the patients had taken 100 mg of L-dopa with dopa-decarboxylase inhibitor (DCI). Levodopa 97-103 enoyl-CoA delta isomerase 1 Homo sapiens 139-142 14593760-5 2003 The treatment of advanced stages of the disease currently requires the application of levodopa combined with other medicines, such as dopamine agonists or catechol-O-methyl transferase (COMT) inhibitors. Levodopa 86-94 catechol-O-methyltransferase Homo sapiens 155-184 14593760-5 2003 The treatment of advanced stages of the disease currently requires the application of levodopa combined with other medicines, such as dopamine agonists or catechol-O-methyl transferase (COMT) inhibitors. Levodopa 86-94 catechol-O-methyltransferase Homo sapiens 186-190 12707709-2 2003 In particular, therapy with L-dopa or dopamine agonists leads to increased dream activity. Levodopa 28-34 potassium voltage-gated channel interacting protein 3 Homo sapiens 75-80 12660477-0 2003 BIA 3-202, a novel catechol-O-methyltransferase inhibitor, reduces the peripheral O-methylation of L-DOPA and enhances its availability to the brain. Levodopa 99-105 catechol-O-methyltransferase Rattus norvegicus 19-47 12802729-2 2003 Mushroom tyrosinase activity was inhibited in a concentration-dependent manner when treated with kinobeon A using L-tyrosine or L-3,4-dihydroxyphenylalannine (L-DOPA) as substrates. Levodopa 159-165 tyrosinase Homo sapiens 9-19 12802729-4 2003 Inhibition of human tyrosinase activity also increased with increasing concentrations of kinobeon A using L-DOPA as the substrate, with an IC50 value of 2.5 microM. Levodopa 106-112 tyrosinase Homo sapiens 20-30 12676374-1 2003 Striatal neurons which are immunoreactive (ir) to aromatic L-amino-acid decarboxylase (AADC) or tyrosine hydrodroxylase (TH) may play a role in the decarboxylation of L-DOPA to dopamine (DA) in advanced stages of Parkinson"s disease (PD). Levodopa 167-173 dopa decarboxylase Rattus norvegicus 50-85 12676374-1 2003 Striatal neurons which are immunoreactive (ir) to aromatic L-amino-acid decarboxylase (AADC) or tyrosine hydrodroxylase (TH) may play a role in the decarboxylation of L-DOPA to dopamine (DA) in advanced stages of Parkinson"s disease (PD). Levodopa 167-173 dopa decarboxylase Rattus norvegicus 87-91 12676374-7 2003 The population of AADC-ir neurons may make a significant contribution to the effects of exogenous L-DOPA in advanced stages of PD. Levodopa 98-104 dopa decarboxylase Rattus norvegicus 18-22 12686106-1 2003 Dopa decarboxylase (DDC) catalyzes as main reaction the stereospecific CO(2) abstraction from L-Dopa and L-5-hydroxytryptophan (5-HTP), generating the corresponding aromatic amines, dopamine and serotonin, respectively. Levodopa 94-100 dopa decarboxylase Sus scrofa 0-18 12707079-2 2003 Autosomal dominantly inherited defects in the GTPCH gene (GCH1) cause a form of dystonia that is responsive to treatment with levodopa (dopa-responsive dystonia [DRD]). Levodopa 126-134 GTP cyclohydrolase 1 Homo sapiens 58-62 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 180-208 catechol-O-methyltransferase Rattus norvegicus 57-85 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 180-208 catechol-O-methyltransferase Rattus norvegicus 87-91 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 210-216 catechol-O-methyltransferase Rattus norvegicus 57-85 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 210-216 catechol-O-methyltransferase Rattus norvegicus 87-91 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 346-352 catechol-O-methyltransferase Rattus norvegicus 57-85 12660477-1 2003 The present study aims at determining the effects of the catechol-O-methyltransferase (COMT) inhibitor BIA 3-202 [1-(3,4-dihydroxy-5-nitrophenyl)-2-phenyl-ethanone] upon levels of L-3,4-dihydroxyphenylalanine (L-DOPA) and metabolites in peripheral circulation (jugular vein), whole brain, and striatal microdialysates in rats orally treated with L-DOPA plus benserazide. Levodopa 346-352 catechol-O-methyltransferase Rattus norvegicus 87-91 12660477-6 2003 In conclusion, inhibition of peripheral COMT by BIA 3-202 may suffice to improve the availability of L-DOPA to the brain. Levodopa 101-107 catechol-O-methyltransferase Rattus norvegicus 40-44 12667651-0 2003 In vivo administration of L-dopa or dopamine decreases the number of splenic IFN gamma-producing cells. Levodopa 26-32 interferon gamma Mus musculus 77-86 12667651-5 2003 However, the number of IFN gamma-, but not IL-4-producing cells was significantly inhibited by L-dopa. Levodopa 95-101 interferon gamma Mus musculus 23-32 12671950-0 2003 SCA2 may present as levodopa-responsive parkinsonism. Levodopa 20-28 ataxin 2 Homo sapiens 0-4 12671950-2 2003 Recent reports have shown trinucleotide repeat expansions in the spinocerebellar ataxia 2 (SCA2) gene in patients with levodopa-responsive parkinsonism. Levodopa 119-127 ataxin 2 Homo sapiens 65-89 12671950-2 2003 Recent reports have shown trinucleotide repeat expansions in the spinocerebellar ataxia 2 (SCA2) gene in patients with levodopa-responsive parkinsonism. Levodopa 119-127 ataxin 2 Homo sapiens 91-95 12591154-8 2003 The increase in NPY mRNA expression observed in patients with PD may reflect the loss of dopaminergic tone on striatal NPY containing interneurones, although a role for chronic L-DOPA therapy cannot be ruled out. Levodopa 177-183 neuropeptide Y Homo sapiens 16-19 12624268-4 2003 The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Levodopa 141-147 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 43-49 12624268-4 2003 The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Levodopa 141-147 tyrosinase Mus musculus 98-108 12624268-6 2003 These experiments raise the possibility that a tyrosinase/l-dopa pathway modifies human PCG, which could open new therapeutic avenues. Levodopa 58-64 tyrosinase Homo sapiens 47-57 12631267-2 2003 Nevertheless, significant problems such as the substrate specificity of PAH and the different susceptibility of TH to feedback inhibition by l-3,4-dihydroxyphenylalanine (l-DOPA) compared with dopamine (DA) remain unresolved. Levodopa 141-169 tyrosine hydroxylase Homo sapiens 112-114 12631267-2 2003 Nevertheless, significant problems such as the substrate specificity of PAH and the different susceptibility of TH to feedback inhibition by l-3,4-dihydroxyphenylalanine (l-DOPA) compared with dopamine (DA) remain unresolved. Levodopa 171-177 tyrosine hydroxylase Homo sapiens 112-114 12614340-0 2003 Cellular and behavioural effects of the adenosine A2a receptor antagonist KW-6002 in a rat model of l-DOPA-induced dyskinesia. Levodopa 100-106 adenosine A2a receptor Rattus norvegicus 40-62 12614926-8 2003 Moreover, a prolonged duration of treatment with L-DOPA in patients with MTHFR T/T genotype enhanced the hypertrophy of IMC, compared with patients with the C/C or C/T genotype. Levodopa 49-55 methylenetetrahydrofolate reductase Homo sapiens 73-78 12631267-8 2003 Two alternative conformations, rotated 180 degrees around an imaginary iron-catecholamine axis, were found for DA and l-DOPA in PAH and for DA in TH. Levodopa 118-124 phenylalanine hydroxylase Homo sapiens 128-131 12631267-9 2003 Electrostatic forces play a key role in hindering the bidentate binding of the immediate reaction product l-DOPA to TH, thereby saving the enzyme from direct feedback inhibition. Levodopa 106-112 tyrosine hydroxylase Homo sapiens 116-118 12703659-1 2003 Benserazide is commonly used for Parkinson"s disease in combination with L-DOPA as a peripheral aromatic L-amino acid decarboxylase (AADC) inhibitor. Levodopa 73-79 dopa decarboxylase Rattus norvegicus 105-131 12703659-1 2003 Benserazide is commonly used for Parkinson"s disease in combination with L-DOPA as a peripheral aromatic L-amino acid decarboxylase (AADC) inhibitor. Levodopa 73-79 dopa decarboxylase Rattus norvegicus 133-137 12703659-8 2003 These results suggest that benserazide reduces the central AADC activity in the striatum of rats with nigrostriatal denervation, which leads to changes in the metabolism of exogenous L-DOPA. Levodopa 183-189 dopa decarboxylase Rattus norvegicus 59-63 12538411-2 2003 This functional cortical deafferentation and its reversibility by levodopa (L-dopa) treatment has been established in previous studies for SMA but remains controversial for M1. Levodopa 66-74 survival of motor neuron 1, telomeric Homo sapiens 139-142 12538411-2 2003 This functional cortical deafferentation and its reversibility by levodopa (L-dopa) treatment has been established in previous studies for SMA but remains controversial for M1. Levodopa 76-82 survival of motor neuron 1, telomeric Homo sapiens 139-142 12538411-6 2003 M1 contralateral to the affected hand and SMA, predominantly of the contralateral side, showed a BOLD signal increase after L-dopa intake. Levodopa 124-130 survival of motor neuron 1, telomeric Homo sapiens 42-45 12538411-8 2003 Signal changes in M1 and SMA were highly correlated with motor performance, which increased after L-dopa intake. Levodopa 98-104 survival of motor neuron 1, telomeric Homo sapiens 25-28 12634922-10 2003 L-Dopa treatment resulted in activation of protein kinase C (PKC). Levodopa 0-6 protein kinase C alpha Homo sapiens 61-64 12631248-7 2003 The melanosomal membrane location of tyrosine hydroxylase together with tyrosinase implies a coupled interaction, where L-dopa production facilitates the activation of tyrosinase. Levodopa 120-126 tyrosinase Homo sapiens 72-82 12631248-7 2003 The melanosomal membrane location of tyrosine hydroxylase together with tyrosinase implies a coupled interaction, where L-dopa production facilitates the activation of tyrosinase. Levodopa 120-126 tyrosinase Homo sapiens 168-178 12421594-0 2003 Catechol-O-methyltransferase inhibition protects against 3,4-dihydroxyphenylalanine (DOPA) toxicity in primary mesencephalic cultures: new insights into levodopa toxicity. Levodopa 153-161 catechol-O-methyltransferase Rattus norvegicus 0-28 12533089-3 2003 However, patients with Parkinson disease (PD) may have elevated homocysteine levels resulting from methylation of levodopa and dopamine by catechol O-methyltransferase, an enzyme that uses S-adenosylmethionine as a methyl donor and yields S-adenosylhomocysteine. Levodopa 114-122 catechol-O-methyltransferase Homo sapiens 139-167 12908845-3 2003 Catechol-O-methyltransferase (COMT) inhibitors reduce levodopa metabolism and enhance the respective plasma levels, resulting in improvements in symptoms and overall quality of life. Levodopa 54-62 catechol-O-methyltransferase Homo sapiens 0-28 12908845-3 2003 Catechol-O-methyltransferase (COMT) inhibitors reduce levodopa metabolism and enhance the respective plasma levels, resulting in improvements in symptoms and overall quality of life. Levodopa 54-62 catechol-O-methyltransferase Homo sapiens 30-34 14526427-0 2003 Effect of levodopa chronic administration on behavioral changes and fos expression in basal ganglia in rat model of PD. Levodopa 10-18 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-71 14526427-5 2003 Fos positive nuclei in the CPU and GP were increased by levodopa acute administration, and more remarkably in the CPU, but not in the cerebral cortex. Levodopa 56-64 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-3 12421594-1 2003 Inhibition of catechol-O-methyltransferase (COMT) has protective effects on levodopa (L-DOPA), but not D-DOPA toxicity towards dopamine (DA) neurons in rat primary mesencephalic cultures [Mol. Levodopa 76-84 catechol-O-methyltransferase Rattus norvegicus 14-42 12421594-1 2003 Inhibition of catechol-O-methyltransferase (COMT) has protective effects on levodopa (L-DOPA), but not D-DOPA toxicity towards dopamine (DA) neurons in rat primary mesencephalic cultures [Mol. Levodopa 76-84 catechol-O-methyltransferase Rattus norvegicus 44-48 12421594-1 2003 Inhibition of catechol-O-methyltransferase (COMT) has protective effects on levodopa (L-DOPA), but not D-DOPA toxicity towards dopamine (DA) neurons in rat primary mesencephalic cultures [Mol. Levodopa 86-92 catechol-O-methyltransferase Rattus norvegicus 14-42 12421594-1 2003 Inhibition of catechol-O-methyltransferase (COMT) has protective effects on levodopa (L-DOPA), but not D-DOPA toxicity towards dopamine (DA) neurons in rat primary mesencephalic cultures [Mol. Levodopa 86-92 catechol-O-methyltransferase Rattus norvegicus 44-48 12421594-9 2003 Increased contamination of the cultures with glial cells attenuated L- and D-DOPA toxicity, but caused significant enhancement of protection by COMT inhibitors against L-DOPA toxicity only. Levodopa 168-174 catechol-O-methyltransferase Rattus norvegicus 144-148 12421594-12 2003 In addition, we demonstrate a second mechanism of L-DOPA toxicity in vitro mediated by a COMT- and glia-dependent pathway, which is blocked by COMT inhibitors, most likely due to enhanced glial uptake of L-DOPA. Levodopa 50-56 catechol-O-methyltransferase Rattus norvegicus 89-93 12421594-12 2003 In addition, we demonstrate a second mechanism of L-DOPA toxicity in vitro mediated by a COMT- and glia-dependent pathway, which is blocked by COMT inhibitors, most likely due to enhanced glial uptake of L-DOPA. Levodopa 50-56 catechol-O-methyltransferase Rattus norvegicus 143-147 12421594-12 2003 In addition, we demonstrate a second mechanism of L-DOPA toxicity in vitro mediated by a COMT- and glia-dependent pathway, which is blocked by COMT inhibitors, most likely due to enhanced glial uptake of L-DOPA. Levodopa 204-210 catechol-O-methyltransferase Rattus norvegicus 89-93 12421594-12 2003 In addition, we demonstrate a second mechanism of L-DOPA toxicity in vitro mediated by a COMT- and glia-dependent pathway, which is blocked by COMT inhibitors, most likely due to enhanced glial uptake of L-DOPA. Levodopa 204-210 catechol-O-methyltransferase Rattus norvegicus 143-147 14673217-1 2003 Catechol-O-methyltransferase (COMT) is an enzyme that inactivates catecholamines, including levodopa. Levodopa 92-100 catechol-O-methyltransferase Homo sapiens 0-28 12835121-7 2003 The melanin-synthetic enzyme tyrosinase in the brain may rapidly oxidize excess amounts of cytosolic DA and L-DOPA, thereby preventing slowly progressive cell damage by auto-oxidation of DA, thus maintainng DA levels. Levodopa 108-114 tyrosinase Homo sapiens 29-39 14673217-1 2003 Catechol-O-methyltransferase (COMT) is an enzyme that inactivates catecholamines, including levodopa. Levodopa 92-100 catechol-O-methyltransferase Homo sapiens 30-34 12535962-0 2003 Effects of oligonucleotide antisense to dopamine D3 receptor mRNA in a rodent model of behavioural sensitization to levodopa. Levodopa 116-124 dopamine receptor D3 Rattus norvegicus 40-60 12535962-3 2003 Elevations in dopamine D(3) receptor mRNA and binding are seen in the denervated striatum of hemiparkinsonian rats treated chronically with levodopa, and these changes correlate well with behavioural sensitization in this model. Levodopa 140-148 dopamine receptor D3 Rattus norvegicus 14-36 12535962-4 2003 Further investigation of dopamine D(3) receptor involvement in levodopa-induced dyskinesias is hampered by the lack of appropriately selective ligands for this receptor. Levodopa 63-71 dopamine receptor D3 Rattus norvegicus 25-47 12835121-8 2003 Since tyrosinase also possesses catecholamine-synthesizing activity in the absence of tyrosine hydroxylase (TH), the double-edged synthesizing and oxidizing functions of tyrosinase in the dopaminergic system suggest its potential for application in the synthesis of DA, instead of TH in the degeneration of dopaminergic neurons, and in the normalization of abnormal DA turnover in the long-term L-DOPA-treated Parkinson"s disease patients. Levodopa 395-401 tyrosinase Homo sapiens 6-16 12573867-11 2003 These primate studies have demonstrated that long-acting dopamine agonists and levodopa given in combination with a catechol-O-methyl transferase (COMT) inhibitor (to increase its relatively short half-life), induce significantly less dyskinesia than occurs with standard levodopa therapy. Levodopa 79-87 catechol-O-methyltransferase Homo sapiens 116-145 12573867-11 2003 These primate studies have demonstrated that long-acting dopamine agonists and levodopa given in combination with a catechol-O-methyl transferase (COMT) inhibitor (to increase its relatively short half-life), induce significantly less dyskinesia than occurs with standard levodopa therapy. Levodopa 79-87 catechol-O-methyltransferase Homo sapiens 147-151 12835121-8 2003 Since tyrosinase also possesses catecholamine-synthesizing activity in the absence of tyrosine hydroxylase (TH), the double-edged synthesizing and oxidizing functions of tyrosinase in the dopaminergic system suggest its potential for application in the synthesis of DA, instead of TH in the degeneration of dopaminergic neurons, and in the normalization of abnormal DA turnover in the long-term L-DOPA-treated Parkinson"s disease patients. Levodopa 395-401 tyrosinase Homo sapiens 170-180 12573867-11 2003 These primate studies have demonstrated that long-acting dopamine agonists and levodopa given in combination with a catechol-O-methyl transferase (COMT) inhibitor (to increase its relatively short half-life), induce significantly less dyskinesia than occurs with standard levodopa therapy. Levodopa 272-280 catechol-O-methyltransferase Homo sapiens 116-145 12573867-11 2003 These primate studies have demonstrated that long-acting dopamine agonists and levodopa given in combination with a catechol-O-methyl transferase (COMT) inhibitor (to increase its relatively short half-life), induce significantly less dyskinesia than occurs with standard levodopa therapy. Levodopa 272-280 catechol-O-methyltransferase Homo sapiens 147-151 12373737-0 2002 Systemic administration of dizocilpine maleate (MK-801) or L-dopa reverses the increases in GAD65 and GAD67 mRNA expression in the globus pallidus in a rat hemiparkinsonian model. Levodopa 59-65 glutamate decarboxylase 2 Rattus norvegicus 92-97 12573869-8 2003 ), both COMT inhibitors significantly increased striatal levels of L-DOPA and DA compared with saline. Levodopa 67-73 catechol-O-methyltransferase Rattus norvegicus 8-12 12373737-0 2002 Systemic administration of dizocilpine maleate (MK-801) or L-dopa reverses the increases in GAD65 and GAD67 mRNA expression in the globus pallidus in a rat hemiparkinsonian model. Levodopa 59-65 glutamate decarboxylase 1 Rattus norvegicus 102-107 12373737-1 2002 This study examined the consequences of systemic treatment with either L-dopa or MK-801 on the levels of mRNAs encoding the 65 and 67 kDa isoforms of glutamate decarboxylase (GAD65 and GAD67) in the striatum and globus pallidus (GP) of rats rendered hemiparkinsonian by intranigral 6-hydroxydopamine injection. Levodopa 71-77 glutamate-ammonia ligase Rattus norvegicus 150-173 12373737-1 2002 This study examined the consequences of systemic treatment with either L-dopa or MK-801 on the levels of mRNAs encoding the 65 and 67 kDa isoforms of glutamate decarboxylase (GAD65 and GAD67) in the striatum and globus pallidus (GP) of rats rendered hemiparkinsonian by intranigral 6-hydroxydopamine injection. Levodopa 71-77 glutamate decarboxylase 2 Rattus norvegicus 175-180 12373737-5 2002 The lesion-induced increases in GAD67 transcripts were potentiated by L-dopa but unaffected by MK-801, whereas the increases in GAD65 were suppressed by MK-801 but unaffected by L-dopa. Levodopa 70-76 glutamate decarboxylase 1 Rattus norvegicus 32-37 12417252-12 2002 It was concluded from this study that L-DOPA contributed to the modulation of iNOS and to the increase of O(2)(-) production in the stimulated glioma cells in vitro. Levodopa 38-44 nitric oxide synthase 2 Homo sapiens 78-82 12622939-2 2002 METHODS: Tyrosinase activity was estimated by measuring the oxidation rate of L-dopa. Levodopa 78-84 tyrosinase Homo sapiens 9-19 12690673-1 2002 The effects of deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the internal pallidum (GPi) on the parkinsonian triad and on levodopa-induced dyskinesias are very similar. Levodopa 141-149 glucose-6-phosphate isomerase Homo sapiens 103-106 12480442-11 2002 This work has been criticised as the SPECT results may have resulted from a differential effect of the agonist and levodopa on the regulation of the dopamine transporter, thereby influencing the imaging outcome measure. Levodopa 115-123 solute carrier family 6 member 3 Homo sapiens 149-169 12417252-3 2002 In this study, lipopolysaccharide (LPS) and interferon-gamma (IFN-g) were used to stimulate C6 glioma cells in the presence of varying concentrations of L-DOPA (1 microM-1 mM). Levodopa 153-159 interferon gamma Homo sapiens 44-60 12466240-9 2002 Protective effects of 100 U ml(-1) catalase (40+/-1% of control) against L-DOPA-induced cell death were lower than those conferred by 200 microM ascorbic acid (70+/-3% of control). Levodopa 73-79 catalase Mus musculus 35-43 12466240-11 2002 L-DOPA-induced neuronal cell death was also accompanied by increases in caspase-3 activity, this being insensitive to ascorbic acid. Levodopa 0-6 caspase 3 Mus musculus 72-81 12466240-14 2002 It is suggested that in addition to generation of H(2)O(2) and quinone formation, L-DOPA- and dopamine-induced cell death may result from induction of apoptosis, as evidenced by increases in caspase-3 activity. Levodopa 82-88 caspase 3 Mus musculus 191-200 12417252-3 2002 In this study, lipopolysaccharide (LPS) and interferon-gamma (IFN-g) were used to stimulate C6 glioma cells in the presence of varying concentrations of L-DOPA (1 microM-1 mM). Levodopa 153-159 interferon gamma Homo sapiens 62-67 12419501-5 2002 Opposite results were obtained concerning the regulation of RGS4 since L-dopa alone was without effect whereas co-administration of L-dopa and R(+)-SCH23390 significantly enhanced the RGS4 mRNA levels (by 38%). Levodopa 132-138 regulator of G-protein signaling 4 Rattus norvegicus 60-64 12417252-5 2002 Western blot analysis corroborated that L-DOPA effects on iNOS was at the level of its protein expression. Levodopa 40-46 nitric oxide synthase 2 Homo sapiens 58-62 12451209-5 2002 Families with autosomal dominant, levodopa-responsive parkinsonism should be tested for the SCA-2 mutation. Levodopa 34-42 ataxin 2 Homo sapiens 92-97 12235154-2 2002 Whereas 3- and 4-fluorophenol react with tyrosinase to give products that undergo a rapid polymerization process, 2-fluorophenol is not reactive and actually acts as a competitive inhibitor in the enzymatic oxidation of 3,4-dihydroxyphenylalanine (L-dopa). Levodopa 248-254 tyrosinase Homo sapiens 41-51 12419501-5 2002 Opposite results were obtained concerning the regulation of RGS4 since L-dopa alone was without effect whereas co-administration of L-dopa and R(+)-SCH23390 significantly enhanced the RGS4 mRNA levels (by 38%). Levodopa 132-138 regulator of G-protein signaling 4 Rattus norvegicus 184-188 12390968-3 2002 We studied variation in the motor short-duration response (SDR) during a levodopa challenge in bilaterally STN-stimulated patients. Levodopa 73-81 caveolae associated protein 2 Homo sapiens 59-62 12390968-12 2002 The main change in the levodopa SDR was a significant reduction in levodopa-induced dyskinesias in both groups. Levodopa 23-31 caveolae associated protein 2 Homo sapiens 32-35 12390968-12 2002 The main change in the levodopa SDR was a significant reduction in levodopa-induced dyskinesias in both groups. Levodopa 67-75 caveolae associated protein 2 Homo sapiens 32-35 12390968-15 2002 On the whole, chronic bilateral STN stimulation tended to decrease the magnitude of the levodopa SDR without changing the duration and latency of the response. Levodopa 88-96 caveolae associated protein 2 Homo sapiens 97-100 12358737-1 2002 Aromatic L-amino acid decarboxylase (AADC) is necessary for conversion of L-DOPA to dopamine. Levodopa 74-80 dopa decarboxylase Rattus norvegicus 0-35 12443929-7 2002 The regions of two genes have been sequenced: D1 dopamine receptor gene (subfamily of the G-protein coupled receptor L-DOPA genes) and the intron 12 of the gene for phenylalanine hydroxylase (PAH) responsible for phenylketonuria or hyperphenylalaninemia. Levodopa 117-123 phenylalanine hydroxylase Homo sapiens 165-190 12443929-7 2002 The regions of two genes have been sequenced: D1 dopamine receptor gene (subfamily of the G-protein coupled receptor L-DOPA genes) and the intron 12 of the gene for phenylalanine hydroxylase (PAH) responsible for phenylketonuria or hyperphenylalaninemia. Levodopa 117-123 phenylalanine hydroxylase Homo sapiens 192-195 12460610-7 2002 In addition, these behavioral measures are correlated to dopamine transporter, vesicular monoamine transporter, and tyrosine hydroxylase expression and are improved following L-DOPA administration. Levodopa 175-181 tyrosine hydroxylase Mus musculus 116-136 12393055-1 2002 Catechol-O-methyl transferase (COMT) inhibitors, entacapone and tolcapone, are used as an adjunctive treatment to L-dopa in Parkinson"s disease. Levodopa 114-120 catechol-O-methyltransferase Rattus norvegicus 0-29 12393055-1 2002 Catechol-O-methyl transferase (COMT) inhibitors, entacapone and tolcapone, are used as an adjunctive treatment to L-dopa in Parkinson"s disease. Levodopa 114-120 catechol-O-methyltransferase Rattus norvegicus 31-35 12420085-6 2002 Baseline PRL values were significantly lower for patients with IPD than for those with MSA, both for levodopa-treated and naive patients ( p < 0.004, estimated decrease 55.1 %, 95 % CI from 29.4 % to 71.52 %). Levodopa 101-109 prolactin Homo sapiens 9-12 12709305-6 2002 Moreover, BDNF triggers D(3) receptor overexpression and behavioral sensitization to levodopa in denervated animals. Levodopa 85-93 brain derived neurotrophic factor Homo sapiens 10-14 12377373-6 2002 In addition, treatment with L-3,4-dihydroxyphenylalanine (L-DOPA) at 20-50 microM increased the intracellular dopamine content in PC12 cells and the increase of dopamine level by L-DOPA was significantly inhibited after exposure to TBTC at 0.5-2.0 microM for 24 h. These results indicate that TBTC decreases dopamine content by the inhibition of TH activity and TH mRNA level in PC12 cells. Levodopa 28-56 tyrosine hydroxylase Rattus norvegicus 346-348 12377373-6 2002 In addition, treatment with L-3,4-dihydroxyphenylalanine (L-DOPA) at 20-50 microM increased the intracellular dopamine content in PC12 cells and the increase of dopamine level by L-DOPA was significantly inhibited after exposure to TBTC at 0.5-2.0 microM for 24 h. These results indicate that TBTC decreases dopamine content by the inhibition of TH activity and TH mRNA level in PC12 cells. Levodopa 28-56 tyrosine hydroxylase Rattus norvegicus 362-364 12377373-6 2002 In addition, treatment with L-3,4-dihydroxyphenylalanine (L-DOPA) at 20-50 microM increased the intracellular dopamine content in PC12 cells and the increase of dopamine level by L-DOPA was significantly inhibited after exposure to TBTC at 0.5-2.0 microM for 24 h. These results indicate that TBTC decreases dopamine content by the inhibition of TH activity and TH mRNA level in PC12 cells. Levodopa 58-64 tyrosine hydroxylase Rattus norvegicus 346-348 12377373-6 2002 In addition, treatment with L-3,4-dihydroxyphenylalanine (L-DOPA) at 20-50 microM increased the intracellular dopamine content in PC12 cells and the increase of dopamine level by L-DOPA was significantly inhibited after exposure to TBTC at 0.5-2.0 microM for 24 h. These results indicate that TBTC decreases dopamine content by the inhibition of TH activity and TH mRNA level in PC12 cells. Levodopa 58-64 tyrosine hydroxylase Rattus norvegicus 362-364 12358737-1 2002 Aromatic L-amino acid decarboxylase (AADC) is necessary for conversion of L-DOPA to dopamine. Levodopa 74-80 dopa decarboxylase Rattus norvegicus 37-41 12358737-2 2002 Therefore, AADC gene therapy has been proposed to enhance pharmacological or gene therapies delivering L-DOPA. Levodopa 103-109 dopa decarboxylase Rattus norvegicus 11-15 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 154-160 dopa decarboxylase Rattus norvegicus 21-25 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 154-160 tyrosine hydroxylase Rattus norvegicus 81-101 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 154-160 tyrosine hydroxylase Rattus norvegicus 103-105 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 154-160 GTP cyclohydrolase 1 Rattus norvegicus 111-131 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 154-160 GTP cyclohydrolase 1 Rattus norvegicus 133-137 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 219-225 tyrosine hydroxylase Rattus norvegicus 81-101 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 219-225 GTP cyclohydrolase 1 Rattus norvegicus 111-131 12358737-3 2002 However, addition of AADC to the grafts of genetically modified cells expressing tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GCH1), which produce L-DOPA in parkinsonian rats, resulted in decreased production of L-DOPA and dopamine owing to feedback inhibition of TH by dopamine. Levodopa 219-225 GTP cyclohydrolase 1 Rattus norvegicus 133-137 12428733-5 2002 In this study, we subjected VMAT2 (+/-) mice to subchronic administration of L-DOPA to determine if it was toxic in this model. Levodopa 77-83 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 28-33 12428733-9 2002 L-DOPA treatment significantly decreased DAT levels in VMAT2 (+/+) mice, but not in VMAT2 (+/-) mice. Levodopa 0-6 solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 Mus musculus 41-44 12428733-9 2002 L-DOPA treatment significantly decreased DAT levels in VMAT2 (+/+) mice, but not in VMAT2 (+/-) mice. Levodopa 0-6 solute carrier family 18 (vesicular monoamine), member 2 Mus musculus 55-60 12236793-1 2002 BIA 3-202, 1-(3,4-dihydroxy-5-nitrophenyl)-2-phenylethanone 3, is a novel, reversible, and tight-binding peripheral inhibitor of the enzyme catechol-O-methyltransferase (COMT), which is currently under clinical evaluation for the treatment of Parkinson"s disease as an adjunct to current L-Dopa/peripheral decarboxylase inhibitor therapy. Levodopa 288-294 catechol-O-methyltransferase Homo sapiens 140-168 12236793-1 2002 BIA 3-202, 1-(3,4-dihydroxy-5-nitrophenyl)-2-phenylethanone 3, is a novel, reversible, and tight-binding peripheral inhibitor of the enzyme catechol-O-methyltransferase (COMT), which is currently under clinical evaluation for the treatment of Parkinson"s disease as an adjunct to current L-Dopa/peripheral decarboxylase inhibitor therapy. Levodopa 288-294 catechol-O-methyltransferase Homo sapiens 170-174 12429227-4 2002 L-DOPA responsiveness was also accompanied by changes at the neuronal level, as shown by changes in the expression of c-fos in the dopamine-depleted striatum. Levodopa 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 118-123 12429227-5 2002 Following 1 week of L-DOPA treatment there was a marked decrease in striatal c-fos expression, compared to single injections, especially evident in the medial and ventral regions and to a lesser extent in the dorsolateral regions of the striatum. Levodopa 20-26 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 77-82 12429227-6 2002 This specific regional expression of c-fos was maintained throughout the 16 weeks of L-DOPA treatment. Levodopa 85-91 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 37-42 12429227-8 2002 Persisting c-fos expression in the dorsolateral striatum might be implicated in the development of dyskinesias when L-DOPA treatment is extended for periods longer than 1 week. Levodopa 116-122 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 11-16 12210799-9 2002 Grip force overflow is a promising parameter to study the desensitizing effect of chronic deep-brain stimulation on levodopa-induced dyskinesias. Levodopa 116-124 glutamate receptor interacting protein 1 Homo sapiens 0-4 12548350-2 2002 After L-dopa administration, the PD patients scored a significantly higher percentage of correct performances ( p<0.05), linked to a decreased BP amplitude ( p<0.001) and an increased SPP amplitude ( p<0.005), than before therapy. Levodopa 6-12 histocompatibility minor 13 Homo sapiens 184-187 12069421-1 2002 Hydroxylation of peptidyl-3,4-dihydroxyphenyl-l-alanine (Dopa) was observed during tyrosinase incubation of a decapeptide related to the mussel adhesive protein mefp1. Levodopa 57-61 tyrosinase Homo sapiens 83-93 12597016-7 2002 L-dopa plus carbidopa or OR-486 (a potent centrally acting COMT inhibitor) completely reversed adenosine-induced catatonia. Levodopa 0-6 catechol-O-methyltransferase Mus musculus 59-63 12083775-0 2002 Behavior of fluorinated analogs of L-(3,4-dihydroxyphenyl)alanine and L-threo-(3,4-dihydroxyphenyl)serine as substrates for Dopa decarboxylase. Levodopa 35-65 dopa decarboxylase Homo sapiens 124-142 12083995-1 2002 Entacapone is one of a new class of drugs, the catechol-O-methyltransferase (COMT) inhibitors, which expand the therapeutic options for Parkinson"s disease by extending the action of levodopa. Levodopa 183-191 catechol-O-methyltransferase Homo sapiens 47-75 12083995-1 2002 Entacapone is one of a new class of drugs, the catechol-O-methyltransferase (COMT) inhibitors, which expand the therapeutic options for Parkinson"s disease by extending the action of levodopa. Levodopa 183-191 catechol-O-methyltransferase Homo sapiens 77-81 12091481-4 2002 Next, AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3,4-dihydroxyphenylalanine into DA, whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells. Levodopa 160-188 tyrosine hydroxylase Mus musculus 78-80 12180806-1 2002 Entacapone and tolcapone, novel catechol-O-methyl-transferase (COMT) inhibitors, have been developed for the treatment of Parkinson"s disease in combination with levodopa. Levodopa 162-170 catechol-O-methyltransferase Rattus norvegicus 32-61 12180806-1 2002 Entacapone and tolcapone, novel catechol-O-methyl-transferase (COMT) inhibitors, have been developed for the treatment of Parkinson"s disease in combination with levodopa. Levodopa 162-170 catechol-O-methyltransferase Rattus norvegicus 63-67 12127155-4 2002 During a course of chronic L-DOPA treatment, rats with intrastriatal 6-OHDA lesions developed abnormal involuntary movements (AIMs), which mapped onto striatal domains exhibiting at least approximately 90% denervation, as judged by DA transporter autoradiography. Levodopa 27-33 solute carrier family 6 member 3 Rattus norvegicus 232-246 12028583-2 2002 Using a neural crest cell (NCC) primary culture system from wild-type mice, we previously demonstrated that KIT-positive and/or L-3, 4-dihydroxyphenylalanine (DOPA)-positive melanocyte precursors proliferate following the addition of SCF to the culture medium. Levodopa 128-157 kit ligand Mus musculus 234-237 12200739-7 2002 The AADC enzyme substrates L-dopa and 5-hydroxytryptophan (5-HTP) were elevated in CSF. Levodopa 27-33 dopa decarboxylase Homo sapiens 4-8 12200739-7 2002 The AADC enzyme substrates L-dopa and 5-hydroxytryptophan (5-HTP) were elevated in CSF. Levodopa 27-33 colony stimulating factor 2 Homo sapiens 83-86 11965353-9 2002 During ontogenesis, the monoenzymatic TH- and AADC-containing neurons established axosomatic and axo-axonal junctions that might facilitate the L-DOPA transport from the former to the latter. Levodopa 144-150 dopa decarboxylase Rattus norvegicus 46-50 12028583-5 2002 More KIT-positive cells and DOPA-positive cells were detected in the presence of SCF on ECM-coated wells than on non-coated wells. Levodopa 28-32 kit ligand Mus musculus 81-84 12028583-6 2002 A statistically significant increase in DOPA-positive cells was evident in FN and CLI wells. Levodopa 40-44 fibronectin 1 Mus musculus 75-77 12028583-10 2002 The number of DOPA-positive cells decreased with RGDS concentration in a dose-dependent fashion. Levodopa 14-18 ral guanine nucleotide dissociation stimulator Mus musculus 49-53 11954048-6 2002 Chronic-intermittent L-dopa (6 mg/kg) treatment increased the striatal levels of GAD67, dynorphin, and enkephalin mRNA in the lesioned side as compared to the vehicle treatment. Levodopa 21-27 proenkephalin Rattus norvegicus 103-113 11954048-0 2002 Differential regulation of GAD67, enkephalin and dynorphin mRNAs by chronic-intermittent L-dopa and A2A receptor blockade plus L-dopa in dopamine-denervated rats. Levodopa 89-95 glutamate decarboxylase 1 Rattus norvegicus 27-32 11954048-0 2002 Differential regulation of GAD67, enkephalin and dynorphin mRNAs by chronic-intermittent L-dopa and A2A receptor blockade plus L-dopa in dopamine-denervated rats. Levodopa 89-95 proenkephalin Rattus norvegicus 34-44 12047348-5 2002 These AADC neurones could uptake exogenously applied L-DOPA and formed dopamine. Levodopa 53-59 dopa decarboxylase Rattus norvegicus 6-10 11954048-0 2002 Differential regulation of GAD67, enkephalin and dynorphin mRNAs by chronic-intermittent L-dopa and A2A receptor blockade plus L-dopa in dopamine-denervated rats. Levodopa 127-133 glutamate decarboxylase 1 Rattus norvegicus 27-32 11954048-0 2002 Differential regulation of GAD67, enkephalin and dynorphin mRNAs by chronic-intermittent L-dopa and A2A receptor blockade plus L-dopa in dopamine-denervated rats. Levodopa 127-133 proenkephalin Rattus norvegicus 34-44 11954048-6 2002 Chronic-intermittent L-dopa (6 mg/kg) treatment increased the striatal levels of GAD67, dynorphin, and enkephalin mRNA in the lesioned side as compared to the vehicle treatment. Levodopa 21-27 glutamate decarboxylase 1 Rattus norvegicus 81-86 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 104-110 catechol-O-methyltransferase Rattus norvegicus 0-28 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 104-110 catechol-O-methyltransferase Rattus norvegicus 30-34 12065640-9 2002 After activation of hTH1 by PKA all the tetrahydro-beta-carbolines investigated in this study decreased l-DOPA formation. Levodopa 104-110 negative elongation factor complex member C/D Homo sapiens 20-24 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 113-141 catechol-O-methyltransferase Rattus norvegicus 0-28 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 113-141 catechol-O-methyltransferase Rattus norvegicus 30-34 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 143-151 catechol-O-methyltransferase Rattus norvegicus 0-28 12111468-1 2002 Catechol-O-methyltransferase (COMT) inhibitors such as entacapone and tolcapone are used as adjuncts to L-DOPA ( l-3,4-dihydroxyphenylalanine, levodopa) in the treatment of Parkinson"s disease. Levodopa 143-151 catechol-O-methyltransferase Rattus norvegicus 30-34 12112191-13 2002 These studies are in line with previous findings suggesting that administration of NR2B-selective NMDA receptor antagonists may be therapeutically beneficial for parkinsonian patients, when given de novo and following L-dopa treatment. Levodopa 218-224 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 83-87 11917105-4 2002 Using new generation high-titer recombinant adeno-associated virus vectors, we show that levels of striatal L-dopa production exceeding this threshold can be obtained provided that tyrosine hydroxylase is coexpressed with the cofactor synthetic enzyme, GTP-cyclohydrolase-1. Levodopa 108-114 GTP cyclohydrolase 1 Homo sapiens 253-273 11959153-9 2002 Of these, one (0.8%) patient had RLS-like symptoms closely correlated to wearing "off" effect of levodopa. Levodopa 97-105 RLS1 Homo sapiens 33-36 12067224-2 2002 We show that exposure of neurons (CSM 14.1) to 5-S-cysteinyl conjugates of dopamine, L-DOPA, DOPAC or DHMA causes neuronal damage, increases in oxidative DNA base modification and an elevation of caspase-3 activity in cells. Levodopa 85-91 caspase 3 Homo sapiens 196-205 12039419-14 2002 Brain monoamine oxidase B inhibition has previously been shown to significantly increases brain PEA and which is capable of releasing dopamine endogenously or that formed from L-dopa. Levodopa 176-182 monoamine oxidase B Rattus norvegicus 6-25 11901210-3 2002 LAT1-mediated [(14)C]phenylalanine uptake was strongly inhibited in a competitive manner by aromatic-amino acid derivatives including L-dopa, alpha-methyldopa, melphalan, triiodothyronine, and thyroxine, whereas phenylalanine methyl ester, N-methyl phenylalanine, dopamine, tyramine, carbidopa, and droxidopa did not inhibit [(14)C]phenylalanine uptake. Levodopa 134-140 solute carrier family 7 member 5 L homeolog Xenopus laevis 0-4 11942697-2 2002 Inhibition of catechol O-methyltransferase (COMT) with tolcapone led to increases in extracellular dopamine levels only when the baseline dopamine level was elevated by administration of L-3,4-dihydroxyphenylalanine in combination with the decarboxylation inhibitor carbidopa. Levodopa 187-215 catechol-O-methyltransferase Rattus norvegicus 14-42 11942697-2 2002 Inhibition of catechol O-methyltransferase (COMT) with tolcapone led to increases in extracellular dopamine levels only when the baseline dopamine level was elevated by administration of L-3,4-dihydroxyphenylalanine in combination with the decarboxylation inhibitor carbidopa. Levodopa 187-215 catechol-O-methyltransferase Rattus norvegicus 44-48 11899548-4 2002 The availability of several newer types of agents--dopamine agonists, monoamine oxidase inhibitors, and catechol-O-methyltransferase inhibitors--gives physicians increased flexibility with regard to first-line therapy, adjunct therapy, and managing or reducing the frequency of motor complications and other side effects associated with chronic levodopa therapy. Levodopa 345-353 catechol-O-methyltransferase Homo sapiens 104-132 11873938-4 2002 When coadministered with levodopa/decarboxylase inhibitor, 2 COMT inhibitors, tolcapone and entacapone have been shown to improve the clinical benefit of levodopa. Levodopa 154-162 catechol-O-methyltransferase Homo sapiens 61-65 11873938-6 2002 Differences in COMT activity may determine the individual response to levodopa and result in ethnic differences in PD susceptibility. Levodopa 70-78 catechol-O-methyltransferase Homo sapiens 15-19 11779580-3 2002 In dogs, intravenous KDR-5169 stimulated upper gastrointestinal motility in the fasting state and also eliminated the depressive effect of 3,4-dihydroxyphenylalanine (L-DOPA) on this motility in the postprandial state. Levodopa 167-173 kinase insert domain receptor Canis lupus familiaris 21-24 11856629-4 2002 RESULTS: After L-dopa administration the PD patients scored a significantly higher percentage of correct performances (P<0.05), linked to a decreased BP amplitude (P<0.001) and an increased SPP amplitude (P<0.005), than before therapy. Levodopa 15-21 histocompatibility minor 13 Homo sapiens 190-193 11856629-5 2002 Dynamic evaluation through the block analysis did not show any learning effect in off-therapy patients but showed that L-dopa intake improved learning, linked to a BP amplitude decrease (P<0.005) and a SPP amplitude increase (P<0.05). Levodopa 119-125 histocompatibility minor 13 Homo sapiens 202-205 11834428-0 2002 The role of endogenous GHRH in arginine-, insulin-, clonidine- and l-dopa-induced GH release in normal subjects. Levodopa 67-73 growth hormone releasing hormone Homo sapiens 23-27 11853020-0 2002 Increase of preproenkephalin mRNA levels in the putamen of Parkinson disease patients with levodopa-induced dyskinesias. Levodopa 91-99 proenkephalin Homo sapiens 12-28 11880864-12 2002 Moreover, bicalutamide therapy significantly reduced PRL increase in response to L-dopa. Levodopa 81-87 prolactin Homo sapiens 53-56 11889758-2 2002 A Combination therapy of a dopamine receptor agonist and levodopa/DCI(DOPA-decarboxylase inhibitor) is commonly used to control the complication. Levodopa 57-65 dopa decarboxylase Homo sapiens 70-88 11889759-3 2002 Based on our previous experimental studies that 8-OH-DPAT, a potent 5-HT1A agonist, attenuates an increase in L-DOPA-induced extracellular DA in the striatum of the rat model of Parkinson"s disease, we hypothesized that L-DOPA-induced dyskinesia in patients with Parkinson"s disease is alleviated by a 5-HT1A agonist. Levodopa 110-116 5-hydroxytryptamine receptor 1A Rattus norvegicus 68-74 11889759-3 2002 Based on our previous experimental studies that 8-OH-DPAT, a potent 5-HT1A agonist, attenuates an increase in L-DOPA-induced extracellular DA in the striatum of the rat model of Parkinson"s disease, we hypothesized that L-DOPA-induced dyskinesia in patients with Parkinson"s disease is alleviated by a 5-HT1A agonist. Levodopa 110-116 5-hydroxytryptamine receptor 1A Homo sapiens 302-308 11889759-15 2002 Further studies such as double-blind trials are needed to confirm the usefulness of a 5-HT1A agonist for L-DOPA-induced dyskinesia. Levodopa 105-111 5-hydroxytryptamine receptor 1A Homo sapiens 86-92 11781109-10 2002 However, replacement of Q (in Tyr) by H (in Tyrps) greatly diminished the affinity for L-dopa, consistent with the low/null tyrosinase activity of the Tyrps. Levodopa 87-93 tyrosinase Homo sapiens 30-33 11781109-10 2002 However, replacement of Q (in Tyr) by H (in Tyrps) greatly diminished the affinity for L-dopa, consistent with the low/null tyrosinase activity of the Tyrps. Levodopa 87-93 tyrosinase Homo sapiens 124-134 11834428-1 2002 OBJECTIVE: The role of endogenous GHRH in arginine-, insulin-, clonidine- and l-dopa-induced GH secretion was studied in man using a GHRH antagonist (GHRH-Ant). Levodopa 78-84 growth hormone releasing hormone Homo sapiens 34-38 11834428-5 2002 When these four agents were sequentially administered 120 min after GHRH injection, the GH responses to clonidine and l-dopa disappeared completely while clear responses were observed to arginine and insulin administration. Levodopa 118-124 growth hormone releasing hormone Homo sapiens 68-72 11821691-5 2002 Radioisotope assays were used to measure the total melanin synthesis and the activity of tyrosinase in converting tyrosine to L-3,4-dihydroxyphenylalanine, which is a rate-limiting reaction in melanogenesis. Levodopa 126-154 tyrosinase Mus musculus 89-99 12075857-1 2002 One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT). Levodopa 33-41 catechol-O-methyltransferase Homo sapiens 88-116 12075857-1 2002 One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT). Levodopa 33-41 catechol-O-methyltransferase Homo sapiens 118-122 11880864-0 2002 Effect of bicalutamide therapy on prolactin response to L-dopa in metastatic prostate cancer patients. Levodopa 56-62 prolactin Homo sapiens 34-43 11880864-1 2002 OBJECTIVES: The secretion of prolactin (PRL), which is a growth factor for prostate cancer cell proliferation, has been proven to present profound alterations in advanced prostate cancer patients, consisting of abnormally elevated baseline levels and paradoxical response to L-dopa. Levodopa 275-281 prolactin Homo sapiens 29-38 11880864-1 2002 OBJECTIVES: The secretion of prolactin (PRL), which is a growth factor for prostate cancer cell proliferation, has been proven to present profound alterations in advanced prostate cancer patients, consisting of abnormally elevated baseline levels and paradoxical response to L-dopa. Levodopa 275-281 prolactin Homo sapiens 40-43 11852293-1 2002 Blockade of the adenosine A2A receptor potentiates the effects of levodopa in experimental animals and may offer a novel nondopaminergic target for drug therapy in Parkinson"s disease (PD). Levodopa 66-74 adenosine A2a receptor Homo sapiens 16-38 12373520-6 2002 In the 1950s, the focus of L-dopa research shifted to its potential for replenishing the experimentally depleted (by insulin or reserpine) peripheral and brain catecholamine stores and the concomitant restoration of normal function. Levodopa 27-33 insulin Homo sapiens 117-124 12373525-8 2002 Both AIM development and the associated upregulation of prodynorphin mRNA by L-DOPA are significantly inhibited by the intrastriatal infusion of fosB antisense. Levodopa 77-83 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 145-149 12373527-6 2002 At the molecular level, transcriptional activation of striatal CREB and cdk5 may contribute to the persistent expression of these levodopa-induced response alterations. Levodopa 130-138 cAMP responsive element binding protein 1 Homo sapiens 63-67 12373527-6 2002 At the molecular level, transcriptional activation of striatal CREB and cdk5 may contribute to the persistent expression of these levodopa-induced response alterations. Levodopa 130-138 cyclin dependent kinase 5 Homo sapiens 72-76 12076493-3 2002 The present study is a systematic review of all randomised controlled trials of bromocriptine/levodopa (BR/LD) combination therapy compared with levodopa (LD) monotherapy in PD. Levodopa 94-102 chromosome 12 open reading frame 73 Homo sapiens 104-106 11978145-2 2002 Drugs that have been used for symptomatic therapy are levodopa, usually combined with a peripheral decarboxylase inhibitor, synthetic dopamine receptor agonists, centrally-acting antimuscarinic drugs, amantadine, monoamine oxidase-B (MAO-B) inhibitors and catechol-O-methyltransferase (COMT) inhibitors. Levodopa 54-62 monoamine oxidase B Homo sapiens 234-239 11978145-2 2002 Drugs that have been used for symptomatic therapy are levodopa, usually combined with a peripheral decarboxylase inhibitor, synthetic dopamine receptor agonists, centrally-acting antimuscarinic drugs, amantadine, monoamine oxidase-B (MAO-B) inhibitors and catechol-O-methyltransferase (COMT) inhibitors. Levodopa 54-62 catechol-O-methyltransferase Homo sapiens 256-284 11978145-2 2002 Drugs that have been used for symptomatic therapy are levodopa, usually combined with a peripheral decarboxylase inhibitor, synthetic dopamine receptor agonists, centrally-acting antimuscarinic drugs, amantadine, monoamine oxidase-B (MAO-B) inhibitors and catechol-O-methyltransferase (COMT) inhibitors. Levodopa 54-62 catechol-O-methyltransferase Homo sapiens 286-290 11978145-16 2002 The COMT inhibitors entacapone and tolcapone dose-dependently inhibit the formation of the major metabolite of levodopa, 3-O-methyldopa, and improve the bioavailability and reduce the clearance of levodopa without significantly affecting its absorption. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 4-8 11978145-16 2002 The COMT inhibitors entacapone and tolcapone dose-dependently inhibit the formation of the major metabolite of levodopa, 3-O-methyldopa, and improve the bioavailability and reduce the clearance of levodopa without significantly affecting its absorption. Levodopa 197-205 catechol-O-methyltransferase Homo sapiens 4-8 12390050-4 2002 Restoring traditional mealtimes and scheduling activities during predicted periods of sleepiness may help alleviate daytime somnolence; the use of controlled-release levodopa preparations or administration of a catechol-O-methyl transferase (COMT) inhibitor with levodopa at bedtime may reduce periods of night-time wakefulness. Levodopa 263-271 catechol-O-methyltransferase Homo sapiens 211-240 12390050-4 2002 Restoring traditional mealtimes and scheduling activities during predicted periods of sleepiness may help alleviate daytime somnolence; the use of controlled-release levodopa preparations or administration of a catechol-O-methyl transferase (COMT) inhibitor with levodopa at bedtime may reduce periods of night-time wakefulness. Levodopa 263-271 catechol-O-methyltransferase Homo sapiens 242-246 11844900-2 2002 We used 123I-iodobenzamide single-photon emission computed tomography to measure the striatal dopamine D2 receptor densities in early levodopa-naive PD, chronic PD with stable levodopa response, and advanced PD with fluctuating levodopa response. Levodopa 134-142 dopamine receptor D2 Homo sapiens 94-114 11849292-7 2002 In contrast, when COMT-deficient mice are challenged with l-dihydroxyphenylalanine, they show an extensive accumulation of 3,4-dihydroxyphenylacetic acid and dihydroxyphenylglycol and even dopamine, revealing an important role for COMT under such situations. Levodopa 58-82 catechol-O-methyltransferase Mus musculus 18-22 11849292-7 2002 In contrast, when COMT-deficient mice are challenged with l-dihydroxyphenylalanine, they show an extensive accumulation of 3,4-dihydroxyphenylacetic acid and dihydroxyphenylglycol and even dopamine, revealing an important role for COMT under such situations. Levodopa 58-82 catechol-O-methyltransferase Mus musculus 231-235 11844900-4 2002 PD patients with fluctuating levodopa response showed a significant decrease in striatal dopamine D2 receptor densities compared to those with early (1.57+/- 0.20 vs. 1.77 +/- 0.12, p = 0.009) or chronic stable PD (1.57 +/- 0.20 vs. 1.77 +/- 0.10, p = 0.024). Levodopa 29-37 dopamine receptor D2 Homo sapiens 89-109 11827462-7 2002 Expression of human TAT1 in Xenopus laevis oocytes demonstrated the Na+-independent transport of tryptophan, tyrosine, phenylalanine, and L-dopa, indicating that human TAT1 is a transporter subserving system T. Because human TAT1 is proposed to be crucial to the efficient absorption of aromatic amino acids from intestine and kidney, its defect could be involved in the disruption of aromatic amino-acid transport, such as in blue diaper syndrome. Levodopa 138-144 solute carrier family 16 member 10 Homo sapiens 20-24 11827462-7 2002 Expression of human TAT1 in Xenopus laevis oocytes demonstrated the Na+-independent transport of tryptophan, tyrosine, phenylalanine, and L-dopa, indicating that human TAT1 is a transporter subserving system T. Because human TAT1 is proposed to be crucial to the efficient absorption of aromatic amino acids from intestine and kidney, its defect could be involved in the disruption of aromatic amino-acid transport, such as in blue diaper syndrome. Levodopa 138-144 solute carrier family 16 member 10 Homo sapiens 168-172 11827462-7 2002 Expression of human TAT1 in Xenopus laevis oocytes demonstrated the Na+-independent transport of tryptophan, tyrosine, phenylalanine, and L-dopa, indicating that human TAT1 is a transporter subserving system T. Because human TAT1 is proposed to be crucial to the efficient absorption of aromatic amino acids from intestine and kidney, its defect could be involved in the disruption of aromatic amino-acid transport, such as in blue diaper syndrome. Levodopa 138-144 solute carrier family 16 member 10 Homo sapiens 168-172 11718747-7 2001 The function of the SMA is closely associated with the nigro-striatal pathway and its impairment can explain the basic akinetic symptoms in PD, which are responsive to L-DOPA treatment. Levodopa 168-174 survival of motor neuron 1, telomeric Homo sapiens 20-23 11980384-13 2002 ), a MAO-B inhibitor potentiated the motor stimulant actions of subthreshold doses of the L-DOPA (100 mg/kg i.p.) Levodopa 90-96 monoamine oxidase B Mus musculus 5-10 11980384-19 2002 It is concluded that COMT and MAO-B enzymes play an important role in the metabolism of dopamine and administration of a COMT or MAO-B inhibitor may prove to be a better adjunct to L-DOPA therapy than a dopamine receptor agonist in Parkinson"s disease. Levodopa 181-187 catechol-O-methyltransferase Mus musculus 21-25 11980384-19 2002 It is concluded that COMT and MAO-B enzymes play an important role in the metabolism of dopamine and administration of a COMT or MAO-B inhibitor may prove to be a better adjunct to L-DOPA therapy than a dopamine receptor agonist in Parkinson"s disease. Levodopa 181-187 catechol-O-methyltransferase Mus musculus 121-125 11980384-19 2002 It is concluded that COMT and MAO-B enzymes play an important role in the metabolism of dopamine and administration of a COMT or MAO-B inhibitor may prove to be a better adjunct to L-DOPA therapy than a dopamine receptor agonist in Parkinson"s disease. Levodopa 181-187 monoamine oxidase B Mus musculus 129-134 12207958-7 2002 Acute oral administration of L-3,4-dihydroxyphenylalanine (L-DOPA) produced a smaller increase in locomotor activity and greater reversal of motor disability in animals treated with SHH than occurred in vehicle-treated common marmosets. Levodopa 29-57 sonic hedgehog protein Callithrix jacchus 182-185 12207958-7 2002 Acute oral administration of L-3,4-dihydroxyphenylalanine (L-DOPA) produced a smaller increase in locomotor activity and greater reversal of motor disability in animals treated with SHH than occurred in vehicle-treated common marmosets. Levodopa 59-65 sonic hedgehog protein Callithrix jacchus 182-185 11793163-2 2002 The aim of the present investigation was to analyse the consequences of subsequent alterations in levodopa metabolism under common treatment conditions when the levodopa dose is adjusted due to the occurrence of dyskinesias after initiation of the COMT-inhibitor. Levodopa 98-106 catechol-O-methyltransferase Homo sapiens 248-252 11793163-8 2002 CONCLUSION: The elevation of DOPAC and the decrease of HVA and HVA / DOPAC reflect a shift of the levodopa metabolism towards the MAO-B dependent oxidative pathway. Levodopa 98-106 monoamine oxidase B Homo sapiens 130-135 11835449-1 2002 Bilateral subthalamic nucleus stimulation (STN-DBS) is used to improve parkinsonian symptoms and attenuate levodopa-induced motor complications. Levodopa 107-115 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 43-46 11835462-1 2002 Two cases of postural asymmetries following unilateral stereotaxic subthalamotomy were observed with head and body tilting to the side contralateral to the STN lesion, which corrected itself completely or partially with levodopa treatment. Levodopa 220-228 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 156-159 11739600-4 2001 Antisense technology was used to produce a local knockdown of CREB in the lateral caudate-putamen, a region that mediates the dyskinetic or stereotypic manifestations associated with l-DOPA or cocaine treatment, respectively. Levodopa 183-189 cAMP responsive element binding protein 1 Rattus norvegicus 62-66 29712241-2 2001 Inhibition of COMT is of significant interest in the therapy of Parkinsonapos;s disease since it ensures that a larger percentage of orally administered L-dopa reaches-in the form of dopamine-its target in the brain. Levodopa 153-159 catechol-O-methyltransferase Homo sapiens 14-18 11739600-8 2001 In behavioral studies, intrastriatal CREB knockdown caused enhanced activity scores in intact control animals and exacerbated the dyskinetic effects of acute l-DOPA treatment in 6-OHDA-lesioned animals. Levodopa 158-164 cAMP responsive element binding protein 1 Rattus norvegicus 37-41 11739600-10 2001 Moreover, our results reveal an unexpected alteration of nuclear signaling mechanisms in the parkinsonian striatum treated with l-DOPA, where AP-1 transcription factors appear to supersede CREB in the activation of CRE-containing genes. Levodopa 128-134 cAMP responsive element binding protein 1 Rattus norvegicus 189-193 11860478-9 2001 The results indicate that a nigro-striatal lesion is associated with an increase in CB1 receptors in the basal ganglia in humans and nonhuman primates and that this increase could be reversed by chronic l-DOPA therapy. Levodopa 203-209 cannabinoid receptor 1 Homo sapiens 84-87 12235825-3 2001 Three enzymes are necessary for efficient dopamine synthesis: tyrosine hydroxylase (TH) converts tyrosine to L-DOPA, aromatic L-amino acid decarboxylase (AADC) then converts L-DOPA to dopamine, and guanosine triphosphate cyclohydrolase I (GCH) is the rate-limiting enzyme for the synthesis of TH co-factor tetrahydrobiopterine. Levodopa 109-115 dopa decarboxylase Homo sapiens 154-158 12235825-3 2001 Three enzymes are necessary for efficient dopamine synthesis: tyrosine hydroxylase (TH) converts tyrosine to L-DOPA, aromatic L-amino acid decarboxylase (AADC) then converts L-DOPA to dopamine, and guanosine triphosphate cyclohydrolase I (GCH) is the rate-limiting enzyme for the synthesis of TH co-factor tetrahydrobiopterine. Levodopa 174-180 dopa decarboxylase Homo sapiens 154-158 11723272-2 2001 OBJECTIVE: To evaluate the possibility that serotoninergic 5-HT1A autoreceptors (by regulating the release of serotonin as well as dopamine formed from exogenous levodopa) affect the response alterations complicating levodopa treatment of PD. Levodopa 162-170 5-hydroxytryptamine receptor 1A Rattus norvegicus 59-65 11723272-2 2001 OBJECTIVE: To evaluate the possibility that serotoninergic 5-HT1A autoreceptors (by regulating the release of serotonin as well as dopamine formed from exogenous levodopa) affect the response alterations complicating levodopa treatment of PD. Levodopa 217-225 5-hydroxytryptamine receptor 1A Rattus norvegicus 59-65 11732751-1 2001 Entacapone is a new inhibitor of catechol-O-methyltransferase (COMT) that is used as an adjunct to L-dopa therapy in the treatment of Parkinson"s disease. Levodopa 99-105 catechol-O-methyltransferase Rattus norvegicus 33-61 11723182-0 2001 Nigrostriatal denervation does not affect glutamate transporter mRNA expression but subsequent levodopa treatment selectively increases GLT1 mRNA and protein expression in the rat striatum. Levodopa 95-103 solute carrier family 1 member 2 Rattus norvegicus 136-140 11723182-3 2001 Given the key role played by uptake processes in glutamate neurotransmission, this study examined the effects of nigrostriatal deafferentation and of levodopa treatment on the striatal expression of the glutamate transporters GLT1, GLAST and EAAC1 in the rat. Levodopa 150-158 solute carrier family 1 member 2 Rattus norvegicus 226-230 11723182-5 2001 In contrast, animals with the lesion subsequently treated with levodopa showed a selective increase (36%) in GLT1 mRNA levels in the denervated striatum versus controls. Levodopa 63-71 solute carrier family 1 member 2 Rattus norvegicus 109-113 11723182-7 2001 These data provide the first evidence that levodopa therapy may interfere with striatal glutamate transmission through change in expression of the primarily glial glutamate transporter GLT1. Levodopa 43-51 solute carrier family 1 member 3 Rattus norvegicus 163-184 11723182-7 2001 These data provide the first evidence that levodopa therapy may interfere with striatal glutamate transmission through change in expression of the primarily glial glutamate transporter GLT1. Levodopa 43-51 solute carrier family 1 member 2 Rattus norvegicus 185-189 11723182-8 2001 We further suggest that levodopa-induced GLT1 overexpression may represent a compensatory mechanism preventing neurotoxic accumulation of endogenous glutamate. Levodopa 24-32 solute carrier family 1 member 2 Rattus norvegicus 41-45 11732751-1 2001 Entacapone is a new inhibitor of catechol-O-methyltransferase (COMT) that is used as an adjunct to L-dopa therapy in the treatment of Parkinson"s disease. Levodopa 99-105 catechol-O-methyltransferase Rattus norvegicus 63-67 11735324-3 2001 In the rat brain model L-DOPA and 3,4-dihydroxybenzoic acid were O-methylated mainly via S-COMT, while dopamine and noradrenaline, at low concentrations, were O-methylated slightly more by MB-COMT. Levodopa 23-29 catechol-O-methyltransferase Homo sapiens 91-95 11685243-1 2001 DOPA decarboxylase (DDC) is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 133-161 dopa decarboxylase Homo sapiens 0-18 11685243-1 2001 DOPA decarboxylase (DDC) is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 133-161 dopa decarboxylase Homo sapiens 20-23 11685243-1 2001 DOPA decarboxylase (DDC) is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 163-169 dopa decarboxylase Homo sapiens 0-18 11685243-1 2001 DOPA decarboxylase (DDC) is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3,4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 163-169 dopa decarboxylase Homo sapiens 20-23 11683909-3 2001 This study investigates the effects of time postdenervation and L-dopa treatment duration on the striatal expression of opioid precursor mRNAs and FosB/DeltaFosB-related proteins. Levodopa 64-70 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 147-151 11683909-7 2001 L-DOPA, but not bromocriptine, induced high striatal levels of FosB/DeltaFosB immunoreactivity and prodynorphin mRNA, and these did not differ between short-term and long-term L-DOPA-treated rats. Levodopa 0-6 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-67 11683909-7 2001 L-DOPA, but not bromocriptine, induced high striatal levels of FosB/DeltaFosB immunoreactivity and prodynorphin mRNA, and these did not differ between short-term and long-term L-DOPA-treated rats. Levodopa 0-6 prodynorphin Rattus norvegicus 99-111 11683909-8 2001 The present data provide the first demonstration that L-DOPA maintains high striatal levels of fosB and prodynorphin gene expression during a prolonged course of treatment, which simulates the clinical practice in Parkinson"s disease more closely than the short-treatment paradigms studied thus far. Levodopa 54-60 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 95-99 11683909-8 2001 The present data provide the first demonstration that L-DOPA maintains high striatal levels of fosB and prodynorphin gene expression during a prolonged course of treatment, which simulates the clinical practice in Parkinson"s disease more closely than the short-treatment paradigms studied thus far. Levodopa 54-60 prodynorphin Rattus norvegicus 104-116 11483656-2 2001 L-DOPA (200 microM) induced differentiation of NB69 cells of more than 4 weeks in vitro, as shown by phase-contrast microscopy and TH immunocytochemistry, and decreased replication, as shown by 5-bromodeoxyuridine immunostaining. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 131-133 11592835-1 2001 In animal models of Parkinson"s disease, gene transfer of aromatic L-amino acid decarboxylase (AADC) leads to an increase in the capacity of the striatum to decarboxylate exogenous L-DOPA. Levodopa 181-187 dopa decarboxylase Homo sapiens 58-93 11592835-1 2001 In animal models of Parkinson"s disease, gene transfer of aromatic L-amino acid decarboxylase (AADC) leads to an increase in the capacity of the striatum to decarboxylate exogenous L-DOPA. Levodopa 181-187 dopa decarboxylase Homo sapiens 95-99 11592835-3 2001 Here, we show that following adeno-associated virus (AAV)-AADC transduction, the transgenic AADC is able to decarboxylate exogenous L-DOPA more efficiently so that a dose of L-DOPA ineffective before gene transfer elicits a motor asymmetry (rotational behavior) following gene transfer. Levodopa 132-138 dopa decarboxylase Homo sapiens 58-62 11592835-3 2001 Here, we show that following adeno-associated virus (AAV)-AADC transduction, the transgenic AADC is able to decarboxylate exogenous L-DOPA more efficiently so that a dose of L-DOPA ineffective before gene transfer elicits a motor asymmetry (rotational behavior) following gene transfer. Levodopa 132-138 dopa decarboxylase Homo sapiens 92-96 11592835-3 2001 Here, we show that following adeno-associated virus (AAV)-AADC transduction, the transgenic AADC is able to decarboxylate exogenous L-DOPA more efficiently so that a dose of L-DOPA ineffective before gene transfer elicits a motor asymmetry (rotational behavior) following gene transfer. Levodopa 174-180 dopa decarboxylase Homo sapiens 58-62 11592835-3 2001 Here, we show that following adeno-associated virus (AAV)-AADC transduction, the transgenic AADC is able to decarboxylate exogenous L-DOPA more efficiently so that a dose of L-DOPA ineffective before gene transfer elicits a motor asymmetry (rotational behavior) following gene transfer. Levodopa 174-180 dopa decarboxylase Homo sapiens 92-96 11693181-1 2001 Catechol-O-methyltransferase (COMT) inactivates neurotransmitters, catechol hormones and drugs such as levodopa and methyldopa. Levodopa 103-111 catechol-O-methyltransferase Homo sapiens 0-28 11693181-1 2001 Catechol-O-methyltransferase (COMT) inactivates neurotransmitters, catechol hormones and drugs such as levodopa and methyldopa. Levodopa 103-111 catechol-O-methyltransferase Homo sapiens 30-34 11520127-0 2001 L-dopa upregulates the expression and activities of methionine adenosyl transferase and catechol-O-methyltransferase. Levodopa 0-6 methionine adenosyltransferase 1A Homo sapiens 52-83 11520127-0 2001 L-dopa upregulates the expression and activities of methionine adenosyl transferase and catechol-O-methyltransferase. Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 88-116 11520127-4 2001 In this study we investigated whether L-dopa increases the transmethylation process by inducing methionine adenosyl transferase (MAT), the enzyme that produces SAM, and catechol-O-methyl transferase (COMT), the enzyme that transfers the methyl group from SAM to L-dopa and DA. Levodopa 38-44 methionine adenosyltransferase 1A Homo sapiens 96-127 11520127-4 2001 In this study we investigated whether L-dopa increases the transmethylation process by inducing methionine adenosyl transferase (MAT), the enzyme that produces SAM, and catechol-O-methyl transferase (COMT), the enzyme that transfers the methyl group from SAM to L-dopa and DA. Levodopa 38-44 methionine adenosyltransferase 1A Homo sapiens 129-132 11520127-4 2001 In this study we investigated whether L-dopa increases the transmethylation process by inducing methionine adenosyl transferase (MAT), the enzyme that produces SAM, and catechol-O-methyl transferase (COMT), the enzyme that transfers the methyl group from SAM to L-dopa and DA. Levodopa 38-44 catechol-O-methyltransferase Homo sapiens 169-198 11520127-4 2001 In this study we investigated whether L-dopa increases the transmethylation process by inducing methionine adenosyl transferase (MAT), the enzyme that produces SAM, and catechol-O-methyl transferase (COMT), the enzyme that transfers the methyl group from SAM to L-dopa and DA. Levodopa 38-44 catechol-O-methyltransferase Homo sapiens 200-204 11520127-16 2001 The highlight of the study is the fact that L-dopa induces the enzymes MAT and COMT. Levodopa 44-50 methionine adenosyltransferase 1A Homo sapiens 71-74 11520127-16 2001 The highlight of the study is the fact that L-dopa induces the enzymes MAT and COMT. Levodopa 44-50 catechol-O-methyltransferase Homo sapiens 79-83 11520127-18 2001 Thus, during PD treatment with L-dopa the induction of MAT and COMT is likely to occur and in turn increase the methylation and reduction of L-dopa and DA that may help cause the tolerance or the wearing-off effect developed to L-dopa. Levodopa 31-37 methionine adenosyltransferase 1A Homo sapiens 55-58 11520127-18 2001 Thus, during PD treatment with L-dopa the induction of MAT and COMT is likely to occur and in turn increase the methylation and reduction of L-dopa and DA that may help cause the tolerance or the wearing-off effect developed to L-dopa. Levodopa 31-37 catechol-O-methyltransferase Homo sapiens 63-67 11520127-18 2001 Thus, during PD treatment with L-dopa the induction of MAT and COMT is likely to occur and in turn increase the methylation and reduction of L-dopa and DA that may help cause the tolerance or the wearing-off effect developed to L-dopa. Levodopa 141-147 methionine adenosyltransferase 1A Homo sapiens 55-58 11520127-18 2001 Thus, during PD treatment with L-dopa the induction of MAT and COMT is likely to occur and in turn increase the methylation and reduction of L-dopa and DA that may help cause the tolerance or the wearing-off effect developed to L-dopa. Levodopa 141-147 methionine adenosyltransferase 1A Homo sapiens 55-58 11483656-0 2001 L-DOPA and glia-conditioned medium have additive effects on tyrosine hydroxylase expression in human catecholamine-rich neuroblastoma NB69 cells. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 60-80 11762703-9 2001 The DA1 antagonist decreased diuresis, natriuresis and urinary L-DOPA in control, but had no effect in Thio treated rats. Levodopa 63-69 RT1 class II, locus Da Rattus norvegicus 4-7 11483656-4 2001 Furthermore, L-DOPA (200 microM) increased Bcl-xL protein expression. Levodopa 13-19 BCL2 like 1 Homo sapiens 43-49 11532645-4 2001 Levodopa is converted to dopamine within the brain by dopa decarboxylase, replenishing central dopamine stores and potentially reversing the motor symptoms of PD. Levodopa 0-8 dopa decarboxylase Homo sapiens 54-72 11445284-1 2001 Levodopa is administered with dopa decarboxylase inhibitors (DDI) to prevent its peripheral degradation. Levodopa 0-8 dopa decarboxylase Homo sapiens 30-48 11445284-2 2001 This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT). Levodopa 29-37 catechol-O-methyltransferase Homo sapiens 67-95 11445284-2 2001 This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT). Levodopa 29-37 catechol-O-methyltransferase Homo sapiens 97-101 11445284-3 2001 S-adenosylmethionine (SAM), which is synthesized from adenosine triphosphate and methionine (MET), serves as methyl donor for this O-metabolisation of levodopa with resulting conversion of SAM to total homocysteine (tHcy) via S-adenosylhomocysteine (SAH). Levodopa 151-159 SAFB like transcription modulator Homo sapiens 93-96 11587490-4 2001 In the model Ro 04-5127 inhibited competitively the L-dopa clearance by AADC. Levodopa 52-58 dopa decarboxylase Rattus norvegicus 72-76 11498717-3 2001 Repeated high dose L-dopa administration was shown to induce marked dyskinesias in monkeys with an intact nigrostriatal system, and the threshold for dyskinesia expression was increased by peripheral catechol-O-methyltransferase inhibition with entacapone. Levodopa 19-25 catechol-O-methyltransferase Homo sapiens 200-228 11452145-9 2001 L-Dopa increased plasma insulin-like growth factor 1 (IGF(1)) concentrations, rates of bone growth, and bone strength measures in controls while having no effect in lead-exposed pups. Levodopa 0-6 insulin-like growth factor 1 Rattus norvegicus 24-52 11452145-9 2001 L-Dopa increased plasma insulin-like growth factor 1 (IGF(1)) concentrations, rates of bone growth, and bone strength measures in controls while having no effect in lead-exposed pups. Levodopa 0-6 insulin-like growth factor 1 Rattus norvegicus 54-60 11445276-0 2001 Dopamine D5 receptor gene polymorphism and the risk of levodopa-induced motor fluctuations in patients with Parkinson"s disease. Levodopa 55-63 dopamine receptor D5 Homo sapiens 0-20 11483656-5 2001 Incubation of cells with L-DOPA (50, 100, 200 microM) for 24 h resulted in an increase in TH protein levels (174, 196 and 212% versus control). Levodopa 25-31 tyrosine hydroxylase Homo sapiens 90-92 11483656-7 2001 L-DOPA (0, 50, 100 and 200 microM) plus GCM further increased the amount of TH protein (346, 446, 472 and 424%). Levodopa 0-6 tyrosine hydroxylase Homo sapiens 76-78 11483656-8 2001 L-DOPA (200 microM) increased TH protein levels to 132, 191 and 245% of controls after incubation for 24, 48 and 72 h. DA metabolism in NB69 cells was increased in cultures treated with either L-DOPA (200-300 microM) or GCM and these two agents had a synergistic effect on DA metabolism. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 30-32 11483656-8 2001 L-DOPA (200 microM) increased TH protein levels to 132, 191 and 245% of controls after incubation for 24, 48 and 72 h. DA metabolism in NB69 cells was increased in cultures treated with either L-DOPA (200-300 microM) or GCM and these two agents had a synergistic effect on DA metabolism. Levodopa 193-199 tyrosine hydroxylase Homo sapiens 30-32 11483656-10 2001 The L-DOPA-induced increase of TH protein expression in NB69 cells was independent of DA production, free radicals and GSH up-regulation. Levodopa 4-10 tyrosine hydroxylase Homo sapiens 31-33 11412836-0 2001 BIA 3-202, a novel catechol-O-methyltransferase inhibitor, enhances the availability of L-DOPA to the brain and reduces its O-methylation. Levodopa 88-94 catechol-O-methyltransferase Rattus norvegicus 19-47 11425590-1 2001 Several benzaldoximes, benzaldehyde-O-ethyloximes, and acetophenonoximes were synthesized and evaluated as tyrosinase inhibitors by an assay based on tyrosinase catalyzed L-DOPA oxidation. Levodopa 171-177 tyrosinase Homo sapiens 107-117 11425590-1 2001 Several benzaldoximes, benzaldehyde-O-ethyloximes, and acetophenonoximes were synthesized and evaluated as tyrosinase inhibitors by an assay based on tyrosinase catalyzed L-DOPA oxidation. Levodopa 171-177 tyrosinase Homo sapiens 150-160 11447722-5 2001 Beside levodopa a variety of alternative treatment options exists which enable a good and longer lasting control of symptoms (e.g. dopamine agonists, COMT-inhibitors etc.). Levodopa 7-15 catechol-O-methyltransferase Homo sapiens 150-154 11440283-3 2001 Inhibition of COMT activity prolongs the action of levodopa and reduces fluctuations in response. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 14-18 11442353-7 2001 l-Dopa and apomorphine (dopaminergic agonists), ropinirole (selective D2 agonist), and selegiline (an monoamino-oxidase B [MAO-B] inhibitor) improve their clinical status. Levodopa 0-6 monoamine oxidase B Homo sapiens 102-121 11481696-2 2001 Preclinical data in the 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP) monkey suggest that alpha-2 antagonists may reduce dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. Levodopa 152-158 glycoprotein hormone subunit alpha 2 Homo sapiens 97-104 11481696-5 2001 These results suggest that blocking alpha-2 receptors in patients with Parkinson"s disease might improve L-DOPA-induced dyskinesia without the cost of a return of parkinsonian symptomatology. Levodopa 105-111 glycoprotein hormone subunit alpha 2 Homo sapiens 36-43 11402115-0 2001 Influence of L-dopa and pramipexole on striatal dopamine transporter in early PD. Levodopa 13-19 solute carrier family 6 member 3 Homo sapiens 48-68 11402115-3 2001 METHODS: A randomized, assessor-blinded, placebo-controlled clinical trial was performed in subjects with early PD to determine whether L-dopa or pramipexole might regulate striatal DAT binding as measured by PET with [(11)C]RTI-32. Levodopa 136-142 solute carrier family 6 member 3 Homo sapiens 182-185 11402115-5 2001 RESULTS: Mean interval change in DAT binding was significantly reduced by 16% to 22% in all striatal regions (caudate, anterior and posterior putamen) of the L-dopa-treated patients, whereas significant changes in the pramipexole-treated patients were limited to the contralateral caudate (-15%), ipsilateral anterior putamen (-14%), and posterior putamen (-20%). Levodopa 158-164 solute carrier family 6 member 3 Homo sapiens 33-36 11402115-8 2001 CONCLUSIONS: Short-term therapy with L-dopa and, to a lesser extent, pramipexole can modestly down-regulate striatal DAT in patients with early PD. Levodopa 37-43 solute carrier family 6 member 3 Homo sapiens 117-120 11278508-2 2001 When expressed in Xenopus oocytes, the encoded protein designated as TAT1 (T-type amino acid transporter 1) exhibited Na+-independent and low-affinity transport of aromatic amino acids such as tryptophan, tyrosine, and phenylalanine (Km values: approximately 5 mm), consistent with the properties of classical amino acid transport system T. TAT1 accepted some variations of aromatic side chains because it interacted with amino acid-related compounds such as l-DOPA and 3-O-methyl-DOPA. Levodopa 459-465 solute carrier family 16 member 10 Rattus norvegicus 69-73 11346370-1 2001 OBJECTIVE: To investigate the range of clinical features to correlate genotypic and phenotypic manifestations in hereditary progressive and/or levodopa-responsive dystonia due to a defect in the guanosine triphosphate-cyclohydrolase (GCH1) gene. Levodopa 143-151 GTP cyclohydrolase 1 Homo sapiens 234-238 11295535-2 2001 L-DOPA (L-dihydroxyphenylalanine), which is metabolized to dopamine by dopa decarboxylase, is the primary therapy for PD, but may also contribute to disease progression. Levodopa 0-6 dopa decarboxylase Rattus norvegicus 71-89 11312565-2 2001 We studied the effects of coadministration of (-)-OSU6162 with l-DOPA on the regulation of striatal preproenkephalin (PPE) and prodynorphin (PDyn) mRNA expression in the primate brain by in situ hybridization histochemistry. Levodopa 63-69 proenkephalin-B Callithrix jacchus 141-145 11312565-9 2001 l-DOPA treatment resulted in an enhancement in PDyn mRNA expression in all functional compartments of the striatum. Levodopa 0-6 proenkephalin-B Callithrix jacchus 47-51 11331406-5 2001 Our results indicate that overexpression of the vesicular monoamine transporter and monoamine oxidase A-induced protection against intracellular dopamine toxicity, and conversely that pharmacological inhibition of these pathways potentiated L-DOPA toxicity in catecholaminergic PC12 cells. Levodopa 241-247 monoamine oxidase A Rattus norvegicus 84-103 11391126-12 2001 The study showed that repeated dosing of entacapone inhibits the COMT activity in a dose-dependent manner and thereby reduces the loss of L-Dopa to 3-OMD. Levodopa 138-144 catechol-O-methyltransferase Homo sapiens 65-69 11295535-2 2001 L-DOPA (L-dihydroxyphenylalanine), which is metabolized to dopamine by dopa decarboxylase, is the primary therapy for PD, but may also contribute to disease progression. Levodopa 8-32 dopa decarboxylase Rattus norvegicus 71-89 11170218-1 2001 The aim was to investigate whether the improved 6-[(18)F]fluoro-L-dopa (FDOPA) availability induced by catechol-O-methyltransferase (COMT) inhibition can be more clearly seen during late than during standard (early) imaging in FDOPA uptake in Parkinson"s disease (PD) patients with severe dopaminergic hypofunction. Levodopa 63-70 catechol-O-methyltransferase Homo sapiens 103-131 11990572-2 2001 The method involves the oxidation of o-dihydroxybenzene derivatives by K2CrO4 followed by oxidative coupling with sulfanilic acid (SPA), leading to the formation of a red or violet colored product having maximum absorbance at 490-495 nm for LD, MD and DP or at 560 nm for PC. Levodopa 241-243 surfactant protein A2 Homo sapiens 131-134 11248589-1 2001 Tolcapone is a catechol-ortho-methyl-tranferase (COMT) inhibitor that increases the L-DOPA half-life and the duration of effect in Parkinson"s disease. Levodopa 84-90 catechol-O-methyltransferase Homo sapiens 15-47 11248589-1 2001 Tolcapone is a catechol-ortho-methyl-tranferase (COMT) inhibitor that increases the L-DOPA half-life and the duration of effect in Parkinson"s disease. Levodopa 84-90 catechol-O-methyltransferase Homo sapiens 49-53 11254447-3 2001 Autosomal recessive juvenile parkinsonism (ARJP) is a clinically and genetically distinct entity; typical PD features are associated with early onset, sustained response to levodopa, and early occurrence of levodopa-induced dyskinesias, which are often severe. Levodopa 173-181 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-47 11254447-3 2001 Autosomal recessive juvenile parkinsonism (ARJP) is a clinically and genetically distinct entity; typical PD features are associated with early onset, sustained response to levodopa, and early occurrence of levodopa-induced dyskinesias, which are often severe. Levodopa 207-215 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-47 11170218-1 2001 The aim was to investigate whether the improved 6-[(18)F]fluoro-L-dopa (FDOPA) availability induced by catechol-O-methyltransferase (COMT) inhibition can be more clearly seen during late than during standard (early) imaging in FDOPA uptake in Parkinson"s disease (PD) patients with severe dopaminergic hypofunction. Levodopa 63-70 catechol-O-methyltransferase Homo sapiens 133-137 11223018-8 2001 We conclude that supplementation with methionine, dimethionine or SAM ameliorates L-dopa neurotoxicity to dopamine neurons, while inhibition of COMT may aggravate or unmask L-dopa neurotoxicity. Levodopa 173-179 catechol-O-methyltransferase Homo sapiens 144-148 11223018-0 2001 COMT-dependent protection of dopaminergic neurons by methionine, dimethionine and S-adenosylmethionine (SAM) against L-dopa toxicity in vitro. Levodopa 117-123 catechol-O-methyltransferase Homo sapiens 0-4 11223018-3 2001 We hypothesized that SAM or SAM-precursors ameliorate L-dopa neurotoxicity, in a COMT-dependent fashion. Levodopa 54-60 catechol-O-methyltransferase Homo sapiens 81-85 11258976-3 2001 L-DOPA, a precursor of eumelanin, was oxidized and oligomerized with tyrosinase. Levodopa 0-6 tyrosinase Homo sapiens 69-79 11223018-7 2001 The COMT inhibitor dinitrocatechol (DNC) completely abolished the protective effect against L-dopa toxicity. Levodopa 92-98 catechol-O-methyltransferase Homo sapiens 4-8 11239919-0 2001 Inhibition by L-3,4-dihydroxyphenylalanine of hippocampal CA1 neurons with facilitation of noradrenaline and gamma-aminobutyric acid release. Levodopa 14-42 carbonic anhydrase 1 Rattus norvegicus 58-61 11239919-1 2001 Electrophysiological studies were performed to elucidate whether L-3,4-dihydroxyphenylalanine (L-DOPA) acted on hippocampal CA1 neurons, since this drug has been reported to act as a neurotransmitter in the hypothalamus and striatum. Levodopa 65-93 carbonic anhydrase 1 Rattus norvegicus 124-127 11239919-1 2001 Electrophysiological studies were performed to elucidate whether L-3,4-dihydroxyphenylalanine (L-DOPA) acted on hippocampal CA1 neurons, since this drug has been reported to act as a neurotransmitter in the hypothalamus and striatum. Levodopa 95-101 carbonic anhydrase 1 Rattus norvegicus 124-127 11239919-11 2001 These results suggested that L-DOPA itself acted on L-DOPA recognition sites to release noradrenaline, and that the latter facilitates gamma-aminobutyric acid (GABA) release via alpha-adrenoceptors located on the GABA-containing cells and/or their nerve terminals, thereby inhibiting the population spikes in the hippocampal CA1 field. Levodopa 29-35 carbonic anhydrase 1 Rattus norvegicus 325-328 11436352-3 2001 Transduction of the gene for GTP cyclohydrolase I, the first and rate-limiting step in BH1 synthesis, along with the TH gene, generated cells that are capable of producing L-DOPA spontaneously both in vitro and in vivo. Levodopa 172-178 GTP cyclohydrolase 1 Rattus norvegicus 29-49 11436352-3 2001 Transduction of the gene for GTP cyclohydrolase I, the first and rate-limiting step in BH1 synthesis, along with the TH gene, generated cells that are capable of producing L-DOPA spontaneously both in vitro and in vivo. Levodopa 172-178 tyrosine hydroxylase Rattus norvegicus 117-119 11436352-6 2001 Gene transfer of the vesicular monoamine transporter was combined with AADC and produced genetically modified cells that can convert L-DOPA to dopamine and store it for gradual release. Levodopa 133-139 dopa decarboxylase Rattus norvegicus 71-75 11436352-4 2001 When the aromatic L-amino acid decarboxylase (AADC) gene was added as a third gene, in an attempt to increase the conversion of L-DOPA to dopamine, feedback inhibition by the end product, dopamine, on TH activity resulted. Levodopa 128-134 dopa decarboxylase Rattus norvegicus 9-44 11436352-4 2001 When the aromatic L-amino acid decarboxylase (AADC) gene was added as a third gene, in an attempt to increase the conversion of L-DOPA to dopamine, feedback inhibition by the end product, dopamine, on TH activity resulted. Levodopa 128-134 dopa decarboxylase Rattus norvegicus 46-50 11436352-4 2001 When the aromatic L-amino acid decarboxylase (AADC) gene was added as a third gene, in an attempt to increase the conversion of L-DOPA to dopamine, feedback inhibition by the end product, dopamine, on TH activity resulted. Levodopa 128-134 tyrosine hydroxylase Rattus norvegicus 201-203 11168568-14 2001 GDNF also diminished L-DOPA-induced dyskinesia, which may relate to its ability to partly restore nigral dopaminergic transmission or to modify the activity of striatal output pathways. Levodopa 21-27 glial cell line-derived neurotrophic factor Callithrix jacchus 0-4 11171088-2 2001 Tyrosinase catalyses the rate-limiting generation of L-dopaquinone from L-tyrosine and is also able to oxidize L-dopa to L-dopaquinone. Levodopa 53-59 tyrosinase Homo sapiens 0-10 11166288-0 2001 Effects of acute and repeated treatment with a novel dopamine D2 receptor ligand on L-DOPA-induced dyskinesias in MPTP monkeys. Levodopa 84-90 dopamine receptor D2 Homo sapiens 53-73 11312883-6 2001 Tyrosinase was purified in a homogeneous form by SDS-PAGE and was characterized: its specific activity toward 3-(3,4-dihydroxyphenyl)-L-alanine (DOPA) increased by a factor of 24 with an overall recovery of 3% of initial activity. Levodopa 110-143 tyrosinase Homo sapiens 0-10 11312883-6 2001 Tyrosinase was purified in a homogeneous form by SDS-PAGE and was characterized: its specific activity toward 3-(3,4-dihydroxyphenyl)-L-alanine (DOPA) increased by a factor of 24 with an overall recovery of 3% of initial activity. Levodopa 145-149 tyrosinase Homo sapiens 0-10 11238719-0 2001 Activation of 5-HT(1A) but not 5-HT(1B) receptors attenuates an increase in extracellular dopamine derived from exogenously administered L-DOPA in the striatum with nigrostriatal denervation. Levodopa 137-143 5-hydroxytryptamine receptor 1A Rattus norvegicus 14-21 11238719-6 2001 These 8-OH-DPAT-induced changes in L-DOPA-derived extracellular DA were antagonized by further pretreatment with WAY-100635, a selective 5-HT(1A) antagonist. Levodopa 35-41 5-hydroxytryptamine receptor 1A Rattus norvegicus 137-144 11238719-8 2001 Thus, stimulation of 5-HT(1A) but not 5-HT(1B) receptors attenuated an increase in extracellular DA derived from exogenous L-DOPA. Levodopa 123-129 5-hydroxytryptamine receptor 1A Rattus norvegicus 21-28 11295799-0 2001 New nonsense mutation in the GTP-cyclohydrolase I gene in L-DOPA responsive dystonia-parkinsonism. Levodopa 58-64 GTP cyclohydrolase 1 Homo sapiens 29-49 11163295-7 2001 Thus, pharmacokinetic or pharmacodynamic factors other than the investigated genetic variant of the COMT enzyme seem to determine the response to levodopa in PD. Levodopa 146-154 catechol-O-methyltransferase Homo sapiens 100-104 11148450-2 2001 Aromatic L-amino acid decarboxylase (AADC) gene, the product of which catalyzes the synthesis of serotonin and dopamine from L-5-hydroxytryptophan and L-3,4-dihydroxyphenylalanine, respectively, was characterized. Levodopa 151-179 dopa decarboxylase Homo sapiens 37-41 11168568-0 2001 GDNF reverses priming for dyskinesia in MPTP-treated, L-DOPA-primed common marmosets. Levodopa 54-60 glial cell line-derived neurotrophic factor Callithrix jacchus 0-4 11168568-4 2001 In this study, we investigate the effects of GDNF on the expression of dyskinesia in L-DOPA-primed MPTP-treated common marmosets, exhibiting dyskinesia. Levodopa 85-91 glial cell line-derived neurotrophic factor Callithrix jacchus 45-49 11271164-0 2001 Plasma homocysteine and MTHFR C677T genotype in levodopa-treated patients with PD. Levodopa 48-56 methylenetetrahydrofolate reductase Homo sapiens 24-29 11168568-8 2001 Following the administration of L-DOPA there was a greater reversal of disability and a reduction in the intensity of L-DOPA-induced dyskinesia in GDNF-treated animals compared to saline-treated controls. Levodopa 32-38 glial cell line-derived neurotrophic factor Callithrix jacchus 147-151 11168568-8 2001 Following the administration of L-DOPA there was a greater reversal of disability and a reduction in the intensity of L-DOPA-induced dyskinesia in GDNF-treated animals compared to saline-treated controls. Levodopa 118-124 glial cell line-derived neurotrophic factor Callithrix jacchus 147-151 11160877-8 2001 Among the catechol drugs used in the L-DOPA treatment of Parkinson"s disease, the COMT inhibitors entacapone and tolcapone were not methylated, whereas the DOPA decarboxylase inhibitor benserazide was 15 times more specific substrate than L-DOPA, the target of COMT inhibition. Levodopa 37-43 catechol-O-methyltransferase Homo sapiens 82-86 11233302-7 2001 At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease. Levodopa 91-99 monoamine oxidase B Homo sapiens 153-158 11487201-5 2001 Priming with L-dopa and SKF38393 significantly increased GAD67 mRNA in the lesioned striatum and reversed dynorphin mRNA reduction, as compared to drug-naive rats, whereas quinpirole failed to produce any effect. Levodopa 13-19 glutamate decarboxylase 1 Rattus norvegicus 57-62 11487207-1 2001 The adenosine A2A receptor antagonist SCH 58261 increases the turning behaviour induced by L-dopa in unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rats. Levodopa 91-97 adenosine A2a receptor Rattus norvegicus 4-26 11160979-0 2001 Plasma homocysteine and MTHFR C677T genotype in levodopa-treated patients with PD. Levodopa 48-56 methylenetetrahydrofolate reductase Homo sapiens 24-29 11764945-0 2001 NAD(P)H:quinone oxidoreductase (NQO1) protects astroglial cells against L-dopa toxicity. Levodopa 72-78 NAD(P)H quinone dehydrogenase 1 Homo sapiens 32-36 11290882-1 2001 We have compared the effects of entacapone, a peripherally acting catechol-O-methyltransferase (COMT) inhibitor, and placebo on cardiovascular autonomic responses in L-Dopa/dopa decarboxylase inhibitor-treated patients with Parkinson"s disease (PD). Levodopa 166-172 catechol-O-methyltransferase Homo sapiens 96-100 11432539-1 2001 OBJECTIVE: To investigate the effect of administration of the catechol-Omethyltransferase (COMT) inhibitor tolcapone on the concentration-effect relationship of levodopa in patients with advanced Parkinson"s disease and on-off fluctuations. Levodopa 161-169 catechol-O-methyltransferase Homo sapiens 62-89 11156574-6 2001 Nevertheless, L-DOPA and two other substrates, namely, catechol and tyramine did produce nitric oxide from Angeli"s salt in the presence of tyrosinase, suggesting involvement of the respective unstable quinones. Levodopa 14-20 tyrosinase Rattus norvegicus 140-150 11352497-0 2001 Inhibition of calcium-independent luminal uptake of L-dopa by calmodulin antagonists in immortalized rat capillary cerebral endothelial cells. Levodopa 52-58 calmodulin 1 Rattus norvegicus 62-72 11352497-4 2001 The Ca(2+)/calmodulin inhibitors calmidazolium and trifluoperazine inhibited L-DOPA (2.5 microM) uptake with IC(50)s of 23 and 33 microM, respectively. Levodopa 77-83 calmodulin 1 Rattus norvegicus 11-21 11352497-7 2001 It is concluded that L-DOPA uptake in RBE-4 cells is promoted through the L-type amino acid transporter and appears to be under the control of calmodulin mediated pathways. Levodopa 21-27 calmodulin 1 Rattus norvegicus 143-153 11290879-0 2001 Catechol-O-methyltransferase decreases levodopa toxicity in vitro. Levodopa 39-47 catechol-O-methyltransferase Homo sapiens 0-28 11290879-1 2001 The purpose of this study was to examine the effects of 3-O-methylation by catechol-O-methyltransferase (COMT) on the toxicity of levodopa in neuronal cultures. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 75-103 11290879-1 2001 The purpose of this study was to examine the effects of 3-O-methylation by catechol-O-methyltransferase (COMT) on the toxicity of levodopa in neuronal cultures. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 105-109 11290879-5 2001 A possible defense mechanism is by means of metabolic shunting of levodopa excess to 3-O-methyldopa by COMT in peripheral and central nervous system tissues. Levodopa 66-74 catechol-O-methyltransferase Homo sapiens 103-107 11290879-6 2001 In this study we examine whether the use of COMT inhibitor, which reduced the levels of 3-O-methyldopa, affect levodopa toxicity. Levodopa 111-119 catechol-O-methyltransferase Homo sapiens 44-48 11432539-1 2001 OBJECTIVE: To investigate the effect of administration of the catechol-Omethyltransferase (COMT) inhibitor tolcapone on the concentration-effect relationship of levodopa in patients with advanced Parkinson"s disease and on-off fluctuations. Levodopa 161-169 catechol-O-methyltransferase Homo sapiens 91-95 11135014-1 2001 The centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor, 3-hydroxybenzyl hydrazine (NSD-1015), is widely used to study the neurotransmitter-like actions of L-DOPA. Levodopa 177-183 dopa decarboxylase Rattus norvegicus 41-59 11290879-10 2001 Addition of purified COMT to levodopa prevented its auto-oxidation and markedly attenuated its cytotoxicity in vitro. Levodopa 29-37 catechol-O-methyltransferase Homo sapiens 21-25 11290879-13 2001 Catechol-O-methyltransferase attenuates toxicity of levodopa in vitro by its metabolism to nontoxic 3-O-methyldopa. Levodopa 52-60 catechol-O-methyltransferase Homo sapiens 0-28 11135014-1 2001 The centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor, 3-hydroxybenzyl hydrazine (NSD-1015), is widely used to study the neurotransmitter-like actions of L-DOPA. Levodopa 177-183 dopa decarboxylase Rattus norvegicus 61-65 11716146-4 2001 Rather, a functional dissociation of D-2 receptor coupling to co-expressed enkephalin/adenosine-2a receptor activity in the striato-GPe indirect pathway may be more important in the development or expression of L-dopa-induced involuntary movements. Levodopa 211-217 immunoglobulin heavy diversity 2-15 Homo sapiens 37-40 11261746-13 2001 Severity of the disease expressed by H&Y stage at "off" was a significant contributing factor for FOG with a significant trend (z = 4.38, p < 0.0001), as was longer duration of levodopa treatment, and confirmed by FOG using the multivariate logistic regression (p = 0.01 and p = 0.004, respectively). Levodopa 177-185 zinc finger protein, FOG family member 1 Homo sapiens 98-101 11261749-1 2001 Entacapone and tolcapone are novel COMT (catechol-O-methyltransferase) inhibitors indicated for the adjunctive treatment of Parkinson"s disease (PD) in combination with levodopa. Levodopa 169-177 catechol-O-methyltransferase Rattus norvegicus 41-69 11716146-1 2001 To assess the role of dopamine receptors in the genesis of dyskinesia, we have used quantitative autoradiography to determine the effect of chronic L-dopa administration on dopamine D-1 (using [3H]SCH 23390), D-2 (using [3H]spiperone) and D-3 (using [3H]7-OH-DPAT) receptor binding levels in the striatum of dyskinetic or non-dyskinetic monkeys. Levodopa 148-154 leiomodin 1 Homo sapiens 182-185 11716146-1 2001 To assess the role of dopamine receptors in the genesis of dyskinesia, we have used quantitative autoradiography to determine the effect of chronic L-dopa administration on dopamine D-1 (using [3H]SCH 23390), D-2 (using [3H]spiperone) and D-3 (using [3H]7-OH-DPAT) receptor binding levels in the striatum of dyskinetic or non-dyskinetic monkeys. Levodopa 148-154 immunoglobulin heavy diversity 2-15 Homo sapiens 209-212 11261749-1 2001 Entacapone and tolcapone are novel COMT (catechol-O-methyltransferase) inhibitors indicated for the adjunctive treatment of Parkinson"s disease (PD) in combination with levodopa. Levodopa 169-177 catechol-O-methyltransferase Rattus norvegicus 35-39 11314772-0 2001 The central catechol-O-methyltransferase inhibitor tolcapone increases striatal hydroxyl radical production in L-DOPA/carbidopa treated rats. Levodopa 111-117 catechol-O-methyltransferase Rattus norvegicus 12-40 11274784-3 2001 After administration of 30mg/kg or 100mg/kg of L-DOPA, rats subjected to unilateral dopaminergic denervation showed intense contraversive rotation and a high density of Fos-immunoreactive nuclei throughout the denervated striatum, with no significant induction of Fos in the intact striatum. Levodopa 47-53 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 169-172 11314772-1 2001 Inhibition of catechol catechol-O-methyltransferase (COMT) in the brains of subjects treated with L-DOPA (L-3,4-dihydroxylphenylalanine) and an aromatic amino acid decarboxylase (AADC) inhibitor is suggested to cause an increase of L-DOPA, which might lead to oxidative damage through enhanced formation of free radicals. Levodopa 98-104 catechol-O-methyltransferase Rattus norvegicus 23-51 11314772-1 2001 Inhibition of catechol catechol-O-methyltransferase (COMT) in the brains of subjects treated with L-DOPA (L-3,4-dihydroxylphenylalanine) and an aromatic amino acid decarboxylase (AADC) inhibitor is suggested to cause an increase of L-DOPA, which might lead to oxidative damage through enhanced formation of free radicals. Levodopa 98-104 catechol-O-methyltransferase Rattus norvegicus 53-57 11314772-1 2001 Inhibition of catechol catechol-O-methyltransferase (COMT) in the brains of subjects treated with L-DOPA (L-3,4-dihydroxylphenylalanine) and an aromatic amino acid decarboxylase (AADC) inhibitor is suggested to cause an increase of L-DOPA, which might lead to oxidative damage through enhanced formation of free radicals. Levodopa 232-238 catechol-O-methyltransferase Rattus norvegicus 53-57 11314772-2 2001 To investigate this hypothesis, the acute effects of two doses of the systemically administered COMT inhibitors entacapone (peripheral) and tolcapone (peripheral and central) on the extracellular formation of hydroxyl radicals in vivo following treatment with L-DOPA and the AADC inhibitor carbidopa were examined. Levodopa 260-266 catechol-O-methyltransferase Rattus norvegicus 96-100 11274784-3 2001 After administration of 30mg/kg or 100mg/kg of L-DOPA, rats subjected to unilateral dopaminergic denervation showed intense contraversive rotation and a high density of Fos-immunoreactive nuclei throughout the denervated striatum, with no significant induction of Fos in the intact striatum. Levodopa 47-53 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 264-267 11274784-4 2001 Injection of the central aromatic L-amino-acid decarboxylase inhibitor NSD-1015 30min before and 15min after the injection of L-DOPA suppressed the rotational behavior and the striatal induction of Fos. Levodopa 126-132 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 198-201 11274784-6 2001 Serotonergic denervation led to slight and statistically non-significant decrease in the rotational behavior and Fos expression induced by high doses of L-DOPA (100mg/kg) in the dopamine-denervated striatum, but totally suppressed the rotational behavior and Fos expression induced by low doses of L-DOPA (30mg/kg). Levodopa 153-159 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 113-116 11085899-5 2000 We found that levodopa significantly decreased regional cerebral blood flow (rCBF) bilaterally in putamen and right cingulate and increased rCBF in right lateral temporal cortex and bilateral frontal cortex. Levodopa 14-22 CCAAT/enhancer binding protein zeta Rattus norvegicus 77-81 11702019-5 2001 Chronic administration of L-dopa resulted in a significant decrease (28%, p < 0.05) in the density of [(3)H]TBZOH binding in the prefrontal cortex but had no effect on VMAT2 and synaptophysin mRNA levels in the substantia nigra. Levodopa 26-32 synaptophysin Rattus norvegicus 181-194 11521741-0 2001 Changes of gastric lipase activity after ethanol and indomethacin administration: influence of pretreatment with allopurinol, pentoxifylline and L-DOPA. Levodopa 145-151 lipase F, gastric type Rattus norvegicus 11-25 11521741-8 2001 L-DOPA administered alone stimulated GL activity, but its administration before IND significantly (p < 0.01) inhibited this enzymatic activity. Levodopa 0-6 lipase F, gastric type Rattus norvegicus 37-39 11346021-5 2001 A more recent strategy has centered on increasing the availability of intracellular levodopa and synaptic dopamine by inhibiting the peripheral and central metabolism of levodopa to 3-O-methyldopa with the use of a catechol-O-methyltransferase inhibitor. Levodopa 84-92 catechol-O-methyltransferase Homo sapiens 215-243 11346021-5 2001 A more recent strategy has centered on increasing the availability of intracellular levodopa and synaptic dopamine by inhibiting the peripheral and central metabolism of levodopa to 3-O-methyldopa with the use of a catechol-O-methyltransferase inhibitor. Levodopa 170-178 catechol-O-methyltransferase Homo sapiens 215-243 11085948-1 2000 Analysis of the reaction of dopa decarboxylase (DDC) with L-dopa reveals that loss of decarboxylase activity with time is observed at enzyme concentrations approximately equal to the binding constant, K(d), of the enzyme for pyridoxal 5"-phosphate (PLP). Levodopa 58-64 dopa decarboxylase Homo sapiens 28-46 11085948-1 2000 Analysis of the reaction of dopa decarboxylase (DDC) with L-dopa reveals that loss of decarboxylase activity with time is observed at enzyme concentrations approximately equal to the binding constant, K(d), of the enzyme for pyridoxal 5"-phosphate (PLP). Levodopa 58-64 pyridoxal phosphatase Homo sapiens 249-252 11672603-0 2001 Up-regulation of secretoneurin immunoreactivity and secretogranin II mRNA in rat striatum following 6-hydroxydopamine lesioning and chronic L-DOPA treatment. Levodopa 140-146 secretogranin II Rattus norvegicus 52-68 11672603-5 2001 Following chronic L-DOPA treatment of 6-hydroxydopamine-lesioned rats, secretogranin II mRNA was further up-regulated to a similar degree to that observed for preproenkephalin A mRNA expression. Levodopa 18-24 secretogranin II Rattus norvegicus 71-87 11672603-6 2001 Immunohistochemical analysis confirmed the increase in secretogranin II peptide levels in striatal neurones in 6-hydroxydopamine-lesioned rats following chronic L-DOPA treatment. Levodopa 161-167 secretogranin II Rattus norvegicus 55-71 11672603-7 2001 The increase in secretogranin II mRNA occurring following destruction of the nigro-striatal pathway and chronic L-DOPA treatment may result in an increase in secretoneurin levels, which could be important for the regulation of striatal output pathways. Levodopa 112-118 secretogranin II Rattus norvegicus 16-32 11113234-2 2000 Analysis of the gene GCH1 in 58 patients with dystonia and a positive response to L-dopa revealed mutations in 30 individuals from 22 families. Levodopa 82-88 GTP cyclohydrolase 1 Homo sapiens 21-25 11085899-5 2000 We found that levodopa significantly decreased regional cerebral blood flow (rCBF) bilaterally in putamen and right cingulate and increased rCBF in right lateral temporal cortex and bilateral frontal cortex. Levodopa 14-22 CCAAT/enhancer binding protein zeta Rattus norvegicus 140-144 11244687-10 2000 Levodopa was prescript to 70.9%, anticholinergic to 51.3%, MAO-B-I to 33.4%, amantadine to 33.1%, D2 stimulants to 18.5%, and COMT-I to 2.6%. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 126-130 11058906-1 2000 Catechol-O-methyltransferase (COMT) catalyses the O-methylation of neurotransmitters, catechol hormones and drugs such as levodopa and methyldopa. Levodopa 122-130 catechol-O-methyltransferase Homo sapiens 0-28 11198128-10 2000 These results demonstrate a synergistic and restorative action of combining certain MAO inhibitors, namely the reversible MAO-A inhibitors, with the suprathreshold dose of L-dopa in MPTP-treated, L-dopa-tolerant mice. Levodopa 172-178 monoamine oxidase A Mus musculus 122-127 11198128-10 2000 These results demonstrate a synergistic and restorative action of combining certain MAO inhibitors, namely the reversible MAO-A inhibitors, with the suprathreshold dose of L-dopa in MPTP-treated, L-dopa-tolerant mice. Levodopa 196-202 monoamine oxidase A Mus musculus 122-127 11058906-1 2000 Catechol-O-methyltransferase (COMT) catalyses the O-methylation of neurotransmitters, catechol hormones and drugs such as levodopa and methyldopa. Levodopa 122-130 catechol-O-methyltransferase Homo sapiens 30-34 11029227-8 2000 Dopamine agonists, catechol-o-methyltransferase inhibitors, amantadine and apomorphine have differing but beneficial roles in the management of levodopa side effects. Levodopa 144-152 catechol-O-methyltransferase Homo sapiens 19-47 11008192-7 2000 Several studies have shown that L-dopa given with a peripheral decarboxylase inhibitor at a 10:4 ratio is effective in treating RLS. Levodopa 32-38 RLS1 Homo sapiens 128-131 11008192-8 2000 Controlled studies using polysomnographic recordings in a double-blind design showed that L-dopa administered at night produces a significant reduction of RLS occurring at bedtime and of PLM, which are often associated with nocturnal arousals. Levodopa 90-96 RLS1 Homo sapiens 155-158 11008192-9 2000 In most cases, L-dopa 100mg, in conjunction with the decarboxylase inhibitor carbidopa or benserazide 25mg, suppresses RLS although a rebound of PLM may be observed in the last part of the night. Levodopa 15-21 RLS1 Homo sapiens 119-122 11011010-7 2000 Furthermore, L-DOPA produced a dramatic induction of c-Fos in the CPu in 6-OHDA-lesioned animals. Levodopa 13-19 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 53-58 11083235-0 2000 Reproducibility and effect of levodopa on dopamine transporter function measurements: a [18F]CFT PET study. Levodopa 30-38 solute carrier family 6 member 3 Homo sapiens 42-62 11083235-1 2000 The objective of this article was to study the reproducibility and effect of levodopa on dopamine transporter function measurements using 2beta-carbomethoxy-3beta-(4-[18F]fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). Levodopa 77-85 solute carrier family 6 member 3 Homo sapiens 89-109 11065139-0 2000 Expression of metallothionein-III mRNA and its regulation by levodopa in the basal ganglia of hemi-parkinsonian rats. Levodopa 61-69 metallothionein 3 Rattus norvegicus 14-33 11065139-2 2000 Here we examined the expression of MT-III mRNA in the basal ganglia of 6-hydroxydopamine (6-OHDA)-lesioned hemi-parkinsonian rats and its regulation by levodopa. Levodopa 152-160 metallothionein 3 Rattus norvegicus 35-41 11065139-4 2000 Levodopa treatment significantly increased the expression of striatal MT-III mRNA in the non-lesioned side, but showed no significant effect in the 6-OHDA-lesioned side. Levodopa 0-8 metallothionein 3 Rattus norvegicus 70-76 11011012-0 2000 The 4F2hc/LAT1 complex transports L-DOPA across the blood-brain barrier. Levodopa 34-40 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 4-9 11011012-1 2000 L-DOPA is transported across the blood-brain barrier (BBB) by an amino acid transporter, system L. Recently, it has been demonstrated that system L consists of two subunits, 4F2hc and either LAT1 or LAT2. Levodopa 0-6 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 174-179 11011012-1 2000 L-DOPA is transported across the blood-brain barrier (BBB) by an amino acid transporter, system L. Recently, it has been demonstrated that system L consists of two subunits, 4F2hc and either LAT1 or LAT2. Levodopa 0-6 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 191-195 11011012-0 2000 The 4F2hc/LAT1 complex transports L-DOPA across the blood-brain barrier. Levodopa 34-40 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 10-14 11002293-6 2000 L-DOPA also protected PC12 cells from cell death induced by depletion of serum and NGF at low concentrations and showed toxicity at high concentration. Levodopa 0-6 nerve growth factor Rattus norvegicus 83-86 11011012-1 2000 L-DOPA is transported across the blood-brain barrier (BBB) by an amino acid transporter, system L. Recently, it has been demonstrated that system L consists of two subunits, 4F2hc and either LAT1 or LAT2. Levodopa 0-6 linker for activation of T cells family, member 2 Mus musculus 199-203 11011012-5 2000 To confirm whether 4F2hc/LAT1 acts as system L to transport L-DOPA, we characterized L-DOPA uptake into the cells. Levodopa 60-66 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 19-24 11011012-5 2000 To confirm whether 4F2hc/LAT1 acts as system L to transport L-DOPA, we characterized L-DOPA uptake into the cells. Levodopa 60-66 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 25-29 11011012-5 2000 To confirm whether 4F2hc/LAT1 acts as system L to transport L-DOPA, we characterized L-DOPA uptake into the cells. Levodopa 85-91 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 19-24 11011012-5 2000 To confirm whether 4F2hc/LAT1 acts as system L to transport L-DOPA, we characterized L-DOPA uptake into the cells. Levodopa 85-91 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 25-29 11011012-11 2000 This is the first report showing that the 4F2hc/LAT1 complex participates in L-DOPA transport across the BBB. Levodopa 77-83 solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2 Mus musculus 42-47 11011012-11 2000 This is the first report showing that the 4F2hc/LAT1 complex participates in L-DOPA transport across the BBB. Levodopa 77-83 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 48-52 10987861-2 2000 In melanocytes, tyrosinase catalyzes both the hydroxylation of tyrosine and the consequent oxidation of L-DOPA to form melanin. Levodopa 104-110 tyrosinase Mus musculus 16-26 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Levodopa 127-133 catechol-O-methyltransferase Homo sapiens 9-37 11068448-15 2000 Monoamine oxidase B inhibitor, Selegiline, is useful as an economizer effect to levodopa. Levodopa 80-88 monoamine oxidase B Homo sapiens 0-19 11052229-4 2000 Administering L-dopa with a catechol-O-methyltransferase (COMT) inhibitor to block its peripheral metabolism increases its plasma half-life and might have a similar effect. Levodopa 14-20 catechol-O-methyltransferase Homo sapiens 28-56 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Levodopa 127-133 catechol-O-methyltransferase Homo sapiens 39-43 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Levodopa 127-133 monoamine oxidase B Homo sapiens 74-93 10900396-1 2000 Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders. Levodopa 127-133 monoamine oxidase B Homo sapiens 95-100 10900397-1 2000 Following the introduction of tolcapone, a potent, reversible Catechol-O-methyltransferase (COMT) inhibitor, it has been possible to optimise the management of Parkinson"s disease (PD) patients in chronic Levodopa (L-dopa) therapy. Levodopa 205-213 catechol-O-methyltransferase Homo sapiens 92-96 10900397-1 2000 Following the introduction of tolcapone, a potent, reversible Catechol-O-methyltransferase (COMT) inhibitor, it has been possible to optimise the management of Parkinson"s disease (PD) patients in chronic Levodopa (L-dopa) therapy. Levodopa 215-221 catechol-O-methyltransferase Homo sapiens 62-90 10900397-1 2000 Following the introduction of tolcapone, a potent, reversible Catechol-O-methyltransferase (COMT) inhibitor, it has been possible to optimise the management of Parkinson"s disease (PD) patients in chronic Levodopa (L-dopa) therapy. Levodopa 215-221 catechol-O-methyltransferase Homo sapiens 92-96 11052229-4 2000 Administering L-dopa with a catechol-O-methyltransferase (COMT) inhibitor to block its peripheral metabolism increases its plasma half-life and might have a similar effect. Levodopa 14-20 catechol-O-methyltransferase Homo sapiens 58-62 10995853-2 2000 l-3,4-Dihydroxyphenylalanine (l-[beta-(11)C]DOPA) and 2beta-carbomethoxy-3beta-(4-fluorophenyl)tropane ([beta-(11)C]CFT) were used to measure dopamine synthesis rate and dopamine transporter (DAT) availability, respectively. Levodopa 0-28 solute carrier family 6 member 3 Homo sapiens 170-190 10993999-1 2000 OBJECTIVE: To describe the clinical and molecular genetic analysis of a large family of northern Chinese descent with a mutation at the SCA2 locus causing carbidopa-levodopa-responsive parkinsonism. Levodopa 165-173 ataxin 2 Homo sapiens 136-140 10995853-2 2000 l-3,4-Dihydroxyphenylalanine (l-[beta-(11)C]DOPA) and 2beta-carbomethoxy-3beta-(4-fluorophenyl)tropane ([beta-(11)C]CFT) were used to measure dopamine synthesis rate and dopamine transporter (DAT) availability, respectively. Levodopa 0-28 solute carrier family 6 member 3 Homo sapiens 192-195 11019859-4 2000 We now show that a Fenton-type OH-generating system is capable of generating L-Dopa (3,4-dihydroxyphenylalanine) in the tyrosine residue of A beta-peptide via aromatic ring hydroxylation, as the result of hydroxyl radical attack on proteins. Levodopa 77-83 amyloid beta precursor protein Homo sapiens 140-146 11019859-5 2000 Since L-Dopa is not a constituent of mammalian proteins and peptides, the formation of L-Dopa in A beta in vitro constitutes a possible important modification caused by hydroxyl radical attack. Levodopa 6-12 amyloid beta precursor protein Homo sapiens 97-103 10981253-6 2000 DATA SYNTHESIS: Entacapone is the second medication of a new class of drugs, the catechol-O-methyltransferase inhibitors, indicated for clinical use as an adjunct to levodopa/carbidopa to treat patients with idiopathic Parkinson"s disease who experience the signs and symptoms of end-of-dose wearing-off. Levodopa 166-174 catechol-O-methyltransferase Homo sapiens 81-109 11019859-5 2000 Since L-Dopa is not a constituent of mammalian proteins and peptides, the formation of L-Dopa in A beta in vitro constitutes a possible important modification caused by hydroxyl radical attack. Levodopa 87-93 amyloid beta precursor protein Homo sapiens 97-103 10981253-7 2000 Entacapone in combination with levodopa/dopa decarboxylase inhibitor has been shown to increase the AUC of levodopa, which leads to less fluctuation of levodopa plasma concentrations. Levodopa 107-115 dopa decarboxylase Homo sapiens 40-58 10984671-1 2000 Autosomal recessive juvenile parkinsonism (AR-JP) is a hereditary neurodegenerative disorder characterized by levodopa-responsive parkinsonism with onset before age 40 years and a slowly progressive course. Levodopa 110-118 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-48 10981253-7 2000 Entacapone in combination with levodopa/dopa decarboxylase inhibitor has been shown to increase the AUC of levodopa, which leads to less fluctuation of levodopa plasma concentrations. Levodopa 107-115 dopa decarboxylase Homo sapiens 40-58 10899290-2 2000 [(3-Chlorophenyl)methyl]amino?ethyl)phenyl]-2-thiophenecarbo ximidamide dihydrochloride (ARL 17477) on recombinant human neuronal NOS (nNOS) and endothelial NOS (eNOS). Levodopa 103-106 nitric oxide synthase 1 Homo sapiens 135-147 11144954-0 2000 The localization and functional contribution of striatal aromatic L-amino acid decarboxylase to L-3,4-dihydroxyphenylalanine decarboxylation in rodent parkinsonian models. Levodopa 96-124 dopa decarboxylase Homo sapiens 66-92 11144954-1 2000 L-3,4-Dihydroxyphenylalanine (L-dopa) is the mainstay of therapy for patients with Parkinson"s disease (PD), and mediates its primary effects through conversion into dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 0-28 dopa decarboxylase Homo sapiens 187-213 11144954-1 2000 L-3,4-Dihydroxyphenylalanine (L-dopa) is the mainstay of therapy for patients with Parkinson"s disease (PD), and mediates its primary effects through conversion into dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 0-28 dopa decarboxylase Homo sapiens 215-219 11144954-1 2000 L-3,4-Dihydroxyphenylalanine (L-dopa) is the mainstay of therapy for patients with Parkinson"s disease (PD), and mediates its primary effects through conversion into dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 30-36 dopa decarboxylase Homo sapiens 187-213 11144954-1 2000 L-3,4-Dihydroxyphenylalanine (L-dopa) is the mainstay of therapy for patients with Parkinson"s disease (PD), and mediates its primary effects through conversion into dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 30-36 dopa decarboxylase Homo sapiens 215-219 11144954-2 2000 Given the loss of AADC-containing nigrostriatal dopaminergic neurons in PD, however, the location of residual AADC that converts L-dopa into dopamine remains controversial. Levodopa 129-135 dopa decarboxylase Homo sapiens 110-114 11144954-8 2000 Understanding the source and localization of AADC is important in understanding the complications of L-dopa therapy and in designing rational therapeutic strategies for PD, including cellular transplantation and gene therapy. Levodopa 101-107 dopa decarboxylase Rattus norvegicus 45-49 11108136-1 2000 The conversion of L-tyrosine to 3,4-dihydroxy-L-phenylalanine by tyrosine hydroxylase (TH) is the first and rate-limiting step in biosynthesis of catecholamine neurotransmitters. Levodopa 32-61 tyrosine hydroxylase Homo sapiens 65-85 11108136-1 2000 The conversion of L-tyrosine to 3,4-dihydroxy-L-phenylalanine by tyrosine hydroxylase (TH) is the first and rate-limiting step in biosynthesis of catecholamine neurotransmitters. Levodopa 32-61 tyrosine hydroxylase Homo sapiens 87-89 10932284-0 2000 Plasma homocysteine and MTHFR C677T genotype in levodopa-treated patients with PD. Levodopa 48-56 methylenetetrahydrofolate reductase Homo sapiens 24-29 10915571-0 2000 The expression of the calcium binding protein calretinin in the rat striatum: effects of dopamine depletion and L-DOPA treatment. Levodopa 112-118 calbindin 2 Rattus norvegicus 46-56 10915571-3 2000 We investigated changes in the neuronal expression of the calcium binding protein calretinin related to dopamine depletion and l-DOPA administration. Levodopa 127-133 calbindin 2 Rattus norvegicus 82-92 10915571-10 2000 In unilaterally lesioned animals, l-DOPA reversed the increase in the number of calretinin-positive cells induced by the lesion. Levodopa 34-40 calbindin 2 Rattus norvegicus 80-90 10899290-2 2000 [(3-Chlorophenyl)methyl]amino?ethyl)phenyl]-2-thiophenecarbo ximidamide dihydrochloride (ARL 17477) on recombinant human neuronal NOS (nNOS) and endothelial NOS (eNOS). Levodopa 103-106 nitric oxide synthase 1 Homo sapiens 149-153 10899290-2 2000 [(3-Chlorophenyl)methyl]amino?ethyl)phenyl]-2-thiophenecarbo ximidamide dihydrochloride (ARL 17477) on recombinant human neuronal NOS (nNOS) and endothelial NOS (eNOS). Levodopa 103-106 nitric oxide synthase 3 Homo sapiens 159-174 10844009-5 2000 Chronic replacement of dopamine to DA-/- mice by repeated l-DOPA administration over 4 d relieved the hypersensitivity of DA-/- mutants in terms of induction of both locomotion and striatal c-fos expression. Levodopa 58-64 FBJ osteosarcoma oncogene Mus musculus 190-195 10884518-8 2000 The present results suggest that novel selective dopamine D(4) receptor antagonists may represent a useful tool to reduce L-Dopa-induced dyskinesias. Levodopa 122-128 dopamine receptor D4 Homo sapiens 49-71 10877910-1 2000 Using an approach that combines gene therapy with aromatic l-amino acid decarboxylase (AADC) gene and a pro-drug (l-dopa), dopamine, the neurotransmitter involved in Parkinson"s disease, can be synthesized and regulated. Levodopa 114-120 dopa decarboxylase Homo sapiens 59-85 10877910-2 2000 Striatal neurons infected with the AADC gene by an adeno-associated viral vector can convert peripheral l-dopa to dopamine and may therefore provide a buffer for unmetabolized l-dopa. Levodopa 104-110 dopa decarboxylase Homo sapiens 35-39 10877910-2 2000 Striatal neurons infected with the AADC gene by an adeno-associated viral vector can convert peripheral l-dopa to dopamine and may therefore provide a buffer for unmetabolized l-dopa. Levodopa 176-182 dopa decarboxylase Homo sapiens 35-39 10890170-0 2000 Synthesis of L-(+)-3-(3-hydroxy-4-pivaloyloxybenzyl)-2,5-diketomorpholine as potential prodrug of L-dopa. Levodopa 98-104 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 13-20 10890170-1 2000 The synthesis and in vitro chemical and enzymatic stability of L-(+)-3-(3-hydroxy-4-pivaloyloxybenzyl)-2,5-diketomorpholine (9) as L-Dopa prodrug are described. Levodopa 131-137 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 63-70 10898900-2 2000 The enzyme catechol-O-methyltransferase (COMT) plays a key role in the degradation of catecholamines such as dopamine, L-DOPA, adrenaline, and noradrenaline and therefore could be considered as a candidate locus for ADHD susceptibility. Levodopa 119-125 catechol-O-methyltransferase Homo sapiens 11-39 10898900-2 2000 The enzyme catechol-O-methyltransferase (COMT) plays a key role in the degradation of catecholamines such as dopamine, L-DOPA, adrenaline, and noradrenaline and therefore could be considered as a candidate locus for ADHD susceptibility. Levodopa 119-125 catechol-O-methyltransferase Homo sapiens 41-45 10825431-0 2000 Involvement of rBAT in Na(+)-dependent and -independent transport of the neurotransmitter candidate L-DOPA in Xenopus laevis oocytes injected with rabbit small intestinal epithelium poly A(+) RNA. Levodopa 100-106 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 15-19 10825431-9 2000 As rBAT is localized at the target regions of L-DOPA in the CNS, rBAT might be one of the components involved in L-DOPAergic neurotransmission. Levodopa 46-52 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 3-7 10825431-9 2000 As rBAT is localized at the target regions of L-DOPA in the CNS, rBAT might be one of the components involved in L-DOPAergic neurotransmission. Levodopa 46-52 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 65-69 10886351-1 2000 Induction of dopamine D3 receptor gene expression in 6-hydroxydopamine-lesioned rats by repeated administration of levodopa had been suggested to be responsible for behavioural sensitization developing in these animals. Levodopa 115-123 dopamine receptor D3 Rattus norvegicus 13-33 10882160-1 2000 When peripheral decarboxylation is blocked by carbidopa or benserazide, the main metabolic pathway of levodopa is O-methylation by catechol-O-methyltransferase (COMT). Levodopa 102-110 catechol-O-methyltransferase Homo sapiens 131-159 10882160-1 2000 When peripheral decarboxylation is blocked by carbidopa or benserazide, the main metabolic pathway of levodopa is O-methylation by catechol-O-methyltransferase (COMT). Levodopa 102-110 catechol-O-methyltransferase Homo sapiens 161-165 10882160-24 2000 COMT inhibitors added to levodopa therapy are beneficial, particularly in patients with fluctuating disease. Levodopa 25-33 catechol-O-methyltransferase Homo sapiens 0-4 10825351-3 2000 We studied 22 families with a phenotype of levodopa-responsive dystonia by sequencing the six coding exons, the 5"-untranslated region and the exon-intron boundaries of the GTPCH I gene. Levodopa 43-51 GTP cyclohydrolase 1 Homo sapiens 173-180 10886351-4 2000 Changes in D3 receptor binding and behavioural sensitization during intermittent administration of levodopa paralleled changes in prodynorphin/preprotachykinin rather than preproenkephalin/prodynorphin and preproenkephalin/preprotachykinin mRNA ratios. Levodopa 99-107 prodynorphin Rattus norvegicus 130-142 10886351-4 2000 Changes in D3 receptor binding and behavioural sensitization during intermittent administration of levodopa paralleled changes in prodynorphin/preprotachykinin rather than preproenkephalin/prodynorphin and preproenkephalin/preprotachykinin mRNA ratios. Levodopa 99-107 prodynorphin Rattus norvegicus 189-201 10886351-5 2000 Behavioural sensitization, induction of D3 receptor binding and changes in prodynorphin/preprotachykinin ratio were all prevented together when levodopa was continuously delivered or intermittently delivered in combination with R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine (SCH 23390), a selective D1 receptor antagonist. Levodopa 144-152 prodynorphin Rattus norvegicus 75-87 10773046-0 2000 Outward transfer of dopamine precursor L-3,4-dihydroxyphenylalanine (L-dopa) by native and human P-glycoprotein in LLC-PK(1) and LLC-GA5 col300 renal cells. Levodopa 39-67 ATP binding cassette subfamily B member 1 Homo sapiens 97-111 10855610-2 2000 COMT inhibitors act by extending the duration of action of levodopa, thus improving the amount of time a patient can experience benefit from levodopa. Levodopa 59-67 catechol-O-methyltransferase Homo sapiens 0-4 10855610-2 2000 COMT inhibitors act by extending the duration of action of levodopa, thus improving the amount of time a patient can experience benefit from levodopa. Levodopa 141-149 catechol-O-methyltransferase Homo sapiens 0-4 10855610-3 2000 COMT inhibitors are only used in conjunction with levodopa. Levodopa 50-58 catechol-O-methyltransferase Homo sapiens 0-4 10855610-7 2000 This article also provides representative case histories for the appropriate use of COMT inhibitors that illustrate how these drugs can be used to manage patients with a fluctuating response to levodopa. Levodopa 194-202 catechol-O-methyltransferase Homo sapiens 84-88 10765095-0 2000 Paradoxical stimulation of prolactin secretion by L-dopa in metastatic prostate cancer and its possible role in prostate-cancer-related hyperprolactinemia. Levodopa 50-56 prolactin Homo sapiens 27-36 10765095-4 2000 This study was carried out to analyze PRL secretion in metastatic prostate cancer patients both at basal conditions and in response to L-Dopa and metoclopramide, which represents the most classical inhibitory and stimulatory tests for PRL secretion, respectively. Levodopa 135-141 prolactin Homo sapiens 38-41 10765095-6 2000 On separate occasions, PRL secretion was evaluated in response to L-Dopa (500 mg orally) and to metoclopramide (10 mg i.v. Levodopa 66-72 prolactin Homo sapiens 23-26 10765095-11 2000 CONCLUSION: By showing a paradoxical stimulatory effect of L-Dopa on PRL secretion and a lack of response to metoclopramide in some patients, this study would suggest the existence of evident alterations in the neuroendocrine regulation of PRL release in advanced prostate cancer. Levodopa 59-65 prolactin Homo sapiens 69-72 10773046-1 2000 The role of P-glycoprotein (P-gp) in the basal-to-apical uptake and flux of L-3,4-dihydroxyphenylalanine (L-dopa) was studied in LLC-PK(1) and LLC-GA5 Col300 cells, a renal cell line expressing the human P-gp in the apical membrane. Levodopa 76-104 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 10773046-1 2000 The role of P-glycoprotein (P-gp) in the basal-to-apical uptake and flux of L-3,4-dihydroxyphenylalanine (L-dopa) was studied in LLC-PK(1) and LLC-GA5 Col300 cells, a renal cell line expressing the human P-gp in the apical membrane. Levodopa 106-112 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 10773046-0 2000 Outward transfer of dopamine precursor L-3,4-dihydroxyphenylalanine (L-dopa) by native and human P-glycoprotein in LLC-PK(1) and LLC-GA5 col300 renal cells. Levodopa 69-75 ATP binding cassette subfamily B member 1 Homo sapiens 97-111 10773046-1 2000 The role of P-glycoprotein (P-gp) in the basal-to-apical uptake and flux of L-3,4-dihydroxyphenylalanine (L-dopa) was studied in LLC-PK(1) and LLC-GA5 Col300 cells, a renal cell line expressing the human P-gp in the apical membrane. Levodopa 106-112 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 10773046-1 2000 The role of P-glycoprotein (P-gp) in the basal-to-apical uptake and flux of L-3,4-dihydroxyphenylalanine (L-dopa) was studied in LLC-PK(1) and LLC-GA5 Col300 cells, a renal cell line expressing the human P-gp in the apical membrane. Levodopa 76-104 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 10773222-1 2000 The present study examined whether the O-methylated derivative of L-DOPA, 3-O-methyl-L-DOPA (3-OM-L-DOPA), inhibits neuronal (brain) and non-neuronal (liver and kidney) aromatic L-amino acid decarboxylase (AADC) activity. Levodopa 66-72 dopa decarboxylase Rattus norvegicus 178-204 10773222-1 2000 The present study examined whether the O-methylated derivative of L-DOPA, 3-O-methyl-L-DOPA (3-OM-L-DOPA), inhibits neuronal (brain) and non-neuronal (liver and kidney) aromatic L-amino acid decarboxylase (AADC) activity. Levodopa 66-72 dopa decarboxylase Rattus norvegicus 206-210 10834300-3 2000 Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). Levodopa 8-14 catechol-O-methyltransferase Homo sapiens 23-51 10834300-3 2000 Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). Levodopa 8-14 catechol-O-methyltransferase Homo sapiens 53-57 10834300-11 2000 L-dopa produces high levels of DA and induces MAT and COMT. Levodopa 0-6 methionine adenosyltransferase 1A Homo sapiens 46-49 10834300-3 2000 Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). Levodopa 8-14 methionine adenosyltransferase 1A Homo sapiens 63-94 10834300-11 2000 L-dopa produces high levels of DA and induces MAT and COMT. Levodopa 0-6 catechol-O-methyltransferase Homo sapiens 54-58 10834300-3 2000 Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). Levodopa 8-14 methionine adenosyltransferase 1A Homo sapiens 96-99 10620706-1 2000 Tyrosine hydroxylase (TH), which converts L-tyrosine to L-3, 4-dihydroxyphenylalanine, is a rate-limiting enzyme in the biosynthesis of catecholamines; its activity is regulated by the feedback inhibition of the catecholamine products including dopamine. Levodopa 56-85 tyrosine hydroxylase Homo sapiens 0-20 10731533-6 2000 A GH stimulation test with oral L-dopa was arranged for controls and for patients with PCOS before and again 6 months later after OWR. Levodopa 32-38 growth hormone 1 Homo sapiens 2-4 10731533-9 2000 The OWR in patients with PCOS obviously reduced their androstenedione and testosterone levels and insulin-glucose ratios, and increased the GH and GH-IGF-1 responses to L-dopa. Levodopa 169-175 growth hormone 1 Homo sapiens 140-142 10731533-9 2000 The OWR in patients with PCOS obviously reduced their androstenedione and testosterone levels and insulin-glucose ratios, and increased the GH and GH-IGF-1 responses to L-dopa. Levodopa 169-175 insulin like growth factor 1 Homo sapiens 150-155 10692500-0 2000 Catechol-O-methyltransferase inhibition attenuates levodopa toxicity in mesencephalic dopamine neurons. Levodopa 51-59 catechol-O-methyltransferase Homo sapiens 0-28 10692500-8 2000 Furthermore, the primary metabolite of L-dopa formed by COMT, 3-O-methyldopa, and the methyl group donor S-adenosyl-L-methionine used by COMT did not alter THir neuron survival and L-dopa-induced toxicity, respectively, with concentrations up to 100 microM. Levodopa 39-45 catechol-O-methyltransferase Homo sapiens 56-60 10692500-9 2000 These data demonstrate that COMT inhibition attenuates L-dopa toxicity toward DA neurons in vitro, but probably not by preventing 3-O-methyldopa production or cellular S-adenosyl-L-methionine depletion. Levodopa 55-61 catechol-O-methyltransferase Homo sapiens 28-32 10833916-4 2000 Further studies are needed to clarify how medication with L-dopa in combination with different diets (relative contributions of protein, fat and carbohydrate) may affect motor fluctuations, nutritional status and cognitive ability. Levodopa 58-64 FAT atypical cadherin 1 Homo sapiens 137-140 10830457-0 2000 Simultaneous stimulation of growth hormone, adrenocorticotropin and cortisol with L-dopa/L-carbidopa and propranolol in children of short stature. Levodopa 82-88 growth hormone 1 Homo sapiens 28-42 10830457-1 2000 In 59 otherwise healthy children of short stature, the simultaneous response of growth hormone, cortisol and plasma adrenocorticotropin (ACTH) to L-dopa/L-carbidopa and propranolol at 45 and 90 min after administration were investigated. Levodopa 146-152 proopiomelanocortin Homo sapiens 137-141 10830457-9 2000 We conclude that the administration of L-dopa/L-carbidopa and propranolol is useful for the simultaneous evaluation of growth hormone, cortisol and ACTH secretion in children of short stature. Levodopa 39-45 growth hormone 1 Homo sapiens 119-133 10830457-9 2000 We conclude that the administration of L-dopa/L-carbidopa and propranolol is useful for the simultaneous evaluation of growth hormone, cortisol and ACTH secretion in children of short stature. Levodopa 39-45 proopiomelanocortin Homo sapiens 148-152 10849837-0 2000 L-DOPA production by immobilized tyrosinase. Levodopa 0-6 tyrosinase Homo sapiens 33-43 10849837-1 2000 The production of L-DOPA using L-tyrosine as substrate, the enzyme tyrosinase (EC 1.14.18.1) as biocatalyst, and L-ascorbate as reducing agent for the o-quinones produced by the enzymatic oxidation of the substrates was studied. Levodopa 18-24 tyrosinase Homo sapiens 67-77 10742291-3 2000 We now investigate the effects of the centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor NSD-1015 (3-hydroxybenzyl hydrazine) on the motor actions of L-DOPA and dopamine agonist drugs in MPTP treated common marmosets. Levodopa 172-178 aromatic-L-amino-acid decarboxylase Callithrix jacchus 75-93 10991665-10 2000 Neurotrophic therapies diminish dyskinesia since glial cell line-derived neurotrophic factor (GDNF) produces a decrease in motor disability in MPTP-treated primates associated with a reduced intensity of levodopa-induced dyskinesia. Levodopa 204-212 glial cell derived neurotrophic factor Homo sapiens 49-92 10991665-10 2000 Neurotrophic therapies diminish dyskinesia since glial cell line-derived neurotrophic factor (GDNF) produces a decrease in motor disability in MPTP-treated primates associated with a reduced intensity of levodopa-induced dyskinesia. Levodopa 204-212 glial cell derived neurotrophic factor Homo sapiens 94-98 10762340-0 2000 Alterations in preproenkephalin and adenosine-2a receptor mRNA, but not preprotachykinin mRNA correlate with occurrence of dyskinesia in normal monkeys chronically treated with L-DOPA. Levodopa 177-183 proenkephalin Homo sapiens 15-31 10762340-3 2000 In the present study, in situ hybridization histochemistry was used to investigate the effect of chronic L-DOPA administration on the activity of the direct and indirect striatal output pathways by measuring striatal preprotachykinin (PPT), preproenkephalin-A (PPE-A) and adenosine-2a (A2a) receptor gene expression in these monkeys. Levodopa 105-111 tachykinin precursor 1 Homo sapiens 217-233 10762340-3 2000 In the present study, in situ hybridization histochemistry was used to investigate the effect of chronic L-DOPA administration on the activity of the direct and indirect striatal output pathways by measuring striatal preprotachykinin (PPT), preproenkephalin-A (PPE-A) and adenosine-2a (A2a) receptor gene expression in these monkeys. Levodopa 105-111 tachykinin precursor 1 Homo sapiens 235-238 10762340-3 2000 In the present study, in situ hybridization histochemistry was used to investigate the effect of chronic L-DOPA administration on the activity of the direct and indirect striatal output pathways by measuring striatal preprotachykinin (PPT), preproenkephalin-A (PPE-A) and adenosine-2a (A2a) receptor gene expression in these monkeys. Levodopa 105-111 proenkephalin Homo sapiens 241-257 10677634-1 2000 Using in vivo microdialysis in freely moving rats, we show that the addition to the dialysis perfusion fluid of the acetylcholinesterase inhibitor neostigmine influences the decarboxylation of levodopa (L-dopa). Levodopa 193-201 acetylcholinesterase Rattus norvegicus 116-136 10677634-1 2000 Using in vivo microdialysis in freely moving rats, we show that the addition to the dialysis perfusion fluid of the acetylcholinesterase inhibitor neostigmine influences the decarboxylation of levodopa (L-dopa). Levodopa 203-209 acetylcholinesterase Rattus norvegicus 116-136 10648644-7 2000 Chronic treatment of lesioned rats with L-dopa normalized the alterations in the abundance and subunit composition of the NMDA receptors in striatal membranes, and produced striking hyperphosphorylation, both of NR1 at serine residues, and NR2A and NR2B at tyrosine residues. Levodopa 40-46 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 212-215 10648644-7 2000 Chronic treatment of lesioned rats with L-dopa normalized the alterations in the abundance and subunit composition of the NMDA receptors in striatal membranes, and produced striking hyperphosphorylation, both of NR1 at serine residues, and NR2A and NR2B at tyrosine residues. Levodopa 40-46 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 240-244 10648644-7 2000 Chronic treatment of lesioned rats with L-dopa normalized the alterations in the abundance and subunit composition of the NMDA receptors in striatal membranes, and produced striking hyperphosphorylation, both of NR1 at serine residues, and NR2A and NR2B at tyrosine residues. Levodopa 40-46 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 249-253 11072750-14 2000 All patients were treated with L-DOPA and those given a higher dose showed a more rapid decrease of dopamine transporter density. Levodopa 31-37 solute carrier family 6 member 3 Homo sapiens 100-120 10908538-4 2000 OBJECTIVES: To assess the efficacy and safety of bromocriptine (BR) monotherapy for delaying the onset of motor complications associated with levodopa (LD) therapy in patients with Parkinson"s disease (PD). Levodopa 142-150 chromosome 12 open reading frame 73 Homo sapiens 64-66 10869844-1 2000 In a previous study, we described a population of striatal cells in the rat brain containing aromatic L-amino acid decarboxylase, the enzyme involved in the conversion of L-DOPA into dopamine. Levodopa 171-177 dopa decarboxylase Rattus norvegicus 93-128 11215752-1 2000 The present study examined the effect of the highly potent and selective MAO B inhibitor PF9601N on L-DOPA-induced rotational behavior in unilateral nigrostriatal 6-hydroxydopamine lesioned rats. Levodopa 100-106 monoamine oxidase B Rattus norvegicus 73-78 11215754-2 2000 Aromatic L-amino acid decarboxylase (AAAD) converts L-DOPA to dopamine. Levodopa 52-58 dopa decarboxylase Mus musculus 0-35 11215754-2 2000 Aromatic L-amino acid decarboxylase (AAAD) converts L-DOPA to dopamine. Levodopa 52-58 dopa decarboxylase Mus musculus 37-41 11215754-7 2000 These studies suggest that it may be possible to enhance the conversion of L-DOPA to dopamine in Parkinson"s disease patients by administering substances that augment brain AAAD. Levodopa 75-81 dopa decarboxylase Mus musculus 173-177 10619466-3 2000 The antiparkinsonian drugs budipine (10 mg/kg) and amantadine (40 mg/kg) enhanced AADC activity in these regions, and prevented or reversed AADC inhibition by L-DOPA. Levodopa 159-165 dopa decarboxylase Rattus norvegicus 140-144 11147506-4 2000 Levodopa is metabolized by both decarboxylase and catechol-O-methyl transferase enzymes. Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 50-79 11147506-6 2000 More recent studies suggest that combination of levodopa with an inhibitor of catechol-O-methyl transferase prolongs the duration of effect of the drug and can prolong the duration of motor response in fluctuating patients. Levodopa 48-56 catechol-O-methyltransferase Homo sapiens 78-107 11147511-1 2000 Two inhibitors of catechol-O-methyl transferase (COMT), tolcapone and entacapone, have recently been introduced as adjuncts to levodopa in the treatment of Parkinson"s disease patients. Levodopa 127-135 catechol-O-methyltransferase Homo sapiens 49-53 11147512-1 2000 Catechol-O-methyl transferase (COMT) inhibitors block the peripheral metabolism of levodopa, increase its plasma half-life, and enhance its brain availability. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 0-29 11147507-2 2000 However, exogenously administered levodopa is extensively metabolized in the periphery by aromatic amino acid decarboxylase (AAAD) and catechol-O-methyltransferase (COMT) so that only 1% of an administered dose gains access to the brain. Levodopa 34-42 catechol-O-methyltransferase Homo sapiens 135-163 10599788-2 1999 BACKGROUND: Mutations of alpha-synuclein have been associated recently with dominantly inherited, levodopa-responsive parkinsonism. Levodopa 98-106 synuclein alpha Homo sapiens 25-40 11147507-2 2000 However, exogenously administered levodopa is extensively metabolized in the periphery by aromatic amino acid decarboxylase (AAAD) and catechol-O-methyltransferase (COMT) so that only 1% of an administered dose gains access to the brain. Levodopa 34-42 catechol-O-methyltransferase Homo sapiens 165-169 11147507-3 2000 Even when levodopa is co-administered with an inhibitor of AAAD such as benserazide or carbidopa, the bulk (90%) of levodopa is converted by COMT to the therapeutically inactive 3-O-methyldopa. Levodopa 10-18 catechol-O-methyltransferase Homo sapiens 141-145 11147507-3 2000 Even when levodopa is co-administered with an inhibitor of AAAD such as benserazide or carbidopa, the bulk (90%) of levodopa is converted by COMT to the therapeutically inactive 3-O-methyldopa. Levodopa 116-124 catechol-O-methyltransferase Homo sapiens 141-145 11147507-4 2000 Two COMT inhibitors, tolcapone and entacapone, have recently been introduced as adjuncts to levodopa to further inhibit peripheral levodopa metabolism and thereby enhance brain levodopa availability. Levodopa 131-139 catechol-O-methyltransferase Homo sapiens 4-8 11147507-4 2000 Two COMT inhibitors, tolcapone and entacapone, have recently been introduced as adjuncts to levodopa to further inhibit peripheral levodopa metabolism and thereby enhance brain levodopa availability. Levodopa 131-139 catechol-O-methyltransferase Homo sapiens 4-8 11147508-0 2000 Effect of COMT inhibition on the pharmacokinetics and pharmacodynamics of levodopa in parkinsonian patients. Levodopa 74-82 catechol-O-methyltransferase Homo sapiens 10-14 11147508-1 2000 Catechol-O-methyl transferase (COMT) is one of the principal levodopa-metabolizing enzymes, particularly when aromatic amino acid decarboxylase (AAAD) is partially inhibited by carbidopa or benserazide. Levodopa 61-69 catechol-O-methyltransferase Homo sapiens 0-29 11147508-1 2000 Catechol-O-methyl transferase (COMT) is one of the principal levodopa-metabolizing enzymes, particularly when aromatic amino acid decarboxylase (AAAD) is partially inhibited by carbidopa or benserazide. Levodopa 61-69 catechol-O-methyltransferase Homo sapiens 31-35 11147509-0 2000 Benefits of COMT inhibitors in levodopa-treated parkinsonian patients: results of clinical trials. Levodopa 31-39 catechol-O-methyltransferase Homo sapiens 12-16 10641989-3 2000 In addition, a new class of drugs, catechol-O-methyltransferase inhibitors, can extend the duration of levodopa action. Levodopa 103-111 catechol-O-methyltransferase Homo sapiens 35-63 10641990-7 2000 Addition of a catechol-O-methyltransferase inhibitor can increase the duration of levodopa"s effect and may prove especially valuable for patients who experience early wearing off of levodopa. Levodopa 82-90 catechol-O-methyltransferase Homo sapiens 14-42 10641990-7 2000 Addition of a catechol-O-methyltransferase inhibitor can increase the duration of levodopa"s effect and may prove especially valuable for patients who experience early wearing off of levodopa. Levodopa 183-191 catechol-O-methyltransferase Homo sapiens 14-42 11147512-1 2000 Catechol-O-methyl transferase (COMT) inhibitors block the peripheral metabolism of levodopa, increase its plasma half-life, and enhance its brain availability. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 31-35 11147512-2 2000 Two COMT inhibitors, tolcapone and entacapone, have recently been made available as adjunctive agents to levodopa. Levodopa 105-113 catechol-O-methyltransferase Homo sapiens 4-8 11147512-7 2000 Finally, there are theoretical reasons to consider administering a COMT inhibitor to patients from the onset of levodopa therapy in order to reduce the likelihood that motor complications will develop. Levodopa 112-120 catechol-O-methyltransferase Homo sapiens 67-71 11147513-4 2000 Administration of levodopa with a catechol-O-methyl transferase (COMT) inhibitor increases its plasma half-life, smoothes out peaks and troughs, and delivers levodopa to the brain in a more continuous fashion. Levodopa 18-26 catechol-O-methyltransferase Homo sapiens 34-63 11147513-4 2000 Administration of levodopa with a catechol-O-methyl transferase (COMT) inhibitor increases its plasma half-life, smoothes out peaks and troughs, and delivers levodopa to the brain in a more continuous fashion. Levodopa 18-26 catechol-O-methyltransferase Homo sapiens 65-69 11147513-4 2000 Administration of levodopa with a catechol-O-methyl transferase (COMT) inhibitor increases its plasma half-life, smoothes out peaks and troughs, and delivers levodopa to the brain in a more continuous fashion. Levodopa 158-166 catechol-O-methyltransferase Homo sapiens 34-63 11147513-4 2000 Administration of levodopa with a catechol-O-methyl transferase (COMT) inhibitor increases its plasma half-life, smoothes out peaks and troughs, and delivers levodopa to the brain in a more continuous fashion. Levodopa 158-166 catechol-O-methyltransferase Homo sapiens 65-69 11147513-5 2000 We hypothesize that the risk of developing motor complications in PD patients when levodopa is introduced can be reduced if the levodopa is coupled with a COMT inhibitor so as to provide more continuous dopaminergic stimulation of dopamine receptors. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 155-159 10619466-2 2000 Acute administration of L-DOPA (25-200 mg/kg) dose-dependently inhibited the activity of aromatic L-amino acid decarboxylase (AADC) in the substantia nigra and corpus striatum. Levodopa 24-30 dopa decarboxylase Rattus norvegicus 98-124 10619466-2 2000 Acute administration of L-DOPA (25-200 mg/kg) dose-dependently inhibited the activity of aromatic L-amino acid decarboxylase (AADC) in the substantia nigra and corpus striatum. Levodopa 24-30 dopa decarboxylase Rattus norvegicus 126-130 10637595-0 2000 US licence for COMT inhibitor to boost levodopa effect in Parkinson"s. Levodopa 39-47 catechol-O-methyltransferase Homo sapiens 15-19 10644014-4 1999 Therefore, the substitution of the lacking tyrosine hydroxylase with tyrosinase might be a novel therapeutical approach that would generate specifically L-DOPA from L-tyrosine. Levodopa 153-159 tyrosinase Rattus norvegicus 69-79 10600402-0 1999 Striatal fosB expression is causally linked with l-DOPA-induced abnormal involuntary movements and the associated upregulation of striatal prodynorphin mRNA in a rat model of Parkinson"s disease. Levodopa 49-55 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 9-13 10600402-3 1999 This effect was paralleled by an induction of FosB-like immunoreactive proteins in striatal subregions somatotopically related to the types of movements that had been elicited by l-DOPA. Levodopa 179-185 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 46-50 10600402-6 1999 These data provide compelling evidence of a causal role for striatal fosB induction in the development of l-DOPA-induced dyskinesia in the rat and of a positive regulation of prodynorphin gene expression by FosB-related transcription factors. Levodopa 106-112 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 69-73 10595790-8 1999 Thus the phosphaturic effect of PTH that was attenuated in respiratory alkalotic rats was enhanced by stimulation of endogenous dopamine synthesis by the infusion of L-DOPA. Levodopa 166-172 parathyroid hormone Rattus norvegicus 32-35 10657530-2 1999 TyrOH activity was determined in vitro by measuring the production of L-dopa with HPLC-ECD. Levodopa 70-76 tyrosine hydroxylase Rattus norvegicus 0-5 10668930-9 1999 Our data suggested that mutations at the -45 locus in the promoter region of the CCK gene may influence vulnerability to hallucinations in PD patients treated with L-dopa. Levodopa 164-170 cholecystokinin Homo sapiens 81-84 10584673-6 1999 In conclusion, in patients with MSA, the GHRH and GH responses to L-dopa were preserved and were similar to responses in age-matched control subjects. Levodopa 66-72 growth hormone releasing hormone Homo sapiens 41-45 10584673-6 1999 In conclusion, in patients with MSA, the GHRH and GH responses to L-dopa were preserved and were similar to responses in age-matched control subjects. Levodopa 66-72 growth hormone 1 Homo sapiens 41-43 10584673-5 1999 In patients with MSA, basal levels of prolactin were elevated (21.1 +/- 5.2 ng/mL [mean +/-standard error]) compared with control subjects (12.1 +/- 1.7, p <0.05), and after L-dopa there was increased variability in prolactin response with less suppression compared with control subjects. Levodopa 174-180 prolactin Homo sapiens 38-47 10555944-7 1999 The catechol-O-methyltransferase inhibitors that block a compensatory metabolic pathway for levodopa and prolong its duration may improve the consistency of the dopaminergic response. Levodopa 92-100 catechol-O-methyltransferase Homo sapiens 4-32 10555945-3 1999 The need to extend the actions of levodopa led to the development of the catechol-O-methyltransferase (COMT) inhibitors, which are the newest agents introduced to manage the symptoms of Parkinson"s disease. Levodopa 34-42 catechol-O-methyltransferase Homo sapiens 73-101 10555945-3 1999 The need to extend the actions of levodopa led to the development of the catechol-O-methyltransferase (COMT) inhibitors, which are the newest agents introduced to manage the symptoms of Parkinson"s disease. Levodopa 34-42 catechol-O-methyltransferase Homo sapiens 103-107 10555945-4 1999 Entacapone and tolcapone are two potent, selective, and reversible COMT inhibitors that effectively augment levodopa"s pharmacokinetics by increasing area under the plasma concentration versus time curve and plasma elimination half-life without significantly affecting peak levodopa concentrations. Levodopa 108-116 catechol-O-methyltransferase Homo sapiens 67-71 10555945-4 1999 Entacapone and tolcapone are two potent, selective, and reversible COMT inhibitors that effectively augment levodopa"s pharmacokinetics by increasing area under the plasma concentration versus time curve and plasma elimination half-life without significantly affecting peak levodopa concentrations. Levodopa 274-282 catechol-O-methyltransferase Homo sapiens 67-71 10555945-8 1999 These data, combined with the potential for delaying the onset of motor fluctuations, suggest that COMT inhibition may enhance levodopa"s short- and long-term efficacy. Levodopa 127-135 catechol-O-methyltransferase Homo sapiens 99-103 10608486-7 1999 In conclusion, when levodopa and carbidopa are given together, COMT inhibition becomes extremely meaningful, and dopamine levels are multiplied by tolcapone. Levodopa 20-28 catechol-O-methyltransferase Rattus norvegicus 63-67 10534246-0 1999 Dopamine D2 receptor gene polymorphism and the risk of levodopa-induced dyskinesias in PD. Levodopa 55-63 dopamine receptor D2 Homo sapiens 0-20 10774572-11 1999 In addition, by showing a paradoxical rise of PRL in response to L-dopa, which inhibits PRL secretion in physiological conditions, this study would suggest that breast cancer-related hyperprolactinemia may depend at least in part on endogenous disease-related neuroendocrine alterations. Levodopa 65-71 prolactin Homo sapiens 46-49 10774572-11 1999 In addition, by showing a paradoxical rise of PRL in response to L-dopa, which inhibits PRL secretion in physiological conditions, this study would suggest that breast cancer-related hyperprolactinemia may depend at least in part on endogenous disease-related neuroendocrine alterations. Levodopa 65-71 prolactin Homo sapiens 88-91 10591873-9 1999 Combined administrations of subthreshold doses of KW-6002 and L-dopa (50 mg/kg, PO) exerted prominent effects on haloperidol-induced and reserpine-induced catalepsy, suggesting that there may be a synergism between the adenosine A2A receptor antagonist KW-6002 and dopaminergic agents. Levodopa 62-68 adenosine A2a receptor Mus musculus 219-241 10534246-11 1999 CONCLUSIONS: Certain alleles of the short tandem repeat polymorphism of the dopamine receptor D2 gene reduce the risk of developing peak-dose dyskinesias and could contribute to varying susceptibility to develop peak-dose dyskinesias during levodopa therapy. Levodopa 241-249 dopamine receptor D2 Homo sapiens 76-96 10514096-2 1999 All 3 subjects self-administered the drug under the impression it was "synthetic heroin" and subsequently developed severe and unremitting parkinsonism, which was L-dopa responsive, at least in the earlier stages of illness. Levodopa 163-169 paired box 5 Homo sapiens 0-5 10451758-2 1999 By inhibiting the enzyme catechol-o-methyl-transferase (COMT), they prevent peripheral degradation of levodopa, allowing a higher concentration to cross the blood-brain barrier. Levodopa 102-110 catechol-O-methyltransferase Homo sapiens 25-54 11139811-5 1999 Dopamine agonists and catechol-O-methyl-transferase (COMT) inhibitors have been valuable adjuncts to levodopa, but until now levodopa has remained the cornerstone of therapy. Levodopa 101-109 catechol-O-methyltransferase Homo sapiens 22-51 11139811-5 1999 Dopamine agonists and catechol-O-methyl-transferase (COMT) inhibitors have been valuable adjuncts to levodopa, but until now levodopa has remained the cornerstone of therapy. Levodopa 101-109 catechol-O-methyltransferase Homo sapiens 53-57 10510160-1 1999 AIMS: Tolcapone is a novel catechol-O-methyltransferase (COMT) inhibitor used as an adjunct to levodopa/carbidopa or levodopa/benserazide therapy to improve treatment of Parkinson"s disease. Levodopa 95-103 catechol-O-methyltransferase Homo sapiens 27-55 10510160-1 1999 AIMS: Tolcapone is a novel catechol-O-methyltransferase (COMT) inhibitor used as an adjunct to levodopa/carbidopa or levodopa/benserazide therapy to improve treatment of Parkinson"s disease. Levodopa 95-103 catechol-O-methyltransferase Homo sapiens 57-61 11096718-5 1999 The optimal initial approach to RLS in the general patient is usually the use of a dopaminergic agent: low-dose levodopa in milder cases, a dopamine agonist in more severe ones. Levodopa 112-120 RLS1 Homo sapiens 32-35 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 88-96 catechol-O-methyltransferase Homo sapiens 0-28 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 88-96 catechol-O-methyltransferase Homo sapiens 30-34 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 201-209 catechol-O-methyltransferase Homo sapiens 0-28 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 201-209 catechol-O-methyltransferase Homo sapiens 30-34 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 201-209 catechol-O-methyltransferase Homo sapiens 0-28 12973467-1 1999 Catechol O-methyltransferase (COMT) inhibition has been proposed as a means to increase levodopa bioavailability in patients with Parkinson"s disease, which may be useful in reducing the total dose of levodopa, diminishing its frequency of administration and, more importantly, improving fluctuations in the response to each individual dose of levodopa, which usually develop after chronic treatment. Levodopa 201-209 catechol-O-methyltransferase Homo sapiens 30-34 12973467-2 1999 Entacapone is a potent, selective peripheral catechol O-methyltransferase inhibitor which effectively inhibits the O-methylation of levodopa, thus increasing its central bioavailability and potentiating its behavioral effects. Levodopa 132-140 catechol-O-methyltransferase Homo sapiens 45-73 10490854-1 1999 OBJECTIVE: To investigate the effect of L-dopa on the PLM/h index of spinal cord injured subjects. Levodopa 40-46 FXYD domain containing ion transport regulator 1 Homo sapiens 54-57 10490854-6 1999 RESULTS: The index of PLM/h on the first night of L-dopa or placebo withdrawal (phase III) was lower than on both the basal night and the first night of L-dopa treatment. Levodopa 50-56 FXYD domain containing ion transport regulator 1 Homo sapiens 22-25 10490854-6 1999 RESULTS: The index of PLM/h on the first night of L-dopa or placebo withdrawal (phase III) was lower than on both the basal night and the first night of L-dopa treatment. Levodopa 153-159 FXYD domain containing ion transport regulator 1 Homo sapiens 22-25 10490854-8 1999 Comparison between L-dopa and placebo treatments revealed that only those volunteers with an index above five revealed a reduction in PLM in L-dopa. Levodopa 19-25 FXYD domain containing ion transport regulator 1 Homo sapiens 134-137 10490854-8 1999 Comparison between L-dopa and placebo treatments revealed that only those volunteers with an index above five revealed a reduction in PLM in L-dopa. Levodopa 141-147 FXYD domain containing ion transport regulator 1 Homo sapiens 134-137 10490854-9 1999 CONCLUSION: These results indicate that despite the spinal cord lesions, L-dopa treatment is capable of minimizing PLM during sleep. Levodopa 73-79 FXYD domain containing ion transport regulator 1 Homo sapiens 115-118 10482268-2 1999 We report that the phenotype of a kindred (Family H) with autosomal dominant, levodopa-responsive parkinsonism maps to chromosomal region 4q21-23 and that affected members of this kindred harbor a previously reported mutation (G209A) in exon 4 of the alpha-synuclein gene. Levodopa 78-86 synuclein alpha Homo sapiens 251-266 10454475-0 1999 Differing effects of N-methyl-D-aspartate receptor subtype selective antagonists on dyskinesias in levodopa-treated 1-methyl-4-phenyl-tetrahydropyridine monkeys. Levodopa 99-107 glutamate ionotropic receptor NMDA type subunit 1 L homeolog Xenopus laevis 21-50 10451758-2 1999 By inhibiting the enzyme catechol-o-methyl-transferase (COMT), they prevent peripheral degradation of levodopa, allowing a higher concentration to cross the blood-brain barrier. Levodopa 102-110 catechol-O-methyltransferase Homo sapiens 56-60 10451758-4 1999 Clinical studies with COMT inhibitors have shown benefit in both stable and fluctuating PD patients with improvement in motor function with lower levodopa doses. Levodopa 146-154 catechol-O-methyltransferase Homo sapiens 22-26 10511474-2 1999 The present work was aimed to study the effect of PKC activation and protein-serine/threonine phosphatase (PP1/PP2 A) inhibition on P-glycoprotein (P-gp) mediated transport of L-DOPA in LLC-GA5 Col300 cells, a renal cell line expressing the human P-glycoprotein in the apical membrane. Levodopa 176-182 ATP binding cassette subfamily B member 1 Homo sapiens 247-261 10439935-3 1999 It has been shown to improve the clinical benefits of levodopa plus an aromatic L-amino acid decarboxylase inhibitor (AADC) when given to patients with Parkinson"s disease and end-of-dose deterioration in the response to levodopa (the "wearing off" phenomenon). Levodopa 221-229 dopa decarboxylase Homo sapiens 118-122 10821639-4 1999 AADC neurons in the human ACC might transform L-DOPA to dopamine, droxidopa to noradrenaline, and/or 5-hydroxytryptophan to serotonin. Levodopa 46-52 dopa decarboxylase Homo sapiens 0-4 10366680-11 1999 These observations complement existing knowledge, and provide novel information about AAAD that may have practical importance for Parkinson"s patients on L-DOPA therapy. Levodopa 154-160 dopa decarboxylase Homo sapiens 86-90 10511474-0 1999 P-glycoprotein phosphorylation/dephosphorylation and cellular accumulation of L-DOPA in LLC-GA5 Col300 cells. Levodopa 78-84 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 10511474-6 1999 Verapamil (25 microM), a P-glycoprotein inhibitor, markedly increased (approximately 40% increase) the accumulation of a non-saturating concentration of L-DOPA (2.5 microM) at both initial rate of uptake (IRU, 6 min incubation) and at steady-state (SS, 30 min incubation). Levodopa 153-159 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 10511474-2 1999 The present work was aimed to study the effect of PKC activation and protein-serine/threonine phosphatase (PP1/PP2 A) inhibition on P-glycoprotein (P-gp) mediated transport of L-DOPA in LLC-GA5 Col300 cells, a renal cell line expressing the human P-glycoprotein in the apical membrane. Levodopa 176-182 ATP binding cassette subfamily B member 1 Homo sapiens 132-146 10511474-13 1999 It is suggested that P-glycoprotein plays a role in regulation of intracellular availability of L-DOPA in renal epithelial cells, and phosphorylation/dephosphorylation of P-glycoprotein may be involved in the regulation of the transporter. Levodopa 96-102 ATP binding cassette subfamily B member 1 Homo sapiens 21-35 10407949-3 1999 COMT inhibitors enhance and prolong the effect of single levodopa doses. Levodopa 57-65 catechol-O-methyltransferase Homo sapiens 0-4 10332097-8 1999 In pulse-chase labelling experiments, the conversion of the amidated gastrin G34 to G17 was inhibited by biogenic amine precursors (L-DOPA and 5-hydroxytryptophan). Levodopa 132-138 gastrin Rattus norvegicus 69-76 10217296-1 1999 Tyrosine hydroxylase (TH), which converts L-tyrosine to L-DOPA, is a rate-limiting enzyme in the biosynthesis of catecholamines; its activity is regulated by feedback inhibition by catecholamine products including dopamine. Levodopa 56-62 tyrosine hydroxylase Homo sapiens 0-20 10212311-1 1999 Catecholamine neurotransmitters are synthesized by hydroxylation of tyrosine to L-dihydroxyphenylalanine (L-Dopa) by tyrosine hydroxylase (TH). Levodopa 80-104 tyrosine hydroxylase Mus musculus 117-137 10229966-0 1999 [Entacapone++ : a new catechol-O-methyltransferase inhibitor which improves the response to levodopa in patients with Parkinson disease and fluctuating motor function]. Levodopa 92-100 catechol-O-methyltransferase Homo sapiens 22-50 10212311-1 1999 Catecholamine neurotransmitters are synthesized by hydroxylation of tyrosine to L-dihydroxyphenylalanine (L-Dopa) by tyrosine hydroxylase (TH). Levodopa 80-104 tyrosine hydroxylase Mus musculus 139-141 10212311-1 1999 Catecholamine neurotransmitters are synthesized by hydroxylation of tyrosine to L-dihydroxyphenylalanine (L-Dopa) by tyrosine hydroxylase (TH). Levodopa 106-112 tyrosine hydroxylase Mus musculus 117-137 10212311-1 1999 Catecholamine neurotransmitters are synthesized by hydroxylation of tyrosine to L-dihydroxyphenylalanine (L-Dopa) by tyrosine hydroxylase (TH). Levodopa 106-112 tyrosine hydroxylase Mus musculus 139-141 10348466-1 1999 The effect of subchronic treatment with L-dopa/carbidopa or L-selegiline on striatal dopamine transporters (DAT) was examined in patients with idiopathic Parkinson"s disease with SPECT (single photon emission computed tomography) using [123I]beta-CIT (2beta-carbomethoxy-3beta-[4-iodophenyl]tropane) as the radiotracer. Levodopa 40-46 solute carrier family 6 member 3 Homo sapiens 85-106 10348466-1 1999 The effect of subchronic treatment with L-dopa/carbidopa or L-selegiline on striatal dopamine transporters (DAT) was examined in patients with idiopathic Parkinson"s disease with SPECT (single photon emission computed tomography) using [123I]beta-CIT (2beta-carbomethoxy-3beta-[4-iodophenyl]tropane) as the radiotracer. Levodopa 40-46 solute carrier family 6 member 3 Homo sapiens 108-111 10191339-0 1999 Vesicular monoamine transporter-2 and aromatic L-amino acid decarboxylase enhance dopamine delivery after L-3, 4-dihydroxyphenylalanine administration in Parkinsonian rats. Levodopa 106-135 solute carrier family 18 member A2 Rattus norvegicus 0-33 10191339-0 1999 Vesicular monoamine transporter-2 and aromatic L-amino acid decarboxylase enhance dopamine delivery after L-3, 4-dihydroxyphenylalanine administration in Parkinsonian rats. Levodopa 106-135 dopa decarboxylase Rattus norvegicus 47-73 10349502-4 1999 Levodopa caused an inhibition of mitogen-induced proliferation, stimulation of IL-6 and TNF-alpha production, whereas the secretion of IL-1 beta and IL-2 was not affected. Levodopa 0-8 interleukin 6 Homo sapiens 79-83 10349502-4 1999 Levodopa caused an inhibition of mitogen-induced proliferation, stimulation of IL-6 and TNF-alpha production, whereas the secretion of IL-1 beta and IL-2 was not affected. Levodopa 0-8 tumor necrosis factor Homo sapiens 88-97 10064831-4 1999 At the same time, levodopa treatment elevated serine phosphorylation of striatal NR2A (p<0.02), but not that of NR2B subunits, without associated changes in subunit protein levels. Levodopa 18-26 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 81-85 10193123-11 1999 L-dopa and clonazepam have been found successful in the treatment of primary RLS, though lifelong treatment is often necessary. Levodopa 0-6 RLS1 Homo sapiens 77-80 10214747-3 1999 Regional striatal dopamine transporter binding was measured in the caudate, anterior putamen, and posterior putamen of six patients with L-dopa-responsive stage 2 PD, six patients with PSP, and six age-comparable healthy controls. Levodopa 137-143 solute carrier family 6 member 3 Homo sapiens 18-38 15992091-3 1999 Entacapone (Comtan) is a selective, reversible catechol-O-methyltransferase inhibitor that dose-dependently increases the peripheral bioavailability of levodopa and prolongs its duration of action. Levodopa 152-160 catechol-O-methyltransferase Homo sapiens 47-75 10078726-4 1999 RESULTS: With the notable exception of the lowest dose of clozapine tested, coadministration of DA D1 or D2 antidopaminergic agents with L-dopa reduced the L-dopa-induced dyskinesias but also caused a return of parkinsonian disability. Levodopa 137-143 defender against cell death 1 Homo sapiens 96-101 10078726-4 1999 RESULTS: With the notable exception of the lowest dose of clozapine tested, coadministration of DA D1 or D2 antidopaminergic agents with L-dopa reduced the L-dopa-induced dyskinesias but also caused a return of parkinsonian disability. Levodopa 156-162 defender against cell death 1 Homo sapiens 96-101 10089382-1 1999 DOPA decarboxylase is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3, 4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 127-156 dopa decarboxylase Sus scrofa 0-18 10089382-1 1999 DOPA decarboxylase is responsible for the synthesis of the key neurotransmitters dopamine and serotonin via decarboxylation of L-3, 4-dihydroxyphenylalanine (L-DOPA) and L-5-hydroxytryptophan, respectively. Levodopa 158-164 dopa decarboxylase Sus scrofa 0-18 10086151-2 1999 Limitations of levodopa therapy have led to development of numerous therapeutic approaches at the level of levodopa/dopamine metabolism, dopamine receptors, dopamine transporter, and other neurotransmitter systems. Levodopa 15-23 solute carrier family 6 member 3 Homo sapiens 157-177 9930741-1 1999 Studies in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys and in parkinsonian patients show elevated preproenkephalin (PPE) mRNA levels, unaltered by chronic L-DOPA therapy, whereas preprotachykinin (PPT) mRNA levels are decreased by the lesion and corrected by L-DOPA. Levodopa 180-186 proenkephalin Homo sapiens 123-139 9930741-1 1999 Studies in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys and in parkinsonian patients show elevated preproenkephalin (PPE) mRNA levels, unaltered by chronic L-DOPA therapy, whereas preprotachykinin (PPT) mRNA levels are decreased by the lesion and corrected by L-DOPA. Levodopa 180-186 proenkephalin Homo sapiens 141-144 9930741-1 1999 Studies in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys and in parkinsonian patients show elevated preproenkephalin (PPE) mRNA levels, unaltered by chronic L-DOPA therapy, whereas preprotachykinin (PPT) mRNA levels are decreased by the lesion and corrected by L-DOPA. Levodopa 284-290 proenkephalin Homo sapiens 123-139 9930741-1 1999 Studies in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys and in parkinsonian patients show elevated preproenkephalin (PPE) mRNA levels, unaltered by chronic L-DOPA therapy, whereas preprotachykinin (PPT) mRNA levels are decreased by the lesion and corrected by L-DOPA. Levodopa 284-290 proenkephalin Homo sapiens 141-144 10069661-2 1999 Insulin secretion in response to an oral glucose tolerance test (OGTT) and a GH stimulation test by L-dopa, growth hormone-binding protein (GHBP) and IGF-I were measured. Levodopa 100-106 insulin Homo sapiens 0-7 10069661-8 1999 GH-AUC to the L-dopa stimulation test was negatively correlated with GHBP levels (r = -0.432. Levodopa 14-20 growth hormone receptor Homo sapiens 69-73 10352397-11 1999 GH response to L-dopa stimulation was blunted in all subjects and it was increased after treatment in both groups. Levodopa 15-21 growth hormone 1 Homo sapiens 0-2 10047930-1 1999 Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels. Levodopa 109-115 catechol-O-methyltransferase Homo sapiens 36-64 10047930-1 1999 Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels. Levodopa 109-115 catechol-O-methyltransferase Homo sapiens 66-70 10047930-1 1999 Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels. Levodopa 188-194 catechol-O-methyltransferase Homo sapiens 66-70 9972388-1 1999 OBJECTIVE: To review published literature investigating the efficacy and safety of levodopa in the management of restless legs syndrome (RLS), with emphasis on the hemodialysis population. Levodopa 83-91 RLS1 Homo sapiens 137-140 9972388-4 1999 STUDY SELECTION AND DATA EXTRACTION: All identified human studies investigating the use of levodopa for the management of RLS in uremic and nonuremic patients were analyzed. Levodopa 91-99 RLS1 Homo sapiens 122-125 9972388-6 1999 Although the benefits of levodopa/(carbidopa/benserazide) in reducing the signs and symptoms of RLS are documented in nonuremic patients, evidence in patients with ESRD is less readily available. Levodopa 25-33 RLS1 Homo sapiens 96-99 9972388-8 1999 CONCLUSIONS: In general, the small amount of published literature supports the empirical use of levodopa/carbidopa as a safe and effective therapy to manage the distressing symptoms of RLS in a hemodialysis population. Levodopa 96-104 RLS1 Homo sapiens 185-188 10343151-0 1999 COMT inhibition by tolcapone further improves levodopa pharmacokinetics when combined with a dual-release formulation of levodopa/benserazide. Levodopa 46-54 catechol-O-methyltransferase Homo sapiens 0-4 10343151-2 1999 The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50). Levodopa 168-176 catechol-O-methyltransferase Homo sapiens 80-109 10343151-2 1999 The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50). Levodopa 168-176 catechol-O-methyltransferase Homo sapiens 111-115 10651109-1 1999 In order to study whether the membrane hyperpolarization and firing inhibition caused by dopamine and levodopa on rat midbrain dopamine cells are affected by the inhibition of brain catechol-O-methyl-transferase (COMT), intracellular electrophysiological recordings were made from these neurons maintained in vitro. Levodopa 102-110 catechol-O-methyltransferase Rattus norvegicus 182-211 9929973-12 1999 When group I was subdivided into group A (with the A1 allele) and group B (with only the A2 allele), group A had a significantly lower peak GH response to the l-dopa test, lower levels of IGF-I, and retarded bone maturation. Levodopa 159-165 growth hormone 1 Homo sapiens 140-142 10370911-12 1999 Addition of dopamine agonists, MAO-B inhibitors, COMT inhibitors and controlled release levodopa preparations may be helpful in prolonging the duration of efficacy of each single levodopa dose. Levodopa 179-187 monoamine oxidase B Homo sapiens 31-36 10370911-12 1999 Addition of dopamine agonists, MAO-B inhibitors, COMT inhibitors and controlled release levodopa preparations may be helpful in prolonging the duration of efficacy of each single levodopa dose. Levodopa 179-187 catechol-O-methyltransferase Homo sapiens 49-53 10051176-2 1999 However, its benefits are limited owing to extensive metabolism by catechol-O-methyltransferase (COMT), especially if levodopa is used in combination with peripheral dopa-decarboxylase inhibitors. Levodopa 118-126 catechol-O-methyltransferase Homo sapiens 67-95 10210287-6 1999 Similar L-DOPA-currents were seen in oocytes co-injected with AMPA receptors, GluRs1,2,3 and 4. Levodopa 8-14 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 78-94 9917075-1 1999 Tolcapone is a selective peripheral and central catechol-O-methyltransferase (COMT) inhibitor recently approved as adjunctive therapy in patients with idiopathic Parkinson"s disease who are already being treated with a levodopa-peripheral dopa decarboxylase inhibitor (DDI) combination. Levodopa 219-227 catechol-O-methyltransferase Homo sapiens 78-82 9917075-1 1999 Tolcapone is a selective peripheral and central catechol-O-methyltransferase (COMT) inhibitor recently approved as adjunctive therapy in patients with idiopathic Parkinson"s disease who are already being treated with a levodopa-peripheral dopa decarboxylase inhibitor (DDI) combination. Levodopa 219-227 dopa decarboxylase Homo sapiens 239-257 10027744-3 1999 The results showed that Vmax values (in nmol mg protein(-1) h(-1)) for AADC, using L-DOPA as the substrate, in rat jejunal epithelial cells (127.3+/-11.4) were found to be 6-fold higher than in Caco-2 cells (22.5+/-2.6). Levodopa 83-89 dopa decarboxylase Rattus norvegicus 71-75 10579213-0 1999 Changes in the regional and compartmental distribution of FosB- and JunB-like immunoreactivity induced in the dopamine-denervated rat striatum by acute or chronic L-dopa treatment. Levodopa 163-169 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 58-62 10579213-0 1999 Changes in the regional and compartmental distribution of FosB- and JunB-like immunoreactivity induced in the dopamine-denervated rat striatum by acute or chronic L-dopa treatment. Levodopa 163-169 JunB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-72 10579213-1 1999 This study was carried out in order to examine the effects of acute or chronic L-DOPA treatment on striatally expressed FosB- and JunB-like proteins in a rat model of Parkinson"s disease. Levodopa 79-85 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 120-124 10579213-1 1999 This study was carried out in order to examine the effects of acute or chronic L-DOPA treatment on striatally expressed FosB- and JunB-like proteins in a rat model of Parkinson"s disease. Levodopa 79-85 JunB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 130-134 10579213-3 1999 Both acute and chronic L-DOPA treatment caused a pronounced, persistent increase in the number of FosB-like immunoreactive cells in the dopamine-denervated striata (five- and seven-fold increase, respectively, above the levels found in lesioned but non-drug-treated controls), but the two treatment groups differed markedly with respect to both the average amount of staining per cell, which was two-fold larger in the chronic L-DOPA cases, and the anatomical distribution of the labeled cells. Levodopa 23-29 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 98-102 10579213-3 1999 Both acute and chronic L-DOPA treatment caused a pronounced, persistent increase in the number of FosB-like immunoreactive cells in the dopamine-denervated striata (five- and seven-fold increase, respectively, above the levels found in lesioned but non-drug-treated controls), but the two treatment groups differed markedly with respect to both the average amount of staining per cell, which was two-fold larger in the chronic L-DOPA cases, and the anatomical distribution of the labeled cells. Levodopa 427-433 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 98-102 10579213-4 1999 After an acute injection of L-DOPA, FosB-positive cells were distributed rather uniformly across all striatal subregions, whereas chronic L-DOPA treatment induced discrete clusters of strongly FosB-like immunoreactive cells within medial and central striatal subregions, as well as in a large, yet sharply defined portion of the lateral caudate-putamen. Levodopa 28-34 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 36-40 10579213-4 1999 After an acute injection of L-DOPA, FosB-positive cells were distributed rather uniformly across all striatal subregions, whereas chronic L-DOPA treatment induced discrete clusters of strongly FosB-like immunoreactive cells within medial and central striatal subregions, as well as in a large, yet sharply defined portion of the lateral caudate-putamen. Levodopa 138-144 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 193-197 10579213-8 1999 Like FosB, JunB was induced in the DA-denervated striatum by both acute and chronic L-DOPA treatment, and exhibited similar distribution patterns. Levodopa 84-90 JunB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 11-15 10579213-9 1999 However, JunB did not exhibit prolonged expression kinetics, and was somewhat down-regulated in the chronically compared with the acutely L-DOPA-treated rats. Levodopa 138-144 JunB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 9-13 10579213-10 1999 The present results show that L-DOPA administration produces a long-lasting increase in the levels of FosB-, but not JunB-like immunoreactivity in the dopamine-denervated striatum. Levodopa 30-36 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 102-106 10579213-11 1999 More importantly, these data show that striatal induction of FosB- and JunB-like proteins by chronic L-DOPA treatment exhibits both regional and compartmental specificity. Levodopa 101-107 FosB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 61-65 10579213-11 1999 More importantly, these data show that striatal induction of FosB- and JunB-like proteins by chronic L-DOPA treatment exhibits both regional and compartmental specificity. Levodopa 101-107 JunB proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 71-75 10051176-2 1999 However, its benefits are limited owing to extensive metabolism by catechol-O-methyltransferase (COMT), especially if levodopa is used in combination with peripheral dopa-decarboxylase inhibitors. Levodopa 118-126 catechol-O-methyltransferase Homo sapiens 97-101 10051176-5 1999 Preclinical and clinical studies have shown that COMT inhibitors markedly enhance levodopa availability and prolong its plasma half-life. Levodopa 82-90 catechol-O-methyltransferase Homo sapiens 49-53 10051176-8 1999 COMT inhibition promises to become an important means of extending the benefits of levodopa therapy in PD. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 0-4 10189264-0 1998 Improvement of L-dopa absorption by dipeptidyl derivation, utilizing peptide transporter PepT1. Levodopa 15-21 solute carrier family 15 member 1 Homo sapiens 89-94 9851438-1 1998 Autosomal recessive juvenile parkinsonism (AR-JP) is a distinct clinical and genetic entity characterized by selective degeneration of nigral dopaminergic neurons and young-onset parkinsonism with remarkable response to levodopa. Levodopa 220-228 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-48 10189264-1 1998 In the present study, possible enhancement of intestinal absorption of L-dopa by utilizing intestinal peptide transporter was examined using Caco-2 cells and Xenopus oocytes expressing human peptide transporter (hPepT1). Levodopa 71-77 solute carrier family 15 member 1 Homo sapiens 212-218 9855559-0 1998 Antiparkinsonian and anti-levodopa-induced dyskinesia effects obtained by stimulating the same site within the GPi in PD. Levodopa 26-34 glucose-6-phosphate isomerase Homo sapiens 111-114 9824689-5 1998 Selective blockade of NR2B subunits with ACEA 10-1244, but not of NR2A subunits with MDL 100,453, reversed the l-DOPA-induced response alterations. Levodopa 111-117 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 22-26 9869170-5 1998 This hypothesis is supported by the finding that the purinergic receptor antagonist ARL 66096, an ATP analogue, reduces in a concentration-dependent fashion the PLD response to thrombin (IC50=28 nM with 0.1 U/ml thrombin). Levodopa 84-87 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 161-164 9869170-5 1998 This hypothesis is supported by the finding that the purinergic receptor antagonist ARL 66096, an ATP analogue, reduces in a concentration-dependent fashion the PLD response to thrombin (IC50=28 nM with 0.1 U/ml thrombin). Levodopa 84-87 coagulation factor II, thrombin Homo sapiens 177-185 9869170-5 1998 This hypothesis is supported by the finding that the purinergic receptor antagonist ARL 66096, an ATP analogue, reduces in a concentration-dependent fashion the PLD response to thrombin (IC50=28 nM with 0.1 U/ml thrombin). Levodopa 84-87 coagulation factor II, thrombin Homo sapiens 212-220 9826227-1 1998 The efficacy of levo-DOPA in the treatment of Parkinson"s disease is potentiated by blockade of its peripheral metabolism with inhibitors of catechol-O-methyltransferase (COMT). Levodopa 16-25 catechol O-methyltransferase Macaca fascicularis 141-169 9826227-1 1998 The efficacy of levo-DOPA in the treatment of Parkinson"s disease is potentiated by blockade of its peripheral metabolism with inhibitors of catechol-O-methyltransferase (COMT). Levodopa 16-25 catechol O-methyltransferase Macaca fascicularis 171-175 9826227-3 1998 We used positron emission tomography (PET) to test the effects of these two COMT inhibitors on the plasma kinetics and brain metabolism of the levo-DOPA analog 6-[18F]fluoro-L-dopa (FDOPA) in cynomolgus monkeys, employing a compartmental model for the assay of DOPA decarboxylase activity in living brain. Levodopa 143-152 catechol O-methyltransferase Macaca fascicularis 76-80 9824689-7 1998 Taken together, these results suggest that augmented tyrosine phosphorylation of NR2B subunits, alone or in combination with the smaller rise in NR2A subunit phosphorylation, contributes to the apparent enhancement in striatal NMDAR sensitivity and thus to the plastic alterations in dopaminergic responses in l-DOPA-treated parkinsonian rats. Levodopa 310-316 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 81-85 9749568-6 1998 By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. Levodopa 118-126 monoamine oxidase B Homo sapiens 13-38 9853519-3 1998 Tyrosine hydroxylase (TH) catalyzes the synthesis of L-dopa, which must be converted to dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 53-59 tyrosine hydroxylase Rattus norvegicus 0-20 9853519-3 1998 Tyrosine hydroxylase (TH) catalyzes the synthesis of L-dopa, which must be converted to dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 53-59 dopa decarboxylase Rattus norvegicus 109-135 9853519-3 1998 Tyrosine hydroxylase (TH) catalyzes the synthesis of L-dopa, which must be converted to dopamine by aromatic L-amino acid decarboxylase (AADC). Levodopa 53-59 dopa decarboxylase Rattus norvegicus 137-141 10079942-1 1998 To increase the solubility of L-3,4-dihydroxyphenylalanine (DOPA) and dopamine (DA) incorporated in liposomes, it was suggested to convert them into ammonium and 1-adamantylammonium borate complexes. Levodopa 60-64 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 30-33 9770541-9 1998 Behaviorally, Atm-deficient mice expressed locomotor abnormalities manifested as stride-length asymmetry, which could be corrected by peripheral application of the dopaminergic precursor L-dopa. Levodopa 187-193 ataxia telangiectasia mutated Mus musculus 14-17 9818851-3 1998 BACKGROUND: Entacapone is a catechol-O-methyltransferase (COMT) inhibitor that has been shown to increase the area under the concentration-time curve of plasma levodopa by decreasing its systemic elimination, thereby promoting and improving therapeutic response to it. Levodopa 160-168 catechol-O-methyltransferase Homo sapiens 28-56 9818851-3 1998 BACKGROUND: Entacapone is a catechol-O-methyltransferase (COMT) inhibitor that has been shown to increase the area under the concentration-time curve of plasma levodopa by decreasing its systemic elimination, thereby promoting and improving therapeutic response to it. Levodopa 160-168 catechol-O-methyltransferase Homo sapiens 58-62 9765511-4 1998 L-DOPA potentiated the outgrowth of processes elicited by NGF. Levodopa 0-6 nerve growth factor Homo sapiens 58-61 9765511-8 1998 L-DOPA potentiation of NGF response was important functionally as seen by increased quantal neurotransmitter release from the L-DOPA/NGF-treated neurite varicosities, which displayed both 2-fold greater quantal size and frequency of quantal release. Levodopa 0-6 nerve growth factor Homo sapiens 23-26 9765511-8 1998 L-DOPA potentiation of NGF response was important functionally as seen by increased quantal neurotransmitter release from the L-DOPA/NGF-treated neurite varicosities, which displayed both 2-fold greater quantal size and frequency of quantal release. Levodopa 0-6 nerve growth factor Homo sapiens 133-136 9765511-8 1998 L-DOPA potentiation of NGF response was important functionally as seen by increased quantal neurotransmitter release from the L-DOPA/NGF-treated neurite varicosities, which displayed both 2-fold greater quantal size and frequency of quantal release. Levodopa 126-132 nerve growth factor Homo sapiens 23-26 9765511-8 1998 L-DOPA potentiation of NGF response was important functionally as seen by increased quantal neurotransmitter release from the L-DOPA/NGF-treated neurite varicosities, which displayed both 2-fold greater quantal size and frequency of quantal release. Levodopa 126-132 nerve growth factor Homo sapiens 133-136 9710269-2 1998 Aromatic L-amino acid decarboxylase (AADC) is a regulated enzyme that catalyzes the decarboxylation of 3,4-dihydroxyphenylalanine (L-Dopa). Levodopa 131-137 dopa decarboxylase Rattus norvegicus 0-35 9741587-2 1998 We investigated the role of glutathione peroxidase (GSHPx) in cellular defense against L-DOPA cytotoxicity. Levodopa 87-93 glutathione peroxidase 1 Rattus norvegicus 52-57 9741587-5 1998 Transfectants over expressing GSHPx were also significantly more resistant to exposure to either L-DOPA or t-butyl hydroperoxide than mock-transfected cells. Levodopa 97-103 glutathione peroxidase 1 Rattus norvegicus 30-35 9710269-2 1998 Aromatic L-amino acid decarboxylase (AADC) is a regulated enzyme that catalyzes the decarboxylation of 3,4-dihydroxyphenylalanine (L-Dopa). Levodopa 131-137 dopa decarboxylase Rattus norvegicus 37-41 9710269-6 1998 The results suggest that the stimulation of AADC mRNA by amantadine may be one of its effects on dopamine metabolism that may have relevance for potentiation of L-Dopa therapy in Parkinsonism. Levodopa 161-167 dopa decarboxylase Rattus norvegicus 44-48 9741396-8 1998 Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson"s disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson"s disease in addition to post-encephalitic parkinsonism as a supportive drug of L-DOPA. Levodopa 325-331 thyrotropin releasing hormone Homo sapiens 187-190 10082378-7 1998 The gene product, fragmentary AADC, was still active with L-dopa as substrate, but its k(cat) value was decreased 57-fold, and the Km value was increased 9-fold compared with those of the wild-type AADC. Levodopa 58-64 dopa decarboxylase Homo sapiens 198-202 9708959-2 1998 OBJECTIVE: To assess the efficacy and tolerability of the catechol-O-methyltransferase inhibitor tolcapone in reducing "off/on" fluctuations in levodopa-treated parkinsonian patients. Levodopa 144-152 catechol-O-methyltransferase Homo sapiens 58-86 9706728-0 1998 Platelet monoamine oxidase B activity in "de novo" and l-dopa treated parkinsonian patients and controls. Levodopa 55-61 monoamine oxidase B Homo sapiens 9-28 9767399-0 1998 L-DOPA-induced dyskinesia in the rat is associated with striatal overexpression of prodynorphin- and glutamic acid decarboxylase mRNA. Levodopa 0-6 prodynorphin Rattus norvegicus 83-95 9767399-6 1998 Among all these markers, PDyn mRNA levels showed the most pronounced treatment-dependence (three times higher in the L-DOPA-treated group than in saline-injected lesion-only controls), and the strongest correlation with the rats" dyskinesia scores (r2 = 0.82). Levodopa 117-123 prodynorphin Rattus norvegicus 25-29 9767399-8 1998 The results show that L-DOPA-induced dyskinesia is associated with overexpression of PDyn and GAD67 mRNA in the striatal projection neurons, and GAD67 mRNA levels in the globus pallidus. Levodopa 22-28 prodynorphin Rattus norvegicus 85-89 9767399-8 1998 The results show that L-DOPA-induced dyskinesia is associated with overexpression of PDyn and GAD67 mRNA in the striatal projection neurons, and GAD67 mRNA levels in the globus pallidus. Levodopa 22-28 glutamate decarboxylase 1 Rattus norvegicus 94-99 9767399-8 1998 The results show that L-DOPA-induced dyskinesia is associated with overexpression of PDyn and GAD67 mRNA in the striatal projection neurons, and GAD67 mRNA levels in the globus pallidus. Levodopa 22-28 glutamate decarboxylase 1 Rattus norvegicus 145-150 10343976-7 1998 The present findings support that one of the effects of L-deprenyl may be to facilitate the decarboxylation of L-DOPA by increasing the availability of AADC. Levodopa 111-117 dopa decarboxylase Rattus norvegicus 152-156 10082378-7 1998 The gene product, fragmentary AADC, was still active with L-dopa as substrate, but its k(cat) value was decreased 57-fold, and the Km value was increased 9-fold compared with those of the wild-type AADC. Levodopa 58-64 dopa decarboxylase Homo sapiens 30-34 9686769-1 1998 We report three patients with bilateral GPi stimulation for stage 4 Parkinson"s disease (PD) with severe levodopa-induced dyskinesias (LID). Levodopa 105-113 glucose-6-phosphate isomerase Homo sapiens 40-43 9667588-3 1998 We conducted genomic DNA sequencing of the GCH gene in two patients (Cases 1 and 2) manifesting generalized dystonia responsive to levodopa and severe developmental motor delay. Levodopa 131-139 GTP cyclohydrolase 1 Homo sapiens 43-46 9667588-8 1998 Our data demonstrate a new phenotype of GCH deficiency associated with compound heterozygosity for GCH gene mutations and suggest the usefulness of combined BH4 and levodopa therapy for this disorder. Levodopa 165-173 GTP cyclohydrolase 1 Homo sapiens 40-43 9695725-3 1998 Doses of 50, 100, 200, or 400 mg entacapone or placebo were given with the patient"s individual levodopa-dopa decarboxylase inhibitor dose. Levodopa 96-104 dopa decarboxylase Homo sapiens 105-123 9628761-2 1998 As GTPCHI is a rate-limiting enzyme in the pathway for synthesis of the essential TH cofactor, tetrahydrobiopterin (BH4), only hTH2 and GTPCHI cotransduced cultured cells produced L-DOPA in the absence of added BH4. Levodopa 180-186 GTP cyclohydrolase 1 Rattus norvegicus 3-9 9667783-2 1998 We measured the P300 in 37 non-demented patients with Parkinson"s disease (19 de novo and 18 levodopa-treated) and 15 age-matched healthy volunteers. Levodopa 93-101 E1A binding protein p300 Homo sapiens 16-20 9667783-6 1998 The levodopa therapy for 6-12 months significantly shortened the P300 latency and reduced the UPDRS-motor examination score in de novo patients. Levodopa 4-12 E1A binding protein p300 Homo sapiens 65-69 9628761-4 1998 Microdialysis experiments showed that those subjects that received cells cotransduced with hTH2 and hGTPCHI produced significantly higher levels of L-DOPA than animals that received either hTH2 or untransduced cells. Levodopa 148-154 GTP cyclohydrolase 1 Homo sapiens 100-107 9592104-6 1998 Microdialysis experiments indicated that only those lesioned animals that received the mixture of MD-TH and MD-GTPCHI vector displayed BH4 independent in vivo L-DOPA production (mean approximately 4-7 ng/ml). Levodopa 159-165 GTP cyclohydrolase 1 Homo sapiens 111-117 9703425-0 1998 A common point mutation in the tyrosine hydroxylase gene in autosomal recessive L-DOPA-responsive dystonia in the Dutch population. Levodopa 80-86 tyrosine hydroxylase Homo sapiens 31-51 9703425-1 1998 This report concerns one new mutation in the tyrosine hydroxylase (TH) gene in three patients originating from three unrelated Dutch families with autosomal recessive L-DOPA-responsive dystonia (DRD). Levodopa 167-173 tyrosine hydroxylase Homo sapiens 45-65 9703425-1 1998 This report concerns one new mutation in the tyrosine hydroxylase (TH) gene in three patients originating from three unrelated Dutch families with autosomal recessive L-DOPA-responsive dystonia (DRD). Levodopa 167-173 tyrosine hydroxylase Homo sapiens 67-69 9633679-5 1998 In the early 1970s, the advantages of adding a dopa decarboxylase inhibitor to treatment were discovered--reducing side effects and gaining better symptom control--and the first levodopa combination, carbidopa/levodopa, became commercially available in 1975. Levodopa 178-186 dopa decarboxylase Homo sapiens 47-65 9633684-0 1998 Extending levodopa action: COMT inhibition. Levodopa 10-18 catechol-O-methyltransferase Homo sapiens 27-31 9633679-5 1998 In the early 1970s, the advantages of adding a dopa decarboxylase inhibitor to treatment were discovered--reducing side effects and gaining better symptom control--and the first levodopa combination, carbidopa/levodopa, became commercially available in 1975. Levodopa 210-218 dopa decarboxylase Homo sapiens 47-65 9633684-3 1998 Therefore, inhibiting COMT activity is one method of extending the action of levodopa. Levodopa 77-85 catechol-O-methyltransferase Homo sapiens 22-26 9633684-5 1998 COMT inhibitors increase patients" duration of response to levodopa and reduce response fluctuations. Levodopa 59-67 catechol-O-methyltransferase Homo sapiens 0-4 9633680-3 1998 Levodopa is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase (COMT). Levodopa 0-8 dopa decarboxylase Homo sapiens 70-105 9633680-3 1998 Levodopa is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase (COMT). Levodopa 0-8 dopa decarboxylase Homo sapiens 107-111 9633680-3 1998 Levodopa is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase (COMT). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 117-145 9633680-3 1998 Levodopa is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase (COMT). Levodopa 0-8 catechol-O-methyltransferase Homo sapiens 147-151 9633680-4 1998 Because gastric AADC and COMT degrade levodopa, the drug is given with inhibitors of AADC (carbidopa or benserazide), and inhibitors of COMT will also enter clinical use. Levodopa 38-46 dopa decarboxylase Homo sapiens 16-20 9633680-4 1998 Because gastric AADC and COMT degrade levodopa, the drug is given with inhibitors of AADC (carbidopa or benserazide), and inhibitors of COMT will also enter clinical use. Levodopa 38-46 catechol-O-methyltransferase Homo sapiens 25-29 9585350-8 1998 Furthermore, the density of TH-positive fibers observed in moderately lesioned rats was higher in those treated chronically with levodopa than in those receiving vehicle. Levodopa 129-137 tyrosine hydroxylase Rattus norvegicus 28-30 9682265-1 1998 Catechol O-methyltransferase (COMT) inactivates neurotransmitters, hormones and drugs such as levodopa. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 0-28 9682265-1 1998 Catechol O-methyltransferase (COMT) inactivates neurotransmitters, hormones and drugs such as levodopa. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 30-34 9593981-0 1998 Stimulatory effects of 4-methylcatechol, dopamine and levodopa on the expression of metallothionein-III (GIF) mRNA in immortalized mouse brain glial cells (VR-2g). Levodopa 54-62 metallothionein 3 Mus musculus 84-103 9593981-0 1998 Stimulatory effects of 4-methylcatechol, dopamine and levodopa on the expression of metallothionein-III (GIF) mRNA in immortalized mouse brain glial cells (VR-2g). Levodopa 54-62 cobalamin binding intrinsic factor Mus musculus 105-108 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 36-44 nerve growth factor Mus musculus 111-130 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 36-44 nerve growth factor Mus musculus 132-135 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 36-44 metallothionein 3 Mus musculus 174-180 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 46-75 nerve growth factor Mus musculus 111-130 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 46-75 nerve growth factor Mus musculus 132-135 9593981-4 1998 4-Methylcatechol, dopamine (DA) and levodopa (l-3, 4-dihydroxyphenylalanine), which stimulate the synthesis of nerve growth factor (NGF), further increased the expression of MT-III mRNA in VR-2g cells. Levodopa 46-75 metallothionein 3 Mus musculus 174-180 9626667-2 1998 As tyrosine hydroxylase (TH) catalyses the formation of L-DOPA, the rate-limiting step in the biosynthesis of DA, the disease can be considered as a TH-deficiency syndrome of the striatum. Levodopa 56-62 tyrosine hydroxylase Homo sapiens 3-23 9626667-2 1998 As tyrosine hydroxylase (TH) catalyses the formation of L-DOPA, the rate-limiting step in the biosynthesis of DA, the disease can be considered as a TH-deficiency syndrome of the striatum. Levodopa 56-62 tyrosine hydroxylase Homo sapiens 25-27 9626667-3 1998 Similarly, some patients with hereditary L-DOPA-responsive dystonia, a neurological disorder with clinical similarities to PD, have mutations in the TH gene and decreased TH activity and/or stability. Levodopa 41-47 tyrosine hydroxylase Homo sapiens 149-151 9626667-3 1998 Similarly, some patients with hereditary L-DOPA-responsive dystonia, a neurological disorder with clinical similarities to PD, have mutations in the TH gene and decreased TH activity and/or stability. Levodopa 41-47 tyrosine hydroxylase Homo sapiens 171-173 9626667-6 1998 Recently, it has been demonstrated that L-DOPA is effectively oxidized by mammalian TH in vitro, possibly contributing to the cytotoxic effects of DOPA. Levodopa 40-46 tyrosine hydroxylase Homo sapiens 84-86 9585355-1 1998 From using in vitro intracellular recordings from mesencephalic neurons and monoamine-depleted rats, we report that the functions of levodopa in the brain are greatly enhanced and prolonged by high doses of the monoamine oxidase (MAO) inhibitor deprenyl. Levodopa 133-141 monoamine oxidase A Rattus norvegicus 211-228 9585355-1 1998 From using in vitro intracellular recordings from mesencephalic neurons and monoamine-depleted rats, we report that the functions of levodopa in the brain are greatly enhanced and prolonged by high doses of the monoamine oxidase (MAO) inhibitor deprenyl. Levodopa 133-141 monoamine oxidase A Rattus norvegicus 230-233 9585355-5 1998 The great increase in levodopa responses by deprenyl suggests a likely therapeutic use of this dopamine precursor with a higher dosage of the MAO inhibitor, to reduce effectively the daily levodopa requirements in Parkinson"s disease patients. Levodopa 22-30 monoamine oxidase A Rattus norvegicus 142-145 9644287-4 1998 The results supported the effectiveness of levodopa therapy in improving lip function. Levodopa 43-51 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 73-76 9591841-1 1998 Tyrosine hydroxylase of catecholamine neurons catalyzes the synthesis of 3,4-dihydroxphenylalanine (DOPA), which is subsequently metabolized to dopamine by DOPA decarboxylase (DDC). Levodopa 100-104 dopa decarboxylase Rattus norvegicus 156-174 9591516-4 1998 This review focuses on the role of the new catechol O-methyltransferase (COMT) inhibitors tolcapone and entacapone as adjuncts to levodopa therapy. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 43-71 9591516-4 1998 This review focuses on the role of the new catechol O-methyltransferase (COMT) inhibitors tolcapone and entacapone as adjuncts to levodopa therapy. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 73-77 9591519-0 1998 Influence of COMT inhibition on levodopa pharmacology and therapy. Levodopa 32-40 catechol-O-methyltransferase Homo sapiens 13-17 9591519-1 1998 Catechol O-methyltransferase (COMT) is an important enzyme that is linked directly to therapy with levodopa. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 0-28 9591519-1 1998 Catechol O-methyltransferase (COMT) is an important enzyme that is linked directly to therapy with levodopa. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 30-34 9591519-4 1998 With COMT inhibition, greater peripheral bioavailability of levodopa occurs in humans without an enhancement of peak plasma levels. Levodopa 60-68 catechol-O-methyltransferase Homo sapiens 5-9 9591519-5 1998 It is reasonable to suggest that COMT inhibition will be associated with prolonged effects of levodopa in PD, without increased peak dose toxicity in the form of dyskinesias and hallucinations. Levodopa 94-102 catechol-O-methyltransferase Homo sapiens 33-37 9591520-1 1998 Tolcapone is a potent, reversible inhibitor of catechol O-methyltransferase (COMT) intended for use as an adjunct to levodopa therapy for Parkinson"s disease (PD). Levodopa 117-125 catechol-O-methyltransferase Homo sapiens 47-75 9591522-0 1998 Catechol-O-methyltransferase inhibition with tolcapone reduces the "wearing off" phenomenon and levodopa requirements in fluctuating parkinsonian patients. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 0-28 9591522-2 1998 Inhibition of catechol-O-methyltransferase by tolcapone has been shown to increase levodopa bioavailability and plasma elimination half life, thereby prolonging the efficacy of levodopa. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 14-42 9591522-2 1998 Inhibition of catechol-O-methyltransferase by tolcapone has been shown to increase levodopa bioavailability and plasma elimination half life, thereby prolonging the efficacy of levodopa. Levodopa 177-185 catechol-O-methyltransferase Homo sapiens 14-42 9545000-8 1998 Conventional treatment of BH4 deficiency, i.e. BH4, 5-hydroxytryptophan, and L-DOPA/carbidopa (the last named given in three doses per day), suppresses prolactin levels merely for a few hours. Levodopa 77-83 prolactin Homo sapiens 152-161 9545000-9 1998 L-DOPA/carbidopa given at shorter intervals or, even better, as a slow release preparation, is more effective in suppressing prolactin levels. Levodopa 0-6 prolactin Homo sapiens 125-134 9545000-12 1998 Treatment with an L-DOPA/carbidopa slow release preparation produces virtually normal prolactin levels. Levodopa 18-24 prolactin Homo sapiens 86-95 9591841-1 1998 Tyrosine hydroxylase of catecholamine neurons catalyzes the synthesis of 3,4-dihydroxphenylalanine (DOPA), which is subsequently metabolized to dopamine by DOPA decarboxylase (DDC). Levodopa 100-104 dopa decarboxylase Rattus norvegicus 176-179 9591841-7 1998 The rate constant for the clearance of DOPA from brain (0.06 min(-1)) and earlier estimates of the rate constant of DDC activity in striatum (0.26 min(-1)) together predict that 80% of DOPA formed in normal rat striatum normally is available for dopamine synthesis. Levodopa 39-43 dopa decarboxylase Rattus norvegicus 116-119 9591841-7 1998 The rate constant for the clearance of DOPA from brain (0.06 min(-1)) and earlier estimates of the rate constant of DDC activity in striatum (0.26 min(-1)) together predict that 80% of DOPA formed in normal rat striatum normally is available for dopamine synthesis. Levodopa 185-189 dopa decarboxylase Rattus norvegicus 116-119 9591841-8 1998 It follows that modulation of DDC activity can influence the rate of DA synthesis by affecting the relative magnitude of the several fates of DOPA in living brain. Levodopa 142-146 dopa decarboxylase Rattus norvegicus 30-33 9591224-1 1998 Clinical pharmacology studies have shown that the catechol-O-methyltransferase inhibitor tolcapone increases the bioavailability area under the plasma concentration-time curve (AUC) and the plasma elimination half-life (t1/2) of levodopa. Levodopa 229-237 catechol-O-methyltransferase Homo sapiens 50-78 9644287-5 1998 In particular, lip pressures recorded during both speech and nonspeech tasks tended to improve after levodopa administration, the lip measures improving somewhat in parallel with the rise and fall of blood plasma levodopa concentrations. Levodopa 101-109 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 15-18 9644287-5 1998 In particular, lip pressures recorded during both speech and nonspeech tasks tended to improve after levodopa administration, the lip measures improving somewhat in parallel with the rise and fall of blood plasma levodopa concentrations. Levodopa 213-221 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 15-18 9469505-8 1998 In addition, the RLS group received a significantly higher number and dosage of psychopharmacological drugs, (ie, L-DOPA), than patients without RLS. Levodopa 114-120 RLS1 Homo sapiens 17-20 9555017-5 1998 In response to NSD-1015 (an inhibitor of aromatic L-amino acid decarboxylase, AADC), 5-hydroxytryptophan (5-HTP) levels were substantially elevated in the SN grafted striata as compared with those in the sham grafted controls, which continued even after subsequent administration of L-3,4-dihydroxyphenylalanine (L-DOPA, 100 mg/kg i.p.). Levodopa 283-311 dopa decarboxylase Rattus norvegicus 78-82 9555017-5 1998 In response to NSD-1015 (an inhibitor of aromatic L-amino acid decarboxylase, AADC), 5-hydroxytryptophan (5-HTP) levels were substantially elevated in the SN grafted striata as compared with those in the sham grafted controls, which continued even after subsequent administration of L-3,4-dihydroxyphenylalanine (L-DOPA, 100 mg/kg i.p.). Levodopa 313-319 dopa decarboxylase Rattus norvegicus 78-82 9583205-4 1998 Growth hormone stimulation tests were done with L-dopa and clonidine before or during acidosis therapy and after the correction of metabolic acidosis. Levodopa 48-54 growth hormone 1 Homo sapiens 0-14 9327843-0 1998 Mutations in the tyrosine hydroxylase gene cause various forms of L-dopa-responsive dystonia. Levodopa 66-72 tyrosine hydroxylase Homo sapiens 17-37 9750925-0 1998 Tetrahydrobiopterin metabolism and GTP cyclohydrolase I mutations in L-dopa-responsive dystonia. Levodopa 69-75 GTP cyclohydrolase 1 Homo sapiens 35-55 9442040-10 1998 ADP or 2-methyl(thio)-ADP-induced intracellular calcium increases were inhibited by the P2Y1 receptor-specific antagonists, adenosine 3"-phosphate 5"-phosphosulfate (A3P5PS), adenosine 3"-phosphate 5"-phosphate (A3P5P), and adenosine 2"-phosphate 5"-phosphate (A2P5P), in a concentration-dependent manner, but not by ARL 66096 or alpha, beta-MeATP. Levodopa 317-320 purinergic receptor P2Y1 Homo sapiens 88-101 9871440-1 1998 This study examines the hypothesis that glutamate tonically suppresses the activity of the enzyme aromatic L-amino acid decarboxylase (AADC), and hence the biosynthesis of dopamine, to explain how antagonists of glutamate receptors might potentiale the motor actions of L-DOPA in animal models of Parkinson"s disease. Levodopa 270-276 dopa decarboxylase Rattus norvegicus 98-133 9458818-6 1998 We have recently shown that chronic ACE inhibition decreases proximal tubule AT1R expression and have also shown that chronic L-3,4-dihydroxyphenylalamine (L-DOPA) administration inhibits AT1R expression in adult Sprague-Dawley proximal tubule and cultured proximal tubule, and this inhibition is mediated via Gs-coupled DA1 receptors. Levodopa 156-162 angiotensin II receptor, type 1a Rattus norvegicus 188-192 9458818-8 1998 Immunoreactive proximal tubule AT1R expression also was increased in 4 wk SHR and was reversed with captopril or L-DOPA treatment. Levodopa 113-119 angiotensin II receptor, type 1a Rattus norvegicus 31-35 9458818-9 1998 Therefore, these results indicate that young, but not adult, SHR have increased expression of proximal tubule AT1R and that chronic L-DOPA or captopril treatment decreased the elevated AT1R expression to control levels. Levodopa 132-138 angiotensin II receptor, type 1a Rattus norvegicus 185-189 9871440-1 1998 This study examines the hypothesis that glutamate tonically suppresses the activity of the enzyme aromatic L-amino acid decarboxylase (AADC), and hence the biosynthesis of dopamine, to explain how antagonists of glutamate receptors might potentiale the motor actions of L-DOPA in animal models of Parkinson"s disease. Levodopa 270-276 dopa decarboxylase Rattus norvegicus 135-139 9720967-1 1998 Putative modulatory effects of L-3,4-dihydroxyphenylalanine (L-DOPA) on D2 dopamine receptor function in the striatum of anaesthetised rats were investigated using both in vivo microdialysis and positron emission tomography (PET) with carbon-11 labelled raclopride as a selective D2 receptor ligand. Levodopa 31-59 dopamine receptor D2 Rattus norvegicus 72-92 9483165-6 1998 In theory, long-acting direct dopamine D2 receptor agonists that also stimulate the D1 receptor should provide a satisfactory alternative to levodopa without the above-mentioned drawbacks. Levodopa 141-149 dopamine receptor D2 Homo sapiens 30-50 9609994-1 1998 Autosomal recessive juvenile parkinsonism (AR-JP) (MIM 600116) is a hereditary neurodegenerative disorder characterized by levodopa-responsive parkinsonism with a mean age at onset of 23.2 years. Levodopa 123-131 parkin RBR E3 ubiquitin protein ligase Homo sapiens 43-48 9564628-0 1998 Increased striatal dopamine production from L-DOPA following selective inhibition of monoamine oxidase B by R(+)-N-propargyl-1-aminoindan (rasagiline) in the monkey. Levodopa 44-50 monoamine oxidase B Macaca mulatta 85-104 9720967-1 1998 Putative modulatory effects of L-3,4-dihydroxyphenylalanine (L-DOPA) on D2 dopamine receptor function in the striatum of anaesthetised rats were investigated using both in vivo microdialysis and positron emission tomography (PET) with carbon-11 labelled raclopride as a selective D2 receptor ligand. Levodopa 61-67 dopamine receptor D2 Rattus norvegicus 72-92 9616770-1 1997 Taken together with electrophysiological data, these results suggest that in states of DA deficiency, systemically administered L-dopa or DA agonist drugs inhibit cell firing in the major output nuclei of the basal ganglia (GPI and SNPR). Levodopa 128-134 glucose-6-phosphate isomerase Homo sapiens 224-227 9489509-8 1998 In conclusion, the results presented here confirm the presence of both MAO-A and MAO-B activity in renal tubular epithelial cells, that MAO-A is the predominant enzyme involved in the deamination of the natriuretic hormone dopamine and that the deamination of newly-formed dopamine is a time-dependent process which occurs early after the decarboxylation of L-DOPA. Levodopa 358-364 monoamine oxidase B Rattus norvegicus 81-86 9489509-8 1998 In conclusion, the results presented here confirm the presence of both MAO-A and MAO-B activity in renal tubular epithelial cells, that MAO-A is the predominant enzyme involved in the deamination of the natriuretic hormone dopamine and that the deamination of newly-formed dopamine is a time-dependent process which occurs early after the decarboxylation of L-DOPA. Levodopa 358-364 monoamine oxidase A Rattus norvegicus 136-141 9396158-10 1997 The urinary excretion of endogenous DA-Fp increased in a rabbit given L-DOPA. Levodopa 70-76 CD55 molecule (Cromer blood group) Homo sapiens 36-41 9403227-1 1997 Tolcapone (Ro 40-7592) is a novel inhibitor of catechol-O-methyltransferase that is being developed for clinical use in the treatment of Parkinson"s disease as add-on therapy to a combination of levodopa and a peripheral amino acid decarboxylase inhibitor (benserazide or carbidopa). Levodopa 195-203 catechol-O-methyltransferase Homo sapiens 47-75 9392574-3 1997 Entacapone, a peripherally acting, reversible inhibitor of catechol-O-methyltransferase, slows the elimination of levodopa in humans by reducing the formation of 3-O-methyldopa. Levodopa 114-122 catechol-O-methyltransferase Homo sapiens 59-87 9349551-6 1997 Grafts containing aromatic L-amino acid decarboxylase produced less L-DOPA and dopamine as monitored by microdialysis. Levodopa 68-74 dopa decarboxylase Rattus norvegicus 18-53 9349551-7 1997 These findings indicate that not only is there sufficient aromatic L-amino acid decarboxylase near striatal grafts producing L-DOPA, but also the close proximity of the enzyme to tyrosine hydroxylase is detrimental for optimal dopamine production. Levodopa 125-131 dopa decarboxylase Rattus norvegicus 58-93 9354586-8 1997 A third group, which consisted of levodopa, D-penicillamine, and muzolimine, inhibited PLK using PL, but not PM, as substrate. Levodopa 34-42 pyridoxal kinase Homo sapiens 87-90 9367815-6 1997 Kinetic constants Km and Vmax of recombinant AADC for the natural substrates L-dihydroxyphenylalanine and 5-hydroxytryptamine were 0.14 mM and 8444 U/mg, and 0.066 mM and 1813 U/mg, respectively. Levodopa 77-101 dopa decarboxylase Rattus norvegicus 45-49 9326301-0 1997 L-DOPA is a substrate for tyrosine hydroxylase. Levodopa 0-6 tyrosine hydroxylase Homo sapiens 26-46 9337447-13 1997 The COMT inhibitors, tolcapone and entacapone, improve the pharmacokinetics of levodopa by preventing its peripheral catabolism and increasing the concentration of brain dopamine; thus, these agents may reduce the incidence of "wearing-off" effects associated with the short half-life of levodopa and the progression of Parkinson"s disease. Levodopa 79-87 catechol-O-methyltransferase Homo sapiens 4-8 9337447-13 1997 The COMT inhibitors, tolcapone and entacapone, improve the pharmacokinetics of levodopa by preventing its peripheral catabolism and increasing the concentration of brain dopamine; thus, these agents may reduce the incidence of "wearing-off" effects associated with the short half-life of levodopa and the progression of Parkinson"s disease. Levodopa 288-296 catechol-O-methyltransferase Homo sapiens 4-8 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 62-86 tyrosine hydroxylase Homo sapiens 27-47 9343116-0 1997 Catechol-O-methyltransferase inhibition with tolcapone reduces the "wearing off" phenomenon and levodopa requirements in fluctuating parkinsonian patients. Levodopa 96-104 catechol-O-methyltransferase Homo sapiens 0-28 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 62-86 tyrosine hydroxylase Homo sapiens 49-51 9343116-2 1997 Inhibition of catechol-O-methyltransferase by tolcapone has been shown to increase levodopa bioavailability and plasma elimination half life, thereby prolonging the efficacy of levodopa. Levodopa 83-91 catechol-O-methyltransferase Homo sapiens 14-42 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 62-86 tyrosine hydroxylase Homo sapiens 219-221 9343116-2 1997 Inhibition of catechol-O-methyltransferase by tolcapone has been shown to increase levodopa bioavailability and plasma elimination half life, thereby prolonging the efficacy of levodopa. Levodopa 177-185 catechol-O-methyltransferase Homo sapiens 14-42 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 88-94 tyrosine hydroxylase Homo sapiens 27-47 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 88-94 tyrosine hydroxylase Homo sapiens 49-51 9326301-1 1997 In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Levodopa 88-94 tyrosine hydroxylase Homo sapiens 219-221 9326301-4 1997 Theoretically, the oxidation of L-DOPA by TH may contribute to the formation of neuromelanin (pheomelanin) in catecholaminergic neurons and in the metabolism of DOPA to reactive intermediates that can react with free thiol groups in cellular proteins. Levodopa 32-38 tyrosine hydroxylase Homo sapiens 42-44 9639745-0 1997 [Responses of growth hormone and prolactin to L-Dopa in women with polycystic ovarian syndrome]. Levodopa 46-52 growth hormone 1 Homo sapiens 14-28 9307256-3 1997 The magnitude of the short-duration response (SDR) to a 2-hour levodopa infusion after an overnight levodopa withdrawal did not differ at 6 and 12 months (16 +/- 8 and 20 +/- 13 taps/min) from that before long-term levodopa (21 +/- taps/min). Levodopa 63-71 caveolae associated protein 2 Homo sapiens 46-49 9307256-4 1997 However, when levodopa was withheld for 3 days, it was evident that the SDR magnitude was increasing in magnitude (19, 23, and 31 taps/min at 0, 6, and 12 months). Levodopa 14-22 caveolae associated protein 2 Homo sapiens 72-75 9333106-8 1997 RESULTS: By inhibiting COMT, tolcapone reduced levodopa metabolism to 3-O-methyldopa, resulting in a twofold increase in levodopa exposure (area under the curve) and elimination half-life, without changing levodopa peak plasma concentration. Levodopa 47-55 catechol-O-methyltransferase Homo sapiens 23-27 9333106-8 1997 RESULTS: By inhibiting COMT, tolcapone reduced levodopa metabolism to 3-O-methyldopa, resulting in a twofold increase in levodopa exposure (area under the curve) and elimination half-life, without changing levodopa peak plasma concentration. Levodopa 121-129 catechol-O-methyltransferase Homo sapiens 23-27 9333106-8 1997 RESULTS: By inhibiting COMT, tolcapone reduced levodopa metabolism to 3-O-methyldopa, resulting in a twofold increase in levodopa exposure (area under the curve) and elimination half-life, without changing levodopa peak plasma concentration. Levodopa 121-129 catechol-O-methyltransferase Homo sapiens 23-27 9266731-0 1997 Glial cell line-derived neurotrophic factor-levodopa interactions and reduction of side effects in parkinsonian monkeys. Levodopa 44-52 glial cell derived neurotrophic factor Macaca mulatta 0-43 9266731-6 1997 In contrast, there was a functional interaction between GDNF and levodopa. Levodopa 65-73 glial cell derived neurotrophic factor Macaca mulatta 56-60 9266731-9 1997 Combined GDNF-Sinemet treatment significantly reduced the occurrence of these levodopa-induced side effects, with a >90% decrease in adverse responses seen at the mid-Sinemet (250 mg levodopa-25 mg carbidopa) dose level. Levodopa 78-86 glial cell derived neurotrophic factor Macaca mulatta 9-13 9266731-9 1997 Combined GDNF-Sinemet treatment significantly reduced the occurrence of these levodopa-induced side effects, with a >90% decrease in adverse responses seen at the mid-Sinemet (250 mg levodopa-25 mg carbidopa) dose level. Levodopa 186-194 glial cell derived neurotrophic factor Macaca mulatta 9-13 9266736-1 1997 The long-duration response (LDR) to chronic levodopa treatment may mask the short-duration response (SDR) to a single dose of the drug in Parkinson"s disease (PD). Levodopa 44-52 caveolae associated protein 2 Homo sapiens 101-104 9266736-2 1997 As a result, the measurement of SDR may be inaccurate for establishing levodopa dosing regimen in individual patients. Levodopa 71-79 caveolae associated protein 2 Homo sapiens 32-35 9266736-3 1997 To evaluate the possible contamination of SDR by LDR, we investigated in 16 patients with PD the characteristics of SDR to a single dose of levodopa administered after a prolonged washout from chronic therapy and after a 15-day treatment period with levodopa. Levodopa 140-148 caveolae associated protein 2 Homo sapiens 116-119 9266736-6 1997 The evaluation of SDR without the interference of LDR is critical in defining the characteristics of the therapeutic response to levodopa. Levodopa 129-137 caveolae associated protein 2 Homo sapiens 18-21 9242453-7 1997 In addition, we used the 3,4-dihydroxy-L-phenylalanine reaction to detect tyrosinase enzyme activity as a confirmation of the tyrosinase immunohistochemical results in a subset of the lesions. Levodopa 25-54 tyrosinase Homo sapiens 74-84 9352569-1 1997 Catechol-O-methyltransferase catalyses the O-methylation of biologically active or toxic catechols and is a major component of the metabolism of drugs and neurotransmitters such as L-dopa, noradrenaline, adrenaline, and dopamine. Levodopa 181-187 catechol-O-methyltransferase Homo sapiens 0-28 9302099-3 1997 The significance of AADC-positive neurons are discussed in relation to the acting sites of L-dopa and antipsychotic drugs. Levodopa 91-97 dopa decarboxylase Homo sapiens 20-24 9639745-0 1997 [Responses of growth hormone and prolactin to L-Dopa in women with polycystic ovarian syndrome]. Levodopa 46-52 prolactin Homo sapiens 33-42 9639745-2 1997 METHODS: Responses of GH and PRL to L-Dopa (L-DA) (500 mg) were observed in two PCOS groups (LH/FSH > or = 3, Group I, n = 15, LH/FSH < 3, Group II, n = 15) and the control (n = 20). Levodopa 36-42 prolactin Homo sapiens 29-32 9639745-2 1997 METHODS: Responses of GH and PRL to L-Dopa (L-DA) (500 mg) were observed in two PCOS groups (LH/FSH > or = 3, Group I, n = 15, LH/FSH < 3, Group II, n = 15) and the control (n = 20). Levodopa 44-48 prolactin Homo sapiens 29-32 9639745-3 1997 RESULTS: Significantly lower GH (P < 0.01) and higher PRL levels (P < 0.05 in group I) in the basal state, and lower responses of GH and PRL to L-DA were found in two PCOS groups as compared with the control. Levodopa 150-154 prolactin Homo sapiens 143-146 9639745-4 1997 CONCLUSION: The altered basal levels and blunted L-DA evoked responses of GH and PRL suggest a relative decrease of the dopaminergic activity in PCOS patients. Levodopa 49-53 prolactin Homo sapiens 81-84 9202290-8 1997 L-DOPA at 50 microM had opposite effects, in that it significantly increased TH-positive, but not GABA neuron numbers in transgenic WT SOD and G93A and in nontransgenic cultures. Levodopa 0-6 superoxide dismutase 1, soluble Mus musculus 135-138 9225735-5 1997 Incubation of mesencephalic cells with 10(-5) to 10(-7) M levodopa on Days 1-6 in vitro produced no significant effects on the number of dopaminergic neurons containing CR, but resulted in the loss of approximately 65% of the dopaminergic cells which did not contain CR. Levodopa 58-66 calbindin 2 Rattus norvegicus 267-269 9225735-9 1997 These results indicate that CR may protect dopaminergic neurons from levodopa-induced toxicity. Levodopa 69-77 calbindin 2 Rattus norvegicus 28-30 9224438-6 1997 RESULTS: Plasma IGF-I concentrations and the GH responses to sumatriptan, sodium valproate and L-Dopa were significantly lower in older than in younger women. Levodopa 95-101 growth hormone 1 Homo sapiens 45-47 9221930-6 1997 Topographical analysis revealed that long-term L-DOPA treatment reversed, in fact, both post-lesional enkephalin and substance P responses to 6-hydroxydopamine lesion, in the ventromedial neostriatum, without significantly modified these peptide responses in the dorsolateral neostriatum. Levodopa 47-53 proenkephalin Rattus norvegicus 102-112 9225735-0 1997 Calretinin-immunoreactive dopaminergic neurons from embryonic rat mesencephalon are resistant to levodopa-induced neurotoxicity. Levodopa 97-105 calbindin 2 Rattus norvegicus 0-10 9202290-9 1997 These results indicate that increased amounts of WT SOD enzyme promote cell survival and protect against L-DOPA-induced dopaminergic neurotoxicity, whereas increased amounts of mutated Cu/Zn-SOD enzyme have inverse effects. Levodopa 105-111 superoxide dismutase 1, soluble Mus musculus 52-55 9202290-10 1997 As the spontaneous loss and L-DOPA-induced loss of postnatal dopaminergic midbrain neurons appear to be mediated by free radicals, our study supports the view that mutated Cu/Zn-SOD enzyme kills cells by oxidative stress. Levodopa 28-34 superoxide dismutase 1, soluble Mus musculus 172-181 9255200-4 1997 Growth hormone reserve was assessed by at least two stimulation tests (clonidine, L-dopa, growth hormone-releasing hormone). Levodopa 82-88 growth hormone 1 Homo sapiens 0-14 9192308-9 1997 The dopamine precursor L-beta-3,4-dihydroxyphenylalanine (L-DOPA) inhibited cleavage of 35S-labelled thirty-four amino acid amidated gastrin, i.e. [35S]G34, and of [35S]G34 with COOH-terminal glycine, i.e. [35S]G34-Gly, at a pair of lysine residues, but did not influence cleavage of progastrin at pairs of arginine residues. Levodopa 23-56 gastrin Rattus norvegicus 133-140 9251066-0 1997 Simultaneous MAO-B and COMT inhibition in L-Dopa-treated patients with Parkinson"s disease. Levodopa 42-48 monoamine oxidase B Homo sapiens 13-18 9251066-0 1997 Simultaneous MAO-B and COMT inhibition in L-Dopa-treated patients with Parkinson"s disease. Levodopa 42-48 catechol-O-methyltransferase Homo sapiens 23-27 9217760-8 1997 In nine people with parkinsonian MSA (MSA-P), the GH response to levodopa was also assessed. Levodopa 65-73 gamma-glutamyl hydrolase Homo sapiens 50-52 9192308-9 1997 The dopamine precursor L-beta-3,4-dihydroxyphenylalanine (L-DOPA) inhibited cleavage of 35S-labelled thirty-four amino acid amidated gastrin, i.e. [35S]G34, and of [35S]G34 with COOH-terminal glycine, i.e. [35S]G34-Gly, at a pair of lysine residues, but did not influence cleavage of progastrin at pairs of arginine residues. Levodopa 58-64 gastrin Rattus norvegicus 133-140 9192308-10 1997 The effect of L-DOPA was reversed by reserpine, which inhibits the amine-proton exchangers VMAT1 and VMAT2, and by carbidopa, which inhibits aromatic L-amino acid decarboxylase. Levodopa 14-20 solute carrier family 18 member A1 Rattus norvegicus 91-96 9192308-10 1997 The effect of L-DOPA was reversed by reserpine, which inhibits the amine-proton exchangers VMAT1 and VMAT2, and by carbidopa, which inhibits aromatic L-amino acid decarboxylase. Levodopa 14-20 solute carrier family 18 member A2 Rattus norvegicus 101-106 9096399-0 1997 Induction of dopamine D3 receptor expression as a mechanism of behavioral sensitization to levodopa. Levodopa 91-99 dopamine receptor D3 Rattus norvegicus 13-33 9197274-0 1997 Protein kinase A inhibitor attenuates levodopa-induced motor response alterations in the hemi-parkinsonian rat. Levodopa 38-46 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 0-16 9426871-1 1997 New medications recently developed for treating Parkinson"s disease include two inhibitors of catechol-O-methyltransferase (COMT), entacapone and tolcapone, which, by decreasing the elimination of levodopa, extend the duration of its effects. Levodopa 197-205 catechol-O-methyltransferase Homo sapiens 94-122 9426871-1 1997 New medications recently developed for treating Parkinson"s disease include two inhibitors of catechol-O-methyltransferase (COMT), entacapone and tolcapone, which, by decreasing the elimination of levodopa, extend the duration of its effects. Levodopa 197-205 catechol-O-methyltransferase Homo sapiens 124-128 9191769-1 1997 To estimate the threshold of nigrostriatal dysfunction required for symptomatic Parkinson"s disease (PD), we employed [11C]RTI-32 and PET to study the dopamine transporter in striatal subdivisions of 11 L-dopa-naive patients with very early parkinsonism. Levodopa 203-209 solute carrier family 6 member 3 Homo sapiens 151-171 9178029-5 1997 In normal adults, although there was no apparent fluctuation in the level of plasma IR-GHRH or of plasma GH during bed rest, a significant increase of plasma IR-GHRH was detected followed by, or synchronized with the surge of plasma GH after oral administration of L-dopa. Levodopa 265-271 growth hormone releasing hormone Homo sapiens 161-165 9178029-8 1997 We conclude that 1) the elevated IR-GHRH in the cord blood plasma originates from the fetus and may have a primary role in enhancing secretion of GH which promotes growth in early human life, and 2) the participations of GHRH in the mechanisms of GH secretion seen after administrations of L-dopa, L-arginine and somatostatin are different. Levodopa 290-296 growth hormone releasing hormone Homo sapiens 36-40 9178029-8 1997 We conclude that 1) the elevated IR-GHRH in the cord blood plasma originates from the fetus and may have a primary role in enhancing secretion of GH which promotes growth in early human life, and 2) the participations of GHRH in the mechanisms of GH secretion seen after administrations of L-dopa, L-arginine and somatostatin are different. Levodopa 290-296 growth hormone 1 Homo sapiens 36-38 9178029-8 1997 We conclude that 1) the elevated IR-GHRH in the cord blood plasma originates from the fetus and may have a primary role in enhancing secretion of GH which promotes growth in early human life, and 2) the participations of GHRH in the mechanisms of GH secretion seen after administrations of L-dopa, L-arginine and somatostatin are different. Levodopa 290-296 growth hormone releasing hormone Homo sapiens 221-225 9084422-1 1997 To study the possibility that increasing striatal activity of aromatic L-amino acid decarboxylase (AADC; EC 4.1.1.28) can increase dopamine production in dopamine denervated striatum in response to L-3,4-dihydroxy-phenylalanine (L-DOPA) administration, we grafted Cos cells stably expressing the human AADC gene (Cos-haadc cells) into 6-hydroxydopamine denervated rat striatum. Levodopa 198-227 dopa decarboxylase Homo sapiens 71-97 9084422-1 1997 To study the possibility that increasing striatal activity of aromatic L-amino acid decarboxylase (AADC; EC 4.1.1.28) can increase dopamine production in dopamine denervated striatum in response to L-3,4-dihydroxy-phenylalanine (L-DOPA) administration, we grafted Cos cells stably expressing the human AADC gene (Cos-haadc cells) into 6-hydroxydopamine denervated rat striatum. Levodopa 198-227 dopa decarboxylase Homo sapiens 99-103 9084422-11 1997 These findings demonstrate that enhancing striatal AADC activity can improve dopamine bioformation in response to systemically administered L-DOPA. Levodopa 140-146 dopa decarboxylase Homo sapiens 51-55 9063681-0 1997 Adenosine A2A receptor antagonism potentiates L-DOPA-induced turning behaviour and c-fos expression in 6-hydroxydopamine-lesioned rats. Levodopa 46-52 adenosine A2a receptor Rattus norvegicus 0-22 9042918-1 1997 An autosomal recessive form of juvenile Parkinsonism (AR-JP) (MIM 600116) is a levodopa-responsive Parkinsonism whose pathological finding is a highly selective degeneration of dopaminergic neurons in the zona compacta of the substantia nigra. Levodopa 79-87 parkin RBR E3 ubiquitin protein ligase Homo sapiens 54-59 9133632-2 1997 On reaction of the normal substrate L-dopa with this mutant AADC, the absorption at around 330 nm gradually increased with concomitant decrease of the absorption of the free PLP molecule at 390 nm. Levodopa 36-42 dopa decarboxylase Homo sapiens 60-64 9175615-7 1997 As compared to peripheral COMT inhibitors, this central effect may help preserve and stabilize the synaptic levels of DA and, thus, further improve the effects of L-DOPA therapy in parkinsonian patients. Levodopa 163-169 catechol-O-methyltransferase Homo sapiens 26-30 9063681-5 1997 Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain. Levodopa 82-88 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 14-19 9063681-5 1997 Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain. Levodopa 127-133 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 14-19 9063681-9 1997 The data also suggest that adenosine A2A receptor antagonists might be useful for potentiating the effects of L-DOPA in Parkinson"s disease. Levodopa 110-116 adenosine A2a receptor Rattus norvegicus 27-49 9252801-1 1997 This double-blind, placebo-controlled, randomized, crossover study was designed to evaluate the effects of catechol-O-methyltransferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa given as four different formulations of levodopa/benserazide: 50/12.5 mg, 100/25 mg, 200/50 mg (all standard release), or 100/25 mg (controlled release). Levodopa 194-202 catechol-O-methyltransferase Homo sapiens 137-141 8987798-6 1997 In PD patients, all of whom had been treated chronically by L-DOPA, COI mRNA expression in the analyzed basal ganglia structures was similar to that in control subjects. Levodopa 60-66 mitochondrially encoded cytochrome c oxidase I Homo sapiens 68-71 9037574-4 1997 In the present study, the ability of the catechol-O-methyltransferase inhibitor Ro 41-0960 to prevent L-Dopa-induced changes in SAM, SAH, and homocysteine concentrations was determined in rats. Levodopa 102-108 catechol-O-methyltransferase Rattus norvegicus 41-69 9121699-1 1997 Catechol-O-methyltransferase (COMT) is an enzyme that inactivates catecholamines such as adrenaline, noradrenaline, dopamine, and levodopa. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 0-28 9121699-1 1997 Catechol-O-methyltransferase (COMT) is an enzyme that inactivates catecholamines such as adrenaline, noradrenaline, dopamine, and levodopa. Levodopa 130-138 catechol-O-methyltransferase Homo sapiens 30-34 9085195-1 1997 Inhibitors of the enzyme catechol-O-methyl transferase (COMT) may be useful adjuncts to L-DOPA in the treatment of Parkinson"s disease as they offer the possibility of increasing the availability of the amino acid. Levodopa 88-94 catechol-O-methyltransferase Rattus norvegicus 25-54 9295168-6 1997 Among the neurotrophic factors GDNF and BDNF totally prevented L-DOPA neurotoxicity, while NGF and bFGF were less effective. Levodopa 63-69 glial cell derived neurotrophic factor Homo sapiens 31-35 8945749-4 1996 Two pathways have been suggested to result in conversion of D-dopa to L-dopa, one involving oxidation of D-dopa to dihydroxyphenylpyruvic acid (DHPPA) by D-amino acid oxidase, the other involving transamination of D-dopa to DHPPA. Levodopa 70-76 D-amino-acid oxidase Rattus norvegicus 154-174 9295168-6 1997 Among the neurotrophic factors GDNF and BDNF totally prevented L-DOPA neurotoxicity, while NGF and bFGF were less effective. Levodopa 63-69 brain derived neurotrophic factor Homo sapiens 40-44 9444560-0 1997 Effect of monoamine oxidase A and B and of catechol-O-methyltransferase inhibition on L-DOPA-induced circling behavior. Levodopa 86-92 monoamine oxidase A Rattus norvegicus 10-71 9444560-6 1997 MAO-A inhibition in conjunction with MAO-B inhibition prolonged the duration of L-DOPA-induced turning but had no effect on the number of turns. Levodopa 80-86 monoamine oxidase A Rattus norvegicus 0-5 9444560-6 1997 MAO-A inhibition in conjunction with MAO-B inhibition prolonged the duration of L-DOPA-induced turning but had no effect on the number of turns. Levodopa 80-86 monoamine oxidase B Rattus norvegicus 37-42 9435379-2 1997 L-dopa, associated with dopa decarboxylase inhibitors and dopaminergic agonists, gave rise to an almost complete standstill of surgical procedures. Levodopa 0-6 dopa decarboxylase Homo sapiens 24-42 9008498-2 1997 Tolcapone is a potent catechol-O-methyltransferase inhibitor that prolongs the plasma half-life of levodopa. Levodopa 99-107 catechol-O-methyltransferase Homo sapiens 22-50 10374498-2 1997 In this study, the tyrosine hydroxylase (TH) gene was introduced into NIH-3T3 cell line and the genetically modified cells reacted positively with TH antiserum and released L-dopa. Levodopa 173-179 tyrosine hydroxylase Mus musculus 19-39 10374498-2 1997 In this study, the tyrosine hydroxylase (TH) gene was introduced into NIH-3T3 cell line and the genetically modified cells reacted positively with TH antiserum and released L-dopa. Levodopa 173-179 tyrosine hydroxylase Mus musculus 41-43 9004111-5 1996 The delta serum GH during levodopa was 5.7 +/- 6.3 ng ml-1 in DS and 13.1 +/- 9.8 ng ml-1 in controls. Levodopa 26-34 growth hormone 1 Homo sapiens 16-18 9004111-11 1996 These results indicate that levodopa and clonidine (drugs stimulating hypothalamic GHRH release and secondary pituitary GH release in normal individuals) do not stimulate GH release in DS. Levodopa 28-36 growth hormone releasing hormone Homo sapiens 83-87 9004111-11 1996 These results indicate that levodopa and clonidine (drugs stimulating hypothalamic GHRH release and secondary pituitary GH release in normal individuals) do not stimulate GH release in DS. Levodopa 28-36 growth hormone 1 Homo sapiens 83-85 8976015-9 1996 CONCLUSIONS: This study has shown a high turnover of L-DOPA in the rat pancreas, which can be modulated to give enhanced levels of DOPAC or dopamine by COMT and MAO inhibition. Levodopa 53-59 catechol-O-methyltransferase Rattus norvegicus 152-156 8976015-9 1996 CONCLUSIONS: This study has shown a high turnover of L-DOPA in the rat pancreas, which can be modulated to give enhanced levels of DOPAC or dopamine by COMT and MAO inhibition. Levodopa 53-59 monoamine oxidase A Rattus norvegicus 161-164 9014452-3 1997 FDOPA is also an efficient tracer to analyze pharmacokinetics of L-DOPA by measuring radioactivities of its metabolites in the peripheral blood by HPLC and to evaluate pharmacological effects on dopamine metabolism by pretreatment of dopa decarboxylase inhibitor or COMT inhibitor. Levodopa 65-71 dopa decarboxylase Homo sapiens 234-252 9014452-3 1997 FDOPA is also an efficient tracer to analyze pharmacokinetics of L-DOPA by measuring radioactivities of its metabolites in the peripheral blood by HPLC and to evaluate pharmacological effects on dopamine metabolism by pretreatment of dopa decarboxylase inhibitor or COMT inhibitor. Levodopa 65-71 catechol-O-methyltransferase Homo sapiens 266-270 9113132-0 1996 Inhibition of catalase in mesencephalic cultures by L-DOPA and dopamine. Levodopa 52-58 catalase Rattus norvegicus 14-22 9113132-1 1996 Catalase activity in cell cultures of fetal rat mesencephalon was decreased by 42 and 50%, respectively, after exposure to L-3,4-dihydroxyphenylalanine (L-DOPA, 100 microM) or dopamine (100 microM) for 48 h. Catalase activity was also decreased 21% by 10 microM hydroquinone. Levodopa 123-151 catalase Rattus norvegicus 0-8 9113132-1 1996 Catalase activity in cell cultures of fetal rat mesencephalon was decreased by 42 and 50%, respectively, after exposure to L-3,4-dihydroxyphenylalanine (L-DOPA, 100 microM) or dopamine (100 microM) for 48 h. Catalase activity was also decreased 21% by 10 microM hydroquinone. Levodopa 123-151 catalase Rattus norvegicus 208-216 9113132-1 1996 Catalase activity in cell cultures of fetal rat mesencephalon was decreased by 42 and 50%, respectively, after exposure to L-3,4-dihydroxyphenylalanine (L-DOPA, 100 microM) or dopamine (100 microM) for 48 h. Catalase activity was also decreased 21% by 10 microM hydroquinone. Levodopa 153-159 catalase Rattus norvegicus 0-8 9113132-1 1996 Catalase activity in cell cultures of fetal rat mesencephalon was decreased by 42 and 50%, respectively, after exposure to L-3,4-dihydroxyphenylalanine (L-DOPA, 100 microM) or dopamine (100 microM) for 48 h. Catalase activity was also decreased 21% by 10 microM hydroquinone. Levodopa 153-159 catalase Rattus norvegicus 208-216 9113132-2 1996 Ascorbic acid (200 microM), an agent that suppresses the autoxidation of L-DOPA and dopamine, blocked the anti-catalase effect of L-DOPA, but not that of dopamine. Levodopa 73-79 catalase Rattus norvegicus 111-119 9113132-2 1996 Ascorbic acid (200 microM), an agent that suppresses the autoxidation of L-DOPA and dopamine, blocked the anti-catalase effect of L-DOPA, but not that of dopamine. Levodopa 130-136 catalase Rattus norvegicus 111-119 9113132-5 1996 However, autoxidation reactions of L-DOPA may play a role since ascorbate suppressed the anti-catalase effect of L-DOPA. Levodopa 35-41 catalase Rattus norvegicus 94-102 9113132-5 1996 However, autoxidation reactions of L-DOPA may play a role since ascorbate suppressed the anti-catalase effect of L-DOPA. Levodopa 113-119 catalase Rattus norvegicus 94-102 9113132-7 1996 L-DOPA and dopamine (25 microM) also inhibited crystalline catalase in solution after incubation for 1 h at neutral pH (40-50% inhibition). Levodopa 0-6 catalase Rattus norvegicus 59-67 9113132-10 1996 Inhibition of catalase may contribute to cell damage during incubation of cultures with L-DOPA, dopamine, or other autoxidizable compounds. Levodopa 88-94 catalase Rattus norvegicus 14-22 8941353-7 1996 However it remains possible that allelic variation in COMT influences severity, type of pathology or treatment response to levodopa or COMT inhibitors. Levodopa 123-131 catechol-O-methyltransferase Homo sapiens 54-58 8891660-3 1996 After administration of L-dopa, EMG responses occurring 30-150 ms after the tendon tap decreased to about 50% of control, and clinical tests revealed a marked decrease in the resistance to muscle stretches and in the degree of clonus. Levodopa 24-30 nuclear RNA export factor 1 Homo sapiens 83-86 9479530-3 1996 To date, only the hair-bulb L-dopa incubation test has been helpful in discriminating between the tyrosinase (ty)-negative and ty-positive forms of OCA. Levodopa 28-34 tyrosinase Homo sapiens 98-108 8915594-0 1996 Effects of L-DOPA-therapy on dopamine D2 receptor mRNA expression in the striatum of MPTP-intoxicated parkinsonian monkeys. Levodopa 11-17 dopamine receptor D2 Homo sapiens 29-49 8913337-1 1996 The effect of L-3,4-dihydroxyphenylalanine (L-DOPA) on dopamine receptor gene expression in the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys was investigated using in situ hybridization histochemistry with measures of changes in relative absorbance. Levodopa 44-50 immunoglobulin kappa variable 2-14 (pseudogene) Homo sapiens 14-17