PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8104402-4 1993 Alterations in glutaminase and glutamine synthetase following aluminum exposure caused increased intracellular glutamine levels, decreased intracellular glutamate levels, and increased conversion of glutamate to glutamine and the release of the latter into the extracellular space. Glutamic Acid 153-162 glutamate-ammonia ligase Rattus norvegicus 31-51 8188174-3 1994 It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Glutamic Acid 103-112 glutamate-ammonia ligase Rattus norvegicus 140-160 7910379-9 1994 Because the concentration of free cytoplasmic Mn(II) is poised near the Kd for Mn(II) with glutamine synthetase, a slight increase in cytoplasmic Mn(II) will directly enhance the activity of glutamine synthetase, which catalyzes removal of neurotoxic glutamate and ammonia. Glutamic Acid 251-260 glutamate-ammonia ligase Rattus norvegicus 191-211 7905447-2 1994 L-Glutamate, a necessary substrate for glutamine synthetase, is transported into muscle cells by Na(+)-dependent and -independent transport systems. Glutamic Acid 0-11 glutamate-ammonia ligase Rattus norvegicus 39-59 8104402-4 1993 Alterations in glutaminase and glutamine synthetase following aluminum exposure caused increased intracellular glutamine levels, decreased intracellular glutamate levels, and increased conversion of glutamate to glutamine and the release of the latter into the extracellular space. Glutamic Acid 199-208 glutamate-ammonia ligase Rattus norvegicus 31-51 1347243-9 1992 The increased capacity for glutamine synthetase may be important in normalizing extracellular glutamate following ischemia and protecting brain from the neurotoxic effects of this excitatory amino acid. Glutamic Acid 94-103 glutamate-ammonia ligase Rattus norvegicus 27-47 1348525-5 1992 Inhibition of GS led to a sustained and greatly elevated intracellular glutamate level, thereby demonstrating the predominance of this pathway in the astrocytic metabolism of glutamate. Glutamic Acid 71-80 glutamate-ammonia ligase Rattus norvegicus 14-16 1348525-5 1992 Inhibition of GS led to a sustained and greatly elevated intracellular glutamate level, thereby demonstrating the predominance of this pathway in the astrocytic metabolism of glutamate. Glutamic Acid 175-184 glutamate-ammonia ligase Rattus norvegicus 14-16 1348527-1 1992 In this study we have investigated the effect of excitatory amino acids on the activity of glutamine synthetase, a glial-specific enzyme that plays a key role in the regulation of glutamate concentration in the CNS. Glutamic Acid 180-189 glutamate-ammonia ligase Rattus norvegicus 91-111 7903184-1 1993 Glutamine synthetase (GS) supposedly inactivates the excitatory neurotransmitter glutamate. Glutamic Acid 81-90 glutamate-ammonia ligase Rattus norvegicus 0-20 1354842-1 1992 Since glutamine synthetase (GS) has been proposed as the primary enzyme in the regulation of glutamate metabolism in the central nervous system and since inhibition of the activity of this enzyme in vivo leads to seizures, it has been proposed that an abnormality in the structure or function of this enzyme could be responsible for the induction of seizures in epilepsy prone rats. Glutamic Acid 93-102 glutamate-ammonia ligase Rattus norvegicus 6-26 1685767-6 1991 As expected from the cycle GAD was inactivated when incubated with glutamate and deoxypyridoxine-P even though cofactor was present, but no inactivation was observed with deoxypyridoxine-P in the absence of glutamate. Glutamic Acid 67-76 glutamate-ammonia ligase Rattus norvegicus 27-30 1727443-2 1992 Rats of different ages were subjected to hyperthermia, and GAD activity was determined in brain homogenates by measuring the release of 14CO2 from labeled glutamate and by measuring the formation of GABA. Glutamic Acid 155-164 glutamate-ammonia ligase Rattus norvegicus 59-62 1680531-4 1991 Here we report that immunoreactivity against glutamine synthetase (GS), one of the glutamate metabolizing enzymes, is localized in the fine astrocytic processes associated with identified glutamatergic synapses in the rat hippocampus. Glutamic Acid 83-92 glutamate-ammonia ligase Rattus norvegicus 45-65 1680531-4 1991 Here we report that immunoreactivity against glutamine synthetase (GS), one of the glutamate metabolizing enzymes, is localized in the fine astrocytic processes associated with identified glutamatergic synapses in the rat hippocampus. Glutamic Acid 83-92 glutamate-ammonia ligase Rattus norvegicus 67-69 1363168-1 1992 Glutamine synthetase (L-glutamate:ammonia ligase; EC 6.3.1.2), an enzyme catalysing the ATP-dependent formation of glutamine from glutamate and ammonia, was detected immunocytochemically only in glial (interstitial) cells of the superficial pineal gland of the rat. Glutamic Acid 24-33 glutamate-ammonia ligase Rattus norvegicus 0-20 1685767-6 1991 As expected from the cycle GAD was inactivated when incubated with glutamate and deoxypyridoxine-P even though cofactor was present, but no inactivation was observed with deoxypyridoxine-P in the absence of glutamate. Glutamic Acid 207-216 glutamate-ammonia ligase Rattus norvegicus 27-30 1671539-3 1991 We previously showed that the specific activity of glutamine synthetase (GS), an astroglial enzyme with a key role in glutamate and ammonia metabolism in the brain, is reduced in fetal guinea pigs exposed to low levels of lead. Glutamic Acid 118-127 glutamate-ammonia ligase Rattus norvegicus 51-71 1674354-1 1991 Glutamine synthetase catalyzes the formation of glutamine from glutamate and ammonia. Glutamic Acid 63-72 glutamate-ammonia ligase Rattus norvegicus 0-20 1968957-5 1990 These results indicate that synaptosomal GAD is not saturated by endogenous levels of its substrate, glutamate, and account for part of the unused catalytic capacity. Glutamic Acid 101-110 glutamate-ammonia ligase Rattus norvegicus 41-44 1982459-7 1990 The results suggest: (1) astrocytes are highly efficient in the conversion of glutamate to glutamine; (2) induction of GS activity increases the rate of glutamate conversion to glutamine by astrocytes and the rate of glutamine release into the medium; (3) endogenous intracellular regulators of GS activity control the flux of glutamate through this enzymatic reaction; and (4) the composition of the medium alters the rate of glutamine synthesis from external glutamate. Glutamic Acid 78-87 glutamate-ammonia ligase Rattus norvegicus 119-121 1982459-7 1990 The results suggest: (1) astrocytes are highly efficient in the conversion of glutamate to glutamine; (2) induction of GS activity increases the rate of glutamate conversion to glutamine by astrocytes and the rate of glutamine release into the medium; (3) endogenous intracellular regulators of GS activity control the flux of glutamate through this enzymatic reaction; and (4) the composition of the medium alters the rate of glutamine synthesis from external glutamate. Glutamic Acid 153-162 glutamate-ammonia ligase Rattus norvegicus 119-121 1982459-7 1990 The results suggest: (1) astrocytes are highly efficient in the conversion of glutamate to glutamine; (2) induction of GS activity increases the rate of glutamate conversion to glutamine by astrocytes and the rate of glutamine release into the medium; (3) endogenous intracellular regulators of GS activity control the flux of glutamate through this enzymatic reaction; and (4) the composition of the medium alters the rate of glutamine synthesis from external glutamate. Glutamic Acid 153-162 glutamate-ammonia ligase Rattus norvegicus 119-121 1982459-7 1990 The results suggest: (1) astrocytes are highly efficient in the conversion of glutamate to glutamine; (2) induction of GS activity increases the rate of glutamate conversion to glutamine by astrocytes and the rate of glutamine release into the medium; (3) endogenous intracellular regulators of GS activity control the flux of glutamate through this enzymatic reaction; and (4) the composition of the medium alters the rate of glutamine synthesis from external glutamate. Glutamic Acid 153-162 glutamate-ammonia ligase Rattus norvegicus 119-121 1973454-0 1990 Glutamate-dependent active-site labeling of brain glutamate decarboxylase. Glutamic Acid 0-9 glutamate-ammonia ligase Rattus norvegicus 50-73 1973454-3 1990 To test this prediction, the effect of glutamate on the incorporation of pyridoxal-P into rat-brain GAD was studied by incubating GAD with [32P]pyridoxal-P, followed by reduction with NaBH4 to link irreversibly the cofactor to the enzyme. Glutamic Acid 39-48 glutamate-ammonia ligase Rattus norvegicus 100-103 1973454-4 1990 Adding glutamate to the reaction mixture strongly stimulated labeling of GAD, as expected. Glutamic Acid 7-16 glutamate-ammonia ligase Rattus norvegicus 73-76 1973454-5 1990 4-Deoxypyridoxine 5"-phosphate (deoxypyridoxine-P), a close structural analogue of pyridoxal-P, was a competitive inhibitor of the activation of glutamate apodecarboxylase by pyridoxal-P (Ki = 0.27 microM) and strongly inhibited glutamate-dependent labeling of GAD. Glutamic Acid 145-154 glutamate-ammonia ligase Rattus norvegicus 261-264 1973454-7 1990 Both proteins could be purified by immunoaffinity chromatography on a column prepared with a monoclonal antibody to GAD, and both were labeled in a glutamate-dependent, deoxypyridoxine-P-sensitive manner, indicating that both were GAD. Glutamic Acid 148-157 glutamate-ammonia ligase Rattus norvegicus 116-119 1973454-7 1990 Both proteins could be purified by immunoaffinity chromatography on a column prepared with a monoclonal antibody to GAD, and both were labeled in a glutamate-dependent, deoxypyridoxine-P-sensitive manner, indicating that both were GAD. Glutamic Acid 148-157 glutamate-ammonia ligase Rattus norvegicus 231-234 1978267-1 1990 Methionine sulfoxime (MS) is an inhibitor of glutamine synthetase, an astroglial enzyme believed to be involved in the maintenance of glutamine, a major precursor for neurotransmitter pools of the excitatory amino acids aspartate and glutamate in striatal afferent axon terminals. Glutamic Acid 234-243 glutamate-ammonia ligase Rattus norvegicus 45-65 1968957-6 1990 The greater stimulation of GABA synthesis by glutamine indicates that the GAD-containing compartment is more accessible to extrasynaptosomal glutamine than glutamate. Glutamic Acid 156-165 glutamate-ammonia ligase Rattus norvegicus 74-77 2305410-4 1990 This protective effect may be mediated by a presynaptic mechanism; methionine sulfoximine profoundly inhibits brain glutamine synthetase, thereby interrupting the astrocyte-neuron glutamate shuttle and impairing neuronal glutamate release. Glutamic Acid 180-189 glutamate-ammonia ligase Rattus norvegicus 116-136 2305410-4 1990 This protective effect may be mediated by a presynaptic mechanism; methionine sulfoximine profoundly inhibits brain glutamine synthetase, thereby interrupting the astrocyte-neuron glutamate shuttle and impairing neuronal glutamate release. Glutamic Acid 221-230 glutamate-ammonia ligase Rattus norvegicus 116-136 1970631-8 1990 A reduction in glutamine synthetase by kainic acid may impair the capacity for astrocytes to metabolize glutamate. Glutamic Acid 104-113 glutamate-ammonia ligase Rattus norvegicus 15-35 1977701-7 1990 The addition of 100 microM glutamate to the culture medium resulted in an increase in GS mRNA in the astrocyte cultures similar to that observed in the cocultures, where the addition of glutamate did not further increase GS mRNA levels. Glutamic Acid 27-36 glutamate-ammonia ligase Rattus norvegicus 86-88 34463828-8 2021 (3) Compared with PD group, the ability of Glu reuptake in the striatum was significantly increased (P < 0.05), the expression levels of GLT-1 and GS mRNA in the striatum were significantly increased (P < 0.05), the protein expression of GLT-1 and GS in the striatum was significantly upregulated (P < 0.05) in PD + Ex group. Glutamic Acid 43-46 glutamate-ammonia ligase Rattus norvegicus 147-149 2424382-14 1985 The finding of both active glutaminase and glutamine synthetase activity in the same liver cells is an evidence of the existence of an active glutamine-glutamate futile cycle. Glutamic Acid 152-161 glutamate-ammonia ligase Rattus norvegicus 43-63 34972242-2 2022 Glutamate decarboxylase (GAD) synthesizes GABA from glutamate, and two isoforms of GAD, GAD65, and GAD67, are separately encoded by the Gad2 and Gad1 genes, respectively. Glutamic Acid 52-61 glutamate-ammonia ligase Rattus norvegicus 0-23 2575901-3 1989 Benzoate-induced glutamate efflux from the liver was not dependent on the concentration (0-1 mM) of ammonia (NH3 + NH4+) in the influent perfusate, but was significantly increased after inhibition of glutamine synthetase by methionine sulphoximine or during the metabolism of added glutamine (5 mM). Glutamic Acid 17-26 glutamate-ammonia ligase Rattus norvegicus 200-220 2572417-6 1989 This was observed in both, antegrade and retrograde perfusions and suggests an almost exclusive uptake of glutamate into perivenous glutamine-synthetase-containing hepatocytes. Glutamic Acid 106-115 glutamate-ammonia ligase Rattus norvegicus 132-152 2572417-19 1989 Comparison of the specific radioactivities of glutamine and glutamate released from perivenous cells indicates that about 60% of total glutamate release from the liver is derived from the perivenous glutamine-synthetase-containing cell population. Glutamic Acid 60-69 glutamate-ammonia ligase Rattus norvegicus 199-219 2572417-19 1989 Comparison of the specific radioactivities of glutamine and glutamate released from perivenous cells indicates that about 60% of total glutamate release from the liver is derived from the perivenous glutamine-synthetase-containing cell population. Glutamic Acid 135-144 glutamate-ammonia ligase Rattus norvegicus 199-219 2572417-22 1989 It is concluded that, in the intact liver, vascular glutamate is almost exclusively taken up by the small perivenous hepatocyte population containing glutamine synthetase. Glutamic Acid 52-61 glutamate-ammonia ligase Rattus norvegicus 150-170 2570341-2 1989 In contrast, mRNA levels of another glutamate cycle enzyme, glutamine synthetase, remained constant. Glutamic Acid 36-45 glutamate-ammonia ligase Rattus norvegicus 60-80 2434618-6 1987 They suggest that Ca2+ and the Na+, K+ pump may serve a role in regulating the activity of ATP-dependent glutamine synthetase, a key enzyme of the glutamate-glutamine cycle, located in the astrocytes. Glutamic Acid 147-156 glutamate-ammonia ligase Rattus norvegicus 105-125 2869109-0 1986 Apparent inhibition of ATP citrate lyase by L-glutamate in vitro is due to the presence of glutamine synthetase. Glutamic Acid 44-55 glutamate-ammonia ligase Rattus norvegicus 91-111 2869109-6 1986 These lines of evidence implicate endogenous glutamine synthetase, and the involvement of this enzyme is established by the use of its inhibitor L-methionine sulphoximine and by the addition of purified glutamine synthetase to restore the glutamate inhibition of purified ATP citrate lyase. Glutamic Acid 239-248 glutamate-ammonia ligase Rattus norvegicus 45-65 2869109-6 1986 These lines of evidence implicate endogenous glutamine synthetase, and the involvement of this enzyme is established by the use of its inhibitor L-methionine sulphoximine and by the addition of purified glutamine synthetase to restore the glutamate inhibition of purified ATP citrate lyase. Glutamic Acid 239-248 glutamate-ammonia ligase Rattus norvegicus 203-223 4062982-1 1985 Twenty conformationally restricted analogues of glutamate including benzoic acids, hydroxy-benzoic acids, pyridine dicarboxylic acids, and pyran dicarboxylic acids were tested as inhibitors of glutamate decarboxylase from rat brain. Glutamic Acid 48-57 glutamate-ammonia ligase Rattus norvegicus 193-216 34681786-2 2021 We hypothesized that the effect of MSO results from a) glutamine synthetase block-mediated inhibition of conversion of Glu/Gln precursors to neurotransmitter Glu, and/or from b) altered synaptic Glu release. Glutamic Acid 119-122 glutamate-ammonia ligase Rattus norvegicus 55-75 34681786-2 2021 We hypothesized that the effect of MSO results from a) glutamine synthetase block-mediated inhibition of conversion of Glu/Gln precursors to neurotransmitter Glu, and/or from b) altered synaptic Glu release. Glutamic Acid 158-161 glutamate-ammonia ligase Rattus norvegicus 55-75 34681786-2 2021 We hypothesized that the effect of MSO results from a) glutamine synthetase block-mediated inhibition of conversion of Glu/Gln precursors to neurotransmitter Glu, and/or from b) altered synaptic Glu release. Glutamic Acid 195-198 glutamate-ammonia ligase Rattus norvegicus 55-75 34324129-6 2021 Glutamate uptake was not changed, but the activities of glutamine synthetase and ATPases were increased. Glutamic Acid 0-9 glutamate-ammonia ligase Rattus norvegicus 56-88 2857768-4 1985 The present study investigates the action of BOAA in vitro on CNS high-affinity transport systems for glutamate, gamma-aminobutyric acid (GABA), aspartate, glycine, and choline and in the activity of glutamate decarboxylase (GAD), the rate-limiting enzyme in the decarboxylation of glutamate to GABA. Glutamic Acid 200-209 glutamate-ammonia ligase Rattus norvegicus 225-228 2859098-6 1985 The development of different enzymes involved in the metabolism of glutamate was also studied; the specific activity of glutaminase increased in culture and was found to be higher in a CDM than in a SCM, while the inverse was true for glutamine synthetase. Glutamic Acid 67-76 glutamate-ammonia ligase Rattus norvegicus 235-255 6149260-0 1984 Alteration of striatal glutamate release after glutamine synthetase inhibition. Glutamic Acid 23-32 glutamate-ammonia ligase Rattus norvegicus 47-67 6113985-0 1981 Inhibition of rat liver glutamine synthetase by phosphonic analogues of glutamic acid. Glutamic Acid 72-85 glutamate-ammonia ligase Rattus norvegicus 24-44 6140923-1 1983 The enzymes of glutamate metabolism were estimated in astrocytes isolated from brains of normal rats and those injected with the potent convulsant, methionine sulfoximine (MSO), which inhibits glutamine synthetase and induces Alzheimer type II astrocytosis. Glutamic Acid 15-24 glutamate-ammonia ligase Rattus norvegicus 193-213 24873689-0 1983 Developing rat cerebellum: Glutamine and glutamate influx correlated to the cellular distribution of glutamine synthetase. Glutamic Acid 41-50 glutamate-ammonia ligase Rattus norvegicus 101-121 6146632-4 1984 Glutamine synthetase activity was increased following incubation (1) in glutamine-free medium (threefold); (2) in medium containing high glutamic acid concentrations (fourfold); and (3) in medium supplemented with dexamethasone (threefold). Glutamic Acid 137-150 glutamate-ammonia ligase Rattus norvegicus 0-20 6146380-8 1984 C6 cells treated with 10 microM hydrocortisone, which is known to induce glutamine synthetase activity, were also resistant to L-glutamate, but not to L-aminoadipate. Glutamic Acid 127-138 glutamate-ammonia ligase Rattus norvegicus 73-93 6105901-1 1980 The subcellular localization of glutamine synthetase, an enzyme fundamental to the compartmentation of glutamate hypothesis, was investigated using brain tissue of adult rats. Glutamic Acid 103-112 glutamate-ammonia ligase Rattus norvegicus 32-52 788859-1 1976 L-Glutamate decarboxylase (GAD, EC 4.1.1.15), the enzyme which catalyzes the alpha-decarboxylation of L-glutamate to form gamma-aminobutyric acid (GABA), was localized both light and electron microscopically in rat substantia nigra by an immunoperoxidase method. Glutamic Acid 102-113 glutamate-ammonia ligase Rattus norvegicus 2-25 488107-2 1979 Decarboxylation of L-glutamate by rat brain glutamate decarboxylase occurs with retention of configuration. Glutamic Acid 19-30 glutamate-ammonia ligase Rattus norvegicus 44-67 39099-5 1979 The glutamine synthetase content correlated well with sites of suspected glutamergic activity in keeping with the view of a critical role of astrocytes in the regulation of the putative neurotransmitter glutamic acid. Glutamic Acid 203-216 glutamate-ammonia ligase Rattus norvegicus 4-24 33492574-9 2021 We showed that rutin inhibited the cell death and loss of glutamine synthetase (GS) induced by glutamate that was associated with an increase in glutamate-aspartate transporter (GLAST) in brain organotypic cultures from post-natal Wistar rats. Glutamic Acid 95-104 glutamate-ammonia ligase Rattus norvegicus 58-78 2155-11 1975 It was concluded that: (a) the alanine aminotransferase and the glutamine synthetase pathways respectively were responsible for 80% of the alanine and glutamine released into the circulation by the extrasplanchnic tissues, and extrahepatic proteolysis could account for a maximum of 20%; (b) alanine formation by the peripheral tissues was dependent on availability of pyruvate and not of glutamate; (c) glutamate availability could influence glutamine formation subject, possibly, to renal control. Glutamic Acid 389-398 glutamate-ammonia ligase Rattus norvegicus 64-84 2155-11 1975 It was concluded that: (a) the alanine aminotransferase and the glutamine synthetase pathways respectively were responsible for 80% of the alanine and glutamine released into the circulation by the extrasplanchnic tissues, and extrahepatic proteolysis could account for a maximum of 20%; (b) alanine formation by the peripheral tissues was dependent on availability of pyruvate and not of glutamate; (c) glutamate availability could influence glutamine formation subject, possibly, to renal control. Glutamic Acid 404-413 glutamate-ammonia ligase Rattus norvegicus 64-84 34048864-5 2021 Downregulated glutamine synthetase (GS) activity, further supports disrupted glutamate metabolism compromising the glutamate-glutamine cycle. Glutamic Acid 77-86 glutamate-ammonia ligase Rattus norvegicus 14-34 34048864-5 2021 Downregulated glutamine synthetase (GS) activity, further supports disrupted glutamate metabolism compromising the glutamate-glutamine cycle. Glutamic Acid 77-86 glutamate-ammonia ligase Rattus norvegicus 36-38 34048864-5 2021 Downregulated glutamine synthetase (GS) activity, further supports disrupted glutamate metabolism compromising the glutamate-glutamine cycle. Glutamic Acid 115-124 glutamate-ammonia ligase Rattus norvegicus 14-34 34048864-5 2021 Downregulated glutamine synthetase (GS) activity, further supports disrupted glutamate metabolism compromising the glutamate-glutamine cycle. Glutamic Acid 115-124 glutamate-ammonia ligase Rattus norvegicus 36-38 33492574-9 2021 We showed that rutin inhibited the cell death and loss of glutamine synthetase (GS) induced by glutamate that was associated with an increase in glutamate-aspartate transporter (GLAST) in brain organotypic cultures from post-natal Wistar rats. Glutamic Acid 95-104 glutamate-ammonia ligase Rattus norvegicus 80-82 31419724-7 2019 GAD was increased and GABA-T was decreased, which resulted in an increase in GABA levels and decrease of the glutamate/GABA ratio in the hippocampus of CUS offspring rats. Glutamic Acid 109-118 glutamate-ammonia ligase Rattus norvegicus 0-3 33238171-7 2021 Protein levels of glutamate-related enzymes such as glutamate dehydrogenase and glutamine synthetase were also increased. Glutamic Acid 18-27 glutamate-ammonia ligase Rattus norvegicus 80-100 32473460-0 2020 Baicalin combats glutamate excitotoxicity via protecting glutamine synthetase from ROS-induced 20S proteasomal degradation. Glutamic Acid 17-26 glutamate-ammonia ligase Rattus norvegicus 57-77 31313857-5 2019 We tested whether the glutamate-glutamine-cycle guides the lasting changes on plasticity observed after juvenile stress by blocking the astrocytic glutamate-degrading enzyme, glutamine synthetase (GS). Glutamic Acid 22-31 glutamate-ammonia ligase Rattus norvegicus 175-195 31313857-5 2019 We tested whether the glutamate-glutamine-cycle guides the lasting changes on plasticity observed after juvenile stress by blocking the astrocytic glutamate-degrading enzyme, glutamine synthetase (GS). Glutamic Acid 147-156 glutamate-ammonia ligase Rattus norvegicus 175-195 30031104-2 2018 Our results showing decreased glutamine synthetase (GS) activity and Ca2+ overload in the cerebral cortex of hypothyroid pups suggest misregulated glutamate metabolism associated with developmentally induced TH deficiency. Glutamic Acid 147-156 glutamate-ammonia ligase Rattus norvegicus 30-50 26188416-1 2016 Astrocytes are most abundant glial cell type in the brain and play a main defensive role in central nervous system against glutamate-induced toxicity by virtue of numerous transporters residing in their membranes and an astrocyte-specific enzyme glutamine synthetase (GS). Glutamic Acid 123-132 glutamate-ammonia ligase Rattus norvegicus 246-266 28238867-8 2017 We propose that glutamate uptake via glutamate transporter 3 could activate expression of glutamate decarboxylase which in turn transforms uptaken glutamate into GABA. Glutamic Acid 16-25 glutamate-ammonia ligase Rattus norvegicus 90-113 28238867-8 2017 We propose that glutamate uptake via glutamate transporter 3 could activate expression of glutamate decarboxylase which in turn transforms uptaken glutamate into GABA. Glutamic Acid 37-46 glutamate-ammonia ligase Rattus norvegicus 90-113 27787475-2 2016 Glu is transformed into glutamine (Gln) by glutamine synthetase (GS) enzyme in glial cells. Glutamic Acid 0-3 glutamate-ammonia ligase Rattus norvegicus 43-63 25579384-5 2016 The excess of glutamate elicited by Pro together with increased glutamate uptake and upregulated glutamine synthetase (GS) activity supported misregulated glutamate homeostasis in astrocytic cells. Glutamic Acid 14-23 glutamate-ammonia ligase Rattus norvegicus 97-117 26709611-6 2016 Corticosterone stimulated astrocyte glutamate recycling by increasing glutamate uptake and glutamine synthetase (GS), and altered the astrocyte cytoskeleton. Glutamic Acid 36-45 glutamate-ammonia ligase Rattus norvegicus 91-111 26727523-9 2016 Also, maternal EtOH exposure decreased glutamine synthetase activity and induced aspartate aminotransferase enzymatic activity, suggesting that in EtOH-exposed offspring hippocampus, glutamate is preferentially used as a fuel in tricarboxylic acid cycle instead of being converted into glutamine. Glutamic Acid 183-192 glutamate-ammonia ligase Rattus norvegicus 39-59 26220375-1 2015 Glutamine synthetase (GS) in astrocytes is critical for metabolism of glutamate and ammonia in the brain, and perturbations in the anatomical distribution and activity of the enzyme are likely to adversely affect synaptic transmission. Glutamic Acid 70-79 glutamate-ammonia ligase Rattus norvegicus 0-20 24955497-6 2014 The activity of glutamate-related metabolic enzymes (glutaminase and glutamine synthetase) in the trigeminal motor nucleus was also investigated. Glutamic Acid 16-25 glutamate-ammonia ligase Rattus norvegicus 69-89 25196365-1 2015 Glutamine synthetase (GS) plays an important role in glutamate neurotransmission or neurological disorder in the brain. Glutamic Acid 53-62 glutamate-ammonia ligase Rattus norvegicus 0-20 24955497-10 2014 These results suggested that increased glutaminase activity and decreased glutamine synthetase activity increased glutamate production and decreased glutamate decomposition, causing an increase in glutamate levels in the trigeminal motor nucleus and eventually increasing masseter muscle tone. Glutamic Acid 114-123 glutamate-ammonia ligase Rattus norvegicus 74-94 24955497-10 2014 These results suggested that increased glutaminase activity and decreased glutamine synthetase activity increased glutamate production and decreased glutamate decomposition, causing an increase in glutamate levels in the trigeminal motor nucleus and eventually increasing masseter muscle tone. Glutamic Acid 149-158 glutamate-ammonia ligase Rattus norvegicus 74-94 24955497-10 2014 These results suggested that increased glutaminase activity and decreased glutamine synthetase activity increased glutamate production and decreased glutamate decomposition, causing an increase in glutamate levels in the trigeminal motor nucleus and eventually increasing masseter muscle tone. Glutamic Acid 149-158 glutamate-ammonia ligase Rattus norvegicus 74-94 24755687-7 2014 Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats. Glutamic Acid 113-122 glutamate-ammonia ligase Rattus norvegicus 0-20 24755687-7 2014 Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats. Glutamic Acid 113-122 glutamate-ammonia ligase Rattus norvegicus 22-24 21756956-4 2011 We found that the TR-MUL cells express the glial specific enzymes, glutamine synthetase, the mitochondrial isoform of branched chain aminotransferase (BCATm) and pyruvate carboxylase, all of which are involved in glutamate metabolism and homeostasis in the retina. Glutamic Acid 213-222 glutamate-ammonia ligase Rattus norvegicus 67-87 24370597-2 2014 Glial glutamine synthetase enzyme synthesizes glutamine, which helps maintain the optimal neuronal glutamate level. Glutamic Acid 99-108 glutamate-ammonia ligase Rattus norvegicus 6-26 23525248-1 2013 Glutamine synthetase (GS) is an enzyme involved in an endogenous mechanism of protection against glutamate neurotoxicity and is important in the regulation of astrocyte migration. Glutamic Acid 97-106 glutamate-ammonia ligase Rattus norvegicus 0-20 23525248-1 2013 Glutamine synthetase (GS) is an enzyme involved in an endogenous mechanism of protection against glutamate neurotoxicity and is important in the regulation of astrocyte migration. Glutamic Acid 97-106 glutamate-ammonia ligase Rattus norvegicus 22-24 22715058-6 2012 This gliosis was accompanied by a persistent cytosolic accumulation of GLU (immunofluorescence quantified by confocal microscope), which persisted for weeks (self-induced glutamate accumulation), and which was associated to a selective decrease of glutamine synthetase activity. Glutamic Acid 71-74 glutamate-ammonia ligase Rattus norvegicus 248-268 21780187-1 2011 Glutamine synthetase (GS) is an astrocytic enzyme, which catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamic Acid 99-108 glutamate-ammonia ligase Rattus norvegicus 0-20 22742831-1 2012 AIM: To investigate the effect of chronic H1-antihistamine treatment on seizure susceptibility after drug withdrawal in nonepileptic rats and to further study its relation to glutamine synthetase (GS), which is the key enzyme for glutamate metabolism and gamma aminobutyric acid (GABA) synthesis. Glutamic Acid 230-239 glutamate-ammonia ligase Rattus norvegicus 175-195 22167234-1 2012 Brain glutamine synthetase (GS) is an integral part of the glutamate-glutamine cycle and occurs in the glial compartment. Glutamic Acid 59-68 glutamate-ammonia ligase Rattus norvegicus 6-26 21626103-1 2011 Glutamine synthetase (GS), a Muller cell specific enzyme in the retina, is the key enzyme involve in glutamate metabolism. Glutamic Acid 101-110 glutamate-ammonia ligase Rattus norvegicus 0-20 20688809-10 2010 The activity of glutamine synthetase, an astrocyte enzyme converting glutamate into glutamine, decreased in parallel, indicating astrocyte dysfunction. Glutamic Acid 69-78 glutamate-ammonia ligase Rattus norvegicus 16-36 21371894-4 2011 Glutamine synthetase (GS) is an enzyme that is expressed in glial cells and may affect glutamate excitotoxicity. Glutamic Acid 87-96 glutamate-ammonia ligase Rattus norvegicus 0-20 21371894-4 2011 Glutamine synthetase (GS) is an enzyme that is expressed in glial cells and may affect glutamate excitotoxicity. Glutamic Acid 87-96 glutamate-ammonia ligase Rattus norvegicus 22-24 20689060-8 2010 The activity of glutamine synthetase (which condenses ammonia and glutamate) was found to be much higher in colonocytes than in small intestine enterocytes and was 1.6-fold higher (P = 0.0304) in colonocytes isolated from HP animals than NP. Glutamic Acid 66-75 glutamate-ammonia ligase Rattus norvegicus 16-36 21193003-2 2011 Glutamine synthetase (GS) is highly expressed by astrocytes, and serves a neuroprotective function by converting cytotoxic glutamate and ammonia into glutamine. Glutamic Acid 123-132 glutamate-ammonia ligase Rattus norvegicus 0-20 20936267-1 2010 Glutamine synthetase is a key enzyme which has a regulatory role in the brain glutamate pool. Glutamic Acid 78-87 glutamate-ammonia ligase Rattus norvegicus 0-20 18421694-3 2008 Serial histological analysis was performed for Mn-superoxide dismutase (Mn-SOD) and glutamine synthetase (GS), which are Mn-binding enzymes against the oxidative stress and glutamate excitotoxicity in neurodegeneration. Glutamic Acid 173-182 glutamate-ammonia ligase Rattus norvegicus 84-104 20384720-1 2010 PURPOSE: The astrocytic enzyme glutamine synthetase (GS) is a key regulator of glutamate and gamma-aminobutyric acid (GABA) metabolism in the glutamate/glutamine cycle (GGC). Glutamic Acid 79-88 glutamate-ammonia ligase Rattus norvegicus 31-51 20384720-1 2010 PURPOSE: The astrocytic enzyme glutamine synthetase (GS) is a key regulator of glutamate and gamma-aminobutyric acid (GABA) metabolism in the glutamate/glutamine cycle (GGC). Glutamic Acid 142-151 glutamate-ammonia ligase Rattus norvegicus 31-51 20567615-6 2010 The decreased activity of glutamine synthetase may favor the prolonged availability of glutamic acid causing excitotoxicity leading to neuronal damage in anoxia. Glutamic Acid 87-100 glutamate-ammonia ligase Rattus norvegicus 26-46 18479397-1 2008 PURPOSE: The astrocyte-specific glutamine synthetase (GS) plays a key role in glutamate recycling and Gamma-aminobutyric acid (GABA) metabolism. Glutamic Acid 78-87 glutamate-ammonia ligase Rattus norvegicus 32-52 18669513-3 2008 We recently reported that the glutamate-metabolizing enzyme glutamine synthetase is deficient in the hippocampus in patients with MTLE, and we postulated that this deficiency is critically involved in the pathophysiology of the disease. Glutamic Acid 30-39 glutamate-ammonia ligase Rattus norvegicus 60-80 20557426-1 2010 Glutamine synthetase (GS) forms glutamine by catalyzing the ATP-dependent amidation of glutamate. Glutamic Acid 87-96 glutamate-ammonia ligase Rattus norvegicus 0-20 20806080-2 2010 Tyrosine nitration may inhibit glutamine synthetase (GS), causing glutamate accumulation and leading to further neuronal cell death. Glutamic Acid 66-75 glutamate-ammonia ligase Rattus norvegicus 31-51 20484951-3 2010 The glutamate clearance function correlated with the expression of glutamine synthetase (GS) mRNA and L-glutamate/L-aspartate transporter (GLAST) mRNA. Glutamic Acid 4-13 glutamate-ammonia ligase Rattus norvegicus 67-87 19299450-3 2009 Here we report that in the arcuate nucleus estradiol significantly increased the protein levels of the two enzymes in the glutamate-glutamine cycle, glutamine synthetase and glutaminase. Glutamic Acid 122-131 glutamate-ammonia ligase Rattus norvegicus 149-169 17710539-9 2008 In entorhinal cortex glutamine labeling and concentration were unchanged despite the reduced glutamate content and label, possibly due to decreased oxidative metabolism and conserved flux of glutamate through glutamine synthetase in astrocytes. Glutamic Acid 191-200 glutamate-ammonia ligase Rattus norvegicus 209-229 18001886-2 2007 Histological analyses were performed using staining for Mn superoxide dismutase (Mn-SOD) and glutamine synthetase (GS), which are Mn-binding enzymes against oxidative stress and glutamate excitotoxicity in neurodegeneration, and the standard hematoxylin and eosin (H&E). Glutamic Acid 178-187 glutamate-ammonia ligase Rattus norvegicus 93-113 17715355-5 2007 We find that pharmacological inhibitors of glutamine synthetase or system A transporters cause an acute depression of basal synaptic transmission that is rapidly reversible, which is unlikely to be attributable to the rapid loss of vesicular glutamate. Glutamic Acid 242-251 glutamate-ammonia ligase Rattus norvegicus 43-63 17600303-5 2007 In interscapular brown adipose tissue as well as in interscapular, mesenteric, perirenal, and epididymal white adipose tissues, we demonstrate robust immunosignals for the excitatory neurotransmitter glutamate, the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), and the GABA-synthesizing enzyme glutamate decarboxylase (GAD) isoforms GAD65 and GAD67. Glutamic Acid 200-209 glutamate-ammonia ligase Rattus norvegicus 308-331 17600303-5 2007 In interscapular brown adipose tissue as well as in interscapular, mesenteric, perirenal, and epididymal white adipose tissues, we demonstrate robust immunosignals for the excitatory neurotransmitter glutamate, the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), and the GABA-synthesizing enzyme glutamate decarboxylase (GAD) isoforms GAD65 and GAD67. Glutamic Acid 200-209 glutamate-ammonia ligase Rattus norvegicus 333-336 16484281-2 2006 Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to glutamine through the enzyme glutamine synthetase (GS). Glutamic Acid 114-123 glutamate-ammonia ligase Rattus norvegicus 175-195 16781745-8 2006 Exposure to glutamate and lead elevated the cellular malondialdehyde (MDA) levels and phospholipase-A(2) (PLA(2)) activity and diminished the glutamine synthetase (GS) activity. Glutamic Acid 12-21 glutamate-ammonia ligase Rattus norvegicus 142-162 16753258-9 2006 The other, glutamine synthetase (GS), catalyzes the metabolism of glutamate to glutamine; its content decreases in proestrus. Glutamic Acid 66-75 glutamate-ammonia ligase Rattus norvegicus 11-31 16688719-0 2006 Ischemic tolerance in chemical preconditioning: possible role of astrocytic glutamine synthetase buffering glutamate-mediated neurotoxicity. Glutamic Acid 107-116 glutamate-ammonia ligase Rattus norvegicus 76-96 16688719-1 2006 Glutamine synthetase (GS), localized to astrocyte is a key enzyme in the glutamate-glutamine pathway in the brain. Glutamic Acid 73-82 glutamate-ammonia ligase Rattus norvegicus 0-20 15114044-1 2004 BACKGROUND/AIMS: Glutamine synthetase is a key enzyme necessary for ammonia detoxification in the brain, but excessive activation of this enzyme can be cytotoxic to neural cells as a consequence of excessive consumption of ATP and glutamate. Glutamic Acid 231-240 glutamate-ammonia ligase Rattus norvegicus 17-37 15834952-8 2005 Glutamine synthetase was shown to be is a key element in the control of glutamate metabolism in astrocytic cultures. Glutamic Acid 72-81 glutamate-ammonia ligase Rattus norvegicus 0-20 15834952-9 2005 The metabolic fate of glutamate depends greatly on the time of endurance to the challenge: in naive cells, glutamate was primarily metabolized through the transaminase pathway, while in well-adapted cells glutamate was converted almost exclusively through glutamine synthetase. Glutamic Acid 22-31 glutamate-ammonia ligase Rattus norvegicus 256-276 15955607-6 2005 Protein expression of glutamine synthetase (GS), which converts toxic glutamate to non-toxic glutamine, was doubly enhanced. Glutamic Acid 70-79 glutamate-ammonia ligase Rattus norvegicus 22-42 15326614-6 2004 Glutamate was also combined with 1 mM ammonia or with methionine sulfoximine (MSO), an inhibitor of glutamine synthetase, the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamic Acid 0-9 glutamate-ammonia ligase Rattus norvegicus 100-120 15326614-6 2004 Glutamate was also combined with 1 mM ammonia or with methionine sulfoximine (MSO), an inhibitor of glutamine synthetase, the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamic Acid 180-189 glutamate-ammonia ligase Rattus norvegicus 100-120 15326127-0 2004 Glutamate-induced glutamine synthetase expression in retinal Muller cells after short-term ocular hypertension in the rat. Glutamic Acid 0-9 glutamate-ammonia ligase Rattus norvegicus 18-38 15326127-1 2004 PURPOSE: To determine the effect of intraocular pressure (IOP) elevation on glutamate-induced expression of glutamine synthetase (GS) in retinal Muller cells of rat eyes. Glutamic Acid 76-85 glutamate-ammonia ligase Rattus norvegicus 108-128 12969269-4 2003 In fimbria and corpus callosum levels of synaptic proteins, synapsin I and synaptophysin were 15-20% of those in cortex; the activities of glutamine synthetase and phosphate-activated glutaminase, enzymes involved in metabolism of transmitter glutamate, were 11-25% of cortical values, and activities of aspartate and alanine aminotransferases were 50-70% of cortical values. Glutamic Acid 243-252 glutamate-ammonia ligase Rattus norvegicus 139-159 11437060-2 2001 Exposure of astrocytes to low levels of organotins produced significant changes in two key components of glutamate homeostasis: glutamine synthetase (CS) activity and the high-affinity transport of L-glutamate. Glutamic Acid 105-114 glutamate-ammonia ligase Rattus norvegicus 128-148 12619185-1 2003 Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. Glutamic Acid 63-72 glutamate-ammonia ligase Rattus norvegicus 0-20 12619185-1 2003 Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. Glutamic Acid 63-72 glutamate-ammonia ligase Rattus norvegicus 22-24 11433423-2 2001 Ammonium ions penetrate from blood to brain, where they form glutamine (Gln) in the reaction with glutamate catalyzed by an astroglia-specific enzyme, glutamine synthetase (GS). Glutamic Acid 98-107 glutamate-ammonia ligase Rattus norvegicus 151-171 11473118-3 2001 The aim of the present study was to impose altered cellular glutamate levels by overexpression of glutamate decarboxylase (GAD) to repress elevation of cytosolic glutamate. Glutamic Acid 60-69 glutamate-ammonia ligase Rattus norvegicus 98-121 11473118-3 2001 The aim of the present study was to impose altered cellular glutamate levels by overexpression of glutamate decarboxylase (GAD) to repress elevation of cytosolic glutamate. Glutamic Acid 60-69 glutamate-ammonia ligase Rattus norvegicus 123-126 11473118-3 2001 The aim of the present study was to impose altered cellular glutamate levels by overexpression of glutamate decarboxylase (GAD) to repress elevation of cytosolic glutamate. Glutamic Acid 98-107 glutamate-ammonia ligase Rattus norvegicus 123-126 11473118-6 2001 Upon GAD overexpression, glutamate concentrations were no longer elevated by 15 mm glucose as compared with controls (-40%). Glutamic Acid 25-34 glutamate-ammonia ligase Rattus norvegicus 5-8 11259512-3 2001 PC12 cells express two glutamate-metabolizing enzymes, glutamine synthetase (GS) and glutamate decarboxylase (GAD), as well as the glutamate-producing enzyme, phosphate-activated glutaminase (PAG). Glutamic Acid 85-94 glutamate-ammonia ligase Rattus norvegicus 110-113 10820157-2 2000 GABA is biosynthesized from glutamate by glutamate decarboxylase (GAD) and from putrescine via diamine oxidase (DAO). Glutamic Acid 28-37 glutamate-ammonia ligase Rattus norvegicus 41-64 10975907-5 2000 Glutamate dehydrogenase (GDH) and glutamine synthetase (GS), which are localized mainly in astrocytes and involved in glutamate catabolism, are shown to be differentially altered. Glutamic Acid 118-127 glutamate-ammonia ligase Rattus norvegicus 34-54 10962139-1 2000 The glial enzyme glutamine synthetase (GS) is critical for central nervous system catabolism of glutamate and glutamine production. Glutamic Acid 96-105 glutamate-ammonia ligase Rattus norvegicus 17-37 10820157-2 2000 GABA is biosynthesized from glutamate by glutamate decarboxylase (GAD) and from putrescine via diamine oxidase (DAO). Glutamic Acid 28-37 glutamate-ammonia ligase Rattus norvegicus 66-69 10811032-3 2000 At 1 x 10(-2) M concentration, the most potent inhibitor of GAD was D-erythro-4-F-Glu with about 70% inhibition in the presence of 1.23 x 10(-2)M L-glutamate. Glutamic Acid 146-157 glutamate-ammonia ligase Rattus norvegicus 60-63 10462368-7 1999 Increased availability of glutamate following OA treatment provides the substrate for the major ammonia-removal mechanism (glutamine synthetase). Glutamic Acid 26-35 glutamate-ammonia ligase Rattus norvegicus 123-143 10533049-8 1999 Additionally, the appearance of (13)C glutamate points to a distortion of glutamine synthetase (GS), leading to the accumulation of glutamate. Glutamic Acid 38-47 glutamate-ammonia ligase Rattus norvegicus 74-94 10533049-8 1999 Additionally, the appearance of (13)C glutamate points to a distortion of glutamine synthetase (GS), leading to the accumulation of glutamate. Glutamic Acid 132-141 glutamate-ammonia ligase Rattus norvegicus 74-94 10445824-1 1999 Glutamine synthetase (GS) is a glucocorticoid-inducible enzyme that has a key role for glutamate metabolism in the central and peripheral nervous system. Glutamic Acid 87-96 glutamate-ammonia ligase Rattus norvegicus 0-20 10383611-4 1999 In addition, we observed that glutamine synthetase, a key enzyme in glutamate metabolism, was localized in oligodendrocytes in situ. Glutamic Acid 68-77 glutamate-ammonia ligase Rattus norvegicus 30-50 10429966-6 1999 Detoxification of ammonia by glutamine synthetase may be limited due to a shortage of glutamate when the nitrogen load is high. Glutamic Acid 86-95 glutamate-ammonia ligase Rattus norvegicus 29-49 10429966-10 1999 On the basis of these changes in mRNA levels, we conclude that: (a) glutamate is produced pericentrally in sufficient amounts to allow ammonia detoxification by glutamine synthetase and (b) in addition to the catalytic role of ornithine in the periportally localized ornithine cycle, pericentral ornithine degradation provides glutamate for ammonia detoxification. Glutamic Acid 68-77 glutamate-ammonia ligase Rattus norvegicus 161-181 9932869-9 1999 Activity of glutamine synthetase, a key glial enzyme involved in glutamate detoxification, was assayed in these cultures in the presence or absence of exogenous glutamate. Glutamic Acid 65-74 glutamate-ammonia ligase Rattus norvegicus 12-32 9495576-1 1997 Glutamine synthetase catalyses the formation of L-Gln from L-Glu and NH4+. Glutamic Acid 59-64 glutamate-ammonia ligase Rattus norvegicus 0-20 9394040-6 1998 Autoradiography of intact and dissociated rat retinae indicates that glutamate uptake by Muller glial cells dominates total retinal glutamate transport and that this uptake is strongly influenced by the activity of glutamine synthetase. Glutamic Acid 69-78 glutamate-ammonia ligase Rattus norvegicus 215-235 9752723-1 1998 Glutamine synthetase, the enzyme that catalyzes the ATP-dependent conversion of glutamate and ammonia into glutamine, is expressed in a tissue-specific and developmentally controlled manner. Glutamic Acid 80-89 glutamate-ammonia ligase Rattus norvegicus 0-20 9086492-1 1996 Glutamine synthetase (GS) is a key enzyme involved in glutamate compartmentalisation which may be pivotal in the course of both central free-radical mediated and excitotoxic events. Glutamic Acid 54-63 glutamate-ammonia ligase Rattus norvegicus 0-20 9435573-2 1997 This response is accompanied by increased enzymatic activity of glutamine synthetase (GS), which catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamic Acid 139-148 glutamate-ammonia ligase Rattus norvegicus 64-84 9283609-8 1997 On starvation, glutamate concentrations increased only in the small rim of pericentral cells that express glutamine synthetase, to approximately 15 mM. Glutamic Acid 15-24 glutamate-ammonia ligase Rattus norvegicus 106-126 9088880-6 1997 In the CNS, GABA is synthesised from glutamic acid by the enzyme glutamate decarboxylase (GAD) and catabolized into succinic semialdehyde by the enzyme GABA-transaminase (GABA-T), which are pyridoxal phosphate (PLP) dependent enzymes. Glutamic Acid 37-50 glutamate-ammonia ligase Rattus norvegicus 65-88 9088880-6 1997 In the CNS, GABA is synthesised from glutamic acid by the enzyme glutamate decarboxylase (GAD) and catabolized into succinic semialdehyde by the enzyme GABA-transaminase (GABA-T), which are pyridoxal phosphate (PLP) dependent enzymes. Glutamic Acid 37-50 glutamate-ammonia ligase Rattus norvegicus 90-93 8690847-1 1995 gamma-Aminobutyric acid (GABA) is a major inhibitory neurotransmitter, synthesised from glutamate by glutamate decarboxylase (GAD), in the central nervous system. Glutamic Acid 88-97 glutamate-ammonia ligase Rattus norvegicus 101-124 7487913-5 1995 A linear increase of 1/v with 1/s permitted estimation of the in vivo glutamine synthetase (GS) activity at a physiological blood ammonia concentration to be 0.4-2.1 mumol/h per g. The observed ammonia-dependence strongly suggests that, under physiological conditions, in vivo GS activity is kinetically limited by sub-optimal in situ concentrations of ammonia as well as glutamate and ATP. Glutamic Acid 372-381 glutamate-ammonia ligase Rattus norvegicus 70-90 8690847-1 1995 gamma-Aminobutyric acid (GABA) is a major inhibitory neurotransmitter, synthesised from glutamate by glutamate decarboxylase (GAD), in the central nervous system. Glutamic Acid 88-97 glutamate-ammonia ligase Rattus norvegicus 126-129 8531222-7 1995 Since endogenous glutamate can only be demonstrated in Muller cells if glutamine synthetase (GS) is inhibited (Pow and Robinson: Neuroscience 60:355-366, 1994), the immunocytochemical localization of GS was determined. Glutamic Acid 17-26 glutamate-ammonia ligase Rattus norvegicus 93-95 7796789-1 1995 Glutamate decarboxylase (EC 4.1.1.15, GAD) activity was studied in the brain of 12-day-old and adult rats treated with 3-mercaptopropionic acid (3-MPA), an inhibitor of GAD competitive with glutamate. Glutamic Acid 190-199 glutamate-ammonia ligase Rattus norvegicus 0-23