PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32149465-0	2020	Induction of apoptosis through extrinsic/intrinsic pathways and suppression of ERK/NF-kappaB signalling participate in anti-glioblastoma of imipramine.	Imipramine	140-150	mitogen-activated protein kinase 1	Homo sapiens	79-82
32149465-0	2020	Induction of apoptosis through extrinsic/intrinsic pathways and suppression of ERK/NF-kappaB signalling participate in anti-glioblastoma of imipramine.	Imipramine	140-150	nuclear factor kappa B subunit 1	Homo sapiens	83-92
32149465-7	2020	The ERK and NF-kappaB inhibitory capacity of imipramine is detected by NF-kappaB reporter gene assay and Western blotting.	Imipramine	45-55	mitogen-activated protein kinase 1	Homo sapiens	4-7
32149465-7	2020	The ERK and NF-kappaB inhibitory capacity of imipramine is detected by NF-kappaB reporter gene assay and Western blotting.	Imipramine	45-55	nuclear factor kappa B subunit 1	Homo sapiens	12-21
32149465-7	2020	The ERK and NF-kappaB inhibitory capacity of imipramine is detected by NF-kappaB reporter gene assay and Western blotting.	Imipramine	45-55	nuclear factor kappa B subunit 1	Homo sapiens	71-80
32149465-10	2020	Furthermore, imipramine effectively suppressed glioblastoma progression in vivo via the inhibition of the ERK/NF-kappaB pathway.	Imipramine	13-23	mitogen-activated protein kinase 1	Homo sapiens	106-109
32149465-10	2020	Furthermore, imipramine effectively suppressed glioblastoma progression in vivo via the inhibition of the ERK/NF-kappaB pathway.	Imipramine	13-23	nuclear factor kappa B subunit 1	Homo sapiens	110-119
32149465-11	2020	In summary, imipramine is a potential anti-glioblastoma drug which induces apoptosis and has the capacity to inhibit ERK/NF-kappaB signalling.	Imipramine	12-22	mitogen-activated protein kinase 1	Homo sapiens	117-120
32149465-11	2020	In summary, imipramine is a potential anti-glioblastoma drug which induces apoptosis and has the capacity to inhibit ERK/NF-kappaB signalling.	Imipramine	12-22	nuclear factor kappa B subunit 1	Homo sapiens	121-130
32198394-2	2020	SERT activity is modulated by antidepressants, e.g., S-citalopram and imipramine, to alleviate symptoms of depression and anxiety.	Imipramine	70-80	solute carrier family 6 member 4	Rattus norvegicus	0-4
32198394-6	2020	The SERT inhibition by Lu AF60097 is demonstrated by the potentiated imipramine binding and increased hippocampal serotonin level in rats.	Imipramine	69-79	solute carrier family 6 member 4	Rattus norvegicus	4-8
31420165-0	2019	Rapid antidepressant actions of imipramine potentiated by zinc through PKA-dependented regulation of mTOR and CREB signaling.	Imipramine	32-42	mechanistic target of rapamycin kinase	Homo sapiens	101-105
32078638-6	2020	Pharmacological studies revealed that enhanced depressive-like behavior in GluD1-KO mice was restored by the serotonin reuptake inhibitors imipramine and fluoxetine, but not the norepinephrine transporter inhibitor desipramine.	Imipramine	139-149	glutamate dehydrogenase 1	Mus musculus	75-80
31866985-3	2019	Both pretreatment of B. mori embryonic cells (BmE) with NPC1 antagonists (imipramine or U18666A) and down-regulation of NPC1 expression resulted in a significant reduction in baculovirus BmNPV (B. mori nuclear polyhedrosis virus) infectivity.	Imipramine	74-84	NPC intracellular cholesterol transporter 1	Homo sapiens	56-60
31656696-3	2019	In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm.	Imipramine	49-59	purinergic receptor P2X 7	Rattus norvegicus	69-74
31656696-3	2019	In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm.	Imipramine	49-59	purinergic receptor P2X 4	Rattus norvegicus	79-84
31656696-3	2019	In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm.	Imipramine	61-64	purinergic receptor P2X 7	Rattus norvegicus	69-74
31656696-3	2019	In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm.	Imipramine	61-64	purinergic receptor P2X 4	Rattus norvegicus	79-84
31656696-4	2019	Repeated, but not acute administration of IMI (15 mg/kg ip) reduced the levels of both P2RX7 and P2RX4 in the ventral, but not in dorsal hippocampus or frontal cortex.	Imipramine	42-45	purinergic receptor P2X 7	Homo sapiens	87-92
31656696-4	2019	Repeated, but not acute administration of IMI (15 mg/kg ip) reduced the levels of both P2RX7 and P2RX4 in the ventral, but not in dorsal hippocampus or frontal cortex.	Imipramine	42-45	purinergic receptor P2X 4	Homo sapiens	97-102
31420165-0	2019	Rapid antidepressant actions of imipramine potentiated by zinc through PKA-dependented regulation of mTOR and CREB signaling.	Imipramine	32-42	cAMP responsive element binding protein 1	Homo sapiens	110-114
31420165-8	2019	Combination of zinc with imipramine rapidly enhanced the phosphorylation of mTOR Ser2448 and CREB Ser133, and increased the expression of mTOR and CREB, which were dependent on the activation of PKA.	Imipramine	25-35	mechanistic target of rapamycin kinase	Homo sapiens	76-80
31420165-8	2019	Combination of zinc with imipramine rapidly enhanced the phosphorylation of mTOR Ser2448 and CREB Ser133, and increased the expression of mTOR and CREB, which were dependent on the activation of PKA.	Imipramine	25-35	cAMP responsive element binding protein 1	Homo sapiens	93-97
31420165-8	2019	Combination of zinc with imipramine rapidly enhanced the phosphorylation of mTOR Ser2448 and CREB Ser133, and increased the expression of mTOR and CREB, which were dependent on the activation of PKA.	Imipramine	25-35	mechanistic target of rapamycin kinase	Homo sapiens	138-142
31420165-8	2019	Combination of zinc with imipramine rapidly enhanced the phosphorylation of mTOR Ser2448 and CREB Ser133, and increased the expression of mTOR and CREB, which were dependent on the activation of PKA.	Imipramine	25-35	cAMP responsive element binding protein 1	Homo sapiens	147-151
31889042-4	2019	After IMI treatment a reduction was noted in the expression of FAAH protein in the dorsal striatum, MAGL in the frontal cortex and DAGLalpha in the cerebellum.	Imipramine	6-9	fatty-acid amide hydrolase-like	Rattus norvegicus	63-67
31278507-10	2019	On the other hand, treatment with combined antidepressants (amitriptyline/imipramine + fluoxetine) initiates p16-dependent cell cycle arrest, overexpression of telomere maintenance proteins and finally restoration of proliferation.	Imipramine	74-84	cyclin dependent kinase inhibitor 2A	Homo sapiens	109-112
31889042-4	2019	After IMI treatment a reduction was noted in the expression of FAAH protein in the dorsal striatum, MAGL in the frontal cortex and DAGLalpha in the cerebellum.	Imipramine	6-9	monoglyceride lipase	Rattus norvegicus	100-104
31889042-4	2019	After IMI treatment a reduction was noted in the expression of FAAH protein in the dorsal striatum, MAGL in the frontal cortex and DAGLalpha in the cerebellum.	Imipramine	6-9	diacylglycerol lipase, alpha	Rattus norvegicus	131-140
31337198-10	2019	Furthermore, imipramine (a selective A-SMase inhibitor) treatment reduced the exercise-induced CK and IL-6 elevations, along with a decrease in cleaved caspase-3 (Cas-3) of gastrocnemius muscles.	Imipramine	13-23	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	37-44
31262782-6	2019	Treatment of mice with pharmacological inhibitors of acid sphingomyelinase (ASMase), desipramine and imipramine, attenuated ATP-induced TF decryption.	Imipramine	101-111	coagulation factor III	Mus musculus	136-138
31181487-3	2019	On MIPBPZ, CPZ, BPZ and imipramine (IMP) gave the maximal retention factors at a mobile-phase pH 8, while the maximal imprinting factors were obtained at a mobile-phase pH 7.	Imipramine	36-39	carboxypeptidase Z	Rattus norvegicus	11-14
31181487-8	2019	The column-switching LC method was validated and applied for the determination of CPZ and its metabolites, DM-CPZ, DDM-CPZ, CPZ-SO and CPZ-NO, in rat plasma after intravenous and oral administration of CPZ using IMP as an internal standard.	Imipramine	212-215	carboxypeptidase Z	Rattus norvegicus	82-85
31061069-6	2019	Compared with RIT alone, the use of RIT with ASMase inhibitor (imipramine) or with a lipid raft disruptor (e.g., methyl-beta-cyclodextrin or filipin) led to an increase in clonogenic cell survival in vitro and to larger tumors and less tissue DNA damage in vivo.	Imipramine	63-73	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	45-51
31337198-10	2019	Furthermore, imipramine (a selective A-SMase inhibitor) treatment reduced the exercise-induced CK and IL-6 elevations, along with a decrease in cleaved caspase-3 (Cas-3) of gastrocnemius muscles.	Imipramine	13-23	interleukin 6	Mus musculus	102-106
30366345-0	2019	Imipramine treatment reverses depressive- and anxiety-like behaviors, normalize adrenocorticotropic hormone, and reduces interleukin-1beta in the brain of rats subjected to experimental periapical lesion.	Imipramine	0-10	interleukin 1 beta	Rattus norvegicus	121-138
30843263-11	2019	Imipramine compared to placebo increased opening urethral pressure in the resting condition with 6.5 cmH2 O (95% confidence interval [CI]: -0.5, 13.5), P = 0.07, and in the squeeze condition with 7.9 cmH 2 O (95% CI: -0.3, 16.1), P = 0.06.	Imipramine	0-10	troponin T2, cardiac type	Homo sapiens	101-105
30877268-12	2019	Elevated levels of phosphorylated insulin signaling proteins were present in the ILPFC of ACTH-pretreated animals that received both imipramine and lithium, together with a concurrent increase in mTOR activation in PBMCs.	Imipramine	133-143	insulin	Homo sapiens	34-41
30419533-6	2019	RESULTS: A single administration of the GPR39 agonist caused an antidepressant-like effect lasting up to 24 h following the injection, which is longer than the effect of imipramine, ZnCl2 and MK-801.	Imipramine	170-180	G protein-coupled receptor 39	Mus musculus	40-45
30366345-13	2019	However, rats treated with imipramine had lower IL-1beta and ACTH levels.	Imipramine	27-37	interleukin 1 beta	Rattus norvegicus	48-56
29378782-3	2018	ASM inhibition with imipramine or sphingomyelin phosphodiesterase 1 (SMPD1) siRNA in human lung cells, or by transgenic Smpd1+/- haploinsufficiency of mouse lungs, markedly reduced mTOR- and P70-S6 kinase (Thr 389)-phosphorylation and modified TFEB in a pattern consistent with its activation.	Imipramine	20-30	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
30091005-10	2018	Moreover, imipramine and reboxetine increased the phosphorylated form of HDAC5 (P-HDAC5), mediating its cytoplasmic export.	Imipramine	10-20	histone deacetylase 5	Mus musculus	73-78
30091005-10	2018	Moreover, imipramine and reboxetine increased the phosphorylated form of HDAC5 (P-HDAC5), mediating its cytoplasmic export.	Imipramine	10-20	histone deacetylase 5	Mus musculus	80-87
29417943-5	2018	Postnatal genetic knock-out of G9a reduces anxiety-related behavior, consistent with the reduction of G9a levels by some medications used to treat anxiety (amitriptyline, imipramine and paroxetine).	Imipramine	171-181	euchromatic histone lysine N-methyltransferase 2	Mus musculus	31-34
29417943-5	2018	Postnatal genetic knock-out of G9a reduces anxiety-related behavior, consistent with the reduction of G9a levels by some medications used to treat anxiety (amitriptyline, imipramine and paroxetine).	Imipramine	171-181	euchromatic histone lysine N-methyltransferase 2	Mus musculus	102-105
30361780-7	2018	All of the six drugs examined, including amitriptyline, fluoxetine, imipramine, irinotecan, ondansetron, and verapamil, were inhibitors of OCT1/2-mediated morphine uptake.	Imipramine	68-78	solute carrier family 22 member 1	Homo sapiens	139-143
29759138-8	2018	One of the most pronounced effect of imipramine is the reduction of vimentin level, this protein is engaged in majority of biological processes which were found to be affected by imipramine.	Imipramine	37-47	vimentin	Rattus norvegicus	68-76
29759138-8	2018	One of the most pronounced effect of imipramine is the reduction of vimentin level, this protein is engaged in majority of biological processes which were found to be affected by imipramine.	Imipramine	179-189	vimentin	Rattus norvegicus	68-76
29151391-10	2018	Moreover, in an independent experimental group, only repeated treatment with 7-NI and imipramine increased BDNF protein levels in the hippocampus.	Imipramine	86-96	brain-derived neurotrophic factor	Rattus norvegicus	107-111
29486339-6	2018	In MDD patient group, the CART levels had a negative correlation with antidepressant dose (imipramine-equivalent dose) (rho = -0.55, p < 0.01) and significantly decreased in antidepressant-treated group (AD-treated group) compared to controls (p < 0.05).	Imipramine	91-101	CART prepropeptide	Homo sapiens	26-30
29358904-6	2017	Other antidepressants (e.g., sertraline and imipramine) also increased the expression of BDNF mRNA with relative potencies similar to those for inhibition of Kir4.1 channels.	Imipramine	44-54	brain derived neurotrophic factor	Mus musculus	89-93
29379286-9	2018	Zuotai or imipramine remarkably decreased levels of corticotropin-releasing hormone, adrenocorticotropic hormone, and corticosterone in the HPA axis, and increased levels of 5-hydroxytryptamine and norepinephrine in the serum in CUMS mice.	Imipramine	10-20	corticotropin releasing hormone	Mus musculus	52-83
29379286-9	2018	Zuotai or imipramine remarkably decreased levels of corticotropin-releasing hormone, adrenocorticotropic hormone, and corticosterone in the HPA axis, and increased levels of 5-hydroxytryptamine and norepinephrine in the serum in CUMS mice.	Imipramine	10-20	pro-opiomelanocortin-alpha	Mus musculus	85-112
27975170-3	2018	In the first part of the study, we found that fluoxetine, imipramine, and milnacipran (i.p., 20 mg/kg/day for 1 week or 3 weeks) upregulated brain-derived neurotrophic factor in the striatum and substantia nigra both at 1 week and 3 weeks.	Imipramine	58-68	brain derived neurotrophic factor	Homo sapiens	141-174
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	carbonic anhydrase 1	Rattus norvegicus	72-75
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	carbonic anhydrase 3	Rattus norvegicus	80-83
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
28398601-0	2017	Antidepressant Imipramine Protects Bupivacaine-Induced Neurotoxicity in Dorsal Root Ganglion Neurons Through Coactivation of TrkA and TrkB.	Imipramine	15-25	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	125-129
28398601-0	2017	Antidepressant Imipramine Protects Bupivacaine-Induced Neurotoxicity in Dorsal Root Ganglion Neurons Through Coactivation of TrkA and TrkB.	Imipramine	15-25	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	134-138
28398601-11	2017	Imipramine protected bupivacaine-induced neurotoxicity in DRG, likely via the co-activation of TrkA and TrkB signaling pathways.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	95-99
28398601-11	2017	Imipramine protected bupivacaine-induced neurotoxicity in DRG, likely via the co-activation of TrkA and TrkB signaling pathways.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	104-108
28722769-7	2017	The imipramine treatment was most prominent among the four antidepressants; it up-regulated hippocampal CHRM2 and frontal cortex CHRM5 in both genotypes, and frontal cortex CHRNA7 only in KIV mice.	Imipramine	4-14	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	173-179
28778545-7	2017	Secondly, the effect of repeated treatment with the selective SIRT2 inhibitor 33i and the antidepressant imipramine on anhedonic behaviour of VGLUT1+/- mice was studied by weekly monitoring of sucrose intake.	Imipramine	105-115	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	142-148
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Imipramine	195-205	NLR family pyrin domain containing 3	Homo sapiens	75-80
28811745-4	2017	The results showed a role for direct and indirect TNF-alpha inhibition through agents such as thalidomide, 3,6-dithiothalidomide, etanercept, infliximab, exendin-4, sodium hydrosulfide, minocycline, imipramine, and atorvastatin.	Imipramine	199-209	tumor necrosis factor	Rattus norvegicus	50-59
28803855-4	2017	A two-week-long pretreatment regime with imipramine (7.5mg/kg/day) or thiamine (200mg/kg/day), which is known to have antidepressant properties, reduced the GSK3beta over-expression and decreased floating behaviour on Day 5.	Imipramine	41-51	glycogen synthase kinase 3 beta	Mus musculus	157-165
28803855-7	2017	In this model, GSK3alpha mRNA changes were prevented by imipramine or thiamine treatment.	Imipramine	56-66	glycogen synthase kinase 3 alpha	Mus musculus	15-24
28093219-11	2017	Imipramine decreased c-Fos expression in the basolateral amygdala and CA1 and CA3 divisions of the hippocampus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
28093219-11	2017	Imipramine decreased c-Fos expression in the basolateral amygdala and CA1 and CA3 divisions of the hippocampus.	Imipramine	0-10	carbonic anhydrase 1	Rattus norvegicus	70-73
28093219-11	2017	Imipramine decreased c-Fos expression in the basolateral amygdala and CA1 and CA3 divisions of the hippocampus.	Imipramine	0-10	carbonic anhydrase 3	Rattus norvegicus	78-81
28481322-4	2017	This effect can be inhibited by imipramine, an inhibitor of acid sphingomyelinase (ASM), which is also known as a member of tricyclic antidepressants (TCAs).	Imipramine	32-42	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	60-81
28238856-7	2017	Additionally, proliferative, but not growth-arrested BAEC, are sensitive to gemcitabine-induced apoptotic death, an effect blocked by inhibiting ASMase with imipramine or by binding ceramide on the cell surface with an anti-ceramide Ab.	Imipramine	157-167	sphingomyelin phosphodiesterase 1	Homo sapiens	145-151
28481322-4	2017	This effect can be inhibited by imipramine, an inhibitor of acid sphingomyelinase (ASM), which is also known as a member of tricyclic antidepressants (TCAs).	Imipramine	32-42	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	83-86
27825907-8	2017	As for imipramine, both compounds inhibited the upregulation of GSK-3beta induced by predator stress or repeated swimming, and reduced floating scores and the predator stress-induced behavioural changes in anxiety and exploration.	Imipramine	7-17	glycogen synthase kinase 3 beta	Mus musculus	64-73
27621227-8	2017	Finally, imipramine, a widely used and effective anti-anxiety medicine, rescued anxiety-like behaviors and excessive self-grooming in Zfp462+/- mice.	Imipramine	9-19	zinc finger protein 462	Mus musculus	134-140
28520379-0	2012	Imipramine Therapy and CYP2D6 and CYP2C19 Genotype Imipramine is a tricyclic antidepressant used in the treatment of several psychiatric disorders including major depression, obsessive-compulsive disorder, generalized anxiety disorder, post-traumatic stress disorder, and bulimia.	Imipramine	51-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
28520379-6	2012	Imipramine is primarily metabolized via CYP2C19 to active metabolites, including desipramine, also a tricyclic antidepressant.	Imipramine	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
28520379-10	2012	The FDA-approved drug label for imipramine states that CYP2D6 poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants when given usual doses.	Imipramine	32-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	55-61
28462695-2	2017	AMPA receptor and cAMP response element-binding protein (CREB) are involved in the antidepressant actions of Ketamine and imipramine, a traditional tricyclic antidepressant.	Imipramine	122-132	cAMP responsive element binding protein 1	Homo sapiens	18-55
28071711-7	2017	While the association between both Per3-/- phenotypes remains unclear, both are alleviated by imipramine treatment during dim night-time light.	Imipramine	94-104	period circadian clock 3	Mus musculus	35-39
27569185-4	2017	Similar to the positive control imipramine (IMI; 10mg/kg), repeated treatment with 10mg/kg MIR but not acute treatment reduced immobility time in the TST, indicating an antidepressant-like effect.	Imipramine	32-42	microRNA 615	Mus musculus	91-94
27569185-4	2017	Similar to the positive control imipramine (IMI; 10mg/kg), repeated treatment with 10mg/kg MIR but not acute treatment reduced immobility time in the TST, indicating an antidepressant-like effect.	Imipramine	44-47	microRNA 615	Mus musculus	91-94
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	175-185	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	108-128
28462695-2	2017	AMPA receptor and cAMP response element-binding protein (CREB) are involved in the antidepressant actions of Ketamine and imipramine, a traditional tricyclic antidepressant.	Imipramine	122-132	cAMP responsive element binding protein 1	Homo sapiens	57-61
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	175-185	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	130-135
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	175-185	cAMP responsive element binding protein 1	Homo sapiens	69-73
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	322-332	cAMP responsive element binding protein 1	Homo sapiens	69-73
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	322-332	cAMP responsive element binding protein 1	Homo sapiens	99-103
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	322-332	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	108-128
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	322-332	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	130-135
28462695-7	2017	CONCLUSION: Our study suggests that differential regulation of CRTC1 expression may contribute to the discrepancy of antidepressant efficacy between ketamine and imipramine, which may lead to a better understanding of ketamine"s fast antidepressant responses.	Imipramine	162-172	CREB regulated transcription coactivator 1	Homo sapiens	63-68
27632988-7	2017	CONCLUSION: CYP2D6 binding subsite A was found to be relatively selective for small molecular weight with higher polarity compared with subsite B which tends to favor larger molecular weight and relatively hydrophobic molecules such as tamoxifen and imipramine.	Imipramine	250-260	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	12-18
28462695-5	2017	RESULTS: Here we show that the enhancement of the phosphorylation of CREB Ser133 and expression of CREB and glutamate receptor 1 (GluR1) are necessary for both ketamine"s and imipramine"s antidepressant actions, but the enhancements at early stage may account for the faster onset of ketamine"s antidepressant action than imipramine.	Imipramine	175-185	cAMP responsive element binding protein 1	Homo sapiens	99-103
27894924-2	2017	administration of glucagon-like peptide-2 (GLP-2) to rodents was shown to have antidepressant-like effects in imipramine-resistant depression-model mice.	Imipramine	110-120	glucagon-like peptide 2 receptor	Mus musculus	18-41
27894924-2	2017	administration of glucagon-like peptide-2 (GLP-2) to rodents was shown to have antidepressant-like effects in imipramine-resistant depression-model mice.	Imipramine	110-120	glucagon-like peptide 2 receptor	Mus musculus	43-48
26915736-8	2016	Treatment with imipramine, an ASMase inhibitor, inhibited the MF-induced EGFR clustering.	Imipramine	15-25	sphingomyelin phosphodiesterase 1	Homo sapiens	30-36
26915736-8	2016	Treatment with imipramine, an ASMase inhibitor, inhibited the MF-induced EGFR clustering.	Imipramine	15-25	epidermal growth factor receptor	Homo sapiens	73-77
27440861-3	2016	Imipramine undergoes N-demethylation to form the active metabolite desipramine, and both imipramine and desipramine are converted to hydroxylated metabolites by the polymorphic enzyme CYP2D6.	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	184-190
27223094-5	2016	Imipramine attenuated stress-induced corticosterone and IL-6 responses in plasma.	Imipramine	0-10	interleukin 6	Mus musculus	56-60
27440861-3	2016	Imipramine undergoes N-demethylation to form the active metabolite desipramine, and both imipramine and desipramine are converted to hydroxylated metabolites by the polymorphic enzyme CYP2D6.	Imipramine	89-99	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	184-190
27440861-9	2016	Moreover, the PBPK model was able to recover simultaneously plasma profiles of imipramine and desipramine in populations with different phenotypes of CYP2D6.	Imipramine	79-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	150-156
27383160-1	2016	The effect of chronic treatment with antidepressant drugs fluoxetine (20 mg/kg) and imipramine (25 mg/kg) on the number of antibody-producing cells and the main T cell subpopulations in ASC mice characterized by genetic predisposition to depression-like states was studied at the peak of the SE-induced immune response (5x10(8)).	Imipramine	84-94	steroid sulfatase	Mus musculus	186-189
27364961-14	2016	Imipramine treatment reversed depressive-like behaviors, re-established hippocampal BDNF and GDNF expression, and normalized ACTH levels in the blood.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	84-88
27364961-14	2016	Imipramine treatment reversed depressive-like behaviors, re-established hippocampal BDNF and GDNF expression, and normalized ACTH levels in the blood.	Imipramine	0-10	glial cell derived neurotrophic factor	Rattus norvegicus	93-97
27373591-0	2016	Effect of acute imipramine administration on the pattern of forced swim-induced c-Fos expression in the mouse brain.	Imipramine	16-26	FBJ osteosarcoma oncogene	Mus musculus	80-85
27373591-5	2016	In the present study, we explored the mouse brain through immunohistochemistry staining for c-Fos after acute administration of imipramine or saline with or without a subsequent swim session.	Imipramine	128-138	FBJ osteosarcoma oncogene	Mus musculus	92-97
27373591-6	2016	Imipramine enhanced the c-Fos density in regions of the central extended amygdala, while forced swim stress increased c-Fos expression in some hypothalamic (the ventrolateral preoptic nucleus and dorsomedial nucleus) and brain stem regions, which is consistent with previous reports.	Imipramine	0-10	FBJ osteosarcoma oncogene	Mus musculus	24-29
27373591-7	2016	In contrast to previous literature with rats, swim stress brought a significant increase in c-Fos expression in the lateral septal nucleus and some other regions in the hypothalamus (the intermediate hypothalamic area, the paraventricular and arcuate nucleus) only in the imipramine-pretreated group, which has not been observed previously.	Imipramine	272-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
27181513-9	2016	Moreover, lithium, carbamazepine, haloperidol and imipramine differently but significantly affected the levels of PGE2, TNF-alpha and P-p65 in plasma and hypothalamus of LPS-treated rats.	Imipramine	50-60	tumor necrosis factor	Rattus norvegicus	120-129
27634008-4	2016	We observed that chronic KOR activation by U50488, a selective KOR agonist, significantly increased depression like symptoms (behavioral despair, anhedonia and sociability) in C57BL/6J mice, which were blocked by KOR antagonist norBNI and antidepressant imipramine, but not by fluoxetine or citalopram.	Imipramine	254-264	opioid receptor, kappa 1	Mus musculus	25-28
27634008-6	2016	Similar to behavioral effects norBNI and imipramine, but not SSRIs, blocked NR2B phosphorylation.	Imipramine	41-51	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	76-80
27208493-0	2016	Evidence for the involvement of neuropeptide Y in the antidepressant effect of imipramine in type 2 diabetes.	Imipramine	79-89	neuropeptide Y	Mus musculus	32-46
27208493-8	2016	Moreover, reduced immobility time by imipramine was potentiated by NPY and [Leu(31), Pro(34)]-NPY, but attenuated by BIBP3226.	Imipramine	37-47	neuropeptide Y	Mus musculus	67-70
27208493-8	2016	Moreover, reduced immobility time by imipramine was potentiated by NPY and [Leu(31), Pro(34)]-NPY, but attenuated by BIBP3226.	Imipramine	37-47	neuropeptide Y	Mus musculus	94-97
27208493-10	2016	A significant reduction in NPY immunoreactivity in the central nucleus of amygdala, nucleus accumbens shell and lateral division of bed nucleus of stria terminalis of the diabetic mice was noticed; the response was ameliorated in imipramine treated animals.	Imipramine	230-240	neuropeptide Y	Mus musculus	27-30
27208493-11	2016	The results suggest that decreased NPY expression in the extended amygdala might be causally linked with the depression induced following type 2 diabetes and that the antidepressant action of imipramine in diabetic mice might be mediated by NPY-NPY Y1 receptor system.	Imipramine	192-202	neuropeptide Y	Mus musculus	241-244
27208493-11	2016	The results suggest that decreased NPY expression in the extended amygdala might be causally linked with the depression induced following type 2 diabetes and that the antidepressant action of imipramine in diabetic mice might be mediated by NPY-NPY Y1 receptor system.	Imipramine	192-202	neuropeptide Y	Mus musculus	241-244
26921875-9	2016	Intraperitoneal injection of imipramine or histone deacetylase inhibitors (HDACi) to the LH mice for 14 consecutive days ameliorated depression-like behaviors and reversed the decrease in BDNF.	Imipramine	29-39	brain derived neurotrophic factor	Mus musculus	188-192
27089947-4	2016	We employ ultraviolet-induced crosslinking with p-azido-L-phenylalanine (azF) at selected positions in hSERT to map the binding site of imipramine, a prototypical tricyclic antidepressant, and vortioxetine, a novel multimodal antidepressant.	Imipramine	136-146	AZF1	Homo sapiens	73-76
27089947-4	2016	We employ ultraviolet-induced crosslinking with p-azido-L-phenylalanine (azF) at selected positions in hSERT to map the binding site of imipramine, a prototypical tricyclic antidepressant, and vortioxetine, a novel multimodal antidepressant.	Imipramine	136-146	solute carrier family 6 member 4	Homo sapiens	103-108
26856855-8	2016	The increased D2 receptor density observed in OBX mice was reversed by imipramine administration.	Imipramine	71-81	dopamine receptor D2	Mus musculus	14-25
26915317-13	2016	The underlying mechanisms of imipramine"s anti-depressive effect may be associated with the down-regulation of betaCaMKII and membrane GluR1 in the habenula, as well as the up-regulation of membrane GluR1 in the prefrontal cortex.	Imipramine	29-39	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	135-140
26641965-1	2016	Homer1a is upregulated by several different antidepressant measures, including non-pharmacological treatments, like sleep deprivation (SD) and electroconvulsive therapy (ECT) and antidepressant drugs, such as imipramine, fluoxetine and ketamine.	Imipramine	209-219	homer scaffold protein 1	Homo sapiens	0-7
26774465-9	2016	Testosterone treatment had no significant effect on neurogenesis, though the combination of testosterone and imipramine increased PSA-NCAM expression in the ventral dentate gyrus.	Imipramine	109-119	neural cell adhesion molecule 1	Rattus norvegicus	134-138
27127489-0	2016	Imipramine protects retinal ganglion cells from oxidative stress through the tyrosine kinase receptor B signaling pathway.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	77-103
27127489-2	2016	In this study, we attempted to examine whether imipramine, a tricyclic antidepressant, may protect hydrogen peroxide (H2O2)-induced RGC degeneration through the activation of the TrkB pathway in RGC-5 cell lines.	Imipramine	47-57	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	179-183
27127489-4	2016	Western blot assay showed that in H2O2 -damaged RGC-5 cells, imipramine activated TrkB pathways through extracellular signal-regulated protein kinase/TrkB phosphorylation.	Imipramine	61-71	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	82-86
27127489-4	2016	Western blot assay showed that in H2O2 -damaged RGC-5 cells, imipramine activated TrkB pathways through extracellular signal-regulated protein kinase/TrkB phosphorylation.	Imipramine	61-71	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	150-154
27127489-6	2016	Finally, TrkB-IgG intervention was able to reverse the protective effect of imipramine on H2O2 -induced RGC-5 apoptosis.	Imipramine	76-86	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	9-13
27127489-7	2016	Imipramine therefore protects RGCs from oxidative stress-induced apoptosis through the TrkB signaling pathway.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	87-91
26915317-13	2016	The underlying mechanisms of imipramine"s anti-depressive effect may be associated with the down-regulation of betaCaMKII and membrane GluR1 in the habenula, as well as the up-regulation of membrane GluR1 in the prefrontal cortex.	Imipramine	29-39	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	199-204
27478647-4	2016	Unexpectedly, floating behaviour and brain glycogen synthase kinase-3 beta (GSK-3beta) mRNA levels, a factor of synaptic plasticity as well as a marker of distress and depression, were increased during the additional swimming session that was prevented by imipramine.	Imipramine	256-266	glycogen synthase kinase 3 beta	Mus musculus	43-74
26620976-0	2016	Imipramine administration induces changes in the phosphorylation of FAK and PYK2 and modulates signaling pathways related to their activity.	Imipramine	0-10	protein tyrosine kinase 2	Rattus norvegicus	68-71
26620976-0	2016	Imipramine administration induces changes in the phosphorylation of FAK and PYK2 and modulates signaling pathways related to their activity.	Imipramine	0-10	protein tyrosine kinase 2 beta	Rattus norvegicus	76-80
26620976-2	2016	We investigated whether the phosphorylation status of focal adhesion kinase (FAK/PTK2) and its homolog, PYK2/PTK2B, and their complex with the downstream effectors (Src kinase, p130Cas, and paxillin) are affected by administration of the antidepressant drug, imipramine.	Imipramine	259-269	protein tyrosine kinase 2	Rattus norvegicus	77-80
26620976-2	2016	We investigated whether the phosphorylation status of focal adhesion kinase (FAK/PTK2) and its homolog, PYK2/PTK2B, and their complex with the downstream effectors (Src kinase, p130Cas, and paxillin) are affected by administration of the antidepressant drug, imipramine.	Imipramine	259-269	protein tyrosine kinase 2	Rattus norvegicus	81-85
26620976-2	2016	We investigated whether the phosphorylation status of focal adhesion kinase (FAK/PTK2) and its homolog, PYK2/PTK2B, and their complex with the downstream effectors (Src kinase, p130Cas, and paxillin) are affected by administration of the antidepressant drug, imipramine.	Imipramine	259-269	protein tyrosine kinase 2 beta	Rattus norvegicus	104-108
26620976-6	2016	RESULTS: Imipramine induced contrasting changes in the phosphorylation of FAK and PYK2 at Tyr397 and Tyr402, respectively.	Imipramine	9-19	protein tyrosine kinase 2	Rattus norvegicus	74-77
26620976-6	2016	RESULTS: Imipramine induced contrasting changes in the phosphorylation of FAK and PYK2 at Tyr397 and Tyr402, respectively.	Imipramine	9-19	protein tyrosine kinase 2 beta	Rattus norvegicus	82-86
26620976-7	2016	The decreased FAK phosphorylation and increased PYK2 phosphorylation were reflected by changes in the levels of their complex with Src and p130Cas, which was observed predominantly after chronic imipramine treatment.	Imipramine	195-205	protein tyrosine kinase 2	Rattus norvegicus	14-17
26620976-7	2016	The decreased FAK phosphorylation and increased PYK2 phosphorylation were reflected by changes in the levels of their complex with Src and p130Cas, which was observed predominantly after chronic imipramine treatment.	Imipramine	195-205	protein tyrosine kinase 2 beta	Rattus norvegicus	48-52
26620976-7	2016	The decreased FAK phosphorylation and increased PYK2 phosphorylation were reflected by changes in the levels of their complex with Src and p130Cas, which was observed predominantly after chronic imipramine treatment.	Imipramine	195-205	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	131-134
26620976-7	2016	The decreased FAK phosphorylation and increased PYK2 phosphorylation were reflected by changes in the levels of their complex with Src and p130Cas, which was observed predominantly after chronic imipramine treatment.	Imipramine	195-205	BCAR1 scaffold protein, Cas family member	Rattus norvegicus	139-146
26620976-8	2016	Similarly only chronic imipramine decreased the Galphaq expression while Galpha11 and Galpha12 proteins were untouched.	Imipramine	23-33	G protein subunit alpha q	Rattus norvegicus	48-55
26620976-9	2016	Acute and chronic treatment with imipramine elevated ERK1 and ERK2 total protein levels, whereas only the pERK1 was significantly affected by the drug.	Imipramine	33-43	mitogen activated protein kinase 3	Rattus norvegicus	53-57
26620976-9	2016	Acute and chronic treatment with imipramine elevated ERK1 and ERK2 total protein levels, whereas only the pERK1 was significantly affected by the drug.	Imipramine	33-43	mitogen activated protein kinase 1	Rattus norvegicus	62-66
26620976-11	2016	GENERAL SIGNIFICANCE: These data demonstrate that treatment with imipramine, which is a routine in counteracting depressive disorders, enhances the phosphorylation of PYK2, a non-receptor kinase instrumental in promoting synaptic plasticity.	Imipramine	65-75	protein tyrosine kinase 2 beta	Rattus norvegicus	167-171
27478647-4	2016	Unexpectedly, floating behaviour and brain glycogen synthase kinase-3 beta (GSK-3beta) mRNA levels, a factor of synaptic plasticity as well as a marker of distress and depression, were increased during the additional swimming session that was prevented by imipramine.	Imipramine	256-266	glycogen synthase kinase 3 beta	Mus musculus	76-85
26427584-10	2015	Increased p11 expression by BDNF and imipramine unraveled a 5-HT4R-mediated modulation of cardiac Ca(2+) handling and ECC associated with deleterious Ca(2+) flux disturbances.	Imipramine	37-47	S100 calcium binding protein A10	Rattus norvegicus	10-13
26427584-3	2015	p11 expression is increased by brain-derived neurotrophic factor (BDNF) or antidepressant drugs (imipramine).	Imipramine	97-107	S100 calcium binding protein A10	Rattus norvegicus	0-3
26208882-6	2015	Moreover, treatment of wild-type mice with the antidepressant drug imipramine reduced the expression of Ndrg2 in the frontal cortex, which was due to the degradation of HIF-1alpha through reduced expression of HSP90 protein.	Imipramine	67-77	N-myc downstream regulated gene 2	Mus musculus	104-109
26427584-5	2015	METHODS AND RESULTS: p11 expression was induced in vivo in healthy Wistar rats by imipramine (10 mg/kg/21 days) and in vitro in left ventricular cardiomyocytes exposed to BDNF (50 ng/ml/8h).	Imipramine	82-92	S100 calcium binding protein A10	Rattus norvegicus	21-24
26427584-7	2015	Both imipramine and BDNF-induced cardiomyocyte p11 expression unmasked a strong response to prucalopride characterized by an increase of both cell shortening and Ca(2+) transient amplitude compared to basal prucalopride associated with a high propensity to trigger diastolic Ca(2+) events.	Imipramine	5-15	S100 calcium binding protein A10	Rattus norvegicus	47-50
26481532-4	2015	OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet.	Imipramine	100-110	cAMP responsive element binding protein 1	Mus musculus	174-178
26481532-4	2015	OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet.	Imipramine	100-110	brain derived neurotrophic factor	Mus musculus	180-184
26481532-4	2015	OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet.	Imipramine	100-110	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	186-190
26481532-4	2015	OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet.	Imipramine	100-110	G protein-coupled receptor 39	Mus musculus	195-200
26481532-5	2015	RESULTS: The administration of acute antidepressants induced diverse effects in the proteins that were examined (namely, GPR39 down-regulation and a reduction in CREB protein after administration of all ADs; a decrease in BDNF after administration of imipramine and escitalopram; an increase in BDNF after administration of reboxetine; no change in BDNF following administration of bupropion; and a decrease in TrkB following the administration of all ADs except bupropion).	Imipramine	251-261	brain derived neurotrophic factor	Mus musculus	222-226
26433268-8	2015	Accordingly, stress and imipramine induced opposite changes on AcH3, AcH4 and CREB expression.	Imipramine	24-34	cAMP responsive element binding protein 1	Homo sapiens	78-82
26521132-0	2015	IL-4/10 prevents stress vulnerability following imipramine discontinuation.	Imipramine	48-58	interleukin 4	Mus musculus	0-4
26521132-11	2015	CONCLUSION: Thus, our results suggest that the reduced IL-4 and IL-10 levels in serum with hippocampal M2 markers may be involved in the stress vulnerability after imipramine discontinuation, and the restoration and modulation of these factors may be useful to some forms of depression-associated conditions.	Imipramine	164-174	interleukin 4	Mus musculus	55-59
26521132-11	2015	CONCLUSION: Thus, our results suggest that the reduced IL-4 and IL-10 levels in serum with hippocampal M2 markers may be involved in the stress vulnerability after imipramine discontinuation, and the restoration and modulation of these factors may be useful to some forms of depression-associated conditions.	Imipramine	164-174	interleukin 10	Mus musculus	64-69
26453619-7	2015	Imipramine, in use as an antidepressant, has been shown to reduce the Mg(2+)E activity of SLC41A1 and OS.	Imipramine	0-10	solute carrier family 41 member 1	Homo sapiens	90-97
26428872-2	2015	Results of biological studies revealed that the majority of compounds exhibited potent to moderately potent activity and among them, 12 displayed potency comparable to that of the imipramine with %DID of 37.95 and 44.84 in the FST and TST, respectively.	Imipramine	180-190	thiosulfate sulfurtransferase	Homo sapiens	235-238
26428872-3	2015	At the same time, imipramine showed %DID of 43.62 and 50.64 in the FST and TST, correspondingly.	Imipramine	18-28	thiosulfate sulfurtransferase	Homo sapiens	75-78
26208882-6	2015	Moreover, treatment of wild-type mice with the antidepressant drug imipramine reduced the expression of Ndrg2 in the frontal cortex, which was due to the degradation of HIF-1alpha through reduced expression of HSP90 protein.	Imipramine	67-77	hypoxia inducible factor 1, alpha subunit	Mus musculus	169-179
26208882-6	2015	Moreover, treatment of wild-type mice with the antidepressant drug imipramine reduced the expression of Ndrg2 in the frontal cortex, which was due to the degradation of HIF-1alpha through reduced expression of HSP90 protein.	Imipramine	67-77	heat shock protein 86, pseudogene 2	Mus musculus	210-215
26208882-7	2015	Furthermore, we found that the down-regulation of Ndrg2 in Ndrg2-deficient mice and imipramine treatment improved mood behavior with enhanced phosphorylation of GSK3beta through activation of PI3K/AKT signaling, suggesting that the expression level of NDRG2 has a causal influence on mood-related phenotypes.	Imipramine	84-94	glycogen synthase kinase 3 beta	Mus musculus	161-169
26730329-11	2015	Imipramine and crocin prevented the decreasing effect of malathion on BDNF.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	70-74
26208882-7	2015	Furthermore, we found that the down-regulation of Ndrg2 in Ndrg2-deficient mice and imipramine treatment improved mood behavior with enhanced phosphorylation of GSK3beta through activation of PI3K/AKT signaling, suggesting that the expression level of NDRG2 has a causal influence on mood-related phenotypes.	Imipramine	84-94	thymoma viral proto-oncogene 1	Mus musculus	197-200
26208882-7	2015	Furthermore, we found that the down-regulation of Ndrg2 in Ndrg2-deficient mice and imipramine treatment improved mood behavior with enhanced phosphorylation of GSK3beta through activation of PI3K/AKT signaling, suggesting that the expression level of NDRG2 has a causal influence on mood-related phenotypes.	Imipramine	84-94	N-myc downstream regulated gene 2	Mus musculus	252-257
26188176-8	2015	Chronic imipramine treatment fully reversed the UCMS-induced increase in methylation of the -681 CpG site in the PFC but not midbrain of stressed animals and also increased 5-HT1A expression in the PFC of control animals.	Imipramine	8-18	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	173-179
26188176-9	2015	Incomplete reversal by imipramine of stress-induced changes in 5-HT1A methylation and expression indicates a persistence of stress vulnerability, and that sustained reversal of behavioral impairments may require additional pathways.	Imipramine	23-33	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	63-69
26398399-10	2015	Plumbagin and imipramine significantly inhibited brain MAO-A activity, decreased plasma nitrite, brain malondialdehyde and catalase levels; and increased reduced glutathione levels of unstressed and stressed mice.	Imipramine	14-24	monoamine oxidase A	Mus musculus	55-60
26398399-10	2015	Plumbagin and imipramine significantly inhibited brain MAO-A activity, decreased plasma nitrite, brain malondialdehyde and catalase levels; and increased reduced glutathione levels of unstressed and stressed mice.	Imipramine	14-24	catalase	Mus musculus	123-131
25975536-8	2015	Serine palmitoyltransferase (SPT) inhibition with myriocin prevented melatonin-induced autophagy and ASMase inhibition with imipramine-impaired autophagy flux.	Imipramine	124-134	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	0-27
26364276-10	2015	CONCLUSIONS: Low S100B levels predict nonresponse to venlafaxine and imipramine with high precision.	Imipramine	69-79	S100 calcium binding protein B	Homo sapiens	17-22
25719307-2	2015	Thus, CYP2D6 catalyzes the 2-hydroxylation, and CYP2C19 in part catalyzes the N-demethylation of imipramine.	Imipramine	97-107	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	6-12
25719307-2	2015	Thus, CYP2D6 catalyzes the 2-hydroxylation, and CYP2C19 in part catalyzes the N-demethylation of imipramine.	Imipramine	97-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
25975536-8	2015	Serine palmitoyltransferase (SPT) inhibition with myriocin prevented melatonin-induced autophagy and ASMase inhibition with imipramine-impaired autophagy flux.	Imipramine	124-134	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	29-32
25975536-8	2015	Serine palmitoyltransferase (SPT) inhibition with myriocin prevented melatonin-induced autophagy and ASMase inhibition with imipramine-impaired autophagy flux.	Imipramine	124-134	sphingomyelin phosphodiesterase 1	Homo sapiens	101-107
26253075-0	2015	Doxepin and imipramine but not fluoxetine reduce the activity of the rat glutamate transporter EAAT3 expressed in Xenopus oocytes.	Imipramine	12-22	solute carrier family 1 member 1	Rattus norvegicus	95-100
26253075-7	2015	Imipramine reduced EAAT3 activity in a concentration-dependent manner at 0.16-0.95 muM.	Imipramine	0-10	solute carrier family 1 member 1	Rattus norvegicus	19-24
26253075-9	2015	At 0.32 muM, imipramine caused an equivalent decrease in EAAT3 activity in the presence or absence of PMA.	Imipramine	13-23	solute carrier family 1 member 1	Rattus norvegicus	57-62
26253075-11	2015	CONCLUSIONS: We showed that doxepin and imipramine, but not fluoxetine, inhibited EAAT3 activity at clinically relevant concentrations.	Imipramine	40-50	solute carrier family 1 member 1	Rattus norvegicus	82-87
25840741-4	2015	The results showed that short- (3 days) or long-term (21 days) systemic treatment with the tricyclic ADs imipramine, clomipramine or desipramine increased BDNF levels in the DPAG.	Imipramine	105-115	brain-derived neurotrophic factor	Rattus norvegicus	155-159
25681757-0	2015	Imipramine protects against the deleterious effects of chronic corticosterone on depression-like behavior, hippocampal reelin expression, and neuronal maturation.	Imipramine	0-10	reelin	Rattus norvegicus	119-125
25681757-8	2015	All of these behavioral and cellular phenotypes were prevented by imipramine, providing further support for the idea that reelin is involved in the pathogenesis of depression.	Imipramine	66-76	reelin	Rattus norvegicus	122-128
25841360-8	2015	The Tubb3 and Htr2A gene expression were up-regulated, Th decreased slightly and Slc6a4 was down-regulated after differentiation We observed a two-fold higher percentage of beta-III-tubulin positive cells after treatment with antidepressants and two-fold increase of neuron-like cells after using CACM with imipramine or fluoxetine simultaneously.	Imipramine	307-317	solute carrier family 6 member 4	Rattus norvegicus	81-87
25840741-8	2015	Imipramine, both after short and long-term administration, and fluoxetine under the latter regimen, raised the levels of phosphorylated TRKB in the DPAG.	Imipramine	0-10	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	136-140
25701613-9	2015	Moreover, 24days of imipramine treatment in RSD mice significantly decreased stress-induced mRNA levels for IL-6 in brain microglia.	Imipramine	20-30	interleukin 6	Mus musculus	108-112
25772791-8	2015	These results suggest that GLP-2 acts on specific brain regions to regulate stress conditions, and induces antidepressant-like effects under imipramine-resistant conditions, which may be associated with the modulation of the hypothalamic-pituitary-adrenal-axis.	Imipramine	141-151	glucagon-like peptide 2 receptor	Mus musculus	27-32
25701613-10	2015	Following ex vivo LPS stimulation, microglia from mice exposed to RSD, had higher mRNA expression of IL-6, TNF-alpha, and IL-1beta, and this was reversed by imipramine treatment.	Imipramine	157-167	interleukin 6	Mus musculus	101-105
25701613-10	2015	Following ex vivo LPS stimulation, microglia from mice exposed to RSD, had higher mRNA expression of IL-6, TNF-alpha, and IL-1beta, and this was reversed by imipramine treatment.	Imipramine	157-167	tumor necrosis factor	Mus musculus	107-116
25701613-10	2015	Following ex vivo LPS stimulation, microglia from mice exposed to RSD, had higher mRNA expression of IL-6, TNF-alpha, and IL-1beta, and this was reversed by imipramine treatment.	Imipramine	157-167	interleukin 1 beta	Mus musculus	122-130
25701613-11	2015	In a second experiment, imipramine was added to drinking water confirming the reversal of social avoidant behavior and decrease in mRNA expression of IL-6 in microglia.	Imipramine	24-34	interleukin 6	Mus musculus	150-154
25617795-0	2015	Involvement of alpha1B-adrenoceptors in the anti-immobility effect of imipramine in the tail suspension test.	Imipramine	70-80	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	15-22
25912579-9	2015	Overall, the summarized studies suggest that some psychotropic drugs (such as lithium and imipramine) exert potent inhibitory effects on NF-kappaB, while the results on other drugs are not conclusive and occasionally contradicting.	Imipramine	90-100	nuclear factor kappa B subunit 1	Homo sapiens	137-146
25826421-0	2015	The effects of antidepressants "fluoxetine and imipramine" on vascular abnormalities and Toll like receptor-4 expression in diabetic and non-diabetic rats exposed to chronic stress.	Imipramine	47-57	toll-like receptor 4	Rattus norvegicus	89-109
25617795-8	2015	However, the anti-immobility effect of imipramine was significantly antagonised by the selective alpha1B-adrenoceptor antagonist (2S)-4-(4-amino-6,7-dimethoxy-2-quinazolinyl)-2-[[(1,1-dimethylethyl)amino]carbonyl]-1-piperazinecarboxylate (L-765,314).	Imipramine	39-49	adrenergic receptor, alpha 1b	Mus musculus	97-117
25617795-10	2015	These results indicate that the selective antagonism of alpha1A- and alpha1D-adrenoceptors results in antidepressant-like effects and that the alpha1B-subtype is the main target for the increased levels of noradrenaline caused by imipramine.	Imipramine	230-240	calcium channel, voltage-dependent, P/Q type, alpha 1A subunit	Mus musculus	56-63
25617795-10	2015	These results indicate that the selective antagonism of alpha1A- and alpha1D-adrenoceptors results in antidepressant-like effects and that the alpha1B-subtype is the main target for the increased levels of noradrenaline caused by imipramine.	Imipramine	230-240	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	143-150
25448279-6	2015	In addition, finasteride strongly inhibited UGT1A4-catalyzed imipramine-N-beta-D-glucuronidation.	Imipramine	61-71	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	44-50
25286136-8	2015	During the 10:10 LD schedule, activity and temperature amplitudes were significantly decreased (paired t test), an effect exacerbated by imipramine (ANOVA/SNK).	Imipramine	137-147	polo like kinase 2	Mus musculus	155-158
25739024-8	2015	Chronic imipramine reversed the lesion-induced decreases in BDNF mRNA in the DG.	Imipramine	8-18	brain-derived neurotrophic factor	Rattus norvegicus	60-64
25218191-11	2014	The SERT inhibitor imipramine similarly blocked AKT activation.	Imipramine	19-29	solute carrier family 6 member 4	Rattus norvegicus	4-8
25832023-6	2015	In accordance with this, Delta60-CPR could mediate metabolism of amitriptyline (AMT) and imipramine (IMP) in the absence of lipids, although activity was diminished.	Imipramine	89-99	cytochrome p450 oxidoreductase	Homo sapiens	33-36
25832023-6	2015	In accordance with this, Delta60-CPR could mediate metabolism of amitriptyline (AMT) and imipramine (IMP) in the absence of lipids, although activity was diminished.	Imipramine	101-104	cytochrome p450 oxidoreductase	Homo sapiens	33-36
25218191-11	2014	The SERT inhibitor imipramine similarly blocked AKT activation.	Imipramine	19-29	AKT serine/threonine kinase 1	Rattus norvegicus	48-51
24647745-2	2014	In rat TAECs, imipramine was biotransformed into N-demethylate and N-oxide by cytochrome P450 (CYP) and flavin-containing monooxygenase (FMO), respectively.	Imipramine	14-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-93
24901414-7	2014	Our findings demonstrated that escitalopram, paroxetine and tranylcypromine significantly increased levels of phospho-mTOR and its down-stream regulators (phospho-4E-BP-1 and phospho-p70S6K); fluoxetine, sertraline and imipramine had no effect.	Imipramine	219-229	mechanistic target of rapamycin kinase	Rattus norvegicus	118-122
25217162-0	2014	Imipramine exploits histone deacetylase 11 to increase the IL-12/IL-10 ratio in macrophages infected with antimony-resistant Leishmania donovani and clears organ parasites in experimental infection.	Imipramine	0-10	interleukin 10	Homo sapiens	65-70
25217162-3	2014	Imipramine, a drug in use for the treatment of depression and nocturnal enuresis in children, inhibits IL-10 production from Sb(R)LD-infected macrophages (Sb(R)LD-Mphis) and favors accumulation of surrogates of antimonials.	Imipramine	0-10	interleukin 10	Homo sapiens	103-108
25217162-8	2014	Instead, a imipramine-mediated decreased IL-10 level allows optimal IL-12 production in Sb(R)LD-Mphis.	Imipramine	11-21	interleukin 10	Homo sapiens	41-46
25217162-10	2014	This observation indicated that reciprocity exists between IL-10 and IL-12 and that imipramine tips the balance toward an increased IL-12/IL-10 ratio in Sb(R)LD-Mphis.	Imipramine	84-94	interleukin 10	Homo sapiens	138-143
25217162-12	2014	Our study deciphers a detailed molecular mechanism of imipramine-mediated regulation of IL-10/IL-12 reciprocity and its impact on Sb(R)LD clearance from infected hosts.	Imipramine	54-64	interleukin 10	Homo sapiens	88-93
25019653-11	2014	Both FLU and IMI treatment reduced the increase of IL-6 and TNF-alpha levels following the FST exposure.	Imipramine	13-16	interleukin 6	Rattus norvegicus	51-55
25019653-11	2014	Both FLU and IMI treatment reduced the increase of IL-6 and TNF-alpha levels following the FST exposure.	Imipramine	13-16	tumor necrosis factor	Rattus norvegicus	60-69
25128275-8	2014	Extent of endocytosis is similar for all TCAs studied so far, and occurs in an arrestin-dependent manner, although imipramine uniquely retains a slight ability to drive alpha2AAR endocytosis in arrestin-null cells.	Imipramine	115-125	adrenoceptor alpha 2A	Homo sapiens	169-178
24495390-5	2014	Finally, levels of HTR2A were lower in the CNS of rats treated with imipramine, but not fluoxetine, for 28 d, but not 10 d. From our current and previous data we conclude cortical HTR2A are lower in schizophrenia, MDD, people with mood disorders who died by suicide, rats treated with some antipsychotic or some antidepressant drugs.	Imipramine	68-78	5-hydroxytryptamine receptor 2A	Rattus norvegicus	19-24
25156823-0	2014	Imipramine ameliorates pain-related negative emotion via induction of brain-derived neurotrophic factor.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	70-103
25268312-12	2014	Chronic treatment with imipramine or pentoxifylline significantly ameliorated the behavioral, neurochemical, immunohistochemical and TNF-alpha gene expression changes induced by the LPS/CMS protocol.	Imipramine	23-33	tumor necrosis factor	Rattus norvegicus	133-142
25116759-10	2014	The behavioral changes well corresponded to a decrease in MEK/ERK immunoreactivity in the medial orbital (MO) cortex and dorsal endopiriform nuclei (DEn), which was averted by imipramine, but not in cingulate, prelimbic, infralimbic, and motor cortex.	Imipramine	176-186	midkine	Mus musculus	58-61
25116759-10	2014	The behavioral changes well corresponded to a decrease in MEK/ERK immunoreactivity in the medial orbital (MO) cortex and dorsal endopiriform nuclei (DEn), which was averted by imipramine, but not in cingulate, prelimbic, infralimbic, and motor cortex.	Imipramine	176-186	mitogen-activated protein kinase 1	Mus musculus	62-65
25116759-11	2014	These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.	Imipramine	225-235	midkine	Mus musculus	27-30
25116759-11	2014	These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.	Imipramine	225-235	mitogen-activated protein kinase 1	Mus musculus	31-34
25116759-11	2014	These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.	Imipramine	225-235	midkine	Mus musculus	183-186
25116759-11	2014	These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.	Imipramine	225-235	mitogen-activated protein kinase 1	Mus musculus	187-190
24786695-9	2014	Additionally, the antidepressants fluoxetine and imipramine, which tend to switch BD depression to mania, each increased AA turnover and cPLA2 IVA expression in rat brain, suggesting that brain AA metabolism is higher in BD mania than depression.	Imipramine	49-59	phospholipase A2 group IVA	Rattus norvegicus	137-142
24495390-5	2014	Finally, levels of HTR2A were lower in the CNS of rats treated with imipramine, but not fluoxetine, for 28 d, but not 10 d. From our current and previous data we conclude cortical HTR2A are lower in schizophrenia, MDD, people with mood disorders who died by suicide, rats treated with some antipsychotic or some antidepressant drugs.	Imipramine	68-78	5-hydroxytryptamine receptor 2A	Homo sapiens	180-185
24647745-2	2014	In rat TAECs, imipramine was biotransformed into N-demethylate and N-oxide by cytochrome P450 (CYP) and flavin-containing monooxygenase (FMO), respectively.	Imipramine	14-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-98
24275045-2	2014	It has been also shown that stimulation of BLA 5-HT2C-Rs underlies the anxiogenic effect caused by acute systemic administration of the antidepressants imipramine or fluoxetine.	Imipramine	152-162	5-hydroxytryptamine receptor 2C	Rattus norvegicus	47-53
24342992-7	2014	Treatment of CUS-exposed mice with either endotoxin, macrophage colony-stimulating factor or granulocyte-macrophage colony-stimulating factor, all of which stimulated hippocampal microglial proliferation, partially or completely reversed the depressive-like behavior and dramatically increased hippocampal neurogenesis, whereas treatment with imipramine or minocycline had minimal or no anti-depressive effects, respectively, in these mice.	Imipramine	343-353	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	93-141
24754268-10	2014	CMS-CCT-induced metabolic and endothelial dysfunctions were improved in the THAL group but were worsened in the IMIP group.	Imipramine	112-116	FLVCR heme transporter 2	Rattus norvegicus	4-7
24458505-5	2014	In both the imipramine- and fluoxetine-treated animals, expression of six genes was down-regulated (ANOVA-filtered gene expression data using dChip [version 2005]): Gpd1; Lrrn3; Sult1A1; Angptl4; Mt1a; Unknown.	Imipramine	12-22	glycerol-3-phosphate dehydrogenase 1	Homo sapiens	165-169
24458505-5	2014	In both the imipramine- and fluoxetine-treated animals, expression of six genes was down-regulated (ANOVA-filtered gene expression data using dChip [version 2005]): Gpd1; Lrrn3; Sult1A1; Angptl4; Mt1a; Unknown.	Imipramine	12-22	leucine rich repeat neuronal 3	Homo sapiens	171-176
24458505-5	2014	In both the imipramine- and fluoxetine-treated animals, expression of six genes was down-regulated (ANOVA-filtered gene expression data using dChip [version 2005]): Gpd1; Lrrn3; Sult1A1; Angptl4; Mt1a; Unknown.	Imipramine	12-22	sulfotransferase family 1A member 1	Homo sapiens	178-185
24458505-5	2014	In both the imipramine- and fluoxetine-treated animals, expression of six genes was down-regulated (ANOVA-filtered gene expression data using dChip [version 2005]): Gpd1; Lrrn3; Sult1A1; Angptl4; Mt1a; Unknown.	Imipramine	12-22	angiopoietin like 4	Homo sapiens	187-194
24458505-5	2014	In both the imipramine- and fluoxetine-treated animals, expression of six genes was down-regulated (ANOVA-filtered gene expression data using dChip [version 2005]): Gpd1; Lrrn3; Sult1A1; Angptl4; Mt1a; Unknown.	Imipramine	12-22	metallothionein 1A	Homo sapiens	196-200
24458505-6	2014	Furthermore, four genes were over-expressed: P4Ha1; RDG1311476; Rgc32; and SLC25A18-like by both imipramine and fluoxetine.	Imipramine	97-107	prolyl 4-hydroxylase subunit alpha 1	Homo sapiens	45-50
24458505-6	2014	Furthermore, four genes were over-expressed: P4Ha1; RDG1311476; Rgc32; and SLC25A18-like by both imipramine and fluoxetine.	Imipramine	97-107	regulator of cell cycle	Homo sapiens	64-69
24458505-6	2014	Furthermore, four genes were over-expressed: P4Ha1; RDG1311476; Rgc32; and SLC25A18-like by both imipramine and fluoxetine.	Imipramine	97-107	solute carrier family 25 member 18	Homo sapiens	75-83
24296153-5	2014	Escitalopram, fluoxetine, paroxetine, sertraline, imipramine, tranylcypromine, and tianeptine significantly prevented B27 deprivation-induced decreases in levels of PSD-95, BDNF, and SYP.	Imipramine	50-60	discs large MAGUK scaffold protein 4	Rattus norvegicus	165-171
24691070-9	2014	The antidepressant imipramine attenuated depressive behaviors and partially restored brain serotonin level in Ahi1 KO mice.	Imipramine	19-29	Abelson helper integration site 1	Mus musculus	110-114
24478625-7	2014	Importantly, antidepressant-like efficacy of the tricyclic antidepressant, imipramine, was maintained in both OX1 and OX2 receptor knock-out mice.	Imipramine	75-85	NAD(P)H dehydrogenase, quinone 1	Mus musculus	110-113
24905304-9	2014	In contrast, imipramine and fluoxetine induced a few-fold weaker suppressing effect on the levels of IL-10.	Imipramine	13-23	interleukin 10	Rattus norvegicus	101-106
25136578-10	2014	Eag1 inhibitor imipramine or Eag1-shRNA significantly suppressed the proliferation of liposarcoma cells in vitro and in vivo, accompanying with accumulation of cells in the G1 phase.	Imipramine	15-25	potassium voltage-gated channel subfamily H member 1	Homo sapiens	0-4
24036107-7	2014	Co-administration of 9h of fasting and imipramine (30mg/kg, i.p) produced the additive antidepressant-like effects in the FST and increased the ratio of p-CREB/CREB.	Imipramine	39-49	cAMP responsive element binding protein 1	Mus musculus	155-159
24036107-7	2014	Co-administration of 9h of fasting and imipramine (30mg/kg, i.p) produced the additive antidepressant-like effects in the FST and increased the ratio of p-CREB/CREB.	Imipramine	39-49	cAMP responsive element binding protein 1	Mus musculus	160-164
24781228-1	2014	OBJECTIVE: To investigate the effect of the neuroleptic aminazine (chlorpromazine) and the antidepressant melipramine on the activity of leukocyte elastase (LE).	Imipramine	106-117	elastase, neutrophil expressed	Homo sapiens	137-155
24492587-5	2014	Reciprocal mutants for both CYP2C19 and 2C9 were produced, and their metabolic activities and spectroscopic properties were examined using three tricyclic antidepressant (TCA) drugs: amitriptyline, imipramine, and dothiepin.	Imipramine	198-208	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-43
24781228-1	2014	OBJECTIVE: To investigate the effect of the neuroleptic aminazine (chlorpromazine) and the antidepressant melipramine on the activity of leukocyte elastase (LE).	Imipramine	106-117	elastase, neutrophil expressed	Homo sapiens	157-159
24781228-4	2014	RESULTS: Aminazine and melipramine inhibited the LE activity.	Imipramine	23-34	elastase, neutrophil expressed	Homo sapiens	49-51
23922220-0	2013	Imipramine-induced c-Fos expression in the medial prefrontal cortex is decreased in the ACTH-treated rats.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
24076182-6	2013	By means of quantitative Real Time PCR experiments we demonstrated that a chronic treatment with either fluoxetine or imipramine resulted in a reduction of IL-6 and IFN-gamma mRNAs and increased IL-4 mRNA expression in the rat hypothalamus.	Imipramine	118-128	interleukin 6	Rattus norvegicus	156-160
24076182-6	2013	By means of quantitative Real Time PCR experiments we demonstrated that a chronic treatment with either fluoxetine or imipramine resulted in a reduction of IL-6 and IFN-gamma mRNAs and increased IL-4 mRNA expression in the rat hypothalamus.	Imipramine	118-128	interleukin 18	Rattus norvegicus	165-174
24076182-6	2013	By means of quantitative Real Time PCR experiments we demonstrated that a chronic treatment with either fluoxetine or imipramine resulted in a reduction of IL-6 and IFN-gamma mRNAs and increased IL-4 mRNA expression in the rat hypothalamus.	Imipramine	118-128	interleukin 4	Rattus norvegicus	195-199
24076182-8	2013	Chronically administered fluoxetine decreased IL-8 and CX3CL1 hypothalamic expression, while a chronic treatment with imipramine decreased p11 mRNA.	Imipramine	118-128	S100 calcium binding protein A10	Rattus norvegicus	139-142
23931269-1	2013	The pharmacological concept that inhibition of the drug efflux pump P-glycoprotein (P-gp) enhances brain distribution of the antidepressant imipramine in the rat has recently been demonstrated.	Imipramine	140-150	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	68-82
23931269-1	2013	The pharmacological concept that inhibition of the drug efflux pump P-glycoprotein (P-gp) enhances brain distribution of the antidepressant imipramine in the rat has recently been demonstrated.	Imipramine	140-150	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	84-88
23931269-2	2013	To determine if these findings are relevant to humans, the present study investigated if imipramine is a transported substrate of human P-gp.	Imipramine	89-99	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
23931269-6	2013	Imipramine was identified as a transported substrate of human P-gp (TR = 1.68, attenuated by P-gp inhibition).	Imipramine	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	62-66
23931269-6	2013	Imipramine was identified as a transported substrate of human P-gp (TR = 1.68, attenuated by P-gp inhibition).	Imipramine	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	93-97
23931269-8	2013	These results offer insight into the role of P-gp in the distribution of antidepressants, revealing that rodent findings pertaining to imipramine may translate to humans.	Imipramine	135-145	ATP binding cassette subfamily B member 1	Homo sapiens	45-49
23922220-4	2013	In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline.	Imipramine	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
23922220-4	2013	In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline.	Imipramine	18-28	complement factor properdin	Mus musculus	117-121
23922220-4	2013	In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline.	Imipramine	18-28	carcinoembryonic antigen gene family 4	Rattus norvegicus	209-212
23922220-5	2013	The imipramine-increased c-Fos immunoreactivity was suppressed in the mPFC of rats repeatedly treated with ACTH.	Imipramine	4-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
23922220-5	2013	The imipramine-increased c-Fos immunoreactivity was suppressed in the mPFC of rats repeatedly treated with ACTH.	Imipramine	4-14	complement factor properdin	Mus musculus	70-74
23922220-7	2013	These results suggest that the mPFC is maybe involved in effects of the imipramine in the ACTH-treated rats.	Imipramine	72-82	complement factor properdin	Mus musculus	31-35
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Imipramine	101-111	latexin	Homo sapiens	67-70
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Imipramine	101-111	latexin	Homo sapiens	84-87
23906970-6	2013	Moreover, Western blot analysis showed the decrease in the activated form of ERK1/2 (p-ERK) after DEX treatment and this effect was inhibited by imipramine.	Imipramine	145-155	mitogen-activated protein kinase 3	Homo sapiens	77-83
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Imipramine	101-111	latexin	Homo sapiens	84-87
23906970-6	2013	Moreover, Western blot analysis showed the decrease in the activated form of ERK1/2 (p-ERK) after DEX treatment and this effect was inhibited by imipramine.	Imipramine	145-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	85-90
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Imipramine	101-111	latexin	Homo sapiens	84-87
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Imipramine	101-111	latexin	Homo sapiens	84-87
23816950-1	2013	UNLABELLED: The effect of long-term administration of imipramine, a tricyclic antidepressant, on the phosphorylation status of cyclic adenosine monophosphate-responsive element-binding protein (CREB), mitogen-activated protein kinase family members, and phospholipase gamma-1 (PLCgamma-1) was investigated in the dorsal horn of the spinal cord following peripheral nerve lesion.	Imipramine	54-64	cAMP responsive element binding protein 1	Mus musculus	127-192
23816950-1	2013	UNLABELLED: The effect of long-term administration of imipramine, a tricyclic antidepressant, on the phosphorylation status of cyclic adenosine monophosphate-responsive element-binding protein (CREB), mitogen-activated protein kinase family members, and phospholipase gamma-1 (PLCgamma-1) was investigated in the dorsal horn of the spinal cord following peripheral nerve lesion.	Imipramine	54-64	cAMP responsive element binding protein 1	Mus musculus	194-198
23816950-1	2013	UNLABELLED: The effect of long-term administration of imipramine, a tricyclic antidepressant, on the phosphorylation status of cyclic adenosine monophosphate-responsive element-binding protein (CREB), mitogen-activated protein kinase family members, and phospholipase gamma-1 (PLCgamma-1) was investigated in the dorsal horn of the spinal cord following peripheral nerve lesion.	Imipramine	54-64	phospholipase C, gamma 1	Mus musculus	277-287
23816950-6	2013	Moreover, imipramine therapy reversed nerve injury-induced CREB and PLCgamma-1 phosphorylation but had no effect on ERK1,2, p38, and c-Jun N-terminal kinase activity.	Imipramine	10-20	cAMP responsive element binding protein 1	Mus musculus	59-63
23816950-6	2013	Moreover, imipramine therapy reversed nerve injury-induced CREB and PLCgamma-1 phosphorylation but had no effect on ERK1,2, p38, and c-Jun N-terminal kinase activity.	Imipramine	10-20	phospholipase C, gamma 1	Mus musculus	68-78
23816950-9	2013	Our data also provide evidence that prolonged imipramine treatment may induce antinociception in neuropathic pain conditions because of its action on the PLCgamma-1/CREB-signaling pathway.	Imipramine	46-56	phospholipase C, gamma 1	Mus musculus	154-164
23816950-9	2013	Our data also provide evidence that prolonged imipramine treatment may induce antinociception in neuropathic pain conditions because of its action on the PLCgamma-1/CREB-signaling pathway.	Imipramine	46-56	cAMP responsive element binding protein 1	Mus musculus	165-169
23615187-8	2013	This reactive increase of Olig1 was confirmed by partly dose-dependent effects of imipramine and amitriptyline in oligodendrocyte cultures.	Imipramine	82-92	oligodendrocyte transcription factor 1	Homo sapiens	26-31
24761678-10	2013	The protein expression of BDNF in brain was more in imipramine, high dose,exercise and joint groups than that of control group, sports group was higher than that of low dose and high dose group, joint group was obviously higher than other groups.	Imipramine	52-62	brain derived neurotrophic factor	Mus musculus	26-30
23722687-12	2013	Based on the data from the competitive binding experiments, the binding affinities of five drugs to calmodulin were obtained in the order: tetrandrine > trifluoperazine > berbamine > chlorpromazine > imipramine.	Imipramine	212-222	calmodulin 1	Homo sapiens	100-110
23914152-11	2013	Taken together, the blunted 5-HT metabolism and reduced levels of SERT are a likely reason for the elevated sensitivity of these mice to the action of imipramine and paroxetine.	Imipramine	151-161	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	66-70
23611809-9	2013	Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, imipramine, and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.	Imipramine	88-98	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	61-68
23706649-7	2013	Inhibitor binding assays showed that both of the thermostabilised SERT mutants bound [(125)I]RTI55 (beta-CIT) with affinity similar to that of the wild-type transporter, although cocaine bound with increased affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower affinity (up to 90-fold).	Imipramine	251-261	solute carrier family 6 member 4	Homo sapiens	66-70
23611809-4	2013	Using recombinant UGT2B10, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, olanzapine, diphenhydramine, tamoxifen, ketoconazole, and midazolam.	Imipramine	94-104	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	18-25
23486447-2	2013	Amitriptyline, clomipramine, doxepin, imipramine, and trimipramine are demethylated by CYP2C19 to pharmacologically active metabolites.	Imipramine	38-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
23474197-3	2013	To investigate whether the GPR39 receptor is involved in the mechanism of antidepressant action, we measured the expression of the GPR39 receptor (Western Blot) in the frontal cortex of mice treated intraperitoneally with imipramine (30 mg/kg), escitalopram (4 mg/kg), reboxetine (10 mg/kg) or bupropion (15 mg/kg) for 14 days.	Imipramine	222-232	G protein-coupled receptor 39	Mus musculus	27-32
23474197-3	2013	To investigate whether the GPR39 receptor is involved in the mechanism of antidepressant action, we measured the expression of the GPR39 receptor (Western Blot) in the frontal cortex of mice treated intraperitoneally with imipramine (30 mg/kg), escitalopram (4 mg/kg), reboxetine (10 mg/kg) or bupropion (15 mg/kg) for 14 days.	Imipramine	222-232	G protein-coupled receptor 39	Mus musculus	131-136
23180303-8	2013	These data indicate that repeated treatment of normal rats with imipramine results in a modification of the release mechanism of GABA from presynaptic terminals and its modulation by mGluR7 receptors as well as in an alteration in GABAA receptor subunit protein levels in the rat cerebral cortex.	Imipramine	64-74	glutamate receptor, ionotropic, kainate 3	Mus musculus	183-189
23238043-0	2013	Imipramine reverses alterations in cytokines and BDNF levels induced by maternal deprivation in adult rats.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	49-53
23333402-2	2013	Chronic ACTH treatment (0.45 mg/kg, s.c., 14 days) weakened the antidepressant-like effects of imipramine (20 mg/kg, i.p., 6 days) in the forced-swim test (FST).	Imipramine	95-105	pro-opiomelanocortin-alpha	Mus musculus	8-12
23333402-7	2013	These results suggest that GLP-2 induced antidepressant-like effects under imipramine-resistant conditions through increase in 5-HT levels.	Imipramine	75-85	glucagon-like peptide 2 receptor	Mus musculus	27-32
23276607-4	2013	Herein, we demonstrate that ACTH-(1-24) (100mug/day; 14 days) blocks the immobility-reducing "antidepressant" effects of a single dose of imipramine (10mg/kg) in the forced swim test.	Imipramine	138-148	proopiomelanocortin	Homo sapiens	28-32
23276607-12	2013	Taken together these results indicate that pre-treatment with ACTH (100mug/day; 14 days) blocks the antidepressant effects of imipramine (10mg/kg), significantly alters key PFC monoamine responses to stress and downregulates glucocorticoid responses.	Imipramine	126-136	proopiomelanocortin	Homo sapiens	62-66
23593136-8	2013	Pdlim5 hetero KO mice showed increased immobility time in the forced swimming test, which was diminished after the chronic administration of imipramine.	Imipramine	141-151	PDZ and LIM domain 5	Mus musculus	0-6
23593136-10	2013	Imipramine increased Pdlim5 mRNA levels in the hippocampus.	Imipramine	0-10	PDZ and LIM domain 5	Mus musculus	21-27
23238043-11	2013	Interestingly, imipramine treatment reversed the effects of maternal deprivation on BDNF and cytokines levels (p<0.05).	Imipramine	15-25	brain-derived neurotrophic factor	Rattus norvegicus	84-88
23785234-0	2013	Effects of pentoxifylline, 7-nitroindazole, and imipramine on tumor necrosis factor-alpha and indoleamine 2,3-dioxygenase enzyme activity in the hippocampus and frontal cortex of chronic mild-stress-exposed rats.	Imipramine	48-58	tumor necrosis factor	Rattus norvegicus	62-89
22310305-9	2013	Finally, chronic administration of imipramine significantly increased mBDNF levels, but not pro-BDNF and protease levels, indicating that the therapeutic mechanism of imipramine differs from that of ECS.	Imipramine	35-45	brain derived neurotrophic factor	Mus musculus	70-75
22310305-9	2013	Finally, chronic administration of imipramine significantly increased mBDNF levels, but not pro-BDNF and protease levels, indicating that the therapeutic mechanism of imipramine differs from that of ECS.	Imipramine	35-45	brain-derived neurotrophic factor	Rattus norvegicus	71-75
23192661-4	2013	In the present study we introduce a novel GalR2 selective agonist and demonstrate its ability to produce actions consistent with theorized GalR2 functions and analogous to that of the anti-depressant, imipramine.	Imipramine	201-211	galanin receptor 2	Homo sapiens	42-47
23385211-5	2013	Imipramine dimers were only found to be moderate inhibitors of the human serotonin transporter (hSERT) having IC(50) values in the micromolar region whilst the induction of cell death occurred independently of hSERT expression.	Imipramine	0-10	solute carrier family 6 member 4	Homo sapiens	73-94
23385211-5	2013	Imipramine dimers were only found to be moderate inhibitors of the human serotonin transporter (hSERT) having IC(50) values in the micromolar region whilst the induction of cell death occurred independently of hSERT expression.	Imipramine	0-10	solute carrier family 6 member 4	Homo sapiens	96-101
23385211-5	2013	Imipramine dimers were only found to be moderate inhibitors of the human serotonin transporter (hSERT) having IC(50) values in the micromolar region whilst the induction of cell death occurred independently of hSERT expression.	Imipramine	0-10	solute carrier family 6 member 4	Homo sapiens	210-215
23098799-0	2013	Effects of chronic treatment with corticosterone and imipramine on fos immunoreactivity and adult hippocampal neurogenesis.	Imipramine	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
23098799-2	2013	Treatment with the tricyclic antidepressant imipramine significantly reversed the anxiogenic effects of CORT, while inhibiting ETM escape, a response related to panic disorder.	Imipramine	44-54	cortistatin	Rattus norvegicus	104-108
23098799-6	2013	Imipramine, on the other hand, increased fos-ir in the medial amygdala and decreased fos-ir in the anterior hypothalamus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
23098799-6	2013	Imipramine, on the other hand, increased fos-ir in the medial amygdala and decreased fos-ir in the anterior hypothalamus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
23098799-7	2013	CORT also decreased the number of DCX-positive cells in the ventral and dorsal hippocampus, an effect antagonized by imipramine.	Imipramine	117-127	cortistatin	Rattus norvegicus	0-4
23098799-7	2013	CORT also decreased the number of DCX-positive cells in the ventral and dorsal hippocampus, an effect antagonized by imipramine.	Imipramine	117-127	doublecortin	Rattus norvegicus	34-37
23785234-0	2013	Effects of pentoxifylline, 7-nitroindazole, and imipramine on tumor necrosis factor-alpha and indoleamine 2,3-dioxygenase enzyme activity in the hippocampus and frontal cortex of chronic mild-stress-exposed rats.	Imipramine	48-58	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	94-121
23785234-8	2013	Likewise, imipramine reduced TNF-alpha immunostaining (P < 0.05) in hippocampus.	Imipramine	10-20	tumor necrosis factor	Rattus norvegicus	29-38
24399720-4	2013	RESULTS: The investigated antidepressant drugs added to control liver microsomes produced certain inhibitory effects on CYP2C11 activity, which were moderate (sertraline, nefazodone and clomipramine: Ki = 39, 56 and 66 muM, respectively), modest (fluoxetine and amitriptyline: Ki = 98 and 108 muM, respectively) or weak (imipramine and desipramine: Ki = 191 and 212 muM, respectively).	Imipramine	321-331	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	120-127
24399720-6	2013	One-day exposure of rats to the antidepressant drugs did not significantly change the activity of CYP2C11 in liver microsomes; however, imipramine, desipramine and fluoxetine showed a tendency to diminish the activity of CYP2C11.	Imipramine	136-146	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	221-228
23041155-4	2012	In mouse cultured hippocampal HT22 cells, imipramine inhibited cell death and caspase-3 activation induced by tunicamycin, although it did not alter the elevated expressions of 78 kDa glucose-regulated protein (GRP78) and C/EBP-homologous protein (CHOP).	Imipramine	42-52	caspase 3	Mus musculus	78-87
23041155-5	2012	Interestingly, in such cells application of imipramine normalized the expression of the sigma-1 receptor, which was decreased by treatment with tunicamycin alone.	Imipramine	44-54	sigma non-opioid intracellular receptor 1	Mus musculus	88-104
23041155-6	2012	Additionally, NE-100, a selective sigma-1 receptor antagonist, abolished the protective effect of imipramine against such tunicamycin-induced cell death.	Imipramine	98-108	sigma non-opioid intracellular receptor 1	Mus musculus	34-50
21796379-7	2012	Effect of alpha- or gamma-tocopherol, but not of delta-tocopherol, on the newly synthesized ceramide content in old cells was correlated with the action of inhibitor of serine palmitoyl transferase (SPT) activity (myriocin) and SMase inhibitors (glutathione, imipramine).	Imipramine	259-269	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	199-202
22868412-9	2012	Hippocampal changes, which correlated these behavioral responses to imipramine, were seen in the extragranule cell layer: the number of calretinin-positive cells was increased by imipramine in females, but not in males, in the normal weaning condition.	Imipramine	68-78	calbindin 2	Mus musculus	136-146
22868412-9	2012	Hippocampal changes, which correlated these behavioral responses to imipramine, were seen in the extragranule cell layer: the number of calretinin-positive cells was increased by imipramine in females, but not in males, in the normal weaning condition.	Imipramine	179-189	calbindin 2	Mus musculus	136-146
23055506-4	2012	Imipramine administration induces phosphorylation of MeCP2 at Ser421 (pMeCP2) selectively in the nucleus accumbens and the lateral habenula, two brain regions important for depressive-like behaviors.	Imipramine	0-10	methyl CpG binding protein 2	Mus musculus	53-58
23055506-8	2012	After chronic social defeat stress, chronic administration of imipramine significantly improved social interaction in the MeCP2 WT mice.	Imipramine	62-72	methyl CpG binding protein 2	Mus musculus	122-127
22718902-6	2012	Consistently, inhibition of acid sphingomyelinase with imipramine disrupts ACEC formation, association of ciliogenic proteins with Rab11a vesicles, and cilium formation.	Imipramine	55-65	RAB11A, member RAS oncogene family	Canis lupus familiaris	131-137
22250926-0	2012	Inhibition of P-glycoprotein enhances transport of imipramine across the blood-brain barrier: microdialysis studies in conscious freely moving rats.	Imipramine	51-61	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	14-28
22743246-14	2012	Genes (>2 fold, p<0.01), affected by WB and/or FR-D and imipramine, included both inflammatory (e.g. IL-3, IL-10) and neurologically relevant targets.	Imipramine	62-72	interleukin 3	Rattus norvegicus	107-111
22250926-9	2012	CONCLUSIONS AND IMPLICATIONS: The present study demonstrated that P-gp inhibition enhanced the intracerebral concentration of imipramine , thus supporting the hypothesis that P-gp activity restricts brain levels of certain antidepressants, including imipramine.	Imipramine	250-260	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	175-179
22250926-3	2012	Therefore, the present study aimed to investigate the effect of P-gp inhibition on the transport of the tricyclic antidepressant imipramine and its active metabolite desipramine across the BBB.	Imipramine	129-139	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	64-68
22250926-9	2012	CONCLUSIONS AND IMPLICATIONS: The present study demonstrated that P-gp inhibition enhanced the intracerebral concentration of imipramine , thus supporting the hypothesis that P-gp activity restricts brain levels of certain antidepressants, including imipramine.	Imipramine	126-136	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	66-70
22250926-9	2012	CONCLUSIONS AND IMPLICATIONS: The present study demonstrated that P-gp inhibition enhanced the intracerebral concentration of imipramine , thus supporting the hypothesis that P-gp activity restricts brain levels of certain antidepressants, including imipramine.	Imipramine	126-136	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	175-179
22250926-9	2012	CONCLUSIONS AND IMPLICATIONS: The present study demonstrated that P-gp inhibition enhanced the intracerebral concentration of imipramine , thus supporting the hypothesis that P-gp activity restricts brain levels of certain antidepressants, including imipramine.	Imipramine	250-260	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	66-70
22160551-7	2012	The meningitis group decreased the sucrose intake and increased the levels of corticosterone and ACTH levels in the serum and TNF-alpha in the cortex; however, the treatment with imipramine reverted the reduction of sweet food consumption, normalized hormonal levels and TNF-alpha in the cortex.	Imipramine	179-189	tumor necrosis factor	Rattus norvegicus	126-135
22237484-8	2012	Adding imipramine and celecoxib abolished the significance for IL-10.	Imipramine	7-17	interleukin 10	Homo sapiens	63-68
22160551-7	2012	The meningitis group decreased the sucrose intake and increased the levels of corticosterone and ACTH levels in the serum and TNF-alpha in the cortex; however, the treatment with imipramine reverted the reduction of sweet food consumption, normalized hormonal levels and TNF-alpha in the cortex.	Imipramine	179-189	tumor necrosis factor	Rattus norvegicus	271-280
22529824-3	2012	RESULTS: Stimulation of astroglial cell culture with imipramine, a tricyclic antidepressant, led to a significant increase of the Bdnf RNA level whereas treatment with escitalopram did not.	Imipramine	53-63	brain-derived neurotrophic factor	Rattus norvegicus	130-134
22764579-2	2012	In this study, the co-expression enzyme of human recombinant CYPOR, CYPb5 and CYP2D6.1 or CYP2D6.10 with the Bac-to-Bac system in baculovirus-infected insect cells was used to study the catalytical activity to imipramine metabolism and stereoselective metabolism of propranolol.	Imipramine	210-220	cytochrome p450 oxidoreductase	Homo sapiens	61-66
22764579-2	2012	In this study, the co-expression enzyme of human recombinant CYPOR, CYPb5 and CYP2D6.1 or CYP2D6.10 with the Bac-to-Bac system in baculovirus-infected insect cells was used to study the catalytical activity to imipramine metabolism and stereoselective metabolism of propranolol.	Imipramine	210-220	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	78-84
22764579-2	2012	In this study, the co-expression enzyme of human recombinant CYPOR, CYPb5 and CYP2D6.1 or CYP2D6.10 with the Bac-to-Bac system in baculovirus-infected insect cells was used to study the catalytical activity to imipramine metabolism and stereoselective metabolism of propranolol.	Imipramine	210-220	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
22590738-2	2012	As the ASM is a key enzyme of the sphingolipid exchange, in the present study we have investigated the effect of an ASM inhibitor imipramine on the ceramide and sphingomyelin content in the tissues of old rats.	Imipramine	130-140	H19, imprinted maternally expressed transcript (non-protein coding)	Rattus norvegicus	7-10
22326584-0	2012	Inhibitory effect of the antidepressant imipramine on NF-kappaB-dependent CXCL1 expression in TNFalpha-exposed astrocytes.	Imipramine	40-50	tumor necrosis factor	Rattus norvegicus	94-102
22326584-4	2012	In this study, rat primary cultured astrocytes were used to elucidate the effect of the imipramine on TNFalpha-induced inflammatory responses.	Imipramine	88-98	tumor necrosis factor	Rattus norvegicus	102-110
22326584-5	2012	The results clearly demonstrated that imipramine reduced TNFalpha-induced CXCL1 expression through suppression of NF-kappaB-dependent CXCL1 promoter activity in primary astrocytes.	Imipramine	38-48	tumor necrosis factor	Rattus norvegicus	57-65
22326584-5	2012	The results clearly demonstrated that imipramine reduced TNFalpha-induced CXCL1 expression through suppression of NF-kappaB-dependent CXCL1 promoter activity in primary astrocytes.	Imipramine	38-48	C-X-C motif chemokine ligand 1	Rattus norvegicus	74-79
22326584-5	2012	The results clearly demonstrated that imipramine reduced TNFalpha-induced CXCL1 expression through suppression of NF-kappaB-dependent CXCL1 promoter activity in primary astrocytes.	Imipramine	38-48	C-X-C motif chemokine ligand 1	Rattus norvegicus	134-139
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	tumor necrosis factor	Rattus norvegicus	49-57
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	NFKB inhibitor alpha	Rattus norvegicus	111-123
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	synaptotagmin 1	Rattus norvegicus	129-132
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	133-137
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	synaptotagmin 1	Rattus norvegicus	213-216
22326584-6	2012	In addition, we found that imipramine suppressed TNFalpha-induced phosphorylation of inhibitor of kappaBalpha (IkappaBalpha) and p65/RelA nuclear factor-kappaB (NF-kappaB), as well as the nuclear translocation of p65/RelA in primary cultured astrocytes.	Imipramine	27-37	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	217-221
22326584-9	2012	This study indicates that the antidepressant imipramine inhibits TNFalpha-induced CXCL1 expression via down-regulation of NF-kappaB signaling pathway in astrocytes and suggests that imipramine has a potential as an anti-inflammatory drug.	Imipramine	45-55	tumor necrosis factor	Rattus norvegicus	65-73
22326584-9	2012	This study indicates that the antidepressant imipramine inhibits TNFalpha-induced CXCL1 expression via down-regulation of NF-kappaB signaling pathway in astrocytes and suggests that imipramine has a potential as an anti-inflammatory drug.	Imipramine	45-55	C-X-C motif chemokine ligand 1	Rattus norvegicus	82-87
22326584-9	2012	This study indicates that the antidepressant imipramine inhibits TNFalpha-induced CXCL1 expression via down-regulation of NF-kappaB signaling pathway in astrocytes and suggests that imipramine has a potential as an anti-inflammatory drug.	Imipramine	182-192	tumor necrosis factor	Rattus norvegicus	65-73
22326584-9	2012	This study indicates that the antidepressant imipramine inhibits TNFalpha-induced CXCL1 expression via down-regulation of NF-kappaB signaling pathway in astrocytes and suggests that imipramine has a potential as an anti-inflammatory drug.	Imipramine	182-192	C-X-C motif chemokine ligand 1	Rattus norvegicus	82-87
22194417-0	2012	Imipramine blocks ethanol-induced ASMase activation, ceramide generation, and PP2A activation, and ameliorates hepatic steatosis in ethanol-fed mice.	Imipramine	0-10	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	34-40
22194417-0	2012	Imipramine blocks ethanol-induced ASMase activation, ceramide generation, and PP2A activation, and ameliorates hepatic steatosis in ethanol-fed mice.	Imipramine	0-10	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	78-82
22194417-3	2012	The effect of ethanol on AMP-activated protein kinase phosphorylation was reversed by imipramine, suggesting that the generation of ceramide via acid sphingomyelinase (ASMase) is stimulated by ethanol.	Imipramine	86-96	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	168-174
22194417-12	2012	The levels of phospho-p38 and phospho-JNK were reduced by treatment with imipramine.	Imipramine	73-83	mitogen-activated protein kinase 8	Mus musculus	38-41
22177663-7	2012	The lipopolysaccharide-induced release of tumor necrosis factor-alpha was inhibited by imipramine at concentrations comparable to those inhibiting the proton current.	Imipramine	87-97	tumor necrosis factor	Mus musculus	42-69
22177663-8	2012	These results support the hypothesis that tumor necrosis factor-alpha inhibition by imipramine is related to its inhibitory effects on proton channels.	Imipramine	84-94	tumor necrosis factor	Mus musculus	42-69
22031603-7	2012	Imipramine and quinidine, known unspecific Na(+)/Mg(2+) exchanger inhibitors, led to a strong 88% to 100% inhibition of hSLC41A1-related Mg(2+) extrusion.	Imipramine	0-10	solute carrier family 41 member 1	Homo sapiens	120-128
23001316-3	2012	Our aim was to investigate the in vitro inhibitory effects of three antidepressants (imipramine, amitriptyline and fluoxetine) on PON1 activity.	Imipramine	85-95	paraoxonase 1	Homo sapiens	130-134
22326584-0	2012	Inhibitory effect of the antidepressant imipramine on NF-kappaB-dependent CXCL1 expression in TNFalpha-exposed astrocytes.	Imipramine	40-50	C-X-C motif chemokine ligand 1	Rattus norvegicus	74-79
21660485-5	2012	RT-PCR studies revealed that Kat1, Kat2 and kynurenine-3-monooxygenase (Kmo) gene expressions were not altered after 2 h. At 24 h, the expression of Kat1 and Kat2 genes was enhanced by all studied drugs, whereas Kmo expression was diminished by citalopram, fluoxetine and amitriptyline, but not imipramine.	Imipramine	295-305	kynurenine aminotransferase 1	Homo sapiens	149-153
21660485-5	2012	RT-PCR studies revealed that Kat1, Kat2 and kynurenine-3-monooxygenase (Kmo) gene expressions were not altered after 2 h. At 24 h, the expression of Kat1 and Kat2 genes was enhanced by all studied drugs, whereas Kmo expression was diminished by citalopram, fluoxetine and amitriptyline, but not imipramine.	Imipramine	295-305	aminoadipate aminotransferase	Homo sapiens	158-162
22590738-2	2012	As the ASM is a key enzyme of the sphingolipid exchange, in the present study we have investigated the effect of an ASM inhibitor imipramine on the ceramide and sphingomyelin content in the tissues of old rats.	Imipramine	130-140	H19, imprinted maternally expressed transcript (non-protein coding)	Rattus norvegicus	116-119
23076128-0	2012	Imipramine induces brain-derived neurotrophic factor mRNA expression in cultured astrocytes.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	19-52
23076128-4	2012	In the present study, we evaluated the effects of imipramine, a classic tricyclic antidepressant drug, on BDNF expression in cultured rat brain astrocytes.	Imipramine	50-60	brain-derived neurotrophic factor	Rattus norvegicus	106-110
21856315-4	2012	Among the factors found to be downregulated after acute (one day) or chronic (21 days) imipramine administration were peptides derived from secretogranin 1 (chromogranin B) as well as peptides derived from cerebellin precursors.	Imipramine	87-97	chromogranin B	Mus musculus	140-155
23076128-5	2012	Imipramine dose-dependently increased BDNF mRNA expression in astrocytes.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	38-42
23076128-6	2012	The imipramine-induced BDNF increase was suppressed with inhibitors for protein kinase A (PKA) or MEK/ERK.	Imipramine	4-14	brain-derived neurotrophic factor	Rattus norvegicus	23-27
23076128-6	2012	The imipramine-induced BDNF increase was suppressed with inhibitors for protein kinase A (PKA) or MEK/ERK.	Imipramine	4-14	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	72-88
23076128-6	2012	The imipramine-induced BDNF increase was suppressed with inhibitors for protein kinase A (PKA) or MEK/ERK.	Imipramine	4-14	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	90-93
23076128-6	2012	The imipramine-induced BDNF increase was suppressed with inhibitors for protein kinase A (PKA) or MEK/ERK.	Imipramine	4-14	Eph receptor B1	Rattus norvegicus	102-105
23076128-7	2012	Moreover, imipramine exposure activated transcription factor cAMP response element binding protein (CREB) in a dose-dependent manner.	Imipramine	10-20	cAMP responsive element binding protein 1	Rattus norvegicus	61-98
23076128-7	2012	Moreover, imipramine exposure activated transcription factor cAMP response element binding protein (CREB) in a dose-dependent manner.	Imipramine	10-20	cAMP responsive element binding protein 1	Rattus norvegicus	100-104
23076128-8	2012	These results suggested that imipramine induced BDNF expression through CREB activation via PKA and/or ERK pathways.	Imipramine	29-39	brain-derived neurotrophic factor	Rattus norvegicus	48-52
23076128-8	2012	These results suggested that imipramine induced BDNF expression through CREB activation via PKA and/or ERK pathways.	Imipramine	29-39	cAMP responsive element binding protein 1	Rattus norvegicus	72-76
23076128-8	2012	These results suggested that imipramine induced BDNF expression through CREB activation via PKA and/or ERK pathways.	Imipramine	29-39	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	92-95
23076128-8	2012	These results suggested that imipramine induced BDNF expression through CREB activation via PKA and/or ERK pathways.	Imipramine	29-39	Eph receptor B1	Rattus norvegicus	103-106
23076128-9	2012	Imipramine treatment in depression might exert antidepressant action through BDNF production from astrocytes, and glial BDNF expression might be a target of developing novel antidepressants.	Imipramine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	77-81
21867718-8	2012	As previously reported, the effects of imipramine in the forced swim test were blunted in heterozygous BDNF knockout (bdnf(+/-)) mice.	Imipramine	39-49	brain derived neurotrophic factor	Mus musculus	103-107
21867718-8	2012	As previously reported, the effects of imipramine in the forced swim test were blunted in heterozygous BDNF knockout (bdnf(+/-)) mice.	Imipramine	39-49	brain derived neurotrophic factor	Mus musculus	118-122
21856315-4	2012	Among the factors found to be downregulated after acute (one day) or chronic (21 days) imipramine administration were peptides derived from secretogranin 1 (chromogranin B) as well as peptides derived from cerebellin precursors.	Imipramine	87-97	chromogranin B	Mus musculus	157-171
21856315-5	2012	In contrast, peptides SRIF-14 and SRIF-28 (1-11) derived from somatostatin (SRIF, somatotropin release inhibiting factor) were significantly upregulated by imipramine in the hypothalamus.	Imipramine	156-166	somatostatin	Mus musculus	22-26
21856315-5	2012	In contrast, peptides SRIF-14 and SRIF-28 (1-11) derived from somatostatin (SRIF, somatotropin release inhibiting factor) were significantly upregulated by imipramine in the hypothalamus.	Imipramine	156-166	somatostatin	Mus musculus	34-38
21856315-5	2012	In contrast, peptides SRIF-14 and SRIF-28 (1-11) derived from somatostatin (SRIF, somatotropin release inhibiting factor) were significantly upregulated by imipramine in the hypothalamus.	Imipramine	156-166	somatostatin	Mus musculus	34-38
21856315-8	2012	Furthermore, chronic co-administration of SRA880 and imipramine synergistically increased BDNF mRNA expression in the cerebral cortex.	Imipramine	53-63	brain derived neurotrophic factor	Mus musculus	90-94
22005597-3	2012	This study assessed whether the antidepressant drugs citalopram, imipramine, and reboxetine, with differing specificity for the serotonin and norepinephrine transporter, altered responding controlled by the conditional stimulus (CS) effects of nicotine.	Imipramine	65-75	solute carrier family 6 member 2	Rattus norvegicus	142-168
22044672-8	2011	The citrate synthase and creatine kinase increased in the amygdala after acute treatment with imipramine.	Imipramine	94-104	citrate synthase	Rattus norvegicus	4-20
21726413-10	2011	Substrate inhibition was observed in lamotrigine, cyproheptadine and imipramine glucuronidation by wild-type UGT1A4 but vanished for p.P364L.	Imipramine	69-79	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	109-115
21930150-13	2011	The results support a role for central BDNF in depressogenic effects of alcohol and antidepressant effects of nomifensine and imipramine.	Imipramine	126-136	brain-derived neurotrophic factor	Rattus norvegicus	39-43
21889492-2	2011	We found that exposure of U-87MG cells to imipramine resulted in the inhibition of PI3K/Akt/mTOR signaling, reduction of clonogenicity, and induction of cell death.	Imipramine	42-52	AKT serine/threonine kinase 1	Homo sapiens	88-91
21961110-4	2011	A good linear correlation is observed for the dependence of the SERS signal at 684 cm(-1) (R(2) = 0.9997) on Imi concentration over the range of 0.75-7.5 muM.	Imipramine	109-112	latexin	Homo sapiens	154-157
21961110-5	2011	The limit of detection of imipramine in the silver colloidal solution is 0.98 muM.	Imipramine	26-36	latexin	Homo sapiens	78-81
21697722-7	2011	Verapamil, carvedilol, imipramine, and cimetidine were competitive inhibitors of OCT3-mediated metformin uptake (Ki 3.6-15.8 muM).	Imipramine	23-33	OCTN3	Homo sapiens	81-85
21697722-7	2011	Verapamil, carvedilol, imipramine, and cimetidine were competitive inhibitors of OCT3-mediated metformin uptake (Ki 3.6-15.8 muM).	Imipramine	23-33	latexin	Homo sapiens	125-128
22803040-5	2011	Ladasten was more potent than imipramine in decreasing the content of proinflammatory cytokines TNF-alpha and IL-6 and preventing the development of behavioral disturbances in mice.	Imipramine	30-40	tumor necrosis factor	Mus musculus	96-105
22803040-5	2011	Ladasten was more potent than imipramine in decreasing the content of proinflammatory cytokines TNF-alpha and IL-6 and preventing the development of behavioral disturbances in mice.	Imipramine	30-40	interleukin 6	Mus musculus	110-114
25379896-0	2011	Administration of cannabidiol and imipramine induces antidepressant-like effects in the forced swimming test and increases brain-derived neurotrophic factor levels in the rat amygdala.	Imipramine	34-44	brain-derived neurotrophic factor	Rattus norvegicus	123-156
22026997-0	2011	Imipramine enhances neuroprotective effect of PEP-1-Catalase against ischemic neuronal damage.	Imipramine	0-10	catalase	Homo sapiens	46-60
22026997-5	2011	Additionally, the group of PEP-1-CAT (+) imipramine showed enhancement of transduction efficiency and therefore increased cellular viability than that of PEP-1-CAT alone.	Imipramine	41-51	catalase	Homo sapiens	33-36
22026997-5	2011	Additionally, the group of PEP-1-CAT (+) imipramine showed enhancement of transduction efficiency and therefore increased cellular viability than that of PEP-1-CAT alone.	Imipramine	41-51	catalase	Homo sapiens	160-163
22026997-7	2011	Interestingly, PEP-1-CAT (+) imipramine prevented neuronal cell death and lipid peroxidation more markedly than PEP-1-CAT alone.	Imipramine	29-39	catalase	Homo sapiens	21-24
21889492-2	2011	We found that exposure of U-87MG cells to imipramine resulted in the inhibition of PI3K/Akt/mTOR signaling, reduction of clonogenicity, and induction of cell death.	Imipramine	42-52	mechanistic target of rapamycin kinase	Homo sapiens	92-96
21889492-3	2011	Imipramine stimulated the formation of acidic vesicular organelles, the conversion of LC3-I to LC3-II, and the redistribution of LC3 to autophagosomes, suggesting that it stimulates the progression of autophagy.	Imipramine	0-10	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	86-89
21889492-3	2011	Imipramine stimulated the formation of acidic vesicular organelles, the conversion of LC3-I to LC3-II, and the redistribution of LC3 to autophagosomes, suggesting that it stimulates the progression of autophagy.	Imipramine	0-10	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	95-98
21889492-3	2011	Imipramine stimulated the formation of acidic vesicular organelles, the conversion of LC3-I to LC3-II, and the redistribution of LC3 to autophagosomes, suggesting that it stimulates the progression of autophagy.	Imipramine	0-10	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	95-98
21889492-5	2011	We further showed that knockdown of Beclin-1 using siRNA abrogated imipramine-induced cell death.	Imipramine	67-77	beclin 1	Homo sapiens	36-44
21889492-6	2011	These results suggest that imipramine exerts antitumor effects on PTEN-null U-87MG human glioma cells by inhibiting PI3K/Akt/mTOR signaling and by inducing autophagic cell death.	Imipramine	27-37	phosphatase and tensin homolog	Homo sapiens	66-70
21889492-6	2011	These results suggest that imipramine exerts antitumor effects on PTEN-null U-87MG human glioma cells by inhibiting PI3K/Akt/mTOR signaling and by inducing autophagic cell death.	Imipramine	27-37	AKT serine/threonine kinase 1	Homo sapiens	121-124
21889492-6	2011	These results suggest that imipramine exerts antitumor effects on PTEN-null U-87MG human glioma cells by inhibiting PI3K/Akt/mTOR signaling and by inducing autophagic cell death.	Imipramine	27-37	mechanistic target of rapamycin kinase	Homo sapiens	125-129
22156682-4	2011	Animal model of depression was developed by chronic administration of Clomipramine and/or Melipramine in rat pups from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Imipramine	90-101	S100 calcium binding protein A9	Rattus norvegicus	151-154
21853482-4	2011	This novel TCA also exhibits an increased selectivity (relative to imipramine) in binding to hSERT versus the human norepinephrine transporter (hNET).	Imipramine	67-77	solute carrier family 6 member 4	Homo sapiens	93-98
21853482-5	2011	Even higher selectivity could be obtained with 3,7-dihydroxymethyl imipramine, which was found to be 167-fold more selective for hSERT over hNET, representative of a 120-fold gain in selectivity relative to the parent imipramine.	Imipramine	67-77	solute carrier family 6 member 4	Homo sapiens	129-134
21853482-5	2011	Even higher selectivity could be obtained with 3,7-dihydroxymethyl imipramine, which was found to be 167-fold more selective for hSERT over hNET, representative of a 120-fold gain in selectivity relative to the parent imipramine.	Imipramine	67-77	solute carrier family 6 member 2	Homo sapiens	140-144
21853482-6	2011	These results further validate our previous model for the binding of imipramine and high-affinity analogues of imipramine to the central binding site of hSERT.	Imipramine	69-79	solute carrier family 6 member 4	Homo sapiens	153-158
21853482-6	2011	These results further validate our previous model for the binding of imipramine and high-affinity analogues of imipramine to the central binding site of hSERT.	Imipramine	111-121	solute carrier family 6 member 4	Homo sapiens	153-158
22156682-4	2011	Animal model of depression was developed by chronic administration of Clomipramine and/or Melipramine in rat pups from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Imipramine	90-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-162
22156682-4	2011	Animal model of depression was developed by chronic administration of Clomipramine and/or Melipramine in rat pups from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Imipramine	90-101	golgi SNAP receptor complex member 1	Rattus norvegicus	170-173
21777907-9	2011	In addition, pharmacological treatments performed in vivo with exogenous NPY and with Y1 receptor antagonist BIBP3226 have indicated that these compounds interact positively with endogenous catecholaminergic and serotoninergic systems, in a way similar to that of the antidepressants imipramine and fluoxetine.	Imipramine	284-294	neuropeptide Y	Homo sapiens	73-76
21777907-10	2011	In addition, the observed decrease of endogenous Peak 5 after treatment with imipramine or fluoxetine could be related to the concomitant stimulation of the catecholaminergic system with consequent reduced need for endogenous NPY.	Imipramine	77-87	neuropeptide Y	Homo sapiens	226-229
21397634-7	2011	Combined treatment with ketamine and imipramine produced stronger increases of CREB and BDNF protein levels in the prefrontal cortex, hippocampus and amygdala, and PKA phosphorylation in the hippocampus and amygdala and PKC phosphorylation in prefrontal cortex.	Imipramine	37-47	cAMP responsive element binding protein 1	Rattus norvegicus	79-83
21397634-0	2011	Ketamine plus imipramine treatment induces antidepressant-like behavior and increases CREB and BDNF protein levels and PKA and PKC phosphorylation in rat brain.	Imipramine	14-24	cAMP responsive element binding protein 1	Rattus norvegicus	86-90
21397634-7	2011	Combined treatment with ketamine and imipramine produced stronger increases of CREB and BDNF protein levels in the prefrontal cortex, hippocampus and amygdala, and PKA phosphorylation in the hippocampus and amygdala and PKC phosphorylation in prefrontal cortex.	Imipramine	37-47	brain-derived neurotrophic factor	Rattus norvegicus	88-92
21397634-0	2011	Ketamine plus imipramine treatment induces antidepressant-like behavior and increases CREB and BDNF protein levels and PKA and PKC phosphorylation in rat brain.	Imipramine	14-24	brain-derived neurotrophic factor	Rattus norvegicus	95-99
21397634-0	2011	Ketamine plus imipramine treatment induces antidepressant-like behavior and increases CREB and BDNF protein levels and PKA and PKC phosphorylation in rat brain.	Imipramine	14-24	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	119-122
21397634-7	2011	Combined treatment with ketamine and imipramine produced stronger increases of CREB and BDNF protein levels in the prefrontal cortex, hippocampus and amygdala, and PKA phosphorylation in the hippocampus and amygdala and PKC phosphorylation in prefrontal cortex.	Imipramine	37-47	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	164-167
21497036-9	2011	This established method was employed to evaluate the inhibitory effects of five target compounds including amitriptyline, hecogenin, imipramine, lamotrigine, and trifluoperazine on enzymatic activity of UGT2B10.	Imipramine	133-143	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	203-210
20572198-5	2011	Subchronic treatment with imipramine showed a tendency (although not statistically significant) to decrease the LH-induced increment of activated astrocytes in the CA3 region and dentate gyrus.	Imipramine	26-36	carbonic anhydrase 3	Rattus norvegicus	164-167
20572198-7	2011	However, the antidepressant-like effects of imipramine in the LH paradigm were blocked when fluorocitrate (a reversible inhibitor of astrocyte function) was injected into the dentate gyrus or CA3 region.	Imipramine	44-54	carbonic anhydrase 3	Rattus norvegicus	192-195
21354245-0	2011	Imipramine activates glial cell line-derived neurotrophic factor via early growth response gene 1 in astrocytes.	Imipramine	0-10	glial cell line derived neurotrophic factor	Mus musculus	21-64
21354245-2	2011	The present study explored early growth response 1 (EGR-1) transcriptional regulation of imipramine-induced glial cell line-derived neurotrophic factor (GDNF) expression in astrocytes.	Imipramine	89-99	early growth response 1	Mus musculus	52-57
21354245-7	2011	Pretreatment of rat primary astrocytes with the MAPK kinase inhibitor U0126 or the JNK inhibitor SP600125 strongly inhibited imipramine-stimulated EGR-1 expression.	Imipramine	125-135	mitogen-activated protein kinase 1	Mus musculus	48-52
21354245-2	2011	The present study explored early growth response 1 (EGR-1) transcriptional regulation of imipramine-induced glial cell line-derived neurotrophic factor (GDNF) expression in astrocytes.	Imipramine	89-99	glial cell line derived neurotrophic factor	Mus musculus	108-151
21354245-7	2011	Pretreatment of rat primary astrocytes with the MAPK kinase inhibitor U0126 or the JNK inhibitor SP600125 strongly inhibited imipramine-stimulated EGR-1 expression.	Imipramine	125-135	mitogen-activated protein kinase 8	Rattus norvegicus	83-86
21354245-2	2011	The present study explored early growth response 1 (EGR-1) transcriptional regulation of imipramine-induced glial cell line-derived neurotrophic factor (GDNF) expression in astrocytes.	Imipramine	89-99	glial cell line derived neurotrophic factor	Mus musculus	153-157
21354245-3	2011	After we observed the induction of GDNF mRNA expression in rat astrocytes in response to imipramine, deletion mutant studies showed that the proximal region between -493 and -114 of the GDNF promoter, which contains three binding sites for EGR-1, was essential for maximal imipramine-induced activation of GDNF promoter.	Imipramine	89-99	glial cell derived neurotrophic factor	Rattus norvegicus	35-39
21354245-7	2011	Pretreatment of rat primary astrocytes with the MAPK kinase inhibitor U0126 or the JNK inhibitor SP600125 strongly inhibited imipramine-stimulated EGR-1 expression.	Imipramine	125-135	early growth response 1	Rattus norvegicus	147-152
21354245-3	2011	After we observed the induction of GDNF mRNA expression in rat astrocytes in response to imipramine, deletion mutant studies showed that the proximal region between -493 and -114 of the GDNF promoter, which contains three binding sites for EGR-1, was essential for maximal imipramine-induced activation of GDNF promoter.	Imipramine	89-99	glial cell derived neurotrophic factor	Rattus norvegicus	186-190
21354245-8	2011	In conclusion, we found that imipramine induction of EGR-1 upregulated GDNF in astrocytes in a dose-dependent manner.	Imipramine	29-39	early growth response 1	Mus musculus	53-58
21354245-3	2011	After we observed the induction of GDNF mRNA expression in rat astrocytes in response to imipramine, deletion mutant studies showed that the proximal region between -493 and -114 of the GDNF promoter, which contains three binding sites for EGR-1, was essential for maximal imipramine-induced activation of GDNF promoter.	Imipramine	89-99	glial cell derived neurotrophic factor	Rattus norvegicus	186-190
21354245-8	2011	In conclusion, we found that imipramine induction of EGR-1 upregulated GDNF in astrocytes in a dose-dependent manner.	Imipramine	29-39	glial cell line derived neurotrophic factor	Mus musculus	71-75
21354245-3	2011	After we observed the induction of GDNF mRNA expression in rat astrocytes in response to imipramine, deletion mutant studies showed that the proximal region between -493 and -114 of the GDNF promoter, which contains three binding sites for EGR-1, was essential for maximal imipramine-induced activation of GDNF promoter.	Imipramine	273-283	glial cell derived neurotrophic factor	Rattus norvegicus	186-190
21354245-3	2011	After we observed the induction of GDNF mRNA expression in rat astrocytes in response to imipramine, deletion mutant studies showed that the proximal region between -493 and -114 of the GDNF promoter, which contains three binding sites for EGR-1, was essential for maximal imipramine-induced activation of GDNF promoter.	Imipramine	273-283	glial cell derived neurotrophic factor	Rattus norvegicus	186-190
21354245-4	2011	The dose-dependent upregulation of EGR-1 by imipramine, the activation of GDNF by the over-expression of EGR-1 without imipramine and the reduction in the imipramine-induced GDNF mRNA expression after silencing of endogenous EGR-1 demonstrated that EGR-1 is upregulated by imipramine to activate the GDNF promoter.	Imipramine	44-54	early growth response 1	Mus musculus	35-40
21354245-4	2011	The dose-dependent upregulation of EGR-1 by imipramine, the activation of GDNF by the over-expression of EGR-1 without imipramine and the reduction in the imipramine-induced GDNF mRNA expression after silencing of endogenous EGR-1 demonstrated that EGR-1 is upregulated by imipramine to activate the GDNF promoter.	Imipramine	119-129	glial cell line derived neurotrophic factor	Mus musculus	74-78
21354245-4	2011	The dose-dependent upregulation of EGR-1 by imipramine, the activation of GDNF by the over-expression of EGR-1 without imipramine and the reduction in the imipramine-induced GDNF mRNA expression after silencing of endogenous EGR-1 demonstrated that EGR-1 is upregulated by imipramine to activate the GDNF promoter.	Imipramine	119-129	glial cell line derived neurotrophic factor	Mus musculus	74-78
21354245-4	2011	The dose-dependent upregulation of EGR-1 by imipramine, the activation of GDNF by the over-expression of EGR-1 without imipramine and the reduction in the imipramine-induced GDNF mRNA expression after silencing of endogenous EGR-1 demonstrated that EGR-1 is upregulated by imipramine to activate the GDNF promoter.	Imipramine	119-129	glial cell line derived neurotrophic factor	Mus musculus	74-78
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	13-23	glial cell line derived neurotrophic factor	Mus musculus	32-36
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	13-23	early growth response 1	Mus musculus	104-109
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	13-23	glial cell line derived neurotrophic factor	Mus musculus	157-161
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	13-23	early growth response 1	Mus musculus	269-274
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	13-23	early growth response 1	Mus musculus	269-274
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	234-244	glial cell line derived neurotrophic factor	Mus musculus	32-36
21354245-5	2011	Furthermore, imipramine-induced GDNF mRNA expression was strongly attenuated in primary astrocytes from Egr-1(-/-) mice, and the immunoreactivity to an anti-GDNF antibody in glial fibrillary acidic protein-positive cells was lower in imipramine-treated astrocytes from Egr-1(-/-) mice than in those from Egr-1(+/-) mice.	Imipramine	234-244	glial cell line derived neurotrophic factor	Mus musculus	157-161
21354245-6	2011	To determine whether mitogen-activated protein kinases (MAPKs) were associated with imipramine-induced EGR-1 expression, we examined the induction of MAPK phosphorylation in response to imipramine.	Imipramine	84-94	early growth response 1	Mus musculus	103-108
21354245-6	2011	To determine whether mitogen-activated protein kinases (MAPKs) were associated with imipramine-induced EGR-1 expression, we examined the induction of MAPK phosphorylation in response to imipramine.	Imipramine	84-94	mitogen-activated protein kinase 1	Mus musculus	56-60
21602609-2	2011	The present study investigates the effect of chronic (16 days) combined treatment with zinc (15 mg/kg zinc hydroaspartate) and imipramine (5 mg/kg) in chronic unpredictable stress (CUS) on the BDNF mRNA level in the rat brain.	Imipramine	127-137	brain-derived neurotrophic factor	Rattus norvegicus	193-197
21488984-8	2011	Treatment with the broad-acting tricyclic antidepressant imipramine, only during the last 3 weeks of the 3-month period after social defeat, completely restored the reduction in neurogenesis by increasing both class I and II DCX(+) cell populations.	Imipramine	57-67	doublecortin	Homo sapiens	225-228
21067755-1	2011	Carbamazepine and imipramine are drugs that have significant binding to human serum albumin (HSA), the most abundant serum protein in blood and a common transport protein for many drugs in the body.	Imipramine	18-28	albumin	Homo sapiens	78-91
21067755-1	2011	Carbamazepine and imipramine are drugs that have significant binding to human serum albumin (HSA), the most abundant serum protein in blood and a common transport protein for many drugs in the body.	Imipramine	18-28	albumin	Homo sapiens	93-96
21067755-3	2011	In this report, an approach based on peak profiling was used with high-performance affinity chromatography to measure the dissociation rate constants for carbamazepine and imipramine with HSA.	Imipramine	172-182	albumin	Homo sapiens	188-191
21067755-6	2011	Dissociation rate constants of 1.7 (+-0.2) s(-1) and 0.67 (+-0.04) s(-1) at pH 7.4 and 37 C were estimated by this approach for HSA in its interactions with carbamazepine and imipramine, respectively.	Imipramine	175-185	albumin	Homo sapiens	128-131
21129485-3	2011	Codon-optimization of this de novo constructed genes and construction of stable cell lines improved expression 3.5-fold and single-step immunoaffinity purification with FLAG-epitope tag yielded around one milligram functional SERT per liter culture medium assessed by [(3)H] imipramine ligand binding.	Imipramine	275-285	solute carrier family 6 member 4	Homo sapiens	226-230
21325831-8	2011	Syk inhibitors also caused a decrease of the monensin-induced 5-HT-efflux from platelets and of imipramine binding to them.	Imipramine	96-106	spleen associated tyrosine kinase	Homo sapiens	0-3
21602609-7	2011	However, combined treatment of zinc and imipramine induced a 12% elevation of the BDNF mRNA level in the stressed but not in the unstressed rats.	Imipramine	40-50	brain-derived neurotrophic factor	Rattus norvegicus	82-86
19921703-6	2010	Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated "depressed" rats) compared with the FSL saline group.	Imipramine	0-10	germ cell-less 1, spermatogenesis associated	Rattus norvegicus	94-97
22358083-1	2011	We have previously reported that chronic imipramine and electroconvulsive treatments increase the alpha(1A)-adrenoceptor (but not the alpha(1B) subtype) mRNA level and the receptor density in the rat cerebral cortex.	Imipramine	41-51	adrenoceptor alpha 1A	Rattus norvegicus	98-120
22358083-3	2011	Here, we report that previous noradrenergic depletion with DSP-4 (50 mg/kg) (a neurotoxin selective for the noradrenergic nerve terminals) significantly attenuated the increase of alpha(1A)-adrenoceptor mRNA induced by a 14-day treatment with imipramine (IMI, 20 mg/kg, ip) and abolished the effect of electroconvulsive shock (ECS, 150 mA, 0.5 s) in the prefrontal cortex of the rat brain.	Imipramine	243-253	adrenoceptor alpha 1A	Rattus norvegicus	180-202
22358083-3	2011	Here, we report that previous noradrenergic depletion with DSP-4 (50 mg/kg) (a neurotoxin selective for the noradrenergic nerve terminals) significantly attenuated the increase of alpha(1A)-adrenoceptor mRNA induced by a 14-day treatment with imipramine (IMI, 20 mg/kg, ip) and abolished the effect of electroconvulsive shock (ECS, 150 mA, 0.5 s) in the prefrontal cortex of the rat brain.	Imipramine	255-258	adrenoceptor alpha 1A	Rattus norvegicus	180-202
22076148-6	2011	In vivo, chronic treatment with the non-selective antidepressant imipramine as well as the norepinephrine-selective reuptake inhibitor desipramine or the serotonin-selective reuptake inhibitor fluoxetine all decrease p21 expression, and this was associated with increased neurogenesis.	Imipramine	65-75	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	217-220
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	76-80
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	brain derived neurotrophic factor	Mus musculus	106-110
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	brain derived neurotrophic factor	Mus musculus	181-185
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	210-214
21720142-1	2011	A facile fluorometric assay using D-kynurenine as a substrate was utilized for evaluating the inhibition of D-amino acid oxidase (DAAO), which is one of the products of a susceptibility gene for schizophrenia, by commercial antipsychotic drugs, namely, chlorpromazine (CPZ), carbamazepine, sulpiride, quetiapine, and imipramine.	Imipramine	317-327	D-amino acid oxidase	Homo sapiens	108-128
21720142-1	2011	A facile fluorometric assay using D-kynurenine as a substrate was utilized for evaluating the inhibition of D-amino acid oxidase (DAAO), which is one of the products of a susceptibility gene for schizophrenia, by commercial antipsychotic drugs, namely, chlorpromazine (CPZ), carbamazepine, sulpiride, quetiapine, and imipramine.	Imipramine	317-327	D-amino acid oxidase	Homo sapiens	130-134
19921703-6	2010	Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated "depressed" rats) compared with the FSL saline group.	Imipramine	0-10	carbonic anhydrase 1	Rattus norvegicus	125-128
19921703-6	2010	Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated "depressed" rats) compared with the FSL saline group.	Imipramine	140-150	carbonic anhydrase 1	Rattus norvegicus	125-128
20829432-5	2010	Two approaches were used subsequently to differentiate between three clusters of potential docking poses: 1) a diagnostic SERT(Y95F) mutation, which greatly reduced the affinity for [(3)H]imipramine but did not affect substrate binding; 2) competition binding experiments in the presence and absence of carbamazepine (i.e., a tricyclic imipramine analog with a short side chain that competes with [(3)H]imipramine binding to SERT).	Imipramine	188-198	solute carrier family 6 member 4	Homo sapiens	122-126
20620184-5	2010	The involvement of ASMase in uptake was confirmed by a pharmacological inhibition of ASMase by imipramine and a subsequent rescue of uptake through external addition of sphingomyelinase, and by using ASMase-deficient cells.	Imipramine	95-105	sphingomyelin phosphodiesterase 1	Homo sapiens	19-25
20680307-9	2010	Imipramine and NOE also restored State 3 respiration to 248.4 +- 2 and 249.0 +- 2, respectively (p < 0.01 vs. TNFalpha alone).	Imipramine	0-10	tumor necrosis factor	Mus musculus	113-121
21273663-4	2010	Imipramine moderately diminished the rate of chlorpromazine 5-sulfoxidation (K(i) = 8.7 muM, competitive inhibition), mono-N-demethylation (K(i) = 16.0 muM, non-competitive inhibition) and di-N-demethylation (K(i) = 13.5 muM mixed inhibition).	Imipramine	0-10	latexin	Homo sapiens	88-91
21273663-4	2010	Imipramine moderately diminished the rate of chlorpromazine 5-sulfoxidation (K(i) = 8.7 muM, competitive inhibition), mono-N-demethylation (K(i) = 16.0 muM, non-competitive inhibition) and di-N-demethylation (K(i) = 13.5 muM mixed inhibition).	Imipramine	0-10	latexin	Homo sapiens	152-155
21273663-4	2010	Imipramine moderately diminished the rate of chlorpromazine 5-sulfoxidation (K(i) = 8.7 muM, competitive inhibition), mono-N-demethylation (K(i) = 16.0 muM, non-competitive inhibition) and di-N-demethylation (K(i) = 13.5 muM mixed inhibition).	Imipramine	0-10	latexin	Homo sapiens	152-155
20620184-5	2010	The involvement of ASMase in uptake was confirmed by a pharmacological inhibition of ASMase by imipramine and a subsequent rescue of uptake through external addition of sphingomyelinase, and by using ASMase-deficient cells.	Imipramine	95-105	sphingomyelin phosphodiesterase 1	Homo sapiens	85-91
20620184-5	2010	The involvement of ASMase in uptake was confirmed by a pharmacological inhibition of ASMase by imipramine and a subsequent rescue of uptake through external addition of sphingomyelinase, and by using ASMase-deficient cells.	Imipramine	95-105	sphingomyelin phosphodiesterase 1	Homo sapiens	85-91
20363235-4	2010	Amitriptyline, nortriptyline and imipramine showed considerably higher affinities for alpha(1A)- (approximately 25- to 80-fold) and alpha(1D)-adrenoceptors (approximately 10- to 25-fold) than for alpha(1B)-adrenoceptors in both contraction and [(3)H]prazosin binding assays with rat native and human receptors, respectively.	Imipramine	33-43	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	86-94
20629583-7	2010	WHAT THE READER WILL GAIN: Insights into the problems associated with determining the contribution of an FMO to the metabolism of a drug and how an Fmo-knockout mouse line has revealed the role of FMO1 in the metabolism of imipramine in vivo.	Imipramine	223-233	flavin containing monooxygenase 1	Mus musculus	197-201
20484120-0	2010	Imipramine-induced cardiac depression is responsible for the increase in intracellular magnesium and the activation of ERK 1/2 in rats.	Imipramine	0-10	mitogen activated protein kinase 3	Rattus norvegicus	119-126
20484120-7	2010	Imipramine also induced activation of ERK 1/2 and increase in the [Mg(2+)]( i), which was inhibited PD98059, ERK 1/2 inhibitor.	Imipramine	0-10	mitogen activated protein kinase 3	Rattus norvegicus	38-45
20484120-7	2010	Imipramine also induced activation of ERK 1/2 and increase in the [Mg(2+)]( i), which was inhibited PD98059, ERK 1/2 inhibitor.	Imipramine	0-10	mitogen activated protein kinase 3	Rattus norvegicus	109-116
20484120-8	2010	These results suggest that imipramine-induced cardiac depression may be partly due to increases of [Mg(2+)](i) that are accompanied by the activation of ERK 1/2 in rats.	Imipramine	27-37	mitogen activated protein kinase 3	Rattus norvegicus	153-160
21150338-5	2010	The SOD and CAT activities increased with acute and chronic treatments with imipramine and harmine, compared to control group in prefrontal cortex and hippocampus.	Imipramine	76-86	catalase	Rattus norvegicus	12-15
21150338-6	2010	In conclusion, our results indicate positive effects of imipramine antidepressant and beta-carboline harmine of oxidative stress parameters, increasing SOD and CAT activities and decreasing lipid and protein oxidation.	Imipramine	56-66	catalase	Rattus norvegicus	160-163
20406626-6	2010	Impramine also significantly attenuated lung inflammation, lung edema, MPO (myeloperoxidase) activity, lung tissue pathological changes and nuclear factor-kappaB DNA binding activity.	Imipramine	0-9	myeloperoxidase	Mus musculus	71-74
20406626-6	2010	Impramine also significantly attenuated lung inflammation, lung edema, MPO (myeloperoxidase) activity, lung tissue pathological changes and nuclear factor-kappaB DNA binding activity.	Imipramine	0-9	myeloperoxidase	Mus musculus	76-91
20073575-9	2010	Finally, exposure of the cells to serotonin promoted an increase in MSCs apoptosis prevented by pargyline and the SERT inhibitor imipramine.	Imipramine	129-139	solute carrier family 6 member 4	Homo sapiens	114-118
19926744-7	2010	Pharmacological inhibition of the ASM pathway with imipramine, D609 or dexamethasone blocked the PAF-induced increase of caveolin-1 and eNOS in caveolae, and the decrease in eNO production and oedema formation.	Imipramine	51-61	PCNA clamp associated factor	Rattus norvegicus	97-100
19926744-7	2010	Pharmacological inhibition of the ASM pathway with imipramine, D609 or dexamethasone blocked the PAF-induced increase of caveolin-1 and eNOS in caveolae, and the decrease in eNO production and oedema formation.	Imipramine	51-61	caveolin 1	Rattus norvegicus	121-131
20363235-5	2010	In addition, amitriptyline, nortriptyline and imipramine were substantially more potent in the inhibition of noradrenaline-induced intracellular Ca(2+) increases in HEK-293 cells expressing alpha(1A)- or a truncated version of alpha(1D)-adrenoceptors which traffics more efficiently towards the cell membrane than in cells expressing alpha(1B)-adrenoceptors.	Imipramine	46-56	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	190-198
20363235-6	2010	Amitriptyline, nortriptyline and imipramine are much weaker antagonists of rat and human alpha(1B)-adrenoceptors than of alpha(1A)- and alpha(1D)-adrenoceptors.	Imipramine	33-43	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	121-129
20224005-8	2010	The activation of PP2A and inhibition of AMPK phosphorylation caused by ethanol was attenuated by fumonisin B1 and imipramine, an acid sphingomyelinase (SMase) inhibitor.	Imipramine	115-125	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	18-22
19884907-0	2010	The CYP2C19*17 genotype is associated with lower imipramine plasma concentrations in a large group of depressed patients.	Imipramine	49-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
20199581-5	2010	Among the antidepressants, antipsychotics, tranquillizers/hypnotic agents and mood stabilizers, the highest SPCC(TDM) scores in the French SPC were reached for imipramine (16), haloperidol (6), clonazepam (8) and lithium (23), respectively.	Imipramine	160-170	proline rich protein gene cluster	Homo sapiens	108-111
19884907-1	2010	CYP2C19 converts the tricyclic antidepressant imipramine to its active metabolite desipramine, which is subsequently inactivated by CYP2D6.	Imipramine	46-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
19884907-1	2010	CYP2C19 converts the tricyclic antidepressant imipramine to its active metabolite desipramine, which is subsequently inactivated by CYP2D6.	Imipramine	46-56	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	132-138
19884907-4	2010	Mean dose-corrected imipramine plasma concentration was significantly dependent on CYP2C19 genotype (Kruskal-Wallis test, P=0.01), with circa 30% lower levels in CYP2C19*17/*17 individuals compared with CYP2C19*1/*1 (wild-type) patients.	Imipramine	20-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-90
19884907-4	2010	Mean dose-corrected imipramine plasma concentration was significantly dependent on CYP2C19 genotype (Kruskal-Wallis test, P=0.01), with circa 30% lower levels in CYP2C19*17/*17 individuals compared with CYP2C19*1/*1 (wild-type) patients.	Imipramine	20-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
19884907-4	2010	Mean dose-corrected imipramine plasma concentration was significantly dependent on CYP2C19 genotype (Kruskal-Wallis test, P=0.01), with circa 30% lower levels in CYP2C19*17/*17 individuals compared with CYP2C19*1/*1 (wild-type) patients.	Imipramine	20-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
19884907-6	2010	In a multivariate analysis, we found a significant, but limited effect (P=0.035, eta(2)=0.031) of the CYP2C19*17 genotype on imipramine+desipramine concentrations.	Imipramine	125-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
19884907-7	2010	Although the CYP2C19*17 allele is associated with a significantly increased metabolism of imipramine, CYP2C19*17 genotyping will, in our view, not importantly contribute to dose management of patients on imipramine therapy guided by imipramine+desipramine plasma concentrations.	Imipramine	90-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
20122921-2	2010	Recently, chronic psychosocial stress as animal model of depression has been shown to stimulate CREB transcriptional activity in the brain; this stimulation was prevented by treatment with the antidepressant imipramine, which inhibits both noradrenaline and serotonin reuptake.	Imipramine	208-218	cAMP responsive element binding protein 1	Mus musculus	96-100
18982003-7	2010	Compared with chronic saline, chronic imipramine but not bupropion significantly increased cortex cPLA(2) mRNA activity, protein and phosphorylation, expression of the cPLA(2) transcription factor, activator protein-2alpha (AP-2alpha) and AA turnover in phospholipids.	Imipramine	38-48	phospholipase A2 group IVA	Rattus norvegicus	98-105
18982003-7	2010	Compared with chronic saline, chronic imipramine but not bupropion significantly increased cortex cPLA(2) mRNA activity, protein and phosphorylation, expression of the cPLA(2) transcription factor, activator protein-2alpha (AP-2alpha) and AA turnover in phospholipids.	Imipramine	38-48	phospholipase A2 group IVA	Rattus norvegicus	168-175
18982003-7	2010	Compared with chronic saline, chronic imipramine but not bupropion significantly increased cortex cPLA(2) mRNA activity, protein and phosphorylation, expression of the cPLA(2) transcription factor, activator protein-2alpha (AP-2alpha) and AA turnover in phospholipids.	Imipramine	38-48	transcription factor AP-2 alpha	Rattus norvegicus	224-233
19762159-0	2010	Hormonal responses to the 5-HT1A agonist buspirone in remitted endogenous depressive patients after long-term imipramine treatment.	Imipramine	110-120	5-hydroxytryptamine receptor 1A	Homo sapiens	26-32
20133892-0	2010	Role of human UGT2B10 in N-glucuronidation of tricyclic antidepressants, amitriptyline, imipramine, clomipramine, and trimipramine.	Imipramine	88-98	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	14-21
20133892-2	2010	The apparent K(m) (S(50)) values for the formation of quaternary N-glucuronides of amitriptyline, imipramine, clomipramine, and trimipramine were 2.60, 16.8, 14.4, and 11.2 microM in UGT2B10 and 448, 262, 112, and 258 microM in UGT1A4, respectively.	Imipramine	98-108	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	183-190
20133892-2	2010	The apparent K(m) (S(50)) values for the formation of quaternary N-glucuronides of amitriptyline, imipramine, clomipramine, and trimipramine were 2.60, 16.8, 14.4, and 11.2 microM in UGT2B10 and 448, 262, 112, and 258 microM in UGT1A4, respectively.	Imipramine	98-108	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	228-234
20133892-3	2010	The kinetics of amitriptyline and imipramine glucuronidation in human liver microsomes exhibited a biphasic character, where the high- and low-affinity components were in good agreement with our results in expressed UGT2B10 and UGT1A4, respectively.	Imipramine	34-44	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	216-223
20133892-3	2010	The kinetics of amitriptyline and imipramine glucuronidation in human liver microsomes exhibited a biphasic character, where the high- and low-affinity components were in good agreement with our results in expressed UGT2B10 and UGT1A4, respectively.	Imipramine	34-44	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	228-234
20133892-5	2010	The in vitro clearances (CL(int) or CL(max)) were comparable between UGT2B10 and UGT1A4 for glucuronidation of imipramine, clomipramine, and trimipramine, whereas CL(int) of amitriptyline glucuronidation by UGT2B10 was more than 10-fold higher than that by UGT1A4.	Imipramine	111-121	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	69-76
20133892-5	2010	The in vitro clearances (CL(int) or CL(max)) were comparable between UGT2B10 and UGT1A4 for glucuronidation of imipramine, clomipramine, and trimipramine, whereas CL(int) of amitriptyline glucuronidation by UGT2B10 was more than 10-fold higher than that by UGT1A4.	Imipramine	111-121	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	81-87
20180829-6	2010	CMS-induced changes in the levels of dynactin 2, Ash 2, non-neuronal SNAP25 and alpha-enolase were reversed by chronic imipramine, but "pulse" treatment was not that effective.	Imipramine	119-129	synaptosome associated protein 25	Rattus norvegicus	69-75
20180829-6	2010	CMS-induced changes in the levels of dynactin 2, Ash 2, non-neuronal SNAP25 and alpha-enolase were reversed by chronic imipramine, but "pulse" treatment was not that effective.	Imipramine	119-129	enolase 1	Rattus norvegicus	80-93
19762159-4	2010	METHODS: A longitudinal design was used in 14 patients with major depressive disorder (DSM-IV) with endogenous features (Newcastle Scale) in order to assess the functional status of post-synaptic 5-HT1A receptors before and after successful antidepressant treatment with imipramine.	Imipramine	271-281	5-hydroxytryptamine receptor 1A	Homo sapiens	196-202
19762159-7	2010	RESULTS: Endogenous depressed patients in remission and currently receiving treatment with imipramine (mean length of treatment 145 days, SD=27) presented significantly lower buspirone responses to ACTH and cortisol than in the pre-treatment condition (Deltamax p< or =.05; AUC p<.001) and to ACTH in comparison with healthy controls (Deltamax p<.01; AUC p<.05).	Imipramine	91-101	proopiomelanocortin	Homo sapiens	198-202
19762159-7	2010	RESULTS: Endogenous depressed patients in remission and currently receiving treatment with imipramine (mean length of treatment 145 days, SD=27) presented significantly lower buspirone responses to ACTH and cortisol than in the pre-treatment condition (Deltamax p< or =.05; AUC p<.001) and to ACTH in comparison with healthy controls (Deltamax p<.01; AUC p<.05).	Imipramine	91-101	proopiomelanocortin	Homo sapiens	299-303
19948720-3	2010	We present an experimentally validated structural model of imipramine and analogous TCAs in the central substrate binding site of hSERT.	Imipramine	59-69	solute carrier family 6 member 4	Homo sapiens	130-135
20436222-8	2010	Chronic treatment with imipramine inhibited the stress-induced decrease in p-JNK1/2, while imipramine, fluoxetine and mirtazapine blocked changes in p-p38.	Imipramine	91-101	mitogen activated protein kinase 14	Rattus norvegicus	151-154
19954760-5	2010	Brain-derived neurotrophic factor (BDNF) hippocampal levels were assessed in imipramine- and memantine-treated rats by ELISA sandwich assay.	Imipramine	77-87	brain-derived neurotrophic factor	Rattus norvegicus	0-33
21200377-7	2010	MAO-A was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > desipramine > amitriptyline > imipramine > citalopram > venlafaxine > reboxetine > olanzapine > mirtazapine > tianeptine > moclobemide, cocaine >> lithium, valproate.	Imipramine	143-153	monoamine oxidase A	Sus scrofa	0-5
20036317-1	2010	This study was aimed to determine whether imipramine chronic treatment promotes neurogenesis in the dentate gyrus (DG) and interferes with neuronal death in the CA1 subfield of the hippocampus after transient global cerebral ischemia (TGCI) in rats.	Imipramine	42-52	carbonic anhydrase 1	Rattus norvegicus	161-164
20036317-9	2010	Chronic imipramine treatment increased cell proliferation in the SGZ of DG and reduced the neurodegeneration in the CA1 of the hippocampus 14 days after TGCI.	Imipramine	8-18	carbonic anhydrase 1	Rattus norvegicus	116-119
19889791-0	2010	Imipramine, in part through tumor necrosis factor alpha inhibition, prevents cognitive decline and beta-amyloid accumulation in a mouse model of Alzheimer"s disease.	Imipramine	0-10	tumor necrosis factor	Mus musculus	28-55
19889791-9	2010	Imipramine significantly prevented memory deficits caused by Abeta25-35 in the water-maze and Y-maze tests, and inhibited the TNF-alpha increase in the frontal cortex.	Imipramine	0-10	tumor necrosis factor	Mus musculus	126-135
19889791-11	2010	So, imipramine prevents memory impairment through its intrinsic property to inhibit TNF-alpha and Abeta accumulation and may represent a potential candidate for AD treatment.	Imipramine	4-14	tumor necrosis factor	Mus musculus	84-93
20089918-7	2010	Furthermore, coadministration of the alpha(2)-adrenoceptor antagonist yohimbine with the antidepressant imipramine significantly accelerates effects on hippocampal progenitor proliferation, the morphological maturation of newborn neurons, and the increase in expression of brain derived neurotrophic factor and vascular endothelial growth factor implicated in the neurogenic and behavioral effects of antidepressants.	Imipramine	104-114	brain derived neurotrophic factor	Mus musculus	273-306
20045935-6	2010	Imipramine treatment at 5 and 20 mg/kg/d enhanced BNIP3 mRNA expression only in the LH group but not in non-LH group or non-stressed group.	Imipramine	0-10	BCL2/adenovirus E1B interacting protein 3	Mus musculus	50-55
21364631-3	2010	Inhibition of JNK activation with sphingomyelinase inhibitors (20 muM desipramine, 20 muM imipramine), with the protein kinase C-delta (PKCdelta) inhibitor rottlerin (10 muM), and with the specific PKCtheta pseudosubstrate inhibitor (30 muM) indicates that ceramide and phosphorylation by PKCdelta and PKCtheta mediate gal-1-induced JNK activation.	Imipramine	90-100	mitogen-activated protein kinase 8	Homo sapiens	14-17
21200377-8	2010	MAO-B was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > venlafaxine > amitriptyline > olanzapine > citalopram > desipramine > reboxetine > imipramine > tianeptine > mirtazapine, cocaine >> moclobemide, lithium, valproate.	Imipramine	208-218	monoamine oxidase B	Sus scrofa	0-5
19632287-3	2009	The present study aims to compare the behavioral effects and the BDNF hippocampus levels of acute administration of harmine and imipramine in rats.	Imipramine	128-138	brain-derived neurotrophic factor	Rattus norvegicus	65-69
19632287-5	2009	Afterwards, hippocampal BDNF protein levels were assessed in imipramine- and harmine-treated rats by ELISA-sandwich assay.	Imipramine	61-71	brain-derived neurotrophic factor	Rattus norvegicus	24-28
19463708-7	2009	Furthermore, imipramine induced a twofold increase of bdnf expression in the dentate gyrus in both genotypes, while bdnf(+/-) mice displayed roughly half-reduced level for the same treatment.	Imipramine	13-23	brain derived neurotrophic factor	Mus musculus	54-58
19632221-7	2009	Furthermore, pre-treatment of mast cells with imipramine or pepstatin A, inhibitors of the intracellular acid sphingomyelinase and cathepsin D pathways respectively, increases survival in IL-15-/- BMMCs.	Imipramine	46-56	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	105-126
19632221-7	2009	Furthermore, pre-treatment of mast cells with imipramine or pepstatin A, inhibitors of the intracellular acid sphingomyelinase and cathepsin D pathways respectively, increases survival in IL-15-/- BMMCs.	Imipramine	46-56	cathepsin D	Mus musculus	131-142
19632221-7	2009	Furthermore, pre-treatment of mast cells with imipramine or pepstatin A, inhibitors of the intracellular acid sphingomyelinase and cathepsin D pathways respectively, increases survival in IL-15-/- BMMCs.	Imipramine	46-56	interleukin 15	Mus musculus	188-193
19787068-6	2009	Imipramine was used for pharmacologic inhibition of acid sphingomyelinase (ASM).	Imipramine	0-10	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	52-73
19787068-6	2009	Imipramine was used for pharmacologic inhibition of acid sphingomyelinase (ASM).	Imipramine	0-10	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	75-78
19787068-14	2009	Induction of MMP-1 by TNF or IL-1beta is completely blocked by inhibition of ASM with imipramine.	Imipramine	86-96	matrix metallopeptidase 13	Mus musculus	13-18
19787068-14	2009	Induction of MMP-1 by TNF or IL-1beta is completely blocked by inhibition of ASM with imipramine.	Imipramine	86-96	tumor necrosis factor	Mus musculus	22-25
19787068-14	2009	Induction of MMP-1 by TNF or IL-1beta is completely blocked by inhibition of ASM with imipramine.	Imipramine	86-96	interleukin 1 beta	Mus musculus	29-37
19787068-14	2009	Induction of MMP-1 by TNF or IL-1beta is completely blocked by inhibition of ASM with imipramine.	Imipramine	86-96	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	77-80
19784492-2	2009	The present study aimed to compare behavioral effects and brain Creatine kinase activity in specific brain regions after administration of ketamine and imipramine in rats.	Imipramine	152-162	creatine kinase B	Rattus norvegicus	58-79
19577549-8	2009	Phenelzine increased locus coeruleus TH and imipramine increased dorsal raphe TPH2 gene expression in a glucocorticoid-dependent manner, suggesting that increases in these enzymes were due to relief of inhibitory glucocorticoid signaling.	Imipramine	44-54	tryptophan hydroxylase 2	Mus musculus	78-82
20137294-8	2009	When FL cells were incubated with ceramide following the imipramine pretreatment for 30 min, EGFR clustering induced by 50-Hz MF exposure could be recovered.	Imipramine	57-67	epidermal growth factor receptor	Homo sapiens	93-97
19904008-8	2009	Hence, taking account of CYP1A2 contribution to the metabolism of endogenous substances (steroids), drugs (xanthine derivatives, phenacetin, propranolol, imipramine, phenothiazine neuroleptics, clozapine) and carcinogenic compounds, the inhibition of CYP1A2 by perazine may be of physiological, pharmacological and toxicological importance.	Imipramine	154-164	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	25-31
19641126-2	2009	Several of these drugs, including imipramine, citalopram, sertraline, and fluoxetine (Prozac), bound more avidly to SERT in the presence of Cl(-).	Imipramine	34-44	solute carrier family 6 member 4	Homo sapiens	116-120
19552509-6	2009	Imipramine, an FMO1-specific inhibitor, selectively inhibited DMA N-oxidation.	Imipramine	0-10	flavin containing dimethylaniline monoxygenase 1	Homo sapiens	15-19
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	Imipramine	133-143	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	93-99
19372226-8	2009	Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1.	Imipramine	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
20043526-0	2009	Imipramine induced elevation of prolactin levels in patients with HIV/AIDS improved their immune status.	Imipramine	0-10	prolactin	Homo sapiens	32-41
19798453-11	2009	Biochemically, both trazodone and imipramine significantly restored depleted reduced glutathione (GSH) levels and catalase activity and attenuated raised lipid peroxidation and nitrite concentrations as compared to untreated sleep-deprived animals.	Imipramine	34-44	catalase	Mus musculus	114-122
20043526-2	2009	Imipramine, a monoamine oxidase inhibitor stimulates prolactin production because it decreases dopamine which inhibits secretion of prolactin.	Imipramine	0-10	prolactin	Homo sapiens	53-62
20043526-2	2009	Imipramine, a monoamine oxidase inhibitor stimulates prolactin production because it decreases dopamine which inhibits secretion of prolactin.	Imipramine	0-10	prolactin	Homo sapiens	132-141
20043526-11	2009	Results showed a trend of prolactin levels decreasing after washout (p = 0.015) and increasing by the end of the trial period once imipramine dispensation had recommenced (p = 0.006).	Imipramine	131-141	prolactin	Homo sapiens	26-35
19328747-0	2009	Studies of imipramine binding to human serum albumin by high-performance affinity chromatography.	Imipramine	11-21	albumin	Homo sapiens	39-52
19268660-6	2009	Gender-specific changes in the glucocorticoid receptor binding parameters in the examined tissues were observed in response to imipramine, and were found to be associated with alterations in the receptor interaction with Hsp70 and Hsp90.	Imipramine	127-137	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	221-226
19268660-6	2009	Gender-specific changes in the glucocorticoid receptor binding parameters in the examined tissues were observed in response to imipramine, and were found to be associated with alterations in the receptor interaction with Hsp70 and Hsp90.	Imipramine	127-137	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	231-236
19254701-0	2009	Neuropeptide Y modulates the antidepressant activity of imipramine in olfactory bulbectomized rats: involvement of NPY Y1 receptors.	Imipramine	56-66	neuropeptide Y	Rattus norvegicus	0-14
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	31-41	neuropeptide Y	Rattus norvegicus	56-70
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	31-41	neuropeptide Y	Rattus norvegicus	72-75
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	31-41	neuropeptide Y	Rattus norvegicus	216-219
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	181-191	neuropeptide Y	Rattus norvegicus	56-70
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	181-191	neuropeptide Y	Rattus norvegicus	72-75
19254701-1	2009	Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors.	Imipramine	181-191	neuropeptide Y	Rattus norvegicus	216-219
19254701-6	2009	The antidepressant actions of imipramine were enhanced by co-administration of NPY or [Leu(31), Pro(34)]-NPY, and antagonized by BIBP3226 given at sub-effective doses.	Imipramine	30-40	neuropeptide Y	Rattus norvegicus	79-82
19254701-6	2009	The antidepressant actions of imipramine were enhanced by co-administration of NPY or [Leu(31), Pro(34)]-NPY, and antagonized by BIBP3226 given at sub-effective doses.	Imipramine	30-40	neuropeptide Y	Rattus norvegicus	105-108
19254701-7	2009	The data suggest that NPY, acting via NPY Y1 receptors, may be involved in antidepressant action of imipramine in OBX rats.	Imipramine	100-110	neuropeptide Y	Rattus norvegicus	22-25
19254701-7	2009	The data suggest that NPY, acting via NPY Y1 receptors, may be involved in antidepressant action of imipramine in OBX rats.	Imipramine	100-110	neuropeptide Y	Rattus norvegicus	38-41
19268660-0	2009	Gender-related differences in the effects of antidepressant imipramine on glucocorticoid receptor binding properties and association with heat shock proteins in the rat liver and kidney.	Imipramine	60-70	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	74-97
19268660-5	2009	Glucocorticoid receptor binding potency (B(max)/K(D) ratio) was significantly higher in males than females both before and after treatment with imipramine.	Imipramine	144-154	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	0-23
19268660-6	2009	Gender-specific changes in the glucocorticoid receptor binding parameters in the examined tissues were observed in response to imipramine, and were found to be associated with alterations in the receptor interaction with Hsp70 and Hsp90.	Imipramine	127-137	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	31-54
19351862-12	2009	Cell proliferation of E6/E7 keratinocytes was decreased by Eag1 antibodies inhibiting channel activity and by the nonspecific Eag1 inhibitors imipramine and astemizole; the latter also increased apoptosis.	Imipramine	142-152	potassium voltage-gated channel subfamily H member 1	Homo sapiens	126-130
19328747-1	2009	Binding by the drug imipramine to the protein human serum albumin (HSA) was studied by using high-performance affinity chromatography.	Imipramine	20-30	albumin	Homo sapiens	52-65
19213730-6	2009	We have identified a residue (Ser-438) located within the 5HT-binding pocket in hSERT to be a critical determinant for the potency of several antidepressants, including the selective serotonin reuptake inhibitor citalopram and the tricyclic antidepressants imipramine, clomipramine, and amitriptyline.	Imipramine	257-267	solute carrier family 6 member 4	Homo sapiens	80-85
19326568-4	2009	Immunohistochemical analysis revealed that chronic CTN-986 treatment increased bromodeoxyuridine (BrdU; thymidine analog as a marker for dividing cells)-positive cells in the hippocampal dentate gyrus in stressed mice, as was the case with chronic IMI treatment.	Imipramine	248-251	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	51-54
19147368-10	2009	Compounds 10a, 10c and 18a exhibited good antidepressant activity, their activities nearly equal to 92.8%, 86.7% and 90.20% of the activity of imipramine, respectively.	Imipramine	143-153	Rho GTPase activating protein 9	Homo sapiens	15-18
18996151-7	2009	In addition, P2X(7) receptor KO mice showed higher responsivity to a subefficacious dose of the antidepressant drug imipramine (15 mg/kg) in forced swim test.	Imipramine	116-126	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	13-28
19189865-5	2009	Serotonin transporter was also labeled with [(3)H]paroxetine, specific binding defined with imipramine.	Imipramine	92-102	solute carrier family 6 member 4	Rattus norvegicus	0-21
19262426-0	2009	Deletion of the mouse Fmo1 gene results in enhanced pharmacological behavioural responses to imipramine.	Imipramine	93-103	flavin containing monooxygenase 1	Mus musculus	22-26
19262426-8	2009	CONCLUSION: The absence of FMO1-mediated N-oxidation of imipramine results in enhanced central nervous system effects of the drug.	Imipramine	56-66	flavin containing monooxygenase 1	Mus musculus	27-31
19302792-7	2009	Inhibition of ASM with imipramine completely abrogated MMP-1 induction.	Imipramine	23-33	sphingomyelin phosphodiesterase 1	Homo sapiens	14-17
19302792-7	2009	Inhibition of ASM with imipramine completely abrogated MMP-1 induction.	Imipramine	23-33	matrix metallopeptidase 1	Homo sapiens	55-60
18608756-3	2008	The antidepressants paroxetine, imipramine, clomipramine and sertraline inhibited both venom AChE as well as human serum BChE in a concentration-dependent manner but had no effect on AChE in the rat brain striatum.	Imipramine	32-42	acetylcholinesterase	Rattus norvegicus	93-97
18823877-9	2009	Chronic, but not acute, treatment with the antidepressant imipramine also increased the phosphorylation of brain FoxO1 and FoxO3a.	Imipramine	58-68	forkhead box O1	Mus musculus	113-118
18657555-9	2009	Altogether, these results indicate that acute elevated platform stress down-regulates a putative BDNF/MEK/MAPK signaling cascade in the frontal cortex in a manner that is reversible by the antidepressants tianeptine and imipramine.	Imipramine	220-230	brain-derived neurotrophic factor	Rattus norvegicus	97-101
18823877-9	2009	Chronic, but not acute, treatment with the antidepressant imipramine also increased the phosphorylation of brain FoxO1 and FoxO3a.	Imipramine	58-68	forkhead box O3	Mus musculus	123-129
20045987-7	2009	Both imipramine (typical substrate of UGT1A3 and 1A4) and flurbiprofen (typical substrate of UGT2B7) inhibit the glucuronidation of glycyrrhetinic acid.	Imipramine	5-15	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	38-52
18789340-5	2009	The antidepressant imipramine, which shows pro-manic properties in patients with bipolar disorder (BPD), also enhanced phospho-MARCKS in prefrontal cortex in vivo.	Imipramine	19-29	myristoylated alanine rich protein kinase C substrate	Homo sapiens	127-133
18608756-3	2008	The antidepressants paroxetine, imipramine, clomipramine and sertraline inhibited both venom AChE as well as human serum BChE in a concentration-dependent manner but had no effect on AChE in the rat brain striatum.	Imipramine	32-42	butyrylcholinesterase	Rattus norvegicus	121-125
18711208-8	2008	U18666A and imipramine, agents that mimic cholesterol trafficking defects of Neimann-Pick type C disease, attenuate cholesterol efflux without altering ABCA1 expression; thus, intestinal NPC1 may facilitate cholesterol movement to ABCA1.	Imipramine	12-22	NPC intracellular cholesterol transporter 1	Homo sapiens	187-191
18705540-8	2008	In low-Mg cells the latter results mainly from a strong TRPM7 related transport component whereas in high-Mg cells the imipramine-sensitive, the Na+/Mg2+ exchanger-mediated transport component causes this effect.	Imipramine	119-129	transient receptor potential cation channel subfamily M member 7	Homo sapiens	56-61
18711208-8	2008	U18666A and imipramine, agents that mimic cholesterol trafficking defects of Neimann-Pick type C disease, attenuate cholesterol efflux without altering ABCA1 expression; thus, intestinal NPC1 may facilitate cholesterol movement to ABCA1.	Imipramine	12-22	ATP binding cassette subfamily A member 1	Homo sapiens	231-236
18801947-1	2008	Although several antidepressants (including fluoxetine, imipramine, citalopram, venlafaxine, and duloxetine) are known to inhibit the serotonin transporter (SERT), whether or not these molecules compete with 5-hydroxytryptamine (serotonin) (5-HT) for binding to SERT has remained controversial.	Imipramine	56-66	solute carrier family 6 member 4	Homo sapiens	134-155
18801947-1	2008	Although several antidepressants (including fluoxetine, imipramine, citalopram, venlafaxine, and duloxetine) are known to inhibit the serotonin transporter (SERT), whether or not these molecules compete with 5-hydroxytryptamine (serotonin) (5-HT) for binding to SERT has remained controversial.	Imipramine	56-66	solute carrier family 6 member 4	Homo sapiens	157-161
18639562-5	2008	The results showed that clomipramine and imipramine significantly decreased the production of nitric oxide or tumor necrosis factor-alpha (TNF-alpha) in microglia and astrocyte cultures.	Imipramine	41-51	tumor necrosis factor	Homo sapiens	110-137
18639562-5	2008	The results showed that clomipramine and imipramine significantly decreased the production of nitric oxide or tumor necrosis factor-alpha (TNF-alpha) in microglia and astrocyte cultures.	Imipramine	41-51	tumor necrosis factor	Homo sapiens	139-148
18639562-6	2008	Clomipramine and imipramine also attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin-1beta and TNF-alpha at mRNA levels.	Imipramine	17-27	interleukin 1 beta	Homo sapiens	132-149
18639562-6	2008	Clomipramine and imipramine also attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin-1beta and TNF-alpha at mRNA levels.	Imipramine	17-27	tumor necrosis factor	Homo sapiens	154-163
18639562-7	2008	In addition, clomipramine and imipramine inhibited IkappaB degradation, nuclear translocation of the p65 subunit of NF-kappaB, and phosphorylation of p38 mitogen-activated protein kinase in the lipopolysaccharide-stimulated microglia cells.	Imipramine	30-40	RELA proto-oncogene, NF-kB subunit	Homo sapiens	101-125
18639562-7	2008	In addition, clomipramine and imipramine inhibited IkappaB degradation, nuclear translocation of the p65 subunit of NF-kappaB, and phosphorylation of p38 mitogen-activated protein kinase in the lipopolysaccharide-stimulated microglia cells.	Imipramine	30-40	mitogen-activated protein kinase 14	Homo sapiens	150-153
18664374-6	2008	Compared to CS treatment, significantly increased mRNA levels were found for JNK1 under imipramine treatment and for GR-alpha after treatment with all AD examined.	Imipramine	88-98	mitogen-activated protein kinase 8	Homo sapiens	77-81
18606473-7	2008	A concentration-dependent increase in the expression of BNIP-3 mRNA was also observed when cells were treated with imipramine, mianserin, or milnacipran.	Imipramine	115-125	BCL2/adenovirus E1B interacting protein 3	Mus musculus	56-62
21499463-13	2008	Propranolol treatment alone produced depression, and antagonized the effects of alprazolam and imipramine, even producing depression in combined treatments.In conclusion, our results reveal that alprazolam may produce antidepressant effects through the release of noradrenaline, which stimulates beta2 receptors to produce an antidepressant action.	Imipramine	95-105	hemoglobin, beta adult minor chain	Mus musculus	296-301
21499463-14	2008	Imipramine may act by activating beta2 receptors by blocking or down-regulating beta1 receptors.	Imipramine	0-10	hemoglobin, beta adult minor chain	Mus musculus	33-38
17667959-3	2008	This retrospective single center study aimed to prove whether CYP2C19 and ample CYP2D6 genotyping (taking into consideration four null alleles and three decreased-activity alleles) could be used to predict imipramine and desipramine plasma concentrations in depressed patients, and whether genotype-based drug dose recommendations might assist in the early management of imipramine pharmacotherapy.	Imipramine	206-216	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
17667959-3	2008	This retrospective single center study aimed to prove whether CYP2C19 and ample CYP2D6 genotyping (taking into consideration four null alleles and three decreased-activity alleles) could be used to predict imipramine and desipramine plasma concentrations in depressed patients, and whether genotype-based drug dose recommendations might assist in the early management of imipramine pharmacotherapy.	Imipramine	206-216	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	80-86
17667959-5	2008	Desipramine and imipramine+desipramine plasma concentration per drug dose unit, imipramine dose at steady state, and imipramine dose requirement significantly depended on CYP2D6 genotype (Kruskal-Wallis test, P<0.0001).	Imipramine	16-26	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	171-177
17667959-5	2008	Desipramine and imipramine+desipramine plasma concentration per drug dose unit, imipramine dose at steady state, and imipramine dose requirement significantly depended on CYP2D6 genotype (Kruskal-Wallis test, P<0.0001).	Imipramine	80-90	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	171-177
17667959-5	2008	Desipramine and imipramine+desipramine plasma concentration per drug dose unit, imipramine dose at steady state, and imipramine dose requirement significantly depended on CYP2D6 genotype (Kruskal-Wallis test, P<0.0001).	Imipramine	80-90	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	171-177
17893702-5	2008	Chronic imipramine treatment (16 mg kg(-1) per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release.	Imipramine	8-18	cholecystokinin	Rattus norvegicus	206-209
18682686-6	2008	Chronic treatment with the tricyclic antidepressant imipramine markedly decreased p21(Cip1) mRNA and protein levels and stimulated neurogenesis in this region.	Imipramine	52-62	cyclin dependent kinase inhibitor 1A	Homo sapiens	82-85
18682686-6	2008	Chronic treatment with the tricyclic antidepressant imipramine markedly decreased p21(Cip1) mRNA and protein levels and stimulated neurogenesis in this region.	Imipramine	52-62	cyclin dependent kinase inhibitor 1A	Homo sapiens	86-90
18310483-3	2008	OBJECTIVES: We investigated the intermediate-term effects (>12 h) of a-SMase inhibition in a neonatal piglet model of repeated airway lavage by the intratracheal use of the a-SMase inhibitor imipramine, together with exogenous surfactant as a carrier substance.	Imipramine	194-204	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	176-183
18310483-10	2008	CONCLUSIONS: We conclude that stabilization of exogenous surfactant by adding imipramine to create a "fortified surfactant preparation" improves lung function in a clinically relevant piglet model, and that this effect can be attributed to the inhibition of a-SMase as evidenced in the mouse model.	Imipramine	78-88	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	258-265
17667959-0	2008	Association of graded allele-specific changes in CYP2D6 function with imipramine dose requirement in a large group of depressed patients.	Imipramine	70-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
17667959-1	2008	The inactivation and clearance of the tricyclic antidepressant imipramine is dependent on CYP2D6 activity.	Imipramine	63-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
17667959-2	2008	First, CYP2C19 converts imipramine into the active metabolite desipramine, which is then inactivated by CYP2D6.	Imipramine	24-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	7-14
17667959-8	2008	Our protocol for CYP2D6 genotyping will thus importantly aid in the prediction of imipramine metabolism, allowing for the use of an adjusted starting dose and faster achievement of predefined imipramine+desipramine plasma levels in all genetic patient subgroups.	Imipramine	82-92	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	17-23
17667959-8	2008	Our protocol for CYP2D6 genotyping will thus importantly aid in the prediction of imipramine metabolism, allowing for the use of an adjusted starting dose and faster achievement of predefined imipramine+desipramine plasma levels in all genetic patient subgroups.	Imipramine	192-202	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	17-23
18446327-2	2008	Long-term treatment with antipanic drugs that nonselectively or selectively blocks the reuptake of serotonin (e.g., imipramine and fluoxetine, respectively) enhances the inhibitory effect on escape caused by intra-DPAG injection of 5-HT(1A) and 5-HT(2A) receptor agonists.	Imipramine	116-126	5-hydroxytryptamine receptor 1A	Rattus norvegicus	232-239
17667959-2	2008	First, CYP2C19 converts imipramine into the active metabolite desipramine, which is then inactivated by CYP2D6.	Imipramine	24-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	104-110
18497958-1	2008	Pharmacological inhibitors of the human ether-a-go-go (hEAG) potassium channel, astemizole and imipramine, have been used to demonstrate that hEAG plays a role in cancer cell proliferation.	Imipramine	95-105	potassium voltage-gated channel subfamily H member 1	Homo sapiens	55-59
18497958-1	2008	Pharmacological inhibitors of the human ether-a-go-go (hEAG) potassium channel, astemizole and imipramine, have been used to demonstrate that hEAG plays a role in cancer cell proliferation.	Imipramine	95-105	potassium voltage-gated channel subfamily H member 1	Homo sapiens	142-146
18497958-2	2008	Astemizole and imipramine are, however, relatively non-specific ion channel blockers, as astemizole can also block the related potassium channel, human ether-a-go-go-related (hERG).	Imipramine	15-25	ETS transcription factor ERG	Homo sapiens	175-179
17950272-2	2008	This study was undertaken to investigate the time-course of the effect of three antidepressants; fluoxetine, imipramine and venlafaxine, which differentially affect monoamine reuptake, on BDNF mRNA expression in the hippocampus.	Imipramine	109-119	brain-derived neurotrophic factor	Rattus norvegicus	188-192
18303133-17	2008	Drugs that interfere with elimination-that is, other drugs utilizing the organic cation transporter-2 in the tubule, such as trimethoprim, metformin, or imipramine-may lead to drug accumulation.	Imipramine	153-163	solute carrier family 22 member 2	Homo sapiens	73-101
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Imipramine	0-10	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	106-112
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Imipramine	0-10	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	199-205
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	213-219
18310890-6	2008	The inhibition constants (Ki values) of imipramine, desipramine, and mazindol against the 21-hydroxylation of PROG and ALLO by CYP2D6 were lower than those by CYP2D4.	Imipramine	40-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	127-133
18310890-6	2008	The inhibition constants (Ki values) of imipramine, desipramine, and mazindol against the 21-hydroxylation of PROG and ALLO by CYP2D6 were lower than those by CYP2D4.	Imipramine	40-50	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	159-165
18172194-11	2008	These results suggest that p21 restrains neurogenesis in the SGZ and imipramine-induced stimulation of neurogenesis might be a consequence of decreased p21 expression and the subsequent release of neuronal progenitor cells from the blockade of proliferation.	Imipramine	69-79	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	27-30
18172194-11	2008	These results suggest that p21 restrains neurogenesis in the SGZ and imipramine-induced stimulation of neurogenesis might be a consequence of decreased p21 expression and the subsequent release of neuronal progenitor cells from the blockade of proliferation.	Imipramine	69-79	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	152-155
18255130-0	2008	Chronic coadministration of carbamazepine together with imipramine produces antidepressant-like effects in an ACTH-induced animal model of treatment-resistant depression: involvement of 5-HT(2A) receptors?	Imipramine	56-66	proopiomelanocortin	Canis lupus familiaris	110-114
18255130-5	2008	The reduction of immobility, induced by chronic administration of imipramine, was blocked by treatment with ACTH.	Imipramine	66-76	proopiomelanocortin	Canis lupus familiaris	108-112
18255130-6	2008	When carbamazepine was administered concurrently with imipramine, we observed a significant decrease in immobility in rats treated with ACTH.	Imipramine	54-64	proopiomelanocortin	Canis lupus familiaris	136-140
18255130-8	2008	This effect of ACTH was significantly increased by the coadministration of carbamazepine and imipramine.	Imipramine	93-103	proopiomelanocortin	Canis lupus familiaris	15-19
18441395-3	2008	Further study revealed that the inhibitor of c-Jun N-terminal kinase - mitogen-activated protein kinase (JNK-MAPK), SP600125 (0.1 microM), reversed the imipramine-induced suppression of GR function, whereas the inhibitor of extracellular signal-regulated kinase (ERK)-MAPK, PD 98059 (15 microM), potentiated the antidepressant action.	Imipramine	152-162	mitogen-activated protein kinase 1	Homo sapiens	224-261
18441395-3	2008	Further study revealed that the inhibitor of c-Jun N-terminal kinase - mitogen-activated protein kinase (JNK-MAPK), SP600125 (0.1 microM), reversed the imipramine-induced suppression of GR function, whereas the inhibitor of extracellular signal-regulated kinase (ERK)-MAPK, PD 98059 (15 microM), potentiated the antidepressant action.	Imipramine	152-162	mitogen-activated protein kinase 1	Homo sapiens	263-266
18441395-6	2008	Moreover, it was found that JNK- and ERK-MAPK were oppositely involved in the regulation of the imipramine-induced inhibition of the GR functional activity.	Imipramine	96-106	mitogen-activated protein kinase 8	Homo sapiens	28-32
18441395-6	2008	Moreover, it was found that JNK- and ERK-MAPK were oppositely involved in the regulation of the imipramine-induced inhibition of the GR functional activity.	Imipramine	96-106	mitogen-activated protein kinase 1	Homo sapiens	37-40
17566715-0	2008	Neuroprotection by Imipramine against lipopolysaccharide-induced apoptosis in hippocampus-derived neural stem cells mediated by activation of BDNF and the MAPK pathway.	Imipramine	19-29	brain-derived neurotrophic factor	Rattus norvegicus	142-146
17950272-6	2008	BDNF mRNA levels in the dentate gyrus (DG) were increased after treatment with venlafaxine (7, 14 and 21 days) and imipramine (14 and 21 days), but not after treatment with fluoxetine, indicating that stimulation of BDNF mRNA expression is dependent on the pharmacological profile and on the time-course of drug treatment.	Imipramine	115-125	brain-derived neurotrophic factor	Rattus norvegicus	0-4
17950272-8	2008	In the CA3 region a reduction of GAP-43 mRNA was observed after treatment with imipramine (21 days) and fluoxetine (7 and 14 days).	Imipramine	79-89	carbonic anhydrase 3	Rattus norvegicus	7-10
17950272-8	2008	In the CA3 region a reduction of GAP-43 mRNA was observed after treatment with imipramine (21 days) and fluoxetine (7 and 14 days).	Imipramine	79-89	growth associated protein 43	Rattus norvegicus	33-39
17950272-9	2008	These results suggest that venlafaxine and imipramine, but not fluoxetine, induce neuroplastic effects in the hippocampus through stimulation of BDNF mRNA expression, and that the effect on BDNF is not directly translated into regulation of synaptophysin and GAP-43 mRNA.	Imipramine	43-53	brain-derived neurotrophic factor	Rattus norvegicus	145-149
17950272-9	2008	These results suggest that venlafaxine and imipramine, but not fluoxetine, induce neuroplastic effects in the hippocampus through stimulation of BDNF mRNA expression, and that the effect on BDNF is not directly translated into regulation of synaptophysin and GAP-43 mRNA.	Imipramine	43-53	brain-derived neurotrophic factor	Rattus norvegicus	190-194
17950272-9	2008	These results suggest that venlafaxine and imipramine, but not fluoxetine, induce neuroplastic effects in the hippocampus through stimulation of BDNF mRNA expression, and that the effect on BDNF is not directly translated into regulation of synaptophysin and GAP-43 mRNA.	Imipramine	43-53	synaptophysin	Rattus norvegicus	241-254
17950272-9	2008	These results suggest that venlafaxine and imipramine, but not fluoxetine, induce neuroplastic effects in the hippocampus through stimulation of BDNF mRNA expression, and that the effect on BDNF is not directly translated into regulation of synaptophysin and GAP-43 mRNA.	Imipramine	43-53	growth associated protein 43	Rattus norvegicus	259-265
17884272-3	2008	Considering that classic antidepressants may take long-lasting time to exhibit their main therapeutic effects, the present study aims to compare the behavioral effects and the BDNF hippocampus levels of acute administration of ketamine and imipramine in rats.	Imipramine	240-250	brain-derived neurotrophic factor	Rattus norvegicus	176-180
18209475-9	2008	Platelet treatment with PP2 or SU6656 also caused a decrease in the imipramine binding to platelets.	Imipramine	68-78	neuropeptide Y receptor Y6 (pseudogene)	Homo sapiens	24-27
18306301-0	2008	Changes in rat hippocampal CA1 synapses following imipramine treatment.	Imipramine	50-60	carbonic anhydrase 1	Rattus norvegicus	27-30
18306301-7	2008	However, the number and percentage of CA1 asymmetric spine synapses increased significantly and, conversely, the percentage of asymmetric shaft synapses significantly decreased in the imipramine treated group.	Imipramine	184-194	carbonic anhydrase 1	Rattus norvegicus	38-41
17884272-5	2008	Afterwards, BDNF protein hippocampal levels were assessed in imipramine- and ketamine-treated rats by ELISA-sandwich assay.	Imipramine	61-71	brain-derived neurotrophic factor	Rattus norvegicus	12-16
17314919-2	2007	We have previously shown that the antidepressants imipramine and fluoxetine produce a rapid autophosphorylation of TrkB in the rodent brain.	Imipramine	50-60	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	115-119
17620344-2	2007	The substrates specific for UGT1A1 (estradiol and bilirubin), UGT1A4 (imipramine and trifluoperazine), and UGT1A6 (serotonin and diclofenac) were used to determine the effects of the coexpression of the other UGT1A isoforms on the enzymatic activity.	Imipramine	70-80	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	62-68
20020918-6	2008	Following rat microsomal incubations with imipramine and analysis of the MS(n) data using the Apex software, strong evidence was found for imipramine and five metabolites and weaker evidence for five additional metabolites.	Imipramine	139-149	apurinic/apyrimidinic endodeoxyribonuclease 1	Rattus norvegicus	94-98
17582397-4	2007	Fourteen day but not acute treatment with citalopram (20 mg/kg), imipramine (10 mg/kg) and amitriptyline (10 mg/kg) in mice significantly elevated hippocampal Bcl-2 protein expression as compared to vehicle treated animals (59, 48 and 42% respectively).	Imipramine	65-75	B cell leukemia/lymphoma 2	Mus musculus	159-164
18048952-6	2007	In our studies, we examined an influence of repeated (21-day) imipramine treatment on the density of group II mGlu receptors and affinity of mGlu2 and mGlu3 receptor radioligand [3H]-LY341495 for group II mGlu receptors in the rat brain hippocampus and frontal cortex.	Imipramine	62-72	glutamate receptor, metabotropic 3	Mus musculus	151-156
17898223-4	2007	Immobility times for Vmat2 heterozygotes were prolonged in forced swim and imipramine normalized this behavior.	Imipramine	75-85	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	21-26
18048960-1	2007	The aim of present study was to examine the effect of repeated co-treatment with imipramine and metyrapone on the development of adaptive changes in the function of central serotonin 5-HT1A and 5-HT2A, dopamine D2/3 and alpha 1-adrenergic receptors in rats.	Imipramine	81-91	5-hydroxytryptamine receptor 1A	Rattus norvegicus	183-195
17582397-7	2007	There was a smaller increase of hippocampal Bax protein levels following treatment with imipramine after 1 or 14 days, and following citalopram and amitriptyline after 14 but not 1 day.	Imipramine	88-98	BCL2-associated X protein	Mus musculus	44-47
17459373-6	2007	These findings suggest that chronic treatment with ACTH enhances the increasing effect release of 5-HT by imipramine through the desensitization of somatodendritic 5-HT1A autoreceptors.	Imipramine	106-116	5-hydroxytryptamine receptor 1A	Rattus norvegicus	164-170
17499240-7	2007	Further, R-citalopram previously thought of as an inactive enantiomer strongly attenuated dissociation of the wild-type [(3)H]-imipramine:hSERT complex, whereas S-citalopram had almost no effect on this complex.	Imipramine	127-137	solute carrier family 6 member 4	Homo sapiens	138-143
17487276-8	2007	Treatment of the stressed mice with the antidepressant imipramine normalized luciferase expression to control levels in all brain regions and likewise reduced CREB-phosphorylation.	Imipramine	55-65	cAMP responsive element binding protein 1	Mus musculus	159-163
17481608-5	2007	Pretreatment with the selective serotonin reuptake inhibitor fluvoxamine, the relatively selective noradrenaline reuptake inhibitor reboxetine, or the non-selective monoaminergic reuptake inhibitor imipramine, significantly inhibited IL-6 and NO production in a dose-dependent manner.	Imipramine	198-208	interleukin 6	Mus musculus	234-238
17622693-0	2007	Repeated co-treatment with imipramine and amantadine induces hippocampal brain-derived neurotrophic factor gene expression in rats.	Imipramine	27-37	brain-derived neurotrophic factor	Rattus norvegicus	73-106
17622693-10	2007	Joint administration of IMI (5 or 10 mg/kg) and AMA (10 mg/kg) induced a more potent increase BDNF gene expression in the hippocampus (but not in cerebral cortex) and either inhibited the behavioral syndrome induced by (+/-)DOI or did not change the action of 8-OH-DPAT (compared to treatment with either drug alone).	Imipramine	24-27	brain-derived neurotrophic factor	Rattus norvegicus	94-98
16936714-2	2007	Chronic treatment with the antimanic agents, lithium and valproate, resulted in reduced synaptic expression of the AMPA(-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor subunit GluR1 in the hippocampus, while treatment with an antidepressant (imipramine) enhanced the synaptic expression of GluR1.	Imipramine	256-266	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	190-195
16936714-9	2007	In addition, lamotrigine and riluzole, as well as the traditional antidepressant imipramine, also increased GluR1 phosphorylation at GluR1 (S845) in the hippocampus after chronic in vivo treatment.	Imipramine	81-91	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	108-113
16936714-9	2007	In addition, lamotrigine and riluzole, as well as the traditional antidepressant imipramine, also increased GluR1 phosphorylation at GluR1 (S845) in the hippocampus after chronic in vivo treatment.	Imipramine	81-91	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	133-138
17071817-7	2007	Other TCAs, such as amitriptyline, desipramine, and imipramine, also inhibited Kir4.1 currents in a similar voltage-dependent fashion.	Imipramine	52-62	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	79-85
17409705-7	2007	The c-Fos immunohistochemical study indicated that the medial prefrontal cortex is an action site of imipramine in ACTH-treated rats.	Imipramine	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
17313964-3	2007	In this test, chronic administration of the non-selective SRI imipramine enhances the inhibitory effect on escape caused by the intra-DPAG injection of the 5-HT1A receptor agonist 8-OH-DPAT.	Imipramine	62-72	sorcin	Rattus norvegicus	58-61
17313964-3	2007	In this test, chronic administration of the non-selective SRI imipramine enhances the inhibitory effect on escape caused by the intra-DPAG injection of the 5-HT1A receptor agonist 8-OH-DPAT.	Imipramine	62-72	5-hydroxytryptamine receptor 1A	Rattus norvegicus	156-162
16672106-7	2007	In addition, combination treatment of mice with risperidone and a monoamine reuptake inhibitor antidepressant imipramine or fluoxetine elicited larger increases in brain phospho-Ser-GSK3 than each agent alone.	Imipramine	110-120	glycogen synthase kinase 3 beta	Mus musculus	182-186
17762163-6	2007	The effects of the drugs on the phosphorylation of Fc gamma RII and NTAL were prominent and correlated with a reduction of the cell surface ceramide production by imipramine and an augmentation of the ceramide generation by B13.	Imipramine	163-173	linker for activation of T cells family member 2	Homo sapiens	68-72
16630709-4	2007	In the modified forced swim test in rats, imipramine (used as a positive control) decreased immobility (MED 40 mg/kg) and increased the duration of escape-oriented (climbing and diving; MED 20 mg/kg) behaviors.	Imipramine	42-52	mediator complex subunit 20	Rattus norvegicus	186-192
17381401-5	2007	Selected cells were pretreated with the acid sphingomyelinase inhibitor imipramine or CD14 neutralizing antibody.	Imipramine	72-82	sphingomyelin phosphodiesterase 1	Homo sapiens	40-61
17049169-6	2007	Since PSA-NCAM and pCREB are expressed in recently-generated neurons in the dentate gyrus, it is likely that chronic imipramine treatment increased their expression in the hippocampus at least partially by increasing neurogenesis.	Imipramine	117-127	neural cell adhesion molecule 1	Rattus norvegicus	10-14
17393067-3	2007	However, imipramine led to opposite changes in the cellular level of GR protein in the brain of female and male rats, as well as to gender- and tissue-specific changes in in vitro dexamethasone binding to GR and mineralocorticoid receptor (MR) in the hippocampus and brain cortex.	Imipramine	9-19	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	69-71
17393067-3	2007	However, imipramine led to opposite changes in the cellular level of GR protein in the brain of female and male rats, as well as to gender- and tissue-specific changes in in vitro dexamethasone binding to GR and mineralocorticoid receptor (MR) in the hippocampus and brain cortex.	Imipramine	9-19	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	205-207
17393067-3	2007	However, imipramine led to opposite changes in the cellular level of GR protein in the brain of female and male rats, as well as to gender- and tissue-specific changes in in vitro dexamethasone binding to GR and mineralocorticoid receptor (MR) in the hippocampus and brain cortex.	Imipramine	9-19	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	212-238
17393067-3	2007	However, imipramine led to opposite changes in the cellular level of GR protein in the brain of female and male rats, as well as to gender- and tissue-specific changes in in vitro dexamethasone binding to GR and mineralocorticoid receptor (MR) in the hippocampus and brain cortex.	Imipramine	9-19	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	240-242
17393067-4	2007	Gender-related differences in the expression of Hsp90 and Hsp70 were noticed mainly in the hippocampus, only after imipramine treatment.	Imipramine	115-125	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	48-53
17393067-4	2007	Gender-related differences in the expression of Hsp90 and Hsp70 were noticed mainly in the hippocampus, only after imipramine treatment.	Imipramine	115-125	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	58-63
17393067-5	2007	The observed changes in the response of GR to imipramine suggest that this antidepressant may affect both the level of the receptor protein and the mechanisms regulating its binding ability in a gender-related manner.	Imipramine	46-56	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	40-42
17873312-4	2007	In addition, imipramine was used to identify the involvement of Eag1 in the growth of SGC-7901 and BGC-823 cells.	Imipramine	13-23	potassium voltage-gated channel subfamily H member 1	Homo sapiens	64-68
17873312-4	2007	In addition, imipramine was used to identify the involvement of Eag1 in the growth of SGC-7901 and BGC-823 cells.	Imipramine	13-23	sarcoglycan beta	Homo sapiens	86-89
17873312-9	2007	Imipramine significantly inhibited the proliferation of SGC-7901 and BGC-823 cells at 12 h and 24 h detected by cells number counting and MTT assay (P < 0.01).	Imipramine	0-10	sarcoglycan beta	Homo sapiens	56-59
16949586-0	2006	Different relevance of inactivation and F468 residue in the mechanisms of hEag1 channel blockage by astemizole, imipramine and dofetilide.	Imipramine	112-122	potassium voltage-gated channel subfamily H member 1	Homo sapiens	74-79
16503401-15	2006	The studied antidepressants increased the CYP2C6 protein level in the liver microsomes of rats after chronic treatment: imipramine to 174.6+/-18.3%, fluoxetine to 159.1+/-13.7%, sertraline to 135.3+/-11.2% and mirtazapine to 138.4+/-10.2% of the control.	Imipramine	120-130	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	42-48
16503401-16	2006	In summary, two different mechanisms of the antidepressant-CYP2C6 interaction have been found to operate in the rat liver: 1) direct inhibition of CYP2C6 shown in vitro mainly for nefazodone and fluoxetine, with their inhibitory effects being somewhat more potent than their action on human CYP2C9; 2) the in vivo induction of CYP2C6 by imipramine, fluoxetine, sertraline and mirtazapine.	Imipramine	337-347	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	59-65
16503401-16	2006	In summary, two different mechanisms of the antidepressant-CYP2C6 interaction have been found to operate in the rat liver: 1) direct inhibition of CYP2C6 shown in vitro mainly for nefazodone and fluoxetine, with their inhibitory effects being somewhat more potent than their action on human CYP2C9; 2) the in vivo induction of CYP2C6 by imipramine, fluoxetine, sertraline and mirtazapine.	Imipramine	337-347	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	147-153
16503401-16	2006	In summary, two different mechanisms of the antidepressant-CYP2C6 interaction have been found to operate in the rat liver: 1) direct inhibition of CYP2C6 shown in vitro mainly for nefazodone and fluoxetine, with their inhibitory effects being somewhat more potent than their action on human CYP2C9; 2) the in vivo induction of CYP2C6 by imipramine, fluoxetine, sertraline and mirtazapine.	Imipramine	337-347	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	147-153
16956981-7	2006	Conversely, although imipramine did not provide significant behavioral analgesia, it significantly blocked both pain- and stress-evoked alterations in hippocampal and spinal NK-1 and BDNF gene expression.	Imipramine	21-31	brain-derived neurotrophic factor	Rattus norvegicus	183-187
16884969-6	2006	Imipramine and fluoxetine, antagonists with specificity for 5-HTT, show the highest potency to antagonize [125I]RTI-55 binding in the MLO-Y4 cells.	Imipramine	0-10	huntingtin	Mus musculus	62-65
16949586-1	2006	The relevance of a point mutation at the C-terminal end of the S6 helix (F468) and the introduction of C-type inactivation in the blockage of hEag1 channels by astemizole, imipramine and dofetilide was tested.	Imipramine	172-182	potassium voltage-gated channel subfamily H member 1	Homo sapiens	142-147
17033092-0	2006	Imipramine and citalopram reverse corticosterone-induced alterations in the effects of the activation of 5-HT(1A) and 5-HT(2) receptors in rat frontal cortex.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	105-112
17172009-8	2006	Na+/Mg2+ antiport is inhibited by amiloride, quinidine and imipramine.	Imipramine	59-69	mucin 7, secreted	Homo sapiens	4-7
17172009-13	2006	Na+-independent Mg2+ efflux via the choline exchanger is also inhibited by amiloride, quinidine and imipramine, and can also be regulated by phosphorylation-dephosphorylation.	Imipramine	100-110	mucin 7, secreted	Homo sapiens	16-19
16814933-4	2006	Subchronic treatment of naive rats with imipramine or fluvoxamine significantly decreased the expression of synapsin I.	Imipramine	40-50	synapsin I	Rattus norvegicus	108-118
16941686-6	2006	ASMase-induced ceramide generation activated JNK resulting in BimL phosphorylation and translocation to mitochondria, as the inhibition of ASMase by imipramine prevented these events.	Imipramine	149-159	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
16941686-6	2006	ASMase-induced ceramide generation activated JNK resulting in BimL phosphorylation and translocation to mitochondria, as the inhibition of ASMase by imipramine prevented these events.	Imipramine	149-159	mitogen-activated protein kinase 8	Mus musculus	45-48
16941686-6	2006	ASMase-induced ceramide generation activated JNK resulting in BimL phosphorylation and translocation to mitochondria, as the inhibition of ASMase by imipramine prevented these events.	Imipramine	149-159	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	139-145
16814933-6	2006	Subchronic treatment of naive rats with fluvoxamine but not imipramine showed a tendency to decrease the expression of synapsin I.	Imipramine	60-70	synapsin I	Rattus norvegicus	119-129
16814933-8	2006	Naive rats subchronically treated with imipramine showed a tendency toward increased expression of MAP-2, but those treated with fluvoxamine did not.	Imipramine	39-49	microtubule-associated protein 2	Rattus norvegicus	99-104
16380238-0	2006	Imipramine treatment ameliorates corticosterone-induced alterations in the effects of 5-HT1A and 5-HT4 receptor activation in the CA1 area of rat hippocampus.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	86-92
16380238-7	2006	In the corticosterone plus imipramine group, the effect of 8-OH-DPAT and zacopride were not different from control, indicating that corticosterone-induced adaptive changes in the reactivity of 5-HT1A and 5-HT4 receptors were reversed by imipramine treatment.	Imipramine	237-247	5-hydroxytryptamine receptor 1A	Rattus norvegicus	193-199
16380238-0	2006	Imipramine treatment ameliorates corticosterone-induced alterations in the effects of 5-HT1A and 5-HT4 receptor activation in the CA1 area of rat hippocampus.	Imipramine	0-10	carbonic anhydrase 1	Rattus norvegicus	130-133
16380238-1	2006	This study tested whether imipramine reverses adaptive modifications in the function of hippocampal 5-HT1A and 5-HT4 receptors induced by repetitive administration of corticosterone.	Imipramine	26-36	5-hydroxytryptamine receptor 1A	Rattus norvegicus	100-106
16380238-7	2006	In the corticosterone plus imipramine group, the effect of 8-OH-DPAT and zacopride were not different from control, indicating that corticosterone-induced adaptive changes in the reactivity of 5-HT1A and 5-HT4 receptors were reversed by imipramine treatment.	Imipramine	27-37	5-hydroxytryptamine receptor 1A	Rattus norvegicus	193-199
15982447-7	2006	Imipramine, amantadine and a combination of amantadine and imipramine enhanced the production of the negative immunoregulator IL-10 in rats subjected to the FST.	Imipramine	0-10	interleukin 10	Rattus norvegicus	126-131
16546220-4	2006	We examined the effects of chronic administration of imipramine, fluvoxamine, maprotiline and, as a negative control, cocaine on the level of G(olf) protein in the rat striatum.	Imipramine	53-63	G protein subunit alpha L	Rattus norvegicus	142-148
16546220-6	2006	Chronic imipramine treatment (10 mg/kg for 2 or 4 weeks) significantly increased the level of G(olf) in the striatum (by 17% or 18%, respectively), although this increase was not apparent after only 1 week of treatment.	Imipramine	8-18	G protein subunit alpha L	Rattus norvegicus	94-100
15982447-7	2006	Imipramine, amantadine and a combination of amantadine and imipramine enhanced the production of the negative immunoregulator IL-10 in rats subjected to the FST.	Imipramine	59-69	interleukin 10	Rattus norvegicus	126-131
16382205-0	2005	Combined treatment with imipramine and metyrapone induces hippocampal and cortical brain-derived neurotrophic factor gene expression in rats.	Imipramine	24-34	brain-derived neurotrophic factor	Rattus norvegicus	83-116
16522641-12	2006	We found that the BDNF-stimulated PLC-gamma activation and the ensued increase in intracellular Ca2+ ([Ca2+]i) were potentiated by pretreatment with imipramine or fluvoxamine, so was the BDNF-induced glutamate release.	Imipramine	149-159	brain derived neurotrophic factor	Homo sapiens	18-22
16522641-12	2006	We found that the BDNF-stimulated PLC-gamma activation and the ensued increase in intracellular Ca2+ ([Ca2+]i) were potentiated by pretreatment with imipramine or fluvoxamine, so was the BDNF-induced glutamate release.	Imipramine	149-159	brain derived neurotrophic factor	Homo sapiens	187-191
16522641-13	2006	Furthermore, enhancement of the interaction between PLC-gamma and TrkB (receptor for BDNF) after imipramine pretreatment was observed.	Imipramine	97-107	neurotrophic receptor tyrosine kinase 2	Homo sapiens	66-70
16522641-13	2006	Furthermore, enhancement of the interaction between PLC-gamma and TrkB (receptor for BDNF) after imipramine pretreatment was observed.	Imipramine	97-107	brain derived neurotrophic factor	Homo sapiens	85-89
16522641-14	2006	Interestingly, BD1047, a potent Sig-1R antagonist, blocked the imipramine-dependent potentiation on the BDNF-induced PLC-gamma activation and glutamate release.	Imipramine	63-73	sigma non-opioid intracellular receptor 1	Homo sapiens	32-38
16522641-14	2006	Interestingly, BD1047, a potent Sig-1R antagonist, blocked the imipramine-dependent potentiation on the BDNF-induced PLC-gamma activation and glutamate release.	Imipramine	63-73	brain derived neurotrophic factor	Homo sapiens	104-108
16501568-4	2006	This hyperacetylation by chronic imipramine was associated with a selective downregulation of histone deacetylase (Hdac) 5.	Imipramine	33-43	histone deacetylase 5	Mus musculus	94-122
16501568-5	2006	Furthermore, viral-mediated HDAC5 overexpression in the hippocampus blocked imipramine"s ability to reverse depression-like behavior.	Imipramine	76-86	histone deacetylase 5	Mus musculus	28-33
16510194-5	2006	Phosducin-like protein levels were measured in brain cortices of rats chronically treated with one of five classes of antidepressants: imipramine, venlafaxine, maprotiline, citalopram, and moclobemide.	Imipramine	135-145	phosducin-like 1	Rattus norvegicus	0-22
16519925-6	2006	Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels.	Imipramine	46-56	brain derived neurotrophic factor	Mus musculus	164-168
16519925-6	2006	Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels.	Imipramine	46-56	cAMP responsive element binding protein 1	Mus musculus	173-177
16519925-6	2006	Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels.	Imipramine	58-61	brain derived neurotrophic factor	Mus musculus	164-168
16519925-6	2006	Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels.	Imipramine	58-61	cAMP responsive element binding protein 1	Mus musculus	173-177
16112691-1	2005	Mutants of serotonin transporter that are altered in their regulation by cGMP were tested for the ability of cocaine and the antidepressant drugs imipramine, sertraline, citalopram and fluoxetine to inhibit serotonin transport.	Imipramine	146-156	solute carrier family 6 member 4	Homo sapiens	11-32
16626519-0	2006	Biosynthesis of imipramine glucuronide and characterization of imipramine glucuronidation catalyzed by recombinant UGT1A4.	Imipramine	16-26	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	115-121
16626519-3	2006	Imipramine N(+)-glucuronide was biosynthesized by incubating imipramine with recombinant UGT1A4 and then purified with solid-phase cartridges.	Imipramine	61-71	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	89-95
16626519-7	2006	The values of apparent K(m), K(i), and V(max) for imipramine glucuronidation via UGT1A4 were 1.39+/-0.09 mmol/L, 6.24+/-0.45 mmol/L and 453.81+/-32.12 pmol/min per mg cell homogenate (n=3), respectively.	Imipramine	50-60	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	81-87
16626519-8	2006	CONCLUSION: As a specific substrate of UGT1A4, imipramine was used as a convenient method to characterize the activity of recombinant UGT1A4 by using HPLC.	Imipramine	47-57	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	39-45
16626519-8	2006	CONCLUSION: As a specific substrate of UGT1A4, imipramine was used as a convenient method to characterize the activity of recombinant UGT1A4 by using HPLC.	Imipramine	47-57	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	134-140
16626519-9	2006	Furthermore, the profile of imipramine glucuronidation was evaluated by using recombinant UGT1A4 in vitro.	Imipramine	28-38	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	90-96
16637596-4	2006	Using real-time quantitative PCR, we demonstrated increased neuroserpin mRNA expression in rat frontal cortex after chronic treatment with several classes of antidepressants, including imipramine, fluoxetine, sertraline, and venlafaxine.	Imipramine	185-195	serpin family I member 2	Rattus norvegicus	60-71
16929962-2	2006	Chronic treatment with imipramine reduced the severity of catalepsy and functional activity of 5-HT1A serotonin receptors, but did not modify their expression in the hippocampus.	Imipramine	23-33	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	95-101
16170231-0	2005	Chronic imipramine treatment sensitizes 5-HT1A and 5-HT 2 A receptors in the dorsal periaqueductal gray matter: evidence from the elevated T-maze test of anxiety.	Imipramine	8-18	5-hydroxytryptamine receptor 1A	Rattus norvegicus	40-52
16170231-3	2005	In the present study we further explore the hypothesis that sensitization of 5-HT1A and 5-HT 2 A receptors in the DPAG is involved in the anti-panic effect of imipramine.	Imipramine	159-169	5-hydroxytryptamine receptor 1A	Rattus norvegicus	77-89
16170231-11	2005	Therefore, chronic imipramine seems to sensitize both 5-HT1A and 5-HT 2 A receptors in the DPAG, strengthening the view that these receptors are involved in the mode of action of anti-panic drugs.	Imipramine	19-29	5-hydroxytryptamine receptor 1A	Rattus norvegicus	54-66
16245071-5	2005	In addition, we demonstrate that the antidepressants imipramine and amitriptyline induce a long-term reduction of the activity of A-SMase in cultured cells.	Imipramine	53-63	sphingomyelin phosphodiesterase 1	Homo sapiens	130-137
16382205-9	2005	Joint administration of IMI (10 mg/kg) and MET (50 mg/kg) induced a more potent increase BDNF gene expression in both the examined brain regions (compared to the treatment with either drug alone).	Imipramine	24-27	brain-derived neurotrophic factor	Rattus norvegicus	89-93
16141545-3	2005	Among the recombinant CYPs, CYP3A4 exhibited the highest metabolic activities of all compounds except for clotiazepam and imipramine.	Imipramine	122-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-34
16141545-4	2005	The metabolism of clotiazepam was catalyzed by CYP2B6, CYP3A4, CYP2C18, and CYP2C19, and imipramine was metabolized by CYP2D6 most efficiently.	Imipramine	89-99	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	119-125
16141545-6	2005	These results suggest that the psychotropic drugs investigated are metabolized predominantly by CYP3A4, except that CYP2D6 catalyzes the metabolism of imipramine.	Imipramine	151-161	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	116-122
15955598-0	2005	Imipramine and citalopram facilitate amyloid precursor protein secretion in vitro.	Imipramine	0-10	amyloid beta precursor protein	Rattus norvegicus	37-62
16077898-8	2005	On the other hand, imipramine, an inhibitor of ASM, caused the accumulation of sphingomyelin.	Imipramine	19-29	sphingomyelin phosphodiesterase 1	Homo sapiens	47-50
15996564-0	2005	Inhibitory effect of imipramine on the human corticotropin-releasing-hormone gene promoter activity operates through a PI3-K/AKT mediated pathway.	Imipramine	21-31	corticotropin releasing hormone	Homo sapiens	45-76
15769300-2	2005	In the present study, we demonstrated that chronic treatment with a tricyclic antidepressant (imipramine) and a selective serotonin reuptake inhibitor (sertraline) reduced the expression of Ndrg2 mRNA and protein in the rat frontal cortex.	Imipramine	94-104	NDRG family member 2	Rattus norvegicus	190-195
15996564-0	2005	Inhibitory effect of imipramine on the human corticotropin-releasing-hormone gene promoter activity operates through a PI3-K/AKT mediated pathway.	Imipramine	21-31	AKT serine/threonine kinase 1	Homo sapiens	125-128
15714225-0	2005	Stress-induced c-Fos expression is differentially modulated by dexamethasone, diazepam and imipramine.	Imipramine	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15996564-2	2005	The aim of the present study was to elucidate the involvement of some intracellular signal transduction pathways in imipramine-induced inhibition of CRH gene activity in the differentiated Neuro-2A cells, stably transfected with a human CRH promoter fragment linked to the chloramphenicol acetyltransferase (CAT) reporter gene.	Imipramine	116-126	corticotropin releasing hormone	Mus musculus	149-152
15996564-2	2005	The aim of the present study was to elucidate the involvement of some intracellular signal transduction pathways in imipramine-induced inhibition of CRH gene activity in the differentiated Neuro-2A cells, stably transfected with a human CRH promoter fragment linked to the chloramphenicol acetyltransferase (CAT) reporter gene.	Imipramine	116-126	corticotropin releasing hormone	Homo sapiens	237-240
15996564-4	2005	Moreover, wortmannin at a low concentration (0.01muM) significantly reversed the inhibitory effect of imipramine on CRH-CAT activity, whereas other protein kinase inhibitors were inactive or even enhanced the imipramine effects.	Imipramine	102-112	corticotropin releasing hormone	Mus musculus	116-119
15996564-5	2005	The involvement of PI3-K/Akt pathway in the imipramine action was confirmed by Western blot study, which showed that this drug increased phospho-Ser-473 Akt level, but had no effect on total Akt and glycogen synthase kinase (GSK-3beta) levels.	Imipramine	44-54	AKT serine/threonine kinase 1	Homo sapiens	25-28
15996564-5	2005	The involvement of PI3-K/Akt pathway in the imipramine action was confirmed by Western blot study, which showed that this drug increased phospho-Ser-473 Akt level, but had no effect on total Akt and glycogen synthase kinase (GSK-3beta) levels.	Imipramine	44-54	AKT serine/threonine kinase 1	Homo sapiens	153-156
15996564-5	2005	The involvement of PI3-K/Akt pathway in the imipramine action was confirmed by Western blot study, which showed that this drug increased phospho-Ser-473 Akt level, but had no effect on total Akt and glycogen synthase kinase (GSK-3beta) levels.	Imipramine	44-54	AKT serine/threonine kinase 1	Homo sapiens	153-156
15996564-5	2005	The involvement of PI3-K/Akt pathway in the imipramine action was confirmed by Western blot study, which showed that this drug increased phospho-Ser-473 Akt level, but had no effect on total Akt and glycogen synthase kinase (GSK-3beta) levels.	Imipramine	44-54	glycogen synthase kinase 3 beta	Homo sapiens	225-234
15996564-6	2005	These results indicate that the inhibitory effect of imipramine on the CRH gene promoter activity in Neuro-2A cells is mainly connected with enhancement of PI-3K/Akt pathway.	Imipramine	53-63	corticotropin releasing hormone	Mus musculus	71-74
15996564-6	2005	These results indicate that the inhibitory effect of imipramine on the CRH gene promoter activity in Neuro-2A cells is mainly connected with enhancement of PI-3K/Akt pathway.	Imipramine	53-63	thymoma viral proto-oncogene 1	Mus musculus	162-165
15946935-4	2005	The putative acid sphingomyelinase (ASMase) inhibitor imipramine inhibited TNF-alpha-induced apoptosis and C16-ceramide increase as did the knock out of ASMase.	Imipramine	54-64	tumor necrosis factor	Rattus norvegicus	75-84
15714225-12	2005	We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression.	Imipramine	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
15687478-10	2005	Fluoxetine is a potent inhibitor of CYP2D6, and imipramine is metabolized by CYP2D6.	Imipramine	48-58	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	77-83
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Imipramine	16-26	sphingomyelin phosphodiesterase 1	Homo sapiens	42-63
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Imipramine	16-26	sphingomyelin phosphodiesterase 1	Homo sapiens	65-71
15935071-6	2005	Conversely, imipramine did not reduce the hippocampal phosphorylation of both ERK subtypes whereas it selectively increased ERK 1 phosphorylation in the cytosolic compartment of frontal cortex suggesting a drug-specific effect on this intracellular target.	Imipramine	12-22	mitogen activated protein kinase 3	Rattus norvegicus	124-129
15625090-6	2005	This effect was mimicked by the tricyclic antidepressants imipramine and clomipramine, and by the SSRI citalopram, with relative efficacies that matched their known relative selectivities for the 5-HT transporter.	Imipramine	58-68	solute carrier family 6 member 4	Homo sapiens	196-212
15869748-0	2005	Subchronic treatment with imipramine ameliorates the decreased number in neuropeptide Y-positive cells in the hippocampus of learned helplessness rats.	Imipramine	26-36	neuropeptide Y	Rattus norvegicus	73-87
15869748-2	2005	Subchronic treatment of learned helplessness rats, but not naive rats, with imipramine ameliorated the decrease in the number of NPY-positive cells.	Imipramine	76-86	neuropeptide Y	Rattus norvegicus	129-132
15796901-7	2005	In addition, blockage of ceramide production by ASM inhibitor imipramine interrupted MNNG-induced receptor clustering.	Imipramine	62-72	sphingomyelin phosphodiesterase 1	Homo sapiens	48-51
15470160-13	2005	Trans-3"-hydroxycotinine O-glucuronosyltransferase activity in human liver microsomes was inhibited by imipramine (a substrate of UGT1A4, IC(50) = 55 microM), androstanediol (a substrate of UGT2B15, IC(50) = 169 microM), and propofol (a substrate of UGT1A9, IC(50) = 296 microM).	Imipramine	103-113	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	130-136
15654117-7	2005	Deletion of SER-1, a 5HT1 receptor, abolishes the response to 5HT but has only a minor effect on the response to imipramine and no effect on the response to fluoxetine.	Imipramine	113-123	G_PROTEIN_RECEP_F1_2 domain-containing protein	Caenorhabditis elegans	12-17
15654117-8	2005	In contrast, deletion of SER-4, a 5HT2 receptor, confers significant resistance to imipramine while leaving the responses to 5HT or fluoxetine intact.	Imipramine	83-93	G_PROTEIN_RECEP_F1_2 domain-containing protein	Caenorhabditis elegans	25-30
15663788-5	2005	In addition, previous studies have shown that the levels of AP-2alpha and AP-2beta in rat whole brain were decreased after 10 days of treatment with citalopram (SSRI) and imipramine (TCA), and were increased with phenelzine (MAO-I).	Imipramine	171-181	transcription factor AP-2 alpha	Rattus norvegicus	60-69
15691529-0	2005	Hypoxia activates glycogen synthase kinase-3 in mouse brain in vivo: protection by mood stabilizers and imipramine.	Imipramine	104-114	glycogen synthase kinase 3 beta	Mus musculus	18-44
15691529-2	2005	METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo.	Imipramine	49-59	glycogen synthase kinase 3 beta	Mus musculus	170-174
15691529-4	2005	Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions.	Imipramine	26-36	glycogen synthase kinase 3 beta	Mus musculus	122-130
15691529-4	2005	Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions.	Imipramine	26-36	glycogen synthase kinase 3 alpha	Mus musculus	135-144
15691529-5	2005	CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects.	Imipramine	44-54	glycogen synthase kinase 3 beta	Mus musculus	157-161
15691529-5	2005	CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects.	Imipramine	44-54	glycogen synthase kinase 3 beta	Mus musculus	237-241
15623560-6	2005	Our findings suggest that imipramine"s proposed activities on forebrain GR function are not essential for its antidepressant effects, and that alteration in GR expression may play a causative role in disease onset of major depressive disorder.	Imipramine	26-36	nuclear receptor subfamily 3, group C, member 1	Mus musculus	72-74
15470160-13	2005	Trans-3"-hydroxycotinine O-glucuronosyltransferase activity in human liver microsomes was inhibited by imipramine (a substrate of UGT1A4, IC(50) = 55 microM), androstanediol (a substrate of UGT2B15, IC(50) = 169 microM), and propofol (a substrate of UGT1A9, IC(50) = 296 microM).	Imipramine	103-113	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	190-197
15470160-13	2005	Trans-3"-hydroxycotinine O-glucuronosyltransferase activity in human liver microsomes was inhibited by imipramine (a substrate of UGT1A4, IC(50) = 55 microM), androstanediol (a substrate of UGT2B15, IC(50) = 169 microM), and propofol (a substrate of UGT1A9, IC(50) = 296 microM).	Imipramine	103-113	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	250-256
15720040-10	2005	Interestingly, amiodarone and imipramine induced apoptosis in U-937 cells as shown by annexin V-FITC staining and DNA fragmentation.	Imipramine	30-40	annexin A5	Homo sapiens	86-95
15720040-11	2005	Enzymatic assays demonstrated that amiodarone and imipramine induced the activity of caspases 2 and 3.	Imipramine	50-60	caspase 2	Homo sapiens	85-101
15470160-14	2005	Interestingly, imipramine (IC(50) = 45 microM), androstanediol (IC(50) = 21 microM), and propofol (IC(50) = 41 microM) also inhibited trans-3"-hydroxycotinine O-glucuronosyltransferase activity by recombinant UGT2B7.	Imipramine	15-25	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	209-215
15365094-0	2004	Mechanism of block of hEag1 K+ channels by imipramine and astemizole.	Imipramine	43-53	potassium voltage-gated channel subfamily H member 1	Homo sapiens	22-27
15662096-0	2004	Effect of imipramine treatment on plasma dopamine beta-hydroxylase activity in chronic mild stress in rats.	Imipramine	10-20	dopamine beta-hydroxylase	Rattus norvegicus	41-66
15662096-5	2004	The data indicate that, similarly to human depression, CMS also affects DBH activity, and, moreover, the CMS-induced alterations are normalized by imipramine treatment.	Imipramine	147-157	dopamine beta-hydroxylase	Homo sapiens	72-75
15662097-1	2004	We previously reported that chronic treatment with imipramine and electroconvulsive shock up-regulate the density and alpha1A-adrenergic receptor (alpha1A-AR) mRNA level in the rat prefrontal cortex, while the expression of the alpha1B subtype was unchanged.	Imipramine	51-61	adrenoceptor alpha 1D	Rattus norvegicus	118-145
15662097-1	2004	We previously reported that chronic treatment with imipramine and electroconvulsive shock up-regulate the density and alpha1A-adrenergic receptor (alpha1A-AR) mRNA level in the rat prefrontal cortex, while the expression of the alpha1B subtype was unchanged.	Imipramine	51-61	adrenoceptor alpha 1D	Rattus norvegicus	147-157
15581848-9	2004	The effects of imipramine on Na+/Mg2+ antiport and choline/Mg2+ antiport are not mediated by PKCalpha but are caused by a direct reaction of imipramine with these transporters.	Imipramine	15-25	protein kinase C, alpha	Rattus norvegicus	93-101
15383576-11	2004	DC apoptosis was significantly higher in inducible NO synthase-deficient mice than in wild-type animals and was significantly reduced by treatment ex vivo with NO, cGMP, or the A-SMase inhibitor imipramine.	Imipramine	195-205	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	177-184
15365094-2	2004	The tricyclic antidepressant imipramine and the antihistamine astemizole inhibit the current through Eag1 channels and reduce the proliferation of cancer cells.	Imipramine	29-39	potassium voltage-gated channel subfamily H member 1	Homo sapiens	101-105
15365094-4	2004	Even if both drugs differ in their affinity for hEag1 channels (IC50s are approximately 2 microM for imipramine and approximately 200 nM for astemizole) and in their blocking kinetics, both drugs permeate the membrane and inhibit the hEag1 current by selectively binding to open channels.	Imipramine	101-111	potassium voltage-gated channel subfamily H member 1	Homo sapiens	48-53
15219641-5	2004	Imipramine at 10 mg/kg daily for 4 weeks by osmotic minipump reduced 5-HT(1A) autoreceptor activity, as measured by the effect of 8-OH-DPAT in the hypothalamus, but the combination of T3 and imipramine given for 2 weeks did not affect either 5-HT(1A) or 5-HT(1B) autoreceptor activity.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	69-76
15150531-4	2004	Here, we report the inhibitory effects of various antidepressants: imipramine, desipramine, amitriptyline, nortriptyline, clomipramine, maprotiline, and citalopram, on GIRK channels.	Imipramine	67-77	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	168-172
15219641-5	2004	Imipramine at 10 mg/kg daily for 4 weeks by osmotic minipump reduced 5-HT(1A) autoreceptor activity, as measured by the effect of 8-OH-DPAT in the hypothalamus, but the combination of T3 and imipramine given for 2 weeks did not affect either 5-HT(1A) or 5-HT(1B) autoreceptor activity.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	242-249
15219641-5	2004	Imipramine at 10 mg/kg daily for 4 weeks by osmotic minipump reduced 5-HT(1A) autoreceptor activity, as measured by the effect of 8-OH-DPAT in the hypothalamus, but the combination of T3 and imipramine given for 2 weeks did not affect either 5-HT(1A) or 5-HT(1B) autoreceptor activity.	Imipramine	0-10	5-hydroxytryptamine receptor 1B	Rattus norvegicus	254-261
15363987-10	2004	The reduction of CRE-binding activities and BDNF levels in the frontal cortex or hippocampus in learned helplessness rats were ameliorated by treatment with imipramine or rolipram alone.	Imipramine	157-167	brain-derived neurotrophic factor	Rattus norvegicus	44-48
15364545-6	2004	On the other hand, CYP4F11 was a better catalyst than CYP4F3A for many drugs such as erythromycin, benzphetamine, ethylmorphine, chlorpromazine, and imipramine.	Imipramine	149-159	cytochrome P450 family 4 subfamily F member 11	Homo sapiens	19-26
15363987-11	2004	CRE-binding activities and/or BDNF levels of the frontal cortex and hippocampus were significantly increased by treatment with a combination of rolipram and imipramine compared to those in imipramine-treated rats.	Imipramine	157-167	brain-derived neurotrophic factor	Rattus norvegicus	30-34
15380377-4	2004	Syt IV (-/-) mice also exhibit reduced depression-like behavior and are highly sensitive to the effects of the anti-depressant imipramine in a modified Porsolt forced swim test.	Imipramine	127-137	synaptotagmin IV	Mus musculus	0-6
15462192-3	2004	The result showed that chlorpromazine (CPZ) and imipramine (IMI) at concentrations of 1x10(-2), 5x10(-3) and 2.5x10(-3) M inhibited rat brain mitochondrial MAO-A activity in vitro by 82, 50, 39 and 86, 74, 38 %, respectively.	Imipramine	48-58	monoamine oxidase A	Rattus norvegicus	156-161
15462192-3	2004	The result showed that chlorpromazine (CPZ) and imipramine (IMI) at concentrations of 1x10(-2), 5x10(-3) and 2.5x10(-3) M inhibited rat brain mitochondrial MAO-A activity in vitro by 82, 50, 39 and 86, 74, 38 %, respectively.	Imipramine	60-63	monoamine oxidase A	Rattus norvegicus	156-161
15205034-6	2004	Imipramine, MBA, and ANF produced significant inhibition in both the wild-type and CYP2E1 knockout mouse liver with minimal effects in lung.	Imipramine	0-10	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	83-89
15039769-4	2004	Treatment with monoamine reuptake inhibitors fluoxetine and imipramine also increased the level of phospho-Ser9-GSK3beta.	Imipramine	60-70	glycogen synthase kinase 3 beta	Mus musculus	112-120
18634600-7	2004	By contrast,imipramine, which can provoke mania, increases synaptic expression of GluR1 in the hippocampus in vivo.	Imipramine	12-22	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	82-87
15212820-8	2004	Diclofenac increased the production of pro-inflammatory cytokines, whereas the production of MCP-1 was increased by minocycline and decreased by imipramine.	Imipramine	145-155	chemokine (C-C motif) ligand 2	Mus musculus	93-98
15269270-9	2004	In contrast, imipramine, an antidepressant that can trigger manic episodes, increased synaptic expression of GluR1 in hippocampus in vivo.	Imipramine	13-23	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	109-114
15205034-5	2004	Chemical inhibitors used to ascertain the contributions made by various cytochromes P450 were imipramine for CYP2C, alpha-methylbenzylaminobenzotriazole (MBA) for CYP2B, alpha-naphthoflavone (ANF) for CYP1A, 5-phenyl-1-pentyne (5P1P) for CYP2F2, and diethyldithiocarbamate (DTTC) for CYP2E1.	Imipramine	94-104	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	109-114
15150117-3	2004	In the present study, we show that the anticancer drug cisplatin induces clustering of CD95 at the surface of the human colon cancer cell line HT29, an event inhibited by the inhibitor of acid sphingomyelinase (aSMase) imipramine.	Imipramine	219-229	Fas cell surface death receptor	Homo sapiens	87-91
15157811-2	2004	Furthermore, we show that both eugenol and imipramine induce brain-derived neurotrophic factor (BDNF) in the hippocampus with and without induction of metallothionein-III (MT-III), respectively.	Imipramine	43-53	brain derived neurotrophic factor	Mus musculus	61-94
15157811-2	2004	Furthermore, we show that both eugenol and imipramine induce brain-derived neurotrophic factor (BDNF) in the hippocampus with and without induction of metallothionein-III (MT-III), respectively.	Imipramine	43-53	brain derived neurotrophic factor	Mus musculus	96-100
15214506-0	2004	Effects of myo-inositol versus fluoxetine and imipramine pretreatments on serotonin 5HT2A and muscarinic acetylcholine receptors in human neuroblastoma cells.	Imipramine	46-56	5-hydroxytryptamine receptor 2A	Homo sapiens	84-128
15181653-0	2004	Decrease of the platelet 5-HT2A receptor function by long-term imipramine treatment in endogenous depression.	Imipramine	63-73	5-hydroxytryptamine receptor 2A	Homo sapiens	25-40
15181653-9	2004	CONCLUSIONS: The results showed a decrease in a platelet functional response mediated by 5-HT2A receptors following effective imipramine treatment, suggesting that desensitization or down-regulation of the 5-HT2A receptor function could be linked to the therapeutic effect of some antidepressants.	Imipramine	126-136	5-hydroxytryptamine receptor 2A	Homo sapiens	89-95
15181653-9	2004	CONCLUSIONS: The results showed a decrease in a platelet functional response mediated by 5-HT2A receptors following effective imipramine treatment, suggesting that desensitization or down-regulation of the 5-HT2A receptor function could be linked to the therapeutic effect of some antidepressants.	Imipramine	126-136	5-hydroxytryptamine receptor 2A	Homo sapiens	89-104
15214506-3	2004	The current study aimed to investigate the possible modulatory role of mI versus fluoxetine or imipramine pretreatments on serotonin-2A receptor (5HT2A-R) and muscarinic acetylcholine receptor (mAChR) function and binding in in vitro systems.	Imipramine	95-105	5-hydroxytryptamine receptor 2A	Homo sapiens	123-144
15150117-3	2004	In the present study, we show that the anticancer drug cisplatin induces clustering of CD95 at the surface of the human colon cancer cell line HT29, an event inhibited by the inhibitor of acid sphingomyelinase (aSMase) imipramine.	Imipramine	219-229	sphingomyelin phosphodiesterase 1	Homo sapiens	188-209
15150117-3	2004	In the present study, we show that the anticancer drug cisplatin induces clustering of CD95 at the surface of the human colon cancer cell line HT29, an event inhibited by the inhibitor of acid sphingomyelinase (aSMase) imipramine.	Imipramine	219-229	sphingomyelin phosphodiesterase 1	Homo sapiens	211-217
15033385-5	2004	These results indicate that the blockade of 5-HT(1B) rather than 5-HT(1A) receptors may facilitate the anti-immobility effect of imipramine, desipramine or moclobemide in the forced swimming test.	Imipramine	129-139	5-hydroxytryptamine receptor 1B	Rattus norvegicus	44-51
15132707-1	2004	Interactions of two amphiphilic antidepressant drugs, imipramine and desipramine hydrochlorides, with the blood protein human serum albumin (HSA) were investigated to gain an understanding of the effects of drug molecular structure on the complex formation of drug-protein molecules.	Imipramine	54-64	albumin	Homo sapiens	126-139
14735130-6	2004	It was found that imipramine, amitryptyline, desipramine, fluoxetine, and mianserin, present in the culture medium for 5 days, in a concentration-dependent manner inhibited basal hCRH gene promoter activity in undifferentiated Neuro-2A cells, while other drugs under study (citalopram, tianeptine, moclobemide, venlafaxine, reboxetine, mirtazapine, and milnacipram) were inactive.	Imipramine	18-28	corticotropin releasing hormone	Homo sapiens	179-183
15023476-3	2004	RESULTS: The platelet 5-HT transporter has been found to have an inconsistent association with suicidality; furthermore, the specificity of imipramine for the 5-HT transporter is most likely low, since the number of platelet impramine binding sites has not been reliably associated with platelet serotonin uptake (Vmax).	Imipramine	140-150	solute carrier family 6 member 4	Homo sapiens	159-175
14735130-10	2004	Moreover, imipramine and fluoxetine, but not tianeptine, showed moderate inhibitory effect on CRH gene promoter activity also in AtT-20 cell line, commonly used in CRH gene regulation studies.	Imipramine	10-20	corticotropin releasing hormone	Mus musculus	94-97
14735130-10	2004	Moreover, imipramine and fluoxetine, but not tianeptine, showed moderate inhibitory effect on CRH gene promoter activity also in AtT-20 cell line, commonly used in CRH gene regulation studies.	Imipramine	10-20	corticotropin releasing hormone	Mus musculus	164-167
14996410-4	2004	imipramine and venlafaxine (at the higher concentration), 5-HTP (at lower and higher concentrations) and a combination of 5-HTP and fluoxetine (both at the lower concentration) increased the production of IL-6; (2).	Imipramine	0-10	interleukin 6	Homo sapiens	205-209
15199661-1	2004	Tricyclic antidepressants are all hydroxylated by cytochrome P450 (CYP) 2D6, but the tertiary amines, amitriptyline, clomipramine and imipramine, are also N-demethylated to the active metabolites, nortriptyline, N-desmethylclomipramine and desipramine, by several CYPs, including the polymorphic CYP2C19, CYP1A2 and CYP3A4.	Imipramine	134-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	296-303
14716684-6	2004	The specificity of tracer uptake was determined by adding the NET inhibitor imipramine.	Imipramine	76-86	solute carrier family 6 member 2	Rattus norvegicus	62-65
13680075-14	2004	(iii) The agreement between mirtazapine and imipramine increases our confidence in the validity of c-fos expression profiling to aid drug classification and predict therapeutic utility.	Imipramine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
15199661-1	2004	Tricyclic antidepressants are all hydroxylated by cytochrome P450 (CYP) 2D6, but the tertiary amines, amitriptyline, clomipramine and imipramine, are also N-demethylated to the active metabolites, nortriptyline, N-desmethylclomipramine and desipramine, by several CYPs, including the polymorphic CYP2C19, CYP1A2 and CYP3A4.	Imipramine	134-144	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	305-311
15199661-1	2004	Tricyclic antidepressants are all hydroxylated by cytochrome P450 (CYP) 2D6, but the tertiary amines, amitriptyline, clomipramine and imipramine, are also N-demethylated to the active metabolites, nortriptyline, N-desmethylclomipramine and desipramine, by several CYPs, including the polymorphic CYP2C19, CYP1A2 and CYP3A4.	Imipramine	134-144	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	316-322
14640711-5	2003	The system was used both to yield the Michaelis constant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 value of a chemical inhibitor (tranylcypromine) for this CYP2C19-mediated reaction.	Imipramine	97-107	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-75
14640711-5	2003	The system was used both to yield the Michaelis constant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 value of a chemical inhibitor (tranylcypromine) for this CYP2C19-mediated reaction.	Imipramine	97-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	208-215
14570768-15	2003	Both propofol, a UGT1A9 substrate, and imipramine, a UGT1A4 substrate, inhibited the glucuronidation of nicotine and cotinine by human liver microsomes.	Imipramine	39-49	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	53-59
14624184-8	2003	However, fasting insulin levels and calculated insulin resistance levels dropped substantially in the imipramine group.	Imipramine	102-112	insulin	Homo sapiens	17-24
14624184-8	2003	However, fasting insulin levels and calculated insulin resistance levels dropped substantially in the imipramine group.	Imipramine	102-112	insulin	Homo sapiens	47-54
12746132-8	2003	Chemical inhibitors were used to ascertain the contributions made by various cytochromes P-450: imipramine for CYP2C, alpha -methylbenzylaminobenzotriazole for CYP2B, alpha -naphthoflavone for CYP1A, 5-phenyl-1-pentyne for CYP2F2, and diethyldithiocar-bamate for CYP2E1.	Imipramine	96-106	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	111-116
14520129-4	2003	All 3 treatments (imipramine, buspirone, and placebo) caused a reduction in anxiety and depression symptoms as measured by changes in the Hamilton Anxiety Rating Scale and Hamilton Depression Rating Scale.	Imipramine	18-28	paired box 5	Homo sapiens	0-5
12943557-5	2003	We have previously shown that treatment with citalopram and imipramin resulted in a decrease in AP-2alpha and AP-2beta levels in rat brain.	Imipramine	60-69	transcription factor AP-2 alpha	Rattus norvegicus	96-105
12963821-5	2003	Insig-1 and Insig-2 also enhance the conformational change in SCAP that occurs upon addition of certain cationic amphiphiles, such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect of cholesterol.	Imipramine	171-181	insulin induced gene 1	Homo sapiens	0-7
12963821-5	2003	Insig-1 and Insig-2 also enhance the conformational change in SCAP that occurs upon addition of certain cationic amphiphiles, such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect of cholesterol.	Imipramine	171-181	insulin induced gene 2	Homo sapiens	12-19
12963821-5	2003	Insig-1 and Insig-2 also enhance the conformational change in SCAP that occurs upon addition of certain cationic amphiphiles, such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect of cholesterol.	Imipramine	171-181	SREBF chaperone	Homo sapiens	62-66
12888916-4	2003	The enhancement of Fas-induced apoptosis by pre-treatment with neuraminidase was inhibited by z-VAD-fmk, a broad caspase inhibitor, and Ac-LEHD-CHO, an inhibitor of caspase-9, but not by Ac-IETD-CHO an inhibitor of caspase-8 or 6, imipramine, an inhibitor of acidic sphingomyelinase, glutathione, an inhibitor of neutral sphingomyelinase and Fumonisin B1, an inhibitor of ceramide synthase.	Imipramine	231-241	neuraminidase 1	Homo sapiens	63-76
12849931-4	2003	Under the conditions of the assays, [(3)H]paroxetine binding in the LC was specific for the SERT, based on the rank order of affinity of compounds for inhibiting [(3)H]paroxetine binding in the LC, i.e. citalopram > imipramine > desipramine > mazindol.	Imipramine	219-229	solute carrier family 6 member 4	Homo sapiens	92-96
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P <0.05).	Imipramine	143-153	mitogen activated protein kinase 3	Rattus norvegicus	19-25
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P <0.05).	Imipramine	143-153	mitogen activated protein kinase 14	Rattus norvegicus	27-30
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P <0.05).	Imipramine	143-153	mitogen-activated protein kinase 8	Rattus norvegicus	45-48
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P <0.05).	Imipramine	143-153	angiotensinogen	Rattus norvegicus	99-105
12725644-9	2003	Quinidine and imipramine reduced the phosphorylation of renal ERK1/2, but did not modify renal p38MAP kinase or JNK.	Imipramine	14-24	mitogen activated protein kinase 3	Rattus norvegicus	62-68
12939530-2	2003	The effects of imipramine, a 5-HT2CR antagonist, on cell growth, cell viability, and the 5-HT2CR mRNA level were investigated in this study.	Imipramine	15-25	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	29-36
12939530-6	2003	Our findings suggest that the effect of imipramine on neuronal growth may be related to its effects on 5-HT2CR.	Imipramine	40-50	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	103-110
12871839-12	2003	We further investigated if nAChR antagonists would influence the antidepressant-like effects of imipramine and citalopram.	Imipramine	96-106	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	27-32
12871839-20	2003	The present results demonstrate an unexpected interaction between nAChR ligands and imipramine and citalopram in the tail-suspension test.	Imipramine	84-94	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	66-71
12742641-0	2003	Effects of chronic exercise and imipramine on mRNA for BDNF after olfactory bulbectomy in rat.	Imipramine	32-42	brain-derived neurotrophic factor	Rattus norvegicus	55-59
12695349-1	2003	The effects of microsomal concentration on the inhibitory potencies of four compounds--fluoxetine, quinidine, imipramine, and ezlopitant--on heterologously expressed recombinant CYP2D6-catalyzed bufuralol 1"-hydroxylase activity were determined.	Imipramine	110-120	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	178-184
12695347-8	2003	The inhibitory effects of 4-nitrophenol (IC(50) = 121.0 microM) as a typical substrate for UGT1A6 and UGT1A9, imipramine (IC(50) = 393.8 microM) as a typical substrate for UGT1A3 and UGT1A4, and morphine (IC(50) = 109.3 microM) as a typical substrate for UGT2B7 were relatively weak.	Imipramine	110-120	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	102-108
12569264-6	2003	The magnitude of the increase was lower ( 0.01) in Ang II groups treated with imipramine (151 +/- 7.4 mmHg) or quinidine (163 +/- 4 mmHg) than in the Ang II only group (205 +/- 4 mmHg).	Imipramine	78-88	angiotensinogen	Rattus norvegicus	51-57
12700885-0	2003	Adaptive changes in the reactivity of 5-HT1A and 5-HT2 receptors induced in rat frontal cortex by repeated imipramine and citalopram.	Imipramine	107-117	5-hydroxytryptamine receptor 1A	Rattus norvegicus	38-50
12700885-7	2003	Both repeated imipramine and citalopram enhanced the effect of the activation of 5-HT(1A) receptor and attenuated the effect related to 5-HT(2) receptor activation, while the effect of the activation of 5-HT(4) receptor remained unchanged.	Imipramine	14-24	5-hydroxytryptamine receptor 1A	Rattus norvegicus	81-88
14506314-2	2003	This study was carried out to compare the effect of imipramine, mianserin and lithium on the in vitro production of Th1-like cytokines, such as IL-2, IFN-gamma, lymphotoxin and Th2-like cytokines such as IL-4, IL-10 as well as IL-12 and TGF-beta.	Imipramine	52-62	interleukin 2	Homo sapiens	144-148
14506314-4	2003	Imipramine and mianserin exhibited similar activities enhancing unstimulated IFN-gamma and IL-10 production.	Imipramine	0-10	interferon gamma	Homo sapiens	77-86
14506314-4	2003	Imipramine and mianserin exhibited similar activities enhancing unstimulated IFN-gamma and IL-10 production.	Imipramine	0-10	interleukin 10	Homo sapiens	91-96
12464250-6	2003	Our findings of the influence of these site-directed mutations of the CYP3A9 active site on its catalysis of testosterone and three other established but structurally different CYP3A substrates (progesterone, imipramine, and carbamazepine) are described.	Imipramine	209-219	cytochrome P450, family 3, subfamily a, polypeptide 9	Rattus norvegicus	70-76
12527797-9	2003	dFMO1 also catalyzed imipramine N-oxidation, with a K(m) of 4.7 microM and a V(max) of 82.1 nmol/min/mg of protein.	Imipramine	21-31	Flavin-containing monooxygenase 1	Drosophila melanogaster	0-5
12856820-2	2003	It was decided to evaluate the influence of imipramine (IMI), amitriptyline (AMI), fluvoxamine (FLU), mianserin (MIA) and tianeptine (TIA) on PLA2 activity after an acute and long-term (4 weeks) drug administration.	Imipramine	44-54	phospholipase A2 group IB	Rattus norvegicus	142-146
12480123-1	2003	This study examines the effects of paroxetine and imipramine on intracellular concentrations of cyclic adenosine monophosphate (cAMP) in human peripheral blood mononuclear cells.	Imipramine	50-60	cathelicidin antimicrobial peptide	Homo sapiens	96-126
12482470-0	2003	Differential effects of fluoxetine and imipramine on the phosphorylation of the transcription factor CREB and cell-viability.	Imipramine	39-49	cAMP responsive element binding protein 1	Homo sapiens	101-105
12482470-3	2003	In the present study we evaluated if the antidepressants imipramine and fluoxetine are capable to influence the translational expression and phosphorylation of CREB (pCREB) in cells known to be apoptosis-inducible by antidepressants.	Imipramine	57-67	cAMP responsive element binding protein 1	Homo sapiens	160-164
12482470-8	2003	Treating cells with lowest concentrations only imipramine revealed an increase of CREB-phosphorylation after long-time treatment over 3 weeks.	Imipramine	47-57	cAMP responsive element binding protein 1	Homo sapiens	82-86
15618734-2	2003	The uptake of L-alanine by cells that express hATB(0) (human amino acid transporter B(0)) was inhibited in the presence of imipramine.	Imipramine	123-133	solute carrier family 1 member 5	Homo sapiens	46-53
15618734-2	2003	The uptake of L-alanine by cells that express hATB(0) (human amino acid transporter B(0)) was inhibited in the presence of imipramine.	Imipramine	123-133	solute carrier family 6 member 14	Homo sapiens	61-88
12435800-6	2002	The kinetics of the up-regulation of Mss4 gene expression measured by Northern blot during the imipramine, tianeptine, or fluoxetine treatments are consistent with an antidepressant effect that occurs after 3 weeks.	Imipramine	95-105	RAB interacting factor	Rattus norvegicus	37-41
12172639-8	2002	hEAG channels were most sensitive to imipramine (IC50: 3.4 microM at +50 mV), followed by KCa (13.8 microM at +50 mV) and Clvol (12 microM at -100 mV), indicating that hEAG expression may be of importance for proliferation of melanoma cells.	Imipramine	37-47	potassium voltage-gated channel subfamily H member 1	Homo sapiens	0-4
12866730-4	2002	Imipramine and fluoxetine present in the medium for 5 days, in a concentration-dependent manner (3-30 microM) inhibited the basal activity of CRH gene promoter, while tianeptine was inactive.	Imipramine	0-10	corticotropin releasing hormone	Homo sapiens	142-145
12866730-5	2002	The obtained results indicate that inhibition of the human CRH gene promoter activity by imipramine and fluoxetine, but not tianeptine, may play a role in a mechanism by which the former drugs attenuate HPA axis activity.	Imipramine	89-99	corticotropin releasing hormone	Homo sapiens	59-62
12228186-7	2002	The tertiary amine TCAs, amitriptyline and imipramine, also inhibited CYP2C19-catalyzed S-mephenytoin 4"-hydroxylation (estimated K(i) of 37.7 and 56.8 micro M, respectively).	Imipramine	43-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
12323383-5	2002	In addition, there was a hyperpolarizing shift in the voltage-dependence of steady-state Na(+) channel inactivation and slowed repriming kinetics consistent with imipramine having a higher affinity for the inactivated state of the Na(+) channel.	Imipramine	162-172	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	89-102
12323383-5	2002	In addition, there was a hyperpolarizing shift in the voltage-dependence of steady-state Na(+) channel inactivation and slowed repriming kinetics consistent with imipramine having a higher affinity for the inactivated state of the Na(+) channel.	Imipramine	162-172	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	231-244
12464448-11	2002	In contrast, 5-HTT-/- mice retained sensitivity to the anti-immobility effects of the norepinephrine reuptake inhibitor, desipramine (20 mg/kg), and the mixed serotonin/norepinephrine reuptake inhibitor, imipramine (25 mg/kg).	Imipramine	204-214	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	13-18
26984461-4	2002	OBJECTIVE: In order to verify the hypothesis that TRH-induced increase of therapeutic efficiency of classical tricyclic antidepressants results from synergistic inhibitory effects of these agents on the secretion of proinflammatory cytokines, we determine the effect of imipramine or fluoxetine with and without TRH on the production of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) by stimulated human whole blood cells.	Imipramine	270-280	thyrotropin releasing hormone	Homo sapiens	50-53
26984461-8	2002	RESULTS: A significant decrease in production of IFN-gamma was observed in cells stimulated with mitogens and co-incubated with imipramine or fluoxetine and TRH.	Imipramine	128-138	interferon gamma	Homo sapiens	49-58
26984461-9	2002	Under the same conditions, TRH alone did not change the production of these cytokines, whereas imipramine alone significantly decreases IFN-gamma production, and fluoxetine alone significantly decreases IFN-gamma and TNF-alpha production.	Imipramine	95-105	interferon gamma	Homo sapiens	136-145
12220539-14	2002	This regulatory site appears to overlap with the activator site occupied by imipramine since activation of the enzyme by this activator is competitively inhibited by compound CT-8.	Imipramine	76-86	leucine zipper protein 4	Homo sapiens	175-179
12144933-0	2002	Inhibition of SK3 channels in the TE671 human medulloblastoma cell line by desipramine and imipramine.	Imipramine	91-101	potassium calcium-activated channel subfamily N member 3	Homo sapiens	14-17
12172639-8	2002	hEAG channels were most sensitive to imipramine (IC50: 3.4 microM at +50 mV), followed by KCa (13.8 microM at +50 mV) and Clvol (12 microM at -100 mV), indicating that hEAG expression may be of importance for proliferation of melanoma cells.	Imipramine	37-47	potassium voltage-gated channel subfamily H member 1	Homo sapiens	168-172
12065442-5	2002	KM values spanned an 80-fold range from 0.12 microM (CYP2D6-catalyzed thioridazine S-oxidation) to 9.8 microM (CYP2C19-catalyzed imipramine N-demethylation).	Imipramine	129-139	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
12065442-5	2002	KM values spanned an 80-fold range from 0.12 microM (CYP2D6-catalyzed thioridazine S-oxidation) to 9.8 microM (CYP2C19-catalyzed imipramine N-demethylation).	Imipramine	129-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
12160695-3	2002	A reduction of the plasma GABA (by administrating a GABA-T agonist, Imipramine) probably results in more axon(s)-to-oligodendrocyte signaling in the corpus callosum and it is postulated that this could result in a reduction of the autistic features for the patient.	Imipramine	68-78	4-aminobutyrate aminotransferase	Homo sapiens	52-58
12128002-9	2002	The expression of mGluR5a increased significantly after chronic imipramine in the CA1 and after chronic ECS in the CA3 region.	Imipramine	64-74	glutamate receptor, ionotropic, kainate 1	Mus musculus	18-24
12062564-0	2002	Chronic imipramine enhances 5-HT(1A) and 5-HT(2) receptors-mediated inhibition of panic-like behavior in the rat dorsal periaqueductal gray.	Imipramine	8-18	5-hydroxytryptamine receptor 1A	Rattus norvegicus	28-35
12062564-6	2002	The results suggest that sensitization of both 5-HT(1A) and 5-HT(2) receptors within the DPAG may be involved in the beneficial effect of imipramine in panic disorder (PD).	Imipramine	138-148	5-hydroxytryptamine receptor 1A	Rattus norvegicus	47-54
12019188-8	2002	The activity in UGT1A4 Supersomes was higher than that in recombinant UGT1A4 expressed in human B-lymphoblastoid cells at all imipramine concentration tested.	Imipramine	126-136	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	16-22
12019188-8	2002	The activity in UGT1A4 Supersomes was higher than that in recombinant UGT1A4 expressed in human B-lymphoblastoid cells at all imipramine concentration tested.	Imipramine	126-136	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	70-76
12089903-6	2002	The reduction of immobility, induced by the chronic administration of imipramine for 15 days, was blocked by treatment with ACTH for 14 days.	Imipramine	70-80	proopiomelanocortin	Homo sapiens	124-128
12128002-9	2002	The expression of mGluR5a increased significantly after chronic imipramine in the CA1 and after chronic ECS in the CA3 region.	Imipramine	64-74	carbonic anhydrase 1	Rattus norvegicus	82-85
12044792-0	2002	Imipramine but not 5-HT(1A) receptor agonists or neuroleptics induces adaptive changes in hippocampal 5-HT(1A) and 5-HT(4) receptors.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	102-109
12063075-0	2002	Repeated imipramine and electroconvulsive shock increase alpha 1A-adrenoceptor mRNA level in rat prefrontal cortex.	Imipramine	9-19	adrenoceptor alpha 1A	Rattus norvegicus	57-78
12044792-1	2002	It has been reported that the treatment with a tricyclic antidepressant imipramine induces an increase in the sensitivity of 5-HT(1A) receptors and a decrease in the sensitivity of 5-HT(4) receptors in the rat hippocampus.	Imipramine	72-82	5-hydroxytryptamine receptor 1A	Rattus norvegicus	125-132
12044792-2	2002	5-HT(1A) receptor agonists and neuroleptics also affect 5-HT(1A) receptors in different brain areas; therefore, it was of interest to compare their effects on hippocampal 5-HT receptors with the influence of the well-established antidepressant imipramine.	Imipramine	244-254	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-7
12044792-11	2002	These findings indicate that adaptive changes in the sensitivity of hippocampal neurons to 5-HT(1A) and 5-HT(4) receptors agonists are specific to imipramine and may thus-at least partly-mediate its effects.	Imipramine	147-157	5-hydroxytryptamine receptor 1A	Rattus norvegicus	91-98
11900811-0	2002	Effects of imipramine and lithium on wet-dog shakes mediated by the 5-HT2A receptor in ACTH-treated rats.	Imipramine	11-21	5-hydroxytryptamine receptor 2A	Canis lupus familiaris	68-83
12141399-1	2002	Drug interactions have previously been reported following the co-administration of methylphenidate (MPH) and drugs metabolized by the cytochrome P450 (CYP450) system such as imipramine.	Imipramine	174-184	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	134-149
12141399-1	2002	Drug interactions have previously been reported following the co-administration of methylphenidate (MPH) and drugs metabolized by the cytochrome P450 (CYP450) system such as imipramine.	Imipramine	174-184	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	151-157
12141399-2	2002	Therefore, this study used the Swiss Webster mouse to determine the effect of MPH on CYP450 isozymes likely to be important in the interaction between MPH and imipramine.	Imipramine	159-169	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	85-91
11900811-0	2002	Effects of imipramine and lithium on wet-dog shakes mediated by the 5-HT2A receptor in ACTH-treated rats.	Imipramine	11-21	proopiomelanocortin	Canis lupus familiaris	87-91
11900811-5	2002	Chronic coadministration of imipramine and lithium, lasting 14 days, decreased the wet-dog shakes response induced by (+/-)-DOI in rats treated with ACTH for 14 days.	Imipramine	28-38	proopiomelanocortin	Canis lupus familiaris	149-153
11900811-6	2002	These findings indicate that lithium inhibits the hyperfunction of the 5-HT2A receptor in rats treated with ACTH when coadministered with imipramine.	Imipramine	138-148	5-hydroxytryptamine receptor 2A	Canis lupus familiaris	71-86
11714871-7	2001	The inactivation of liver microsomal CYP1A2 by trans-resveratrol required NADPH, was not reversible by dialysis, and was not affected by the trapping agents glutathione, N-acetylcysteine, catalase, or superoxide dismutase, but was attenuated by a CYP1A2 substrate, imipramine.	Imipramine	265-275	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	37-43
11958526-6	2002	The most potent of inhibition of SSAO in monkey brain was observed by tricyclic antidepressant drug imipramine, as compared to tetracyclic drug maprotiline or non-cyclic drug nomifensine.	Imipramine	100-110	amine oxidase, copper containing 3	Rattus norvegicus	33-37
12139115-0	2002	Effect of imipramine on brain D-1 and 5-HT-2A receptors in a chronic unpredictable stress model in rats.	Imipramine	10-20	5-hydroxytryptamine receptor 2A	Rattus norvegicus	24-45
12139115-2	2002	In this paper, we report the results of investigations into dopaminergic D-1 and serotonergic 5-HT-2A receptors in the brain of rats subjected to CUS procedure and treated chronically with imipramine.	Imipramine	189-199	5-hydroxytryptamine receptor 2A	Rattus norvegicus	94-101
12139115-5	2002	Also a 21% increase in the density of 5-HT-2A receptors in the cerebral cortex induced by CUS was reduced by chronic imipramine treatment.	Imipramine	117-127	5-hydroxytryptamine receptor 2A	Rattus norvegicus	38-45
12139115-6	2002	The present data indicate that the increases in the density of brain D-1 and 5-HT-2A receptors of rats subjected to CUS, which are "normalized" by imipramine, might be involved in the pathophysiology of "animal depression" (and, thus, in pathophysiology of human depression) and in the mechanism of antidepressant therapy.	Imipramine	147-157	5-hydroxytryptamine receptor 2A	Rattus norvegicus	63-84
11817516-7	2002	In addition, chronic pretreatment with imipramine, but not lithium or paroxetine, downregulated the induction of AP-1 binding activity in response to acute restraint stress in the frontal cortex.	Imipramine	39-49	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-117
11746710-11	2001	Although the affinities of several non-amines were unchanged in the mutant SERT, the affinity of imipramine was decreased, revealing possible differences in amine and non-amine binding domains on the SERT.	Imipramine	97-107	solute carrier family 6 member 4	Homo sapiens	200-204
11899840-1	2001	Tricyclic antidepressants, amitriptyline, doxepin--derivatives of cycloheptadiene as well as imipramine and clomipramine, derivatives of dibenzazepine inhibit the activity of glutathione-S-transferase pi isolated from different regions of human brain (parietal cortex, frontal cortex, brain stem).	Imipramine	93-103	glutathione S-transferase kappa 1	Homo sapiens	175-200
11704501-6	2001	Imipramine and fluoxetine, antagonists with specificity for 5-HTT, showed the highest potency to antagonize [125I]RTI-55 binding in ROS and UMR cells.	Imipramine	0-10	huntingtin	Rattus norvegicus	62-65
11990081-12	2001	In summary, CYP1A2 was distinctly inhibited by imipramine and amitriptyline, CYP3A by imipramine and fluoxetine, while other CYP isoenzymes (CYP2B and/or 2E1) by imipramine and fluoxetine.	Imipramine	86-96	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	12-18
11985330-3	2001	The aim of the present study was to investigate the effect of imipramine (IMI), administered repeatedly, on the hyperactivity induced by 7-OH-DPAT, a dopamine D3 receptor-preferring agonist.	Imipramine	62-72	dopamine receptor D3	Rattus norvegicus	150-170
11985330-3	2001	The aim of the present study was to investigate the effect of imipramine (IMI), administered repeatedly, on the hyperactivity induced by 7-OH-DPAT, a dopamine D3 receptor-preferring agonist.	Imipramine	74-77	dopamine receptor D3	Rattus norvegicus	150-170
11990081-4	2001	The aim of the present study was to investigate the influence of imipramine, amitriptyline and fluoxetine on cytochrome P-450 activity measured by caffeine oxidation in rat liver microsomes.	Imipramine	65-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Imipramine	285-295	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Imipramine	285-295	tumor necrosis factor	Homo sapiens	141-149
11677251-5	2001	The potencies of the antidepressants citalopram, fluoxetine, paroxetine and imipramine were several-fold higher at hSERT compared with bSERT.	Imipramine	76-86	solute carrier family 6 member 4	Homo sapiens	115-120
11526465-12	2001	We conclude that monoamine-uptake inhibitors reduce ACh-currents and that imipramine regulates reversibly and non- competitively neuronal alpha2beta4 and muscle AChRs through similar mechanisms, perhaps by interacting externally on a non-conducting state of the AChR and by blocking the open receptor-channel complex close to the vestibule of the channel.	Imipramine	74-84	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	161-165
11526469-10	2001	Long-term pre-treatment with either imipramine or Hypericum reduced to control levels the stress-induced increases in gene transcription of GAD in the BST, CREB in the hippocampus, and POMC in the pituitary.	Imipramine	36-46	cAMP responsive element binding protein 1	Rattus norvegicus	156-160
11526469-10	2001	Long-term pre-treatment with either imipramine or Hypericum reduced to control levels the stress-induced increases in gene transcription of GAD in the BST, CREB in the hippocampus, and POMC in the pituitary.	Imipramine	36-46	proopiomelanocortin	Rattus norvegicus	185-189
11526469-11	2001	The stress-induced increases in mRNA levels of CRH in the PVN and TH in the locus coeruleus were reduced by imipramine but not by Hypericum.	Imipramine	108-118	corticotropin releasing hormone	Rattus norvegicus	47-50
11513817-8	2001	Measurements obtained before ingestion of the AA drink indicated that, relative to control subjects URs exhibited lower serotonin platelet concentrations, lower affinity, and fewer binding sites of the serotonin transporter for imipramine; these differences were unaffected by ATD.	Imipramine	228-238	solute carrier family 6 member 4	Homo sapiens	202-223
11425914-4	2001	We have observed that the genetic knock-out of the alpha(2A)-AR makes mice less active in a modified version of Porsolt"s forced swim test and insensitive to the antidepressant effects of the tricyclic drug imipramine in this paradigm.	Imipramine	207-217	adrenergic receptor, alpha 2a	Mus musculus	51-63
11425914-6	2001	These findings suggest that the alpha(2A)-AR may play a protective role in some forms of depression and anxiety and that the antidepressant effects of imipramine may be mediated by the alpha(2A)-AR.	Imipramine	151-161	adrenergic receptor, alpha 2a	Mus musculus	185-197
11990081-12	2001	In summary, CYP1A2 was distinctly inhibited by imipramine and amitriptyline, CYP3A by imipramine and fluoxetine, while other CYP isoenzymes (CYP2B and/or 2E1) by imipramine and fluoxetine.	Imipramine	47-57	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	12-18
11990081-12	2001	In summary, CYP1A2 was distinctly inhibited by imipramine and amitriptyline, CYP3A by imipramine and fluoxetine, while other CYP isoenzymes (CYP2B and/or 2E1) by imipramine and fluoxetine.	Imipramine	86-96	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	77-82
11990081-12	2001	In summary, CYP1A2 was distinctly inhibited by imipramine and amitriptyline, CYP3A by imipramine and fluoxetine, while other CYP isoenzymes (CYP2B and/or 2E1) by imipramine and fluoxetine.	Imipramine	86-96	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	12-18
11990081-12	2001	In summary, CYP1A2 was distinctly inhibited by imipramine and amitriptyline, CYP3A by imipramine and fluoxetine, while other CYP isoenzymes (CYP2B and/or 2E1) by imipramine and fluoxetine.	Imipramine	86-96	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	77-82
11331145-5	2001	On day 21, the combination did not change imipramine- or T3-induced decrease in 5-HT transporter density whereas it prevented imipramine-induced increase in 5-HT(1A) receptor density.	Imipramine	126-136	5-hydroxytryptamine receptor 1A	Rattus norvegicus	157-164
11282253-4	2001	Chronic treatment with imipramine also attenuated LPS-induced adrenocortical activation.	Imipramine	23-33	toll-like receptor 4	Mus musculus	50-53
11282253-6	2001	The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFalpha and IL-1beta mRNA in the spleen (assessed by semiquantitative in situ hybridization) was not altered following chronic treatment with either fluoxetine or imipramine.	Imipramine	352-362	toll-like receptor 4	Mus musculus	56-59
11282253-6	2001	The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFalpha and IL-1beta mRNA in the spleen (assessed by semiquantitative in situ hybridization) was not altered following chronic treatment with either fluoxetine or imipramine.	Imipramine	352-362	toll-like receptor 4	Mus musculus	162-165
11383709-6	2001	Both repeated ECS and imipramine enhanced the effects related to 5-HT1A receptor activation and attenuated the effects of 5-HT4 receptor activation.	Imipramine	22-32	5-hydroxytryptamine receptor 1A	Rattus norvegicus	65-71
11270917-2	2001	This study was carried out to examine the effects of antidepressive agents, i.e., imipramine, venlafaxine, L-5-hydroxytryptophan, and fluoxetine on the production of interferon-gamma (IFN-gamma), a proinflammatory cytokine, and interleukin-10 (IL-10), a negative immunoregulatory cytokine.	Imipramine	82-92	interferon gamma	Homo sapiens	166-182
11785930-2	2001	In the present study we attempted to find out whether imipramine, one of the most frequently used antidepressant drugs, interfered with glucocorticoids, modulating the production of IFN-gamma and IL-10, pro-inflammatory and anti-inflammatory cytokines, respectively.	Imipramine	54-64	interferon gamma	Homo sapiens	182-191
11785930-2	2001	In the present study we attempted to find out whether imipramine, one of the most frequently used antidepressant drugs, interfered with glucocorticoids, modulating the production of IFN-gamma and IL-10, pro-inflammatory and anti-inflammatory cytokines, respectively.	Imipramine	54-64	interleukin 10	Homo sapiens	196-201
11785930-4	2001	Imipramine at doses of 10(-6) and 10(-5) M did not modulate IFN-gamma or IL-10 production, whereas at a dose of 10(-5) M it increased the production of IL- 10 and decreased that of IFN-gamma, those results being statistically insignificant, though.	Imipramine	0-10	interleukin 10	Homo sapiens	152-158
11785930-5	2001	A combination of imipramine and dexamethasone or hydrocortisone at doses of 10(-6) or 10(-5) M significantly suppressed the production of IFN-gamma and IL-10, the level of inhibition being similar to that observed for glucocorticoids alone.	Imipramine	17-27	interferon gamma	Homo sapiens	138-147
11785930-5	2001	A combination of imipramine and dexamethasone or hydrocortisone at doses of 10(-6) or 10(-5) M significantly suppressed the production of IFN-gamma and IL-10, the level of inhibition being similar to that observed for glucocorticoids alone.	Imipramine	17-27	interleukin 10	Homo sapiens	152-157
11278387-6	2001	Imipramine and quinidine (putative inhibitors of the Na(+)/Mg(2+) exchanger) and removal of extracellular Na(+) abrogated Ang II-mediated [Mg(2+)](i) effects.	Imipramine	0-10	ANG	Canis lupus familiaris	122-125
11257428-4	2001	In the present study, reverse transcription-polymerase chain reaction analysis confirmed the induction of CSP at mRNA levels in rat frontal cortex after chronic treatment with two different classes of antidepressants, imipramine or sertraline.	Imipramine	218-228	DnaJ heat shock protein family (Hsp40) member C5	Rattus norvegicus	106-109
11115741-5	2000	Chronic severe serotonin depletion combined with treatment with the antidepressant imipramine leads to enhanced NET(Long) mRNA levels.	Imipramine	83-93	solute carrier family 6 member 2	Homo sapiens	112-115
11205881-6	2000	Chronic administration of citalopram (10 mg/kg), imipramin (10 mg/kg) and lithium-chloride (40 mg/kg) significantly decreased DNA-binding activity of AP-2.	Imipramine	49-58	fatty acid binding protein 4	Rattus norvegicus	150-154
11205881-7	2000	Furthermore, citalopram (10 mg/kg) and imipramin (10 mg/kg) significantly decreased the amount of AP-2alpha protein as determined by ELISA.	Imipramine	39-48	transcription factor AP-2 alpha	Rattus norvegicus	98-107
11334244-0	2000	Suppressive effect of TRH and imipramine on human interferon-gamma and interleukin-10 production in vitro.	Imipramine	30-40	interferon gamma	Homo sapiens	50-66
11334244-0	2000	Suppressive effect of TRH and imipramine on human interferon-gamma and interleukin-10 production in vitro.	Imipramine	30-40	interleukin 10	Homo sapiens	71-85
11334244-3	2000	In order to verify the hypothesis that the TRH-induced increase in the therapeutic efficiency of classic tricyclic antidepressants results from synergistic inhibitory effects of those two agents on the secretion of pro-inflammatory cytokines, we studied the effect of imipramine appliedjointly with TRH on the production of IFN-gamma and IL-10 by human whole blood cells stimulated in vitro by mitogens.	Imipramine	268-278	thyrotropin releasing hormone	Homo sapiens	43-46
11334244-4	2000	A significant decrease in the production of IFN-gamma and IL-10 cytokines, by 36% and 34%, respectively, was observed in cells stimulated with mitogens and co-incubated with imipramine and TRH (either given at a dose of 10(-5) M).	Imipramine	174-184	interferon gamma	Homo sapiens	44-53
11334244-4	2000	A significant decrease in the production of IFN-gamma and IL-10 cytokines, by 36% and 34%, respectively, was observed in cells stimulated with mitogens and co-incubated with imipramine and TRH (either given at a dose of 10(-5) M).	Imipramine	174-184	interleukin 10	Homo sapiens	58-63
11334244-6	2000	Furthermore, imipramine alone decreased, not statistically significantly, though, the production of IFN-gamma.	Imipramine	13-23	interferon gamma	Homo sapiens	100-109
11334244-7	2000	Hence our data only partly support the above-mentioned hypothesis, since TRH and imipramine applied jointly suppress the production of both the pro-inflammatory IFN-gamma and the anti-inflammatory IL-10 cytokines.	Imipramine	81-91	interferon gamma	Homo sapiens	161-170
11334244-7	2000	Hence our data only partly support the above-mentioned hypothesis, since TRH and imipramine applied jointly suppress the production of both the pro-inflammatory IFN-gamma and the anti-inflammatory IL-10 cytokines.	Imipramine	81-91	interleukin 10	Homo sapiens	197-202
10915830-3	2000	Amitriptyline, carbamazepine, chlorpromazine, cyproheptadine, imipramine, tacrine and trifluperazine blocked SK2 channel currents with micromolar affinity.	Imipramine	62-72	potassium calcium-activated channel subfamily N member 2	Rattus norvegicus	109-112
11334224-3	2000	The aim of the present study was to investigate the effect of two antidepressant drugs with different pharmacological profile, i.e. imipramine and citalopram, administered repeatedly, on the hypoactivity induced by low dose (0.05 mg/kg sc) of (+/-)7-hydroxy-dipropylaminotetralin (7-OH-DPAT), a dopamine D3 receptor preferring agonist.	Imipramine	132-142	dopamine receptor D3	Rattus norvegicus	295-315
10930579-5	2000	Reconstitution of ceramide, the product of acid sphingomyelinase activity, in imipramine- or SR33557-treated cells restores internalization of the bacteria.	Imipramine	78-88	sphingomyelin phosphodiesterase 1	Homo sapiens	43-64
10886465-8	2000	CYP2C19 enzyme participates in the metabolism of omeprazole, propranolol and psychotropic drugs such as hexobarbital, diazepam, citalopram, imipramine, clomipramine and amitriptyline.	Imipramine	140-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
10825654-4	2000	The most potent of inhibition of SSAO was observed by imipramine, followed by maprotiline, zimeldine and nomifensine.	Imipramine	54-64	amine oxidase copper containing 2	Homo sapiens	33-37
10903980-14	2000	Phorbol ester (an activator of PKC) attenuates the inhibitory effect of imipramine on the GR-induced gene transcription.	Imipramine	72-82	nuclear receptor subfamily 3 group C member 1	Homo sapiens	90-92
10957931-9	2000	Until further information is available, treatment with imipramine or trazodone has been shown to offer effective relief of chest pain for subgroups of patients with UCP.	Imipramine	55-65	uncoupling protein 1	Homo sapiens	165-168
10869387-3	2000	5-HT reuptake blockers (e.g., imipramine, paroxetine) also raised [(3)H]5-HT efflux, reaching approximately one-third of the maximal effect of the hSERT substrates.	Imipramine	30-40	solute carrier family 6 member 4	Homo sapiens	147-152
10693966-3	2000	5-HT reuptake blockers (e.g., imipramine, citalopram) also caused an enhancement of [3H]5-HT efflux, reaching about half the maximal effect of the rSERT substrates.	Imipramine	30-40	solute carrier family 6 member 4	Rattus norvegicus	147-152
10764890-5	2000	This paradoxical response to imipramine was significantly correlated with serum PRL (r = 0.59, p<0.01) but not with estradiol levels.	Imipramine	29-39	prolactin	Rattus norvegicus	80-83
10618463-0	1999	Neutrophil beta(2)-adrenoceptor function in major depression: G(s) coupling, effects of imipramine and relationship to treatment outcome.	Imipramine	88-98	adrenoceptor beta 2	Homo sapiens	11-31
10604946-10	2000	These results suggest that IFN-alpha centrally induces depression-like behavior in mice that can be alleviated with imipramine.	Imipramine	116-126	interferon alpha	Mus musculus	27-36
10764890-6	2000	These findings suggest that, at least in female rats submitted to the forced swimming model, PRL may induce reversed behavioral effects in response to imipramine, independently of circulating estrogen levels.	Imipramine	151-161	prolactin	Rattus norvegicus	93-96
10877531-1	2000	The involvement of alpha2-adrenoceptors in the antinociception induced by the tricyclic antidepressants amitriptyline and imipramine was investigated in mice by using the hot-plate and abdominal constriction tests.	Imipramine	122-132	adrenergic receptor, alpha 2a	Mus musculus	19-39
10877531-10	2000	On the basis of the above data, it can be postulated that amitriptyline and imipramine exerted their antinociceptive effect by activation of alpha2-adrenoceptors.	Imipramine	76-86	adrenergic receptor, alpha 2a	Mus musculus	141-161
11268375-8	2000	Chronic treatment with antidepressants (imipramine or fluoxetine) attenuated many of the behavioral effects of LPS, as well as LPS-induced changes in body temperature, adrenocortical activation, hypothalamic serotonin release, and the expression of splenic TNF-alpha mRNA.	Imipramine	40-50	tumor necrosis factor	Homo sapiens	257-266
10653987-6	2000	Furthermore, all the various hormone and drug ligands are mutually inhibitory in their binding to cytochrome P-450; e.g., K(i) values of androstenedione and progesterone, to inhibit imipramine binding to P-450 (determined by spectral analysis), are 11 nM and 26 nM, respectively.	Imipramine	182-192	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	98-117
10618463-4	1999	We investigated beta(2)-adrenoceptor coupling to G(s) protein in 25 controls, 23 major depressive disorder drug-free patients and 16 major depressive disorder patients after chronic imipramine treatment using agonist displacement experiments.	Imipramine	182-192	adrenoceptor beta 2	Homo sapiens	16-36
10624553-5	1999	RESULTS: Unaffected relatives manifested lower platelet 5-HTT function than control participants as revealed both by reduced number and diminished affinity of imipramine binding sites and diminished platelet 5-HT content.	Imipramine	159-169	solute carrier family 6 member 4	Homo sapiens	56-61
10618463-6	1999	Chronic imipramine induced beta(2)-adrenoceptor uncoupling.	Imipramine	8-18	adrenoceptor beta 2	Homo sapiens	27-47
10618463-8	1999	Beta(2)-adrenoceptor density decreased after imipramine treatment.	Imipramine	45-55	adrenoceptor beta 2	Homo sapiens	0-20
10618467-7	1999	The results of the time-course experiment demonstrated that the imipramine-induced decrease in the responsiveness of CA1 cells to DHPG was apparent after a 7-day treatment; there was a further decrease after 14 days of treatment to a level which was not changed by longer (21-day) administration of imipramine.	Imipramine	64-74	carbonic anhydrase 1	Rattus norvegicus	117-120
10618467-7	1999	The results of the time-course experiment demonstrated that the imipramine-induced decrease in the responsiveness of CA1 cells to DHPG was apparent after a 7-day treatment; there was a further decrease after 14 days of treatment to a level which was not changed by longer (21-day) administration of imipramine.	Imipramine	299-309	carbonic anhydrase 1	Rattus norvegicus	117-120
10618467-9	1999	It is concluded that repeated treatment with imipramine induces a decrease in the responsiveness of rat CA1 hippocampal neurons to group I mGlu receptor activation with a time course which correlates with the delayed onset of the therapeutic effect of antidepressants in humans.	Imipramine	45-55	carbonic anhydrase 1	Rattus norvegicus	104-107
10669046-0	1999	Influence of chronic treatment with imipramine on mRNA levels in rat brain: elevation of glyceraldehyde-3-phosphate dehydrogenase levels.	Imipramine	36-46	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	89-129
10606630-9	1999	Reduction of epidermal A-SMase activity by the inhibitor imipramine resulted in delayed permeability barrier repair after SC injury.	Imipramine	57-67	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-30
10625117-0	1999	Effect of imipramine on enkephalin-degrading peptidases.	Imipramine	10-20	proenkephalin	Rattus norvegicus	24-34
10625117-2	1999	In this work, we have measured the effect of imipramine on enkephalin-degrading peptidases in several rat brain areas.	Imipramine	45-55	proenkephalin	Rattus norvegicus	59-69
10625117-7	1999	These results suggest to us that enkephalin-degrading peptidases are involved in the acute and chronic action mechanism of imipramine and reinforce the idea that the central enkephalinergic activity is dynamically changed during the treatment of depressive illness.	Imipramine	123-133	proenkephalin	Rattus norvegicus	33-43
10669046-5	1999	Quantitative PCR showed that imipramine treatment significantly elevated the GAPDH/beta-actin ratio in the cortex.	Imipramine	29-39	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	77-82
10669046-5	1999	Quantitative PCR showed that imipramine treatment significantly elevated the GAPDH/beta-actin ratio in the cortex.	Imipramine	29-39	actin, beta	Rattus norvegicus	83-93
10669046-6	1999	These findings suggest that long-term treatment with imipramine stimulates GAPDH mRNA expression.	Imipramine	53-63	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	75-80
10612700-4	1999	Immobilisation for 1 h caused an approximately 60% increase in the number of dendritic processes undergoing NK(1) receptor endocytosis in the basolateral amygdala that was inhibited by acute pretreatment of animals with L-760,735 (3 mg/kg), but not by imipramine (10 mg/kg).	Imipramine	252-262	tachykinin receptor 1	Homo sapiens	108-122
10559392-0	1999	Block of an ether-a-go-go-like K(+) channel by imipramine rescues egl-2 excitation defects in Caenorhabditis elegans.	Imipramine	47-57	Uncharacterized protein	Caenorhabditis elegans	66-71
10559392-5	1999	We verified this by showing that EGL-2 currents are inhibited by imipramine.	Imipramine	65-75	Uncharacterized protein	Caenorhabditis elegans	33-38
10411572-1	1999	Cytochrome P-450 (CYP) 2C19 is responsible for the metabolism of a number of therapeutic agents such as S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine.	Imipramine	202-212	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-27
12609461-0	1999	Differential effect of a single high dose of the tricyclic antidepressant imipramine on interleukin-1beta and tumor necrosis factor-alpha secretion following an in vivo lipopolysaccharide challenge in rats.	Imipramine	74-84	interleukin 1 beta	Rattus norvegicus	88-137
12609461-6	1999	The results demonstrated that imipramine pretreatment inhibits LPS-induced increases in serum concentrations of the proinflammatory cytokine, tumor necrosis factor (TNF)-alpha both 3 and 6 h, following administration.	Imipramine	30-40	tumor necrosis factor	Rattus norvegicus	142-175
12609461-10	1999	Furthermore, the suppressive effects of imipramine on LPS-induced TNF-alpha secretion could not be attributed to either increased glucocorticoid levels, or increased secretion of the antiinflammatory cytokine IL-10.	Imipramine	40-50	tumor necrosis factor	Rattus norvegicus	66-75
10534316-12	1999	Taken together, the results indicated that CYP3A7 was the major if not sole isoform responsible for catalysis of the N-demethylation of imipramine in human hepatic tissues during embryogenesis.	Imipramine	136-146	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	43-49
10580379-3	1999	Imipramine inhibited MAO-B more potently than MAO-A activity in mouse and rat brains.	Imipramine	0-10	monoamine oxidase B	Mus musculus	21-26
10580379-4	1999	When dog and monkey brains were investigated, MAO-A activity was inhibited more potently than MAO-B activity at high concentrations of imipramine, while at low concentrations, MAO-B activity was more potently inhibited.	Imipramine	135-145	monoamine oxidase A	Canis lupus familiaris	46-51
10580379-4	1999	When dog and monkey brains were investigated, MAO-A activity was inhibited more potently than MAO-B activity at high concentrations of imipramine, while at low concentrations, MAO-B activity was more potently inhibited.	Imipramine	135-145	monoamine oxidase B	Canis lupus familiaris	94-99
20654512-0	1999	Imipramine for Cytochrome P450 Activity Determination: a Multiple-species Metabolic Probe.	Imipramine	0-10	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-30
20654512-6	1999	To conclude, the metabolic profile of imipramine can be used to reveal a number of cytochrome P450 enzymes active in microsomal fractions.	Imipramine	38-48	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	83-98
10401680-0	1999	Imipramine- and mianserin-induced acute cell injury in primary cultured rat hepatocytes: implication of different cytochrome P450 enzymes.	Imipramine	0-10	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-129
10445381-0	1999	The effect of arginine-428 mutation on modulation of activity of human liver flavin monooxygenase 3 (FMO3) by imipramine and chlorpromazine.	Imipramine	110-120	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	77-99
10445381-0	1999	The effect of arginine-428 mutation on modulation of activity of human liver flavin monooxygenase 3 (FMO3) by imipramine and chlorpromazine.	Imipramine	110-120	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	101-105
10445381-1	1999	This study was carried out to investigate the molecular basis for modulation of recombinant FMO3-catalyzed activity by the tricyclic antidepressants, imipramine and chlorpromazine.	Imipramine	150-160	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	92-96
10445381-5	1999	Imipramine modulated the activities of the native and T428R human FMO3s differently; the activity of the native FMO3 was increased at all concentrations, whereas the activity of the mutant enzyme was inhibited at concentrations above 300 microM.	Imipramine	0-10	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	66-70
10445381-5	1999	Imipramine modulated the activities of the native and T428R human FMO3s differently; the activity of the native FMO3 was increased at all concentrations, whereas the activity of the mutant enzyme was inhibited at concentrations above 300 microM.	Imipramine	0-10	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	112-116
10401680-7	1999	These findings indicated that CYP-mediated metabolic activation was involved in acute cell injury induced by the antidepressants; namely a CYP2D enzyme(s), which is deficient in Dark Agouti rats, and a male specific CYP enzyme(s) were suggested to be responsible for the cytotoxicity of imipramine and mianserin, respectively.	Imipramine	287-297	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-33
9861783-4	1998	RESULTS: The results showed that Imipramine (IMIP), a tricyclic antidepressant (TCA), decreased the TRH content in a dose-dependent manner (from 80.7 +/- 4.9, at 10(-9) mol/L, to 14.1 +/- 0.6, at 10(-5) mol/L, fmol/well; P < 0.05).	Imipramine	33-43	thyrotropin releasing hormone	Rattus norvegicus	100-103
10487422-0	1999	The antidepressants imipramine, clomipramine, and citalopram induce apoptosis in human acute myeloid leukemia HL-60 cells via caspase-3 activation.	Imipramine	20-30	caspase 3	Homo sapiens	126-135
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	caspase 3	Homo sapiens	165-174
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	caspase 3	Homo sapiens	175-184
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	poly(ADP-ribose) polymerase 1	Homo sapiens	239-266
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	poly(ADP-ribose) polymerase 1	Homo sapiens	268-272
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	caspase 3	Homo sapiens	175-184
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	caspase 3	Homo sapiens	308-313
10487422-4	1999	Treatment with apoptosis-inducing concentrations of the antidepressants (80 microM imipramine, 35 microM clomipramine, or 220 microM citalopram) caused induction of caspase-3/caspase-3-like activity, which was monitored by the cleavage of poly(ADP-ribose) polymerase (PARP), the loss of the 32 kD caspase-3 (CPP32) precursor, and the cleavage of the fluorescent CPP32-like substrate PhiPhiLux.	Imipramine	83-93	caspase 3	Homo sapiens	362-367
10025677-1	1999	The induction of the early gene c-fos was evaluated through Fos immunohistochemistry in areas belonging to the extended amygdala after acute administration of two antidepressants, citalopram and imipramine.	Imipramine	195-205	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
10025677-2	1999	Both citalopram and imipramine at the dose of 5 and 20 mg/kg, respectively, induced Fos-like immunoreactivity (FLI) in the central amygdaloid nucleus, lateral division of the bed nucleus of the stria terminalis (BSTL), and interstitial nucleus of the posterior limb of the anterior commissure (IPAC).	Imipramine	20-30	FLII actin remodeling protein	Homo sapiens	84-109
10025677-2	1999	Both citalopram and imipramine at the dose of 5 and 20 mg/kg, respectively, induced Fos-like immunoreactivity (FLI) in the central amygdaloid nucleus, lateral division of the bed nucleus of the stria terminalis (BSTL), and interstitial nucleus of the posterior limb of the anterior commissure (IPAC).	Imipramine	20-30	FLII actin remodeling protein	Homo sapiens	111-114
10025677-3	1999	The shell of the nucleus accumbens, which forms a continuum with the central extended amygdala, showed a decrease of FLI after administration of either citalopram or imipramine.	Imipramine	166-176	FLII actin remodeling protein	Homo sapiens	117-120
9861783-4	1998	RESULTS: The results showed that Imipramine (IMIP), a tricyclic antidepressant (TCA), decreased the TRH content in a dose-dependent manner (from 80.7 +/- 4.9, at 10(-9) mol/L, to 14.1 +/- 0.6, at 10(-5) mol/L, fmol/well; P < 0.05).	Imipramine	45-49	thyrotropin releasing hormone	Rattus norvegicus	100-103
9861783-8	1998	IMIP, DESIP and FLUO at 10(-6) mol/L reduced the TRH response to glucocorticoid stimulation (36.4 +/- 4.0, 56.6 +/- 2.4, 23.75 +/- 4.0, respectively vs 107 +/- 7.5 fmol/well; P < 0.05).	Imipramine	0-4	thyrotropin releasing hormone	Rattus norvegicus	49-52
9923577-11	1998	CONCLUSIONS: Fluvoxamine is a fairly potent inhibitor of CYP2C19 and it has the potential for causing drug-drug interactions with substrates for CYP2C19 such as imipramine, clomipramine, amitriptyline and diazepam.	Imipramine	161-171	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
9868741-1	1998	The selective serotonin re-uptake inhibitor, fluvoxamine, is a very potent inhibitor of CYP1A2, and accordingly causes pharmacokinetic interactions with drugs metabolised by CYP1A2, such as caffeine, theophylline, imipramine, tacrine and clozapine.	Imipramine	214-224	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	88-94
9868741-1	1998	The selective serotonin re-uptake inhibitor, fluvoxamine, is a very potent inhibitor of CYP1A2, and accordingly causes pharmacokinetic interactions with drugs metabolised by CYP1A2, such as caffeine, theophylline, imipramine, tacrine and clozapine.	Imipramine	214-224	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	174-180
9832351-4	1998	Using the human neuroblastoma cell line IMR32 we demonstrate a GBR-12909 and cocaine-sensitive specific uptake of dopamine, whereas dopamine uptake in platelets is performed by an imipramine-sensitive serotonin transporter.	Imipramine	180-190	solute carrier family 6 member 4	Homo sapiens	201-222
9750169-2	1998	Imipramine activates FMO3-catalyzed metabolism of methimazole at all substrate concentrations tested.	Imipramine	0-10	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	21-25
9750169-4	1998	The response of FMO3 is also unique in that chlorpromazine is markedly more effective as a modulator than is imipramine.	Imipramine	109-119	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	16-20
9845280-0	1998	Imipramine inhibits soluble enkephalin-degrading aminopeptidase activity in vitro.	Imipramine	0-10	proenkephalin	Rattus norvegicus	28-38
9845280-2	1998	Imipramine in vitro inhibits the enkephalin-degrading aminopeptidase MII and interacts with the enzyme in a mixed competitive-noncompetitive manner.	Imipramine	0-10	proenkephalin	Rattus norvegicus	33-43
9845280-3	1998	The present work shows that imipramine in vitro also inhibits reversibly soluble enkephalin-degrading aminopeptidase activity in rat brain.	Imipramine	28-38	proenkephalin	Rattus norvegicus	81-91
9792215-8	1998	AChE activity was altered by imipramine (1.0-2.0 mM) and by diazepam (0.5-2.0 mM).	Imipramine	29-39	acetylcholinesterase	Rattus norvegicus	0-4
9724254-6	1998	min-1), Na+-dependent mechanism that was inhibited by chlorimipramine > imipramine > fluoxetine > desipramine > zimelidine.	Imipramine	59-69	CD59 molecule (CD59 blood group)	Homo sapiens	0-5
9558327-0	1998	Identification of amino acid residues associated with modulation of flavin-containing monooxygenase (FMO) activity by imipramine: structure/function studies with FMO1 from pig and rabbit.	Imipramine	118-128	flavin containing dimethylaniline monoxygenase 1	Sus scrofa	162-166
9754440-5	1998	When all four brain regions were taken together, a down-regulation was noted between presynaptic [3H]imipramine binding and the postsynaptic 5-HT2A receptor (r = -0.40; P = 0.0013) in the control group.	Imipramine	101-111	5-hydroxytryptamine receptor 2A	Homo sapiens	141-156
9770644-8	1998	Conversely, imipramine treatment produced widespread reductions in epsilon 2-subunit mRNA levels (e.g., in cortex, CA1-4 of hippocampus, and amygdala), whereas the effects of citalopram on levels of this transcript were largely restricted to amygdala.	Imipramine	12-22	carbonic anhydrase 1	Mus musculus	115-118
9709400-5	1998	RESULTS: Imipramine (1 and 5 microM) strongly inhibited INa.	Imipramine	9-19	internexin neuronal intermediate filament protein alpha	Homo sapiens	56-59
9709400-11	1998	CONCLUSIONS: Alkalinization antagonizes the INa-blocking action of imipramine by promoting unbinding from the receptor.	Imipramine	67-77	internexin neuronal intermediate filament protein alpha	Homo sapiens	44-47
9776709-5	1998	Clomipramine and imipramine reduced the numbers of Th1 cells secreting IFN-gamma in response to the neuritogenic myelin proteins BPM, P0 and P2 among lymph node mononuclear cells (MNC) from rats with EAN.	Imipramine	17-27	interferon gamma	Rattus norvegicus	71-80
9776709-7	1998	The action of clomipramine and imipramine on induced IFN-gamma and anti-myelin antibodies suggests that the mechanism for the suppressive effect of those substances on EAN symptoms may be due to an action on myelin T and B cell autoreactivity.	Imipramine	31-41	interferon gamma	Rattus norvegicus	53-62
9711811-9	1998	Methimazole, imipramine and thiobenzamide are much better substrates for FMO1 than for FMO3 or FMO5.	Imipramine	13-23	flavin containing monooxygenase 1	Mus musculus	73-77
9711811-9	1998	Methimazole, imipramine and thiobenzamide are much better substrates for FMO1 than for FMO3 or FMO5.	Imipramine	13-23	flavin containing monooxygenase 3	Mus musculus	87-91
9711811-9	1998	Methimazole, imipramine and thiobenzamide are much better substrates for FMO1 than for FMO3 or FMO5.	Imipramine	13-23	flavin containing monooxygenase 5	Mus musculus	95-99
9603221-0	1998	Distinct effects of imipramine on 5-hydroxytryptamine uptake mediated by the recombinant rat serotonin transporter SERT1.	Imipramine	20-30	Sertoli cell protein 1	Rattus norvegicus	115-120
9603221-2	1998	Here, we show that both the tricyclic antidepressant imipramine and the nontricyclic antidepressant citalopram competitively inhibit 5-HT transport mediated by the recombinant rat 5-HT transporter SERT1.	Imipramine	53-63	solute carrier family 6 member 4	Rattus norvegicus	180-196
9603221-2	1998	Here, we show that both the tricyclic antidepressant imipramine and the nontricyclic antidepressant citalopram competitively inhibit 5-HT transport mediated by the recombinant rat 5-HT transporter SERT1.	Imipramine	53-63	Sertoli cell protein 1	Rattus norvegicus	197-202
9603221-6	1998	Occupation of the high-affinity imipramine binding site on SERT1 did not affect 5-HT transport but allosterically displaced citalopram from the substrate recognition site.	Imipramine	32-42	Sertoli cell protein 1	Rattus norvegicus	59-64
9603221-9	1998	Thus, depending on which of its binding sites on SERT1 is occupied, imipramine may exert distinct effects on 5-HT uptake mediated by the recombinant rat 5-HT transporter.	Imipramine	68-78	Sertoli cell protein 1	Rattus norvegicus	49-54
9603221-9	1998	Thus, depending on which of its binding sites on SERT1 is occupied, imipramine may exert distinct effects on 5-HT uptake mediated by the recombinant rat 5-HT transporter.	Imipramine	68-78	solute carrier family 6 member 4	Rattus norvegicus	153-169
9558327-3	1998	Imipramine activates methimazole metabolism catalyzed by rabbit FMO1 or FMO2 at methimazole concentrations greater than 50 or 100 microM, respectively, and inhibits at lower methimazole concentrations.	Imipramine	0-10	dimethylaniline monooxygenase [N-oxide-forming] 1	Oryctolagus cuniculus	64-68
9558327-3	1998	Imipramine activates methimazole metabolism catalyzed by rabbit FMO1 or FMO2 at methimazole concentrations greater than 50 or 100 microM, respectively, and inhibits at lower methimazole concentrations.	Imipramine	0-10	dimethylaniline monooxygenase [N-oxide-forming] 2	Oryctolagus cuniculus	72-76
9558327-6	1998	In contrast, imipramine inhibits the metabolism of methimazole catalyzed by pig FMO1 at all substrate concentrations.	Imipramine	13-23	flavin containing dimethylaniline monoxygenase 1	Sus scrofa	80-84
9558327-7	1998	The structural basis for this unique ortholog difference between the responses of rabbit and pig FMO1 to imipramine was studied by random chimeragenesis and site-directed mutagenesis.	Imipramine	105-115	flavin containing dimethylaniline monoxygenase 1	Sus scrofa	97-101
9558327-8	1998	Results with chimeras indicated that modulation of FMO1 activity by imipramine is controlled to a great extent by two areas of the FMO primary structure (residues 381-432 and 433-465).	Imipramine	68-78	flavin containing dimethylaniline monoxygenase 1	Sus scrofa	51-55
9558327-11	1998	Our results suggest that the response of FMO1 to imipramine involves a distribution between two sites that is regulated by structural features that do not alter the overall binding.	Imipramine	49-59	flavin containing dimethylaniline monoxygenase 1	Sus scrofa	41-45
9564441-10	1998	The decreases in 5-HT1A mRNA and binding, as well as the MR/GR alterations, were prevented in animals that received imipramine or desipramine antidepressant treatment.	Imipramine	116-126	5-hydroxytryptamine receptor 1A	Rattus norvegicus	17-23
9490065-7	1998	In liver microsomes, the demethylation of imipramine was essentially due to CYP1A2 and to a smaller extent to CYP3A.	Imipramine	42-52	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	76-82
9625487-0	1998	Kinetic interaction between fluoxetine and imipramine as a function of elevated serum alpha-1-acid glycoprotein levels.	Imipramine	43-53	nitrogen permease regulator-like 3	Mus musculus	86-111
9625487-1	1998	The effect of elevated serum alpha-1-acid glycoprotein (AAG) levels on the pharmacokinetic interaction between imipramine and fluoxetine has been examined by utilizing a novel strain of transgenic mice which express serum AAG levels several times greater than normal.	Imipramine	111-121	nitrogen permease regulator-like 3	Mus musculus	56-59
9625487-8	1998	These findings indicate that the extent of increases in imipramine and desipramine serum and brain levels are greater during elevated serum AAG states than during normal AAG states when imipramine is co-administered with fluoxetine.	Imipramine	56-66	nitrogen permease regulator-like 3	Mus musculus	140-143
9625487-8	1998	These findings indicate that the extent of increases in imipramine and desipramine serum and brain levels are greater during elevated serum AAG states than during normal AAG states when imipramine is co-administered with fluoxetine.	Imipramine	56-66	nitrogen permease regulator-like 3	Mus musculus	170-173
9519934-4	1998	In the patients with depression, 5 months of treatment with imipramine and/or nortriptyline significantly reduced EPO concentrations in the CSF (1.56+/-0.34 mU/ mL, P < 0.01).	Imipramine	60-70	erythropoietin	Homo sapiens	114-117
9535010-6	1998	Radioligand binding studies with the D2 receptor agonist, [3H]-N-0437, indicated, that following imipramine administration, the affinity of the agonist for the D2 dopamine receptor significantly increased, though without any alterations in the Bmax.	Imipramine	97-107	dopamine receptor D2	Rattus norvegicus	160-180
9490065-7	1998	In liver microsomes, the demethylation of imipramine was essentially due to CYP1A2 and to a smaller extent to CYP3A.	Imipramine	42-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-115
9490065-8	1998	In fetuses and early neonates, CYP3A proteins were responsible for the low demethylation of imipramine (3-4% of the adult activity) before the onset of CYP1A2 and the subsequent rise of activity.	Imipramine	92-102	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-36
9459570-0	1998	Effects of phenelzine and imipramine on the steady-state levels of mRNAs that encode glutamic acid decarboxylase (GAD67 and GAD65), the GABA transporter GAT-1 and GABA transaminase in rat cortex.	Imipramine	26-36	glutamate decarboxylase 1	Rattus norvegicus	114-119
9504424-5	1998	Although the expressed dog CYP2D15 showed high catalytic activity for the hydroxylations of bunitrolol and imipramine at low substrate concentration (10 microM), the catalytic activity for that of debrisoquine (50 microM) was extremely low as compared with that of CYP2D from other species.	Imipramine	107-117	cytochrome P450 2D15	Canis lupus familiaris	27-34
9504424-5	1998	Although the expressed dog CYP2D15 showed high catalytic activity for the hydroxylations of bunitrolol and imipramine at low substrate concentration (10 microM), the catalytic activity for that of debrisoquine (50 microM) was extremely low as compared with that of CYP2D from other species.	Imipramine	107-117	cytochrome P450 2D15	Canis lupus familiaris	27-32
9504424-7	1998	In addition, the expressed CYP2D showed high catalytic activity for imipramine N-demethylation.	Imipramine	68-78	cytochrome P450 2D15	Canis lupus familiaris	27-32
9459570-0	1998	Effects of phenelzine and imipramine on the steady-state levels of mRNAs that encode glutamic acid decarboxylase (GAD67 and GAD65), the GABA transporter GAT-1 and GABA transaminase in rat cortex.	Imipramine	26-36	glutamate decarboxylase 2	Rattus norvegicus	124-129
9452181-2	1997	In this test, a reduction of duration of immobility after treatment with imipramine is obtained in mice of the NMRI strain but not of the CD1 strain.	Imipramine	73-83	CD1 antigen complex	Mus musculus	138-141
9481618-9	1997	The observation that chronic, but not acute treatment with imipramine and electroconvulsive shock produces a region-specific change in the levels of mRNA encoding cytochrome b suggests that this enzyme may be involved in the sequence of events resulting in an antidepressant action.	Imipramine	59-69	cytochrome b, mitochondrial	Mus musculus	163-175
9452183-9	1997	5-HT1A autoreceptors in the raphe nuclei, which this study suggests to be tonically active, may be stimulated after systemic administration of high doses of imipramine.	Imipramine	157-167	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-6
9351907-6	1997	Other substrates of CYP1A2, such as phenacetin, imipramine, caffeine, and estradiol, are also inhibitors of flutamide metabolism by CYP1A2.	Imipramine	48-58	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	20-26
9351907-6	1997	Other substrates of CYP1A2, such as phenacetin, imipramine, caffeine, and estradiol, are also inhibitors of flutamide metabolism by CYP1A2.	Imipramine	48-58	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	132-138
9566055-0	1997	Influence of imipramine treatment on the group I of metabotropic glutamate receptors in CA1 region of hippocampus.	Imipramine	13-23	carbonic anhydrase 1	Rattus norvegicus	88-91
9316857-8	1997	P450 ML2d had the oxidation activities for the rat CYP2D-substrates, such as propranolol 4-hydroxylation and imipramine 2-hydroxylation, in higher rates than those of the microsomes, but did not exhibit debrisoquine 4-hydroxylase activity.	Imipramine	109-119	cytochrome P450, 2d region	Mus musculus	51-56
9505989-3	1997	Imipramine pharmacokinetics serve as a marker for hepatic CYP2D6, CYP1A2, CYP3A activity.	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	58-64
9505989-3	1997	Imipramine pharmacokinetics serve as a marker for hepatic CYP2D6, CYP1A2, CYP3A activity.	Imipramine	0-10	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	66-72
9505989-3	1997	Imipramine pharmacokinetics serve as a marker for hepatic CYP2D6, CYP1A2, CYP3A activity.	Imipramine	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-79
9512923-2	1997	Imipramine possesses such characteristics and is both a substrate and an inhibitor of the CYP2D6 enzyme.	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
9512923-4	1997	Imipramine inhibited the 1"-hydroxylation of bufuralol (10 microM), an in vitro marker of CYP2D6 activity, in a CYP2D6 cell line (IC50 = 2.4 microM).	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
9512923-4	1997	Imipramine inhibited the 1"-hydroxylation of bufuralol (10 microM), an in vitro marker of CYP2D6 activity, in a CYP2D6 cell line (IC50 = 2.4 microM).	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
9566035-0	1997	Imipramine induces alterations in proenkephalin and prodynorphin mRNAs level in the nucleus accumbens and striatum in the rat.	Imipramine	0-10	proenkephalin	Rattus norvegicus	34-47
9258093-11	1997	CONCLUSIONS: Imipramine has a vasopressin independent antidiuretic effect if nocturnal polyuria is present.	Imipramine	13-23	arginine vasopressin	Homo sapiens	30-41
9566035-2	1997	In this study, we evaluated effects of single and repeated imipramine administration on proenkephalin and prodynorphin gene expression in the rat nucleus accumbens and striatum.	Imipramine	59-69	proenkephalin	Rattus norvegicus	88-101
9566034-1	1997	The effects of repeated treatment with imipramine on the reactivity of CA1 neurons in the rat hippocampus to the 5-HT4 receptor agonist zacopride and the direct adenylate cyclase activator forskolin were compared ex vivo to assess whether a modulation of signal transduction pathway may contribute to the antidepressant-induced adaptive changes in the responsiveness of pyramidal neurons to 5-HT4 receptor activation.	Imipramine	39-49	carbonic anhydrase 1	Rattus norvegicus	71-74
9264550-7	1997	In addition, UGT1A7l possesses catalytic activity toward tertiary amines like the tricyclic antidepressant imipramine.	Imipramine	107-117	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	13-19
9566034-6	1997	It is concluded that the reduction in the responsiveness of CA1 cells to zacopride, induced by repeated administration of imipramine, may be due to modifications of the signal transduction pathway, i.e. adenylate cyclase and protein kinase A, which is responsible for the 5-HT4 receptor-mediated decrease in the activity of potassium channels.	Imipramine	122-132	carbonic anhydrase 1	Rattus norvegicus	60-63
9324197-6	1997	Imipramine is metabolized in the liver by the cytochrome P-450 (CYP 1A2) system, and barbiturates are known inducers of this enzyme subset.	Imipramine	0-10	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	46-71
9316174-0	1997	Effects of genetic defects in the CYP2C19 gene on the N-demethylation of imipramine, and clinical outcome of imipramine therapy.	Imipramine	73-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
9361724-0	1997	Chronic imipramine treatment-induced changes in acetylcholinesterase (EC 3.1.1.7) activity in discrete rat brain regions.	Imipramine	8-18	acetylcholinesterase	Rattus norvegicus	48-68
9361724-8	1997	Membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) after chronic imipramine treatment was significantly decreased in the hippocampus (control = 188.8 +/- 19.4, imipramine = 154.4 +/- 7.5, P < 0.005) and striatum (control = 850.9 +/- 59.6, imipramine = 742.5 +/- 34.7, P < 0.005).	Imipramine	90-100	acetylcholinesterase	Rattus norvegicus	15-21
9361724-8	1997	Membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) after chronic imipramine treatment was significantly decreased in the hippocampus (control = 188.8 +/- 19.4, imipramine = 154.4 +/- 7.5, P < 0.005) and striatum (control = 850.9 +/- 59.6, imipramine = 742.5 +/- 34.7, P < 0.005).	Imipramine	185-195	acetylcholinesterase	Rattus norvegicus	15-21
9361724-8	1997	Membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) after chronic imipramine treatment was significantly decreased in the hippocampus (control = 188.8 +/- 19.4, imipramine = 154.4 +/- 7.5, P < 0.005) and striatum (control = 850.9 +/- 59.6, imipramine = 742.5 +/- 34.7, P < 0.005).	Imipramine	185-195	acetylcholinesterase	Rattus norvegicus	15-21
9253341-2	1997	Although chronic administration of imipramine to experimental animals significantly decreases CRH messenger RNA levels in the paraventricular nucleus, it is generally thought that resolution of hypercortisolism following recovery from depression is related to the improvement in mood and decrease in anxiety that accompanies recovery rather than an intrinsic effect of imipramine.	Imipramine	35-45	corticotropin releasing hormone	Homo sapiens	94-97
9253341-5	1997	Imipramine was associated with decreased responses in peak ACTH and cortisol to ovine CRH and in peak ACTH to arginine vasopressin (P = 0.02, P = 0.003, and P = 0.02, respectively) without changes in indices of basal HPA axis function.	Imipramine	0-10	corticotropin releasing hormone	Homo sapiens	86-89
9253341-5	1997	Imipramine was associated with decreased responses in peak ACTH and cortisol to ovine CRH and in peak ACTH to arginine vasopressin (P = 0.02, P = 0.003, and P = 0.02, respectively) without changes in indices of basal HPA axis function.	Imipramine	0-10	arginine vasopressin	Homo sapiens	119-130
9278210-1	1997	AIMS: In vitro data indicate that imipramine (IMI), a widely used tricyclic antidepressant drug, is N-demethylated by several isoforms of cytochrome P450, which include CYP3A4.	Imipramine	34-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	169-175
9278210-1	1997	AIMS: In vitro data indicate that imipramine (IMI), a widely used tricyclic antidepressant drug, is N-demethylated by several isoforms of cytochrome P450, which include CYP3A4.	Imipramine	46-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	169-175
9316174-0	1997	Effects of genetic defects in the CYP2C19 gene on the N-demethylation of imipramine, and clinical outcome of imipramine therapy.	Imipramine	109-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
9316174-1	1997	The relationship between the genetic polymorphism of S-mephenytoin 4"-hydroxylation catalyzed by CYP2C19 and the N-demethylation of imipramine was examined in 10 Japanese depressed patients.	Imipramine	132-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
9316174-6	1997	This suggests that the N-demethylation of imipramine is impaired in patients with genetic defects in the CYP2C19 gene, and that genotype determination may be useful in preventing side effects induced by unexpectedly elevated levels of imipramine.	Imipramine	42-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
9316174-6	1997	This suggests that the N-demethylation of imipramine is impaired in patients with genetic defects in the CYP2C19 gene, and that genotype determination may be useful in preventing side effects induced by unexpectedly elevated levels of imipramine.	Imipramine	235-245	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Imipramine	154-164	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
9207145-5	1997	These results indicate that serine-545 is a crucial determinant of both the cation dependence of serotonin transport by SERT and the imipramine binding properties of SERT.	Imipramine	133-143	solute carrier family 6 member 4	Rattus norvegicus	166-170
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Imipramine	154-164	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-37
9242843-4	1997	Venlafaxine was significantly superior to both imipramine and placebo for the SARS total score and the items "social/leisure" and "extended family."	Imipramine	47-57	seryl-tRNA synthetase 1	Homo sapiens	78-82
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	72-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9226733-0	1997	Effect of imipramine treatments on the 5-HT1A-receptor-mediated inhibition of panic-like behaviours in rats.	Imipramine	10-20	5-hydroxytryptamine receptor 1A	Rattus norvegicus	39-45
9226733-5	1997	In contrast, long-term treatment with imipramine enhanced the 5-HT1A-mediated inhibition, as the decrement in the amplitude of the flight response produced by 8-OH-DPAT was 96% after this treatment compared to 41% in controls.	Imipramine	38-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	62-68
9226733-9	1997	It is suggested that an alteration at the level of the DPAG-5-HT1A receptor system is implicated in the therapeutic and withdrawal effect of imipramine in panic disorder.	Imipramine	141-151	5-hydroxytryptamine receptor 1A	Rattus norvegicus	60-66
9205822-0	1997	Venlafaxine: in vitro inhibition of CYP2D6 dependent imipramine and desipramine metabolism; comparative studies with selected SSRIs, and effects on human hepatic CYP3A4, CYP2C9 and CYP1A2.	Imipramine	53-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	36-42
9205822-1	1997	AIMS: In order to anticipate drug-interactions of potential clinical significance the ability of the novel antidepressant, venlafaxine, to inhibit CYP2D6 dependent imipramine and desipramine 2-hydroxylation was investigated in human liver microsomes.	Imipramine	164-174	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	147-153
9205822-5	1997	The inhibitory effect of imipramine and desipramine on liver microsomal CYP2D6 dependent venlafaxine O-demethylation was determined similarly.	Imipramine	25-35	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-78
9205822-10	1997	Imipramine and desipramine gave marked inhibition of CYP2D6 dependent venlafaxine O-demethylase activity (Ki values of 3.9 +/- 1.7 and 1.7 +/- 0.9 microM, respectively).	Imipramine	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	60-70	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	60-70	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	60-70	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	202-205
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	72-75	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	72-75	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
9190854-1	1997	Cytochrome P450 (CYP) involved in the two major pathways of imipramine (IMI) was reappraised using human liver microsomes phenotyped for S-mephenytoin 4"-hydroxylation in vitro and 11 recombinant human CYP isoforms.	Imipramine	72-75	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	202-205
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	72-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	332-337
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	291-301	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9088587-6	1997	CONCLUSIONS: These findings indicate that ketoconazole, a relatively specific inhibitor of CYP3A4, inhibits the N-demethylation of imipramine without affecting the 2-hydroxylation of imipramine and desipramine.	Imipramine	131-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
9084457-0	1997	Imipramine demethylation in vivo: impact of CYP1A2, CYP2C19, and CYP3A4.	Imipramine	0-10	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-50
9084457-0	1997	Imipramine demethylation in vivo: impact of CYP1A2, CYP2C19, and CYP3A4.	Imipramine	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Imipramine	83-93	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	118-124
9084457-0	1997	Imipramine demethylation in vivo: impact of CYP1A2, CYP2C19, and CYP3A4.	Imipramine	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Imipramine	83-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
9465283-8	1996	Treatment with imipramine decreased auditory P300 latencies and increased auditory P300 amplitudes.	Imipramine	15-25	E1A binding protein p300	Homo sapiens	83-87
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Imipramine	83-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	139-145
9076656-6	1997	Mouse FMO1 expressed in yeast showed activities of thiobenzamide S-oxidation, and NADPH oxidation associated with the S- or N-oxidation of chlorpromazine, N,N-dimethylaniline, N,N-dimethyl-hydrazine, imipramine, nicotine, thioacetamide, thiourea and trimethylamine.	Imipramine	200-210	flavin containing monooxygenase 1	Mus musculus	6-10
20654293-4	1997	Optimal concentrations for the formation of these structures were 20 muM for clomipramine and 40 muM for imipramine.	Imipramine	105-115	latexin	Homo sapiens	97-100
9395259-0	1997	Interaction mechanisms of imipramine and desipramine with enkephalin-degrading aminopeptidases in vitro.	Imipramine	26-36	proenkephalin	Rattus norvegicus	58-68
9395259-3	1997	In this sense, imipramine treatment in vivo increases the enkephalin levels, and this effect is enhanced by inhibitors of enkephalin-degrading enzymes.	Imipramine	15-25	proenkephalin	Rattus norvegicus	58-68
9395259-3	1997	In this sense, imipramine treatment in vivo increases the enkephalin levels, and this effect is enhanced by inhibitors of enkephalin-degrading enzymes.	Imipramine	15-25	proenkephalin	Rattus norvegicus	122-132
9395259-4	1997	The present work shows the effects in vitro of imipramine and its active metabolite desipramine on the activities of two membrane-bound enkephalin-degrading aminopeptidases present in rat brain.	Imipramine	47-57	proenkephalin	Rattus norvegicus	136-146
8910433-6	1996	Furthermore, the CYP2D18-expressed COS cell lysate showed N-demethylation activity toward imipramine, whereas another brain P-450 CYP4F6-expressed COS cell lysate showed 10-hydroxylation activity.	Imipramine	90-100	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	17-24
9465283-10	1996	Thus, P300 topography and latency classifies ADHD into three groups: group 1 with normal P300 topography, and good response to pemoline; group 2 with small right frontocentral auditory P300 amplitudes, poor response to pemoline, and good response to imipramine; and group 3 with long auditory and visual P300 latencies and small right frontocentral auditory P300 amplitudes, and poor response to pemoline and imipramine.	Imipramine	250-260	E1A binding protein p300	Homo sapiens	6-10
9465283-10	1996	Thus, P300 topography and latency classifies ADHD into three groups: group 1 with normal P300 topography, and good response to pemoline; group 2 with small right frontocentral auditory P300 amplitudes, poor response to pemoline, and good response to imipramine; and group 3 with long auditory and visual P300 latencies and small right frontocentral auditory P300 amplitudes, and poor response to pemoline and imipramine.	Imipramine	409-419	E1A binding protein p300	Homo sapiens	6-10
9364202-0	1997	Chronic imipramine treatment downregulates IR1-imidazoline receptors in rat brainstem.	Imipramine	8-18	nischarin	Rattus norvegicus	43-46
9364202-5	1997	Herein, the prototypic antidepressant, imipramine (IMI), has been studied in regard to its treatment effects on [125I]p-iodoclonidine binding to both alpha 2 AR and IR1 in rat brainstem membranes.	Imipramine	39-49	nischarin	Rattus norvegicus	150-168
9364202-5	1997	Herein, the prototypic antidepressant, imipramine (IMI), has been studied in regard to its treatment effects on [125I]p-iodoclonidine binding to both alpha 2 AR and IR1 in rat brainstem membranes.	Imipramine	51-54	nischarin	Rattus norvegicus	150-168
9413893-7	1997	Chlorpromazine, imipramine, fluoxetine, doxepin, amitriptyline and hydroxyzine used in the practice of dermatology may exert their therapeutic effects by modulating skin PKC activity.	Imipramine	16-26	proline rich transmembrane protein 2	Homo sapiens	170-173
8949923-0	1996	In vitro metabolism of imipramine by brain microsomes: effects of inhibitors and exogenous cytochrome P450 reductase.	Imipramine	23-33	cytochrome p450 oxidoreductase	Rattus norvegicus	91-116
8949923-6	1996	Results from studies on the incorporation of cytochrome P450 reductase into the brain microsomal system reveal a reductase concentration-dependent increase in imipramine metabolism and suggest that the reductase level in brain is an important factor for the study of catalytic activities in brain microsomal systems.	Imipramine	159-169	cytochrome p450 oxidoreductase	Rattus norvegicus	45-70
9465283-0	1996	Prolonged P300 latency in attention deficit hyperactivity disorder predicts poor response to imipramine.	Imipramine	93-103	E1A binding protein p300	Homo sapiens	10-14
9465283-7	1996	Poor imipramine responders had longer auditory and visual P300 latencies than good responders.	Imipramine	5-15	E1A binding protein p300	Homo sapiens	58-62
9465283-8	1996	Treatment with imipramine decreased auditory P300 latencies and increased auditory P300 amplitudes.	Imipramine	15-25	E1A binding protein p300	Homo sapiens	45-49
8923121-5	1996	Also, concurrent inhibition of the 5-HT and noradrenaline transporters with 20 mg/kg imipramine increases cortical extracellular 5-HT concentration more than SSRI doses which maximally block the 5-HT transporter.	Imipramine	85-95	solute carrier family 6 member 4	Homo sapiens	195-211
8863842-2	1996	Previously, using chimeric proteins, we determined that domains or residues distal to transmembrane domain 11 (amino acid 531) dictate the increased sensitivity of human SERT to imipramine.	Imipramine	178-188	solute carrier family 6 member 4	Homo sapiens	170-174
8893267-0	1996	Steady-state kinetics of imipramine in transgenic mice with elevated serum AAG levels.	Imipramine	25-35	nitrogen permease regulator-like 3	Mus musculus	75-78
8893267-1	1996	PURPOSE: The effect of elevated serum alpha-1-acid glycoprotein (AAG) concentrations on the steady-state serum and brain levels of imipramine and its metabolite desipramine was assessed.	Imipramine	131-141	nitrogen permease regulator-like 3	Mus musculus	38-63
9112692-0	1996	Effect of chronic treatment with imipramine on interleukin 1 and interleukin 2 production by splenocytes obtained from rats subjected to a chronic mild stress model of depression.	Imipramine	33-43	interleukin 2	Rattus norvegicus	65-78
8893267-1	1996	PURPOSE: The effect of elevated serum alpha-1-acid glycoprotein (AAG) concentrations on the steady-state serum and brain levels of imipramine and its metabolite desipramine was assessed.	Imipramine	131-141	nitrogen permease regulator-like 3	Mus musculus	65-68
8880946-8	1996	5-HTP-induced head twitches (a 5-HT2A effect) were inhibited by repeated paroxetine or imipramine.	Imipramine	87-97	5-hydroxytryptamine receptor 2A	Rattus norvegicus	31-37
8893267-11	1996	CONCLUSIONS: Elevated serum AAG impedes the transport of imipramine and desipramine into the brain.	Imipramine	57-67	nitrogen permease regulator-like 3	Mus musculus	28-31
8880223-6	1996	IL-2 release was suppressed to 60% of the control values by clomipramine and imipramine (p = 0.001; p = 0.000), but citalopram was found to cause a much weaker inhibition (only 18%) (p = 0.16).	Imipramine	77-87	interleukin 2	Homo sapiens	0-4
8880223-12	1996	Citalopram was equality as potent as imipramine and clomipramine in inhibiting IL-6 release after long-term exposure of monocytes to LPS.	Imipramine	37-47	interleukin 6	Homo sapiens	79-83
8835703-6	1996	In conclusion, by taking into account that the incidence of the PMs of CYP2C19 is much greater (18-23%) than that of CYP2D6 (< 1%) in Japanese population, the individually predetermined assessment of the CYP2C19-mediated metabolic capacity of imipramine would be more valuable than that of the CYP2D6-mediated capacity for forecasting the steady-state concentrations of imipramine and desipramine in Japanese depressive patients, thereby attaining an individualized optimization of imipramine therapy.	Imipramine	373-383	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
8835703-6	1996	In conclusion, by taking into account that the incidence of the PMs of CYP2C19 is much greater (18-23%) than that of CYP2D6 (< 1%) in Japanese population, the individually predetermined assessment of the CYP2C19-mediated metabolic capacity of imipramine would be more valuable than that of the CYP2D6-mediated capacity for forecasting the steady-state concentrations of imipramine and desipramine in Japanese depressive patients, thereby attaining an individualized optimization of imipramine therapy.	Imipramine	373-383	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
8835703-5	1996	This index correlated with the 4"-hydroxylation of S-mephenytoin (rs = -0.51, p < 0.01), but not with the alpha-hydroxylation of metoprolol, implying that imipramine N-demethylation is under a coregulatory pharmacogenetic control of CYP2C19, but not of CYP2D6.	Imipramine	158-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	236-243
8835703-5	1996	This index correlated with the 4"-hydroxylation of S-mephenytoin (rs = -0.51, p < 0.01), but not with the alpha-hydroxylation of metoprolol, implying that imipramine N-demethylation is under a coregulatory pharmacogenetic control of CYP2C19, but not of CYP2D6.	Imipramine	158-168	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	256-262
8842678-10	1996	MAO-A was inhibited by the following drugs (in ascending order of potency) : nortriptyline, amitriptyline, imipramine, maprotiline, zimeldine, nomifensine, and viloxazine.	Imipramine	107-117	monoamine oxidase A	Mus musculus	0-5
8835703-6	1996	In conclusion, by taking into account that the incidence of the PMs of CYP2C19 is much greater (18-23%) than that of CYP2D6 (< 1%) in Japanese population, the individually predetermined assessment of the CYP2C19-mediated metabolic capacity of imipramine would be more valuable than that of the CYP2D6-mediated capacity for forecasting the steady-state concentrations of imipramine and desipramine in Japanese depressive patients, thereby attaining an individualized optimization of imipramine therapy.	Imipramine	246-256	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
8842333-0	1996	Different effects of the antidepressant drugs imipramine, maprotiline and bupropion on insulin secretion from mouse pancreatic islets.	Imipramine	46-56	insulin	Oryctolagus cuniculus	87-94
8842333-4	1996	On the other hand, in presence of 16.7 mmol/l imipramine and maprotiline suppressed the stimulated insulin secretion.	Imipramine	46-56	insulin	Oryctolagus cuniculus	99-106
8842678-12	1996	MAO-B was inhibited by the following drugs (in ascending order of potency): nortriptyline, imipramine, maprotiline, amitriptyline, zimeldine, nomifensine, and viloxazine.	Imipramine	91-101	monoamine oxidase B	Mus musculus	0-5
8601816-6	1996	Moreover, coadministration of rolipram with imipramine resulted in a more rapid induction of CREB than with either treatment alone.	Imipramine	44-54	cAMP responsive element binding protein 1	Rattus norvegicus	93-97
8736433-4	1996	After 14 and 56 days of imipramine treatment, Arc NPY mRNA levels are decreased to 85% and 75% of control levels, but are unchanged compared to control after one or five days of treatment.	Imipramine	24-34	neuropeptide Y	Rattus norvegicus	50-53
8736433-7	1996	The divergent effects of imipramine vs the other 3 antidepressant drugs on Arc NPY mRNA expression are similar to the pattern of changes in tyrosine hydroxylase (TH) mRNA expression levels in the locus coeruleus (LC) using the same experimental paradigm, but are different from the unidirectional depressive effects of all four drugs on CRH mRNA expression in the PVN.	Imipramine	25-35	neuropeptide Y	Rattus norvegicus	79-82
8813535-0	1996	Imipramine increases the 5-HT1A receptor-mediated inhibition of hippocampal neurons without changing the 5-HT1A receptor binding.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Rattus norvegicus	25-31
8813535-1	1996	The effect of repeated treatment with imipramine on the 5-HT1A receptor-mediated inhibition of a population spike was studied in the rat CA1 hippocampal region ex vivo.	Imipramine	38-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	56-62
8813535-1	1996	The effect of repeated treatment with imipramine on the 5-HT1A receptor-mediated inhibition of a population spike was studied in the rat CA1 hippocampal region ex vivo.	Imipramine	38-48	carbonic anhydrase 1	Rattus norvegicus	137-140
8813535-5	1996	The latter findings indicate that the imipramine-induced increase in the responsiveness of hippocampal neurons to stimulation of 5-HT1A receptors may not involve an increase in the density of this receptor subtype.	Imipramine	38-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	129-135
8813535-8	1996	Our results suggest that repeated treatment with imipramine induces sensitization to the inhibitory effects of 5-HT1A receptor agonists in the hippocampus.	Imipramine	49-59	5-hydroxytryptamine receptor 1A	Rattus norvegicus	111-117
8627519-5	1996	Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis.	Imipramine	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8627519-8	1996	Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices.	Imipramine	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	Imipramine	73-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8627519-12	1996	Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine.	Imipramine	196-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
21043654-5	1996	Inhibition of the reuptake of serotonin by imipramine during thrombin-induced secretion increased the secretion in stored platelets.	Imipramine	43-53	coagulation factor II, thrombin	Homo sapiens	61-69
8661340-1	1996	The commonly used antidepressants imipramine, amitriptyline, and nortriptyline were found to significantly inhibit human natural killer (NK) cell-mediated cytolysis in vitro and suppress the stimulation of NK cells by IFN-gamma.	Imipramine	34-44	interferon gamma	Homo sapiens	218-227
8820428-11	1996	The results show that detergents (such as Lubrol PX, Emulgen 911, and Triton X-100) are inhibitory for the quaternary ammonium-linked glucuronidation of chlorpromazine and imipramine catalyzed by expressed human UDP-glucuronosyltransferase 1.4.	Imipramine	172-182	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	212-243
9160649-8	1996	Imipramine induced a decrease in growth hormone secretion during the first half of the night.	Imipramine	0-10	growth hormone 1	Homo sapiens	33-47
8593584-6	1995	5-HTt mRNA levels decreased to 81.1% (P = 0.05) and 76.0% (P = 0.05) of the control level for PCPA treated animals without and with concomitant imipramine treatment, respectively.	Imipramine	144-154	solute carrier family 6 member 4	Rattus norvegicus	0-5
8597444-3	1995	Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents.	Imipramine	18-28	corticotropin releasing hormone	Homo sapiens	145-148
8929926-0	1996	Imipramine-induced increase in 5-HT2C receptor mRNA level in the rat brain.	Imipramine	0-10	5-hydroxytryptamine receptor 2C	Rattus norvegicus	31-37
8929926-1	1996	Repeated oral administration of 20 mg/kg imipramine elevated the level of 5-HT2C mRNA in the rat brain.	Imipramine	41-51	5-hydroxytryptamine receptor 2C	Rattus norvegicus	74-80
8929926-3	1996	These results suggest that long-term treatment with imipramine stimulates 5-HT2C receptor gene expression.	Imipramine	52-62	5-hydroxytryptamine receptor 2C	Rattus norvegicus	74-80
8580224-4	1995	Imipramine caused an increase in the GH ratio in all subgroups.	Imipramine	0-10	growth hormone 1	Homo sapiens	37-39
8580224-5	1995	Protocol completers had a significantly larger imipramine-induced increase in the GH ratio than did recurrers.	Imipramine	47-57	growth hormone 1	Homo sapiens	82-84
8593584-8	1995	The isolated effect of 21 days of imipramine treatment was a 5-HTt mRNA level of 89.4%, which was not significantly different from the control level.	Imipramine	34-44	solute carrier family 6 member 4	Rattus norvegicus	61-66
8565792-7	1995	These results indicate that imipramine has two actions on the liver CYP system (i.e. as an inhibitor of the CYP2D enzyme and as a phenobarbital-type inducer).	Imipramine	28-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-71
8521680-9	1995	While CYP2D6 catalyses the metabolism of lipophilic bases only, CYP2C19 is involved in the metabolism of acids (e.g. S-mephenytoin), bases (e.g. imipramine and omeprazole) and neutral drugs (e.g. diazepam).	Imipramine	145-155	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	6-12
8521680-9	1995	While CYP2D6 catalyses the metabolism of lipophilic bases only, CYP2C19 is involved in the metabolism of acids (e.g. S-mephenytoin), bases (e.g. imipramine and omeprazole) and neutral drugs (e.g. diazepam).	Imipramine	145-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
8565792-0	1995	Inhibition and induction of cytochrome P450 isozymes after repetitive administration of imipramine in rats.	Imipramine	88-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-43
7478203-9	1995	Imipramine binding could be inhibited by potent non-tricyclic inhibitors of the serotonin transporter such as paroxetine and fluoxetine but also by the tricyclic antidepressant drugs clomipramine and desipramine.	Imipramine	0-10	solute carrier family 6 member 4	Homo sapiens	80-101
8565792-1	1995	Repetitive oral administration of imipramine (100 mg/kg/day for 5 days) caused a decrease in rat liver microsomal debrisoquine 4-hydroxylase activity, a characteristic reaction catalyzed by cytochrome P450 (CYP) 2D1.	Imipramine	34-44	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	114-140
8565792-1	1995	Repetitive oral administration of imipramine (100 mg/kg/day for 5 days) caused a decrease in rat liver microsomal debrisoquine 4-hydroxylase activity, a characteristic reaction catalyzed by cytochrome P450 (CYP) 2D1.	Imipramine	34-44	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	190-215
8565792-4	1995	Imipramine pretreatment also resulted in an increase in total CYP content and in formation of a ferrous CYP metabolic intermediate (MI)-complex absorbing at 454 nm.	Imipramine	0-10	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-65
8565792-4	1995	Imipramine pretreatment also resulted in an increase in total CYP content and in formation of a ferrous CYP metabolic intermediate (MI)-complex absorbing at 454 nm.	Imipramine	0-10	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-107
7675318-0	1995	Chronic imipramine, L-sulpiride and mianserin decrease corticotropin releasing factor levels in the rat brain.	Imipramine	8-18	corticotropin releasing hormone	Rattus norvegicus	55-85
7779239-0	1995	Chronic imipramine administration alters the activity and phosphorylation state of tyrosine hydroxylase in dopaminergic regions of rat brain.	Imipramine	8-18	tyrosine hydroxylase	Rattus norvegicus	83-103
7640151-11	1995	This indicates that CYP1A2, which is induced by cigarette smoking, also catalyzes the N-demethylation of imipramine.	Imipramine	105-115	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	20-26
7779239-5	1995	However, imipramine treatment increased levels of TH back phosphorylation in VTA, suggesting that the antidepressant-induced decrease in levels of TH activity is a result of decreased phosphorylation of the enzyme.	Imipramine	9-19	tyrosine hydroxylase	Rattus norvegicus	147-149
7779239-6	1995	These results demonstrate that imipramine treatment regulates levels of TH enzyme activity in dopaminergic brain regions, and may account for some of the previously observed effects of these drugs on dopaminergic function.	Imipramine	31-41	tyrosine hydroxylase	Rattus norvegicus	72-74
7612155-6	1995	Chronic administration of ECS, tranylcypromine, or imipramine also decreased stressed-induced levels of NGFI-A mRNA, another immediate early gene transcription factor, whereas levels of c-jun mRNA were not influenced by either stress or antidepressant treatments.	Imipramine	51-61	early growth response 1	Rattus norvegicus	104-110
7633328-1	1995	We have previously reported elevated brain tissue contents of neuropeptide Y-like immunoreactivity (NPY-LI) following 3 weeks of oral treatment with the antidepressants zimelidine and imipramine.	Imipramine	184-194	neuropeptide Y	Rattus norvegicus	62-76
7779239-7	1995	Finally, imipramine regulation of TH enzyme activity in VTA and immunoreactivity in LC was observed in Sprague Dawley, but not Wistar rats, demonstrating that different rat strains exhibit different biochemical responses to antidepressant treatment.	Imipramine	9-19	tyrosine hydroxylase	Rattus norvegicus	34-36
7779239-1	1995	In the present study the influence of imipramine, a tricyclic antidepressant, on the expression and function of tyrosine hydroxylase (TH) in dopaminergic rat brain regions was examined.	Imipramine	38-48	tyrosine hydroxylase	Rattus norvegicus	112-132
7633328-1	1995	We have previously reported elevated brain tissue contents of neuropeptide Y-like immunoreactivity (NPY-LI) following 3 weeks of oral treatment with the antidepressants zimelidine and imipramine.	Imipramine	184-194	neuropeptide Y	Rattus norvegicus	100-103
7779239-1	1995	In the present study the influence of imipramine, a tricyclic antidepressant, on the expression and function of tyrosine hydroxylase (TH) in dopaminergic rat brain regions was examined.	Imipramine	38-48	tyrosine hydroxylase	Rattus norvegicus	134-136
7779239-2	1995	Chronic administration of imipramine (18 days) decreased levels of TH enzyme activity in ventral tegmental area (VTA) and substantia nigra (SN), dopaminergic cell body regions, as well as in caudate-putamen (CP), nucleus accumbens (ACB), prefrontal cortex (PFC), and olfactory tubercle (OT), dopaminergic terminal fields.	Imipramine	26-36	tyrosine hydroxylase	Rattus norvegicus	67-69
7779239-5	1995	However, imipramine treatment increased levels of TH back phosphorylation in VTA, suggesting that the antidepressant-induced decrease in levels of TH activity is a result of decreased phosphorylation of the enzyme.	Imipramine	9-19	tyrosine hydroxylase	Rattus norvegicus	50-52
7628292-4	1995	However, expressed human UGT1.4 protein exhibited glucuronidation activity toward tertiary amine substrates, such as imipramine, cyproheptadine, tripelennamine, and chlorpromazine, which form quaternary ammonium-linked glucuronides.	Imipramine	117-127	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	25-31
7711157-2	1995	Decreased platelet serotonin (5-HT) transport and reduced binding of imipramine or paroxetine to brain and platelet 5-HT uptake sites/transporters in patients with depression and suicide victims define the 5-HT transporter (5-HTT) as a candidate gene.	Imipramine	69-79	solute carrier family 6 member 4	Homo sapiens	206-222
7741768-6	1995	The reconstituted system containing P450(b-1) catalyzed the metabolism of aminopyrine, benzo[a]pyrene, 7-ethoxycoumarin, imipramine and propranolol, of which P450(b-1) most strongly catalyzed aminopyrine N-demethylation and imipramine N-demethylation.	Imipramine	121-131	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	36-44
7741768-6	1995	The reconstituted system containing P450(b-1) catalyzed the metabolism of aminopyrine, benzo[a]pyrene, 7-ethoxycoumarin, imipramine and propranolol, of which P450(b-1) most strongly catalyzed aminopyrine N-demethylation and imipramine N-demethylation.	Imipramine	121-131	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	158-166
7613100-0	1995	The effect of chronic treatment with imipramine on the responsiveness of hippocampal CA1 neurons to phenylephrine and serotonin in a chronic mild stress model of depression.	Imipramine	37-47	carbonic anhydrase 1	Rattus norvegicus	85-88
7758754-0	1995	Dithiothreithol promotes a higher affinity state of the serotonin transporter for the tricyclic antidepressant, imipramine.	Imipramine	112-122	solute carrier family 6 member 4	Homo sapiens	56-77
8846618-11	1995	Consistent with its minimal in vitro effect on CYP2D6, fluvoxamine shows minimal in vivo pharmacokinetic interaction with desipramine, but does interact with imipramine (approximately 3- to 4-fold increase in AUC) through inhibition of CYP3A3/4, CYP1A2, and CYP2C19.	Imipramine	158-168	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	246-252
7777221-3	1995	The present experiment tested whether the MAO inhibitor antidepressant phenelzine shares this common effect of anxiolytics and imipramine on hippocampal RSA.	Imipramine	127-137	monoamine oxidase A	Rattus norvegicus	42-45
8846618-11	1995	Consistent with its minimal in vitro effect on CYP2D6, fluvoxamine shows minimal in vivo pharmacokinetic interaction with desipramine, but does interact with imipramine (approximately 3- to 4-fold increase in AUC) through inhibition of CYP3A3/4, CYP1A2, and CYP2C19.	Imipramine	158-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	258-265
8846619-2	1995	Cytochrome P450 1A2 (CYP1A2) accounts for about 10 to 15% of the total CYP content of human liver and is the major enzyme involved in the metabolism of imipramine, propranolol, clozapine, theophylline, and caffeine.	Imipramine	152-162	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	0-19
8846619-2	1995	Cytochrome P450 1A2 (CYP1A2) accounts for about 10 to 15% of the total CYP content of human liver and is the major enzyme involved in the metabolism of imipramine, propranolol, clozapine, theophylline, and caffeine.	Imipramine	152-162	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	21-27
8846619-2	1995	Cytochrome P450 1A2 (CYP1A2) accounts for about 10 to 15% of the total CYP content of human liver and is the major enzyme involved in the metabolism of imipramine, propranolol, clozapine, theophylline, and caffeine.	Imipramine	152-162	peptidylprolyl isomerase G	Homo sapiens	21-24
8806399-5	1995	The remaining interactions (felbamate, omeprazole, cimetidine, fluoxetine, imipramine, and diazepam) were attributed to inhibition of CYP2C19.	Imipramine	75-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	134-141
7623967-7	1995	Pretreatment with (+)WAY100135 to block 5-HT1A autoreceptors, abolished the inhibition of 5-HT release produced by systemic sertraline, clomipramine and imipramine.	Imipramine	153-163	5-hydroxytryptamine receptor 1A	Rattus norvegicus	40-46
7760982-4	1994	The present experiments tested the possibility that buspirone, chlordiazepoxide and imipramine reduce RSA frequency via 5-HT1A autoreceptors.	Imipramine	84-94	5-hydroxytryptamine receptor 1A	Rattus norvegicus	120-126
7847180-1	1994	Imipramine was administered chronically to LEW/N, outbred and F344/N rats which were then exposed to the aseptic irritant carrageenin in order to determine whether the decreased hypothalamic expression of CRH m-RNA previously shown to be associated with imipramine affects peripheral immune processes.	Imipramine	0-10	corticotropin releasing hormone	Rattus norvegicus	205-208
7894333-8	1994	Preincubation of the cytosol with anti-PLC-beta 1 antibody prevented the imipramine-mediated activation of PLC.	Imipramine	73-83	phospholipase C beta 1	Rattus norvegicus	39-49
7894333-10	1994	These results suggest that imipramine activates PLC-beta 1 directly without receptor or guanine nucleotide binding protein mediation.	Imipramine	27-37	phospholipase C beta 1	Rattus norvegicus	48-58
7813561-3	1994	Moreover we found that the "antidepressant" effect of imipramine in the behavioural despair test was antagonized by SCH 23390, a selective dopamine D1 receptor blocker.	Imipramine	54-64	dopamine receptor D1	Homo sapiens	139-159
8073046-2	1994	These experiments examined the effects of cocaine and imipramine, drugs known to decrease NE uptake, on the changes in arterial pressure and total peripheral resistance (TPR) in response to NE and arginine vasopressin (AVP) in conscious rabbits.	Imipramine	54-64	vasopressin-neurophysin 2-copeptin	Oryctolagus cuniculus	219-222
8073046-5	1994	The infusion of AVP caused significantly larger increases in arterial pressure and in TPR following cocaine or imipramine administration than was seen after the administration of AVP to control rabbits not treated with these drugs.	Imipramine	111-121	vasopressin-neurophysin 2-copeptin	Oryctolagus cuniculus	16-19
8073046-6	1994	These studies demonstrated that cocaine and imipramine, substances known to decrease NE uptake by the sympathetic nerve terminals, will induce pressor and vascular hyperresponsiveness to NE and AVP in rabbits.	Imipramine	44-54	vasopressin-neurophysin 2-copeptin	Oryctolagus cuniculus	194-197
8182048-2	1994	Treatment of JAR and BeWo cells with the selective calmodulin antagonist 1,3-dihydro-1-[1-((4-methyl-4H, 6H-pyrrolo[1,2-a][4,1]-benzoxapin-4-yl)-methyl)-4-piperindinyl+ ++]- 2H-benzimidazol-2-one (CGS93-43B (CGS)) for 1 h decreased the imipramine-sensitive serotonin transport activity markedly.	Imipramine	236-246	calmodulin 1	Homo sapiens	51-61
7928004-4	1994	The uptake of [3H]5-HT was temperature, sodium and chloride dependent and was potently inhibited by the antidepressants clomipramine, imipramine, fluoxetine and fluvoxamine, which are specific for the 5-HT transporter.	Imipramine	134-144	solute carrier family 6 member 4	Homo sapiens	201-217
8016192-3	1994	Among the compounds tested, indatraline, imipramine and fluoxetine, selective inhibitors of neuronal serotonin transporter, were the most potent inhibitors of [3H]-dopamine uptake in lymphocytes.	Imipramine	41-51	solute carrier family 6 member 4	Homo sapiens	101-122
8050484-3	1994	Many of these compounds are derivatives with modified naphthalenesulfonamide or isoquinolinesulfonamide structures, which appear to compete directly with imipramine for binding to the serotonin transporter.	Imipramine	154-164	solute carrier family 6 member 4	Homo sapiens	184-205
8000448-0	1994	Prolonged administration of imipramine and (+)-oxaprotiline, but not citalopram, results in sensitization of the rat hippocampal CA1 neurons to serotonin ex vivo.	Imipramine	28-38	carbonic anhydrase 1	Rattus norvegicus	129-132
8000448-1	1994	Prolonged (14 days, twice daily), but not acute, application of imipramine and (+)-oxaprotiline (10 mg/kg) induced sensitization of hippocampal CA1 neurons to the inhibitory effect of 5-hydroxytryptamine (5-HT), as studied ex vivo in the rat hippocampal slice preparation.	Imipramine	64-74	carbonic anhydrase 1	Rattus norvegicus	144-147
7838924-4	1994	Imipramine decreased Bmax, reversing the effect of CMS, for beta-adrenergic and 5HT2 receptor binding, but increased Bmax for 5HT1A receptor binding.	Imipramine	0-10	5-hydroxytryptamine receptor 1A	Homo sapiens	126-140
8198931-0	1994	The role of S-mephenytoin 4"-hydroxylase in imipramine metabolism by human liver microsomes: a two-enzyme kinetic analysis of N-demethylation and 2-hydroxylation.	Imipramine	44-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-40
8198931-2	1994	The metabolism of imipramine (N-demethylation and 2-hydroxylation) was studied in relation to the activity of S-mephenytoin 4"-hydroxylase in human liver microsomes.	Imipramine	18-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	110-138
8198931-7	1994	kinetic parameters for the N-demethylation and 2-hydroxylation of imipramine derived from a two-enzyme kinetic analysis were: Km1 = 1.1 +/- 0.4 and 1.6 +/- 0.6 microM, Vmax1 = 0.11 +/- 0.03 and 0.15 +/- 0.07 nmol mg-1 min-1, and Vmax1/Km1 = 0.10 +/- 0.02 and 0.09 +/- 0.04 ml mg-1 min-1; Km2 = 214 +/- 84 and 257 +/- 148 microM, Vmax2 = 2.22 +/- 0.69 and 0.53 +/- 0.15 nmol mg-1 min-1, and Vmax2/Km2 = 0.011 +/- 0.001 and 0.003 +/- 0.002 ml mg-1 min-1.	Imipramine	66-76	CD59 molecule (CD59 blood group)	Homo sapiens	218-223
8198931-7	1994	kinetic parameters for the N-demethylation and 2-hydroxylation of imipramine derived from a two-enzyme kinetic analysis were: Km1 = 1.1 +/- 0.4 and 1.6 +/- 0.6 microM, Vmax1 = 0.11 +/- 0.03 and 0.15 +/- 0.07 nmol mg-1 min-1, and Vmax1/Km1 = 0.10 +/- 0.02 and 0.09 +/- 0.04 ml mg-1 min-1; Km2 = 214 +/- 84 and 257 +/- 148 microM, Vmax2 = 2.22 +/- 0.69 and 0.53 +/- 0.15 nmol mg-1 min-1, and Vmax2/Km2 = 0.011 +/- 0.001 and 0.003 +/- 0.002 ml mg-1 min-1.	Imipramine	66-76	CD59 molecule (CD59 blood group)	Homo sapiens	281-286
8198931-7	1994	kinetic parameters for the N-demethylation and 2-hydroxylation of imipramine derived from a two-enzyme kinetic analysis were: Km1 = 1.1 +/- 0.4 and 1.6 +/- 0.6 microM, Vmax1 = 0.11 +/- 0.03 and 0.15 +/- 0.07 nmol mg-1 min-1, and Vmax1/Km1 = 0.10 +/- 0.02 and 0.09 +/- 0.04 ml mg-1 min-1; Km2 = 214 +/- 84 and 257 +/- 148 microM, Vmax2 = 2.22 +/- 0.69 and 0.53 +/- 0.15 nmol mg-1 min-1, and Vmax2/Km2 = 0.011 +/- 0.001 and 0.003 +/- 0.002 ml mg-1 min-1.	Imipramine	66-76	CD59 molecule (CD59 blood group)	Homo sapiens	281-286
8198931-7	1994	kinetic parameters for the N-demethylation and 2-hydroxylation of imipramine derived from a two-enzyme kinetic analysis were: Km1 = 1.1 +/- 0.4 and 1.6 +/- 0.6 microM, Vmax1 = 0.11 +/- 0.03 and 0.15 +/- 0.07 nmol mg-1 min-1, and Vmax1/Km1 = 0.10 +/- 0.02 and 0.09 +/- 0.04 ml mg-1 min-1; Km2 = 214 +/- 84 and 257 +/- 148 microM, Vmax2 = 2.22 +/- 0.69 and 0.53 +/- 0.15 nmol mg-1 min-1, and Vmax2/Km2 = 0.011 +/- 0.001 and 0.003 +/- 0.002 ml mg-1 min-1.	Imipramine	66-76	CD59 molecule (CD59 blood group)	Homo sapiens	281-286
8296900-3	1994	This study demonstrates that imipramine can antagonize the panicogenic effects of CCK-4.	Imipramine	29-39	protein tyrosine kinase 7 (inactive)	Homo sapiens	82-87
8199869-2	1994	To further characterize these strains, we investigated the effect of chronic (8 wk) imipramine administration (5 mg/kg/day) on 5-HT1A and 5-HT2 receptor densities and mRNA in the cortex and hippocampus and 5-HT transporter mRNA in the dorsal raphe of LEW/N, HSD, and F344/N rats, using quantitative autoradiography and in situ hybridization histochemistry.	Imipramine	84-94	5-hydroxytryptamine receptor 1A	Rattus norvegicus	127-139
8199869-3	1994	After imipramine treatment, a significant increase in the levels of hippocampal 5-HT1A receptors, but not mRNA, was observed in LEW/N rats while the abundance of hippocampal 5-HT1A receptor mRNA, but not 5-HT1A receptor densities, decreased in F344/N rats.	Imipramine	6-16	5-hydroxytryptamine receptor 1A	Rattus norvegicus	80-86
8199869-3	1994	After imipramine treatment, a significant increase in the levels of hippocampal 5-HT1A receptors, but not mRNA, was observed in LEW/N rats while the abundance of hippocampal 5-HT1A receptor mRNA, but not 5-HT1A receptor densities, decreased in F344/N rats.	Imipramine	6-16	5-hydroxytryptamine receptor 1A	Rattus norvegicus	174-180
8199869-3	1994	After imipramine treatment, a significant increase in the levels of hippocampal 5-HT1A receptors, but not mRNA, was observed in LEW/N rats while the abundance of hippocampal 5-HT1A receptor mRNA, but not 5-HT1A receptor densities, decreased in F344/N rats.	Imipramine	6-16	5-hydroxytryptamine receptor 1A	Rattus norvegicus	174-180
8199869-6	1994	The effects of imipramine on the levels of cortical and hippocampal 5-HT1A and 5-HT2 receptors and their transcripts, therefore, appear to be strain-dependent.	Imipramine	15-25	5-hydroxytryptamine receptor 1A	Rattus norvegicus	68-80
8304470-12	1994	Imipramine, fluoxetine, staurosporine, and cholera toxin inhibited the stimulations of both DNA synthesis and c-myc and actin mRNA expressions by 5-HT.	Imipramine	0-10	MYC proto-oncogene, bHLH transcription factor	Bos taurus	110-115
8373164-3	1993	The uptake was sensitive to reserpine (1 microM) and bafilomycin (50 nM) (inhibitors of the vesicular monoamine transporter and vacuolar-type H(+)-ATPase, respectively) and substrates for monoamine transporters, but insensitive to imipramine (an inhibitor of the monoamine transporter present in the plasma membrane).	Imipramine	231-241	solute carrier family 18 member A2	Homo sapiens	188-209
8218295-10	1993	The ligands of the serotonin transporter (imipramine, paroxetine, and fluoxetine) showed intermediate inhibitory potencies, whereas the ligands of the dopamine transporter (bupropion and GBR 12909) were the least potent.	Imipramine	42-52	solute carrier family 6 member 4	Homo sapiens	19-40
8148368-3	1994	The density of 5-HT1A receptors, labelled with [3H]8-OH-DPAT, in the rat hippocampus was enhanced after citalopram, imipramine, mianserin and levoprotiline, but not altered after fluoxetine administration.	Imipramine	116-126	5-hydroxytryptamine receptor 1A	Rattus norvegicus	15-21
8310712-0	1993	Analysis of imipramine and three metabolites produced by isozyme CYP2D6 expressed in a human cell line.	Imipramine	12-22	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	65-71
8310712-2	1993	A commercially-available human cytochrome P450 isozyme (CYP2D6) preparation was used in imipramine metabolism studies.	Imipramine	88-98	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	31-46
8310712-2	1993	A commercially-available human cytochrome P450 isozyme (CYP2D6) preparation was used in imipramine metabolism studies.	Imipramine	88-98	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
8310712-14	1993	CYP2D6 catalyses C-hydroxylation of imipramine to 2-hydroxyimipramine more efficiently than its N-demethylation to desipramine.	Imipramine	36-46	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
8366353-9	1993	Administration of imipramine alone under basal conditions produced a robust induction of Fos-LI in the central nucleus of the amygdala and in the dorsal lateral subdivision of the bed nucleus of the stria terminalis.	Imipramine	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
8110987-4	1993	Acetylcholinesterase (AChE) was inhibited by CPZ, 3,7,8-trihydroxy-CPZ, acridine orange partially saturated desipramine, imipramine, trans-clopenthixol and tetrahydrocannabidiolic at 10(-4) to 10(-5).	Imipramine	121-131	acetylcholinesterase	Rattus norvegicus	0-20
8110987-4	1993	Acetylcholinesterase (AChE) was inhibited by CPZ, 3,7,8-trihydroxy-CPZ, acridine orange partially saturated desipramine, imipramine, trans-clopenthixol and tetrahydrocannabidiolic at 10(-4) to 10(-5).	Imipramine	121-131	acetylcholinesterase	Rattus norvegicus	22-26
7906990-8	1993	It is concluded that prolonged treatment with imipramine, mianserin and citalopram produces an increase in the responsiveness of hippocampal CA1 neurons to stimulation of the dopamine D-2 receptor.	Imipramine	46-56	carbonic anhydrase 1	Rattus norvegicus	141-144
8295156-0	1993	An association between the lysosomal enzyme NAG and urinary free cortisol and platelet imipramine binding.	Imipramine	87-97	N-acetyl-alpha-glucosaminidase	Homo sapiens	44-47
8295156-2	1993	In a separate study of healthy controls NAG levels showed a trend toward association with platelet imipramine binding density.	Imipramine	99-109	N-acetyl-alpha-glucosaminidase	Homo sapiens	40-43
8354888-3	1993	Imipramine and desipramine were structurally modified by the attachment of spacer arms to the aromatic ring which were subsequently attached to bovine serum albumin.	Imipramine	0-10	albumin	Oryctolagus cuniculus	151-164
8429827-9	1993	[3H]Imipramine binding to the platelet serotonin transporter and [3H]GBR-12935 binding to the dopamine transporter were not inhibited by decreasing the pH from 8 to 6.5.	Imipramine	4-14	solute carrier family 6 member 4	Rattus norvegicus	39-60
8335704-0	1993	Metabolism of imipramine in vitro by isozyme CYP2D6 expressed in a human cell line, and observations on metabolite stability.	Imipramine	14-24	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	45-51
8335704-1	1993	A metabolism study of imipramine (IMI) has been conducted in vitro with commercially available human CYP2D6 isozyme expressed in a human AHH-1 TK +/- cell line.	Imipramine	22-32	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	101-107
8335704-1	1993	A metabolism study of imipramine (IMI) has been conducted in vitro with commercially available human CYP2D6 isozyme expressed in a human AHH-1 TK +/- cell line.	Imipramine	34-37	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	101-107
8384247-1	1993	The number of beta 1-adrenergic receptor (beta 1AR) binding sites is decreased by chronic antidepressant treatments, including electroconvulsive seizure (ECS) and imipramine, whereas administration of agents that deplete norepinephrine (NE) increases the number of beta 1AR binding sites in cerebral cortex.	Imipramine	163-173	adrenoceptor beta 1	Rattus norvegicus	14-40
8384247-1	1993	The number of beta 1-adrenergic receptor (beta 1AR) binding sites is decreased by chronic antidepressant treatments, including electroconvulsive seizure (ECS) and imipramine, whereas administration of agents that deplete norepinephrine (NE) increases the number of beta 1AR binding sites in cerebral cortex.	Imipramine	163-173	adrenoceptor beta 1	Rattus norvegicus	42-50
8384247-6	1993	However, imipramine administration regulated levels of beta 1AR mRNA in a biphasic manner, with treatments for 7-14 days increasing and treatments for 18-21 days decreasing levels of beta 1AR mRNA in frontal cortex.	Imipramine	9-19	adrenoceptor beta 1	Rattus norvegicus	55-63
8466541-5	1993	Our findings explain the mechanism of the pharmacokinetic interactions between fluvoxamine and drugs that are metabolized by CYP1A2, e.g. theophylline and imipramine.	Imipramine	155-165	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	125-131
8449936-7	1993	Catalytic similarity to the native FMO 1B1 was demonstrated by the ability of the expressed enzymes to metabolize methimazole, thiourea, dimethylaniline, and cysteamine, but not chlorpromazine or imipramine.	Imipramine	196-206	dimethylaniline monooxygenase [N-oxide-forming] 2	Oryctolagus cuniculus	35-42
8401777-2	1993	An in situ hybridization histochemistry showed that imipramine decreased the Go alpha mRNA level in CA1 (by ca.	Imipramine	52-62	carbonic anhydrase 1	Rattus norvegicus	100-103
8364729-4	1993	[3H]paroxetine-binding to serotonin transporter sites was decreased by tianeptine treatment as well as by imipramine in both hippocampus and cerebral cortex, with some overlap of the fields that were significantly affected, whereas there were no effects of stress per se and no evidence of a stress x drug interaction.	Imipramine	106-116	solute carrier family 6 member 4	Rattus norvegicus	26-47
8502233-4	1993	Correlations were obtained between rates of imipramine demethylation and cytochrome P-450 (P-450) 1A2 (r = 0.88, p < 0.001) and P-450 3A (r = 0.80, p < 0.02) concentrations in human liver microsomal preparations from 13 different subjects.	Imipramine	44-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	73-89
8439771-1	1993	The effects of acute and chronic treatment with the tricyclic antidepressant drugs, imipramine, clomipramine and desipramine on levels of neuropeptide Y (NPY) and prepro-NPY-mRNA were studied in different areas of the rat brain.	Imipramine	84-94	neuropeptide Y	Rattus norvegicus	138-152
1610412-1	1992	The effects of long-term (28-day) administration of several antidepressant/antipanic drugs [imipramine, desipramine, tranylcypromine and phenelzine (PLZ)] on gamma-aminobutyric acid-tranaminase (GABA-T) activity and GABA levels were investigated in rat frontal cortex.	Imipramine	92-102	4-aminobutyrate aminotransferase	Rattus norvegicus	158-193
1494903-5	1992	Moreover, chronic administration of the antidepressant imipramine or tranylcypromine produced a similar increase in levels of DARPP-32 in frontal cortex, whereas other types of psychotropic drugs, including haloperidol, morphine, and cocaine, did not influence DARPP-32 levels.	Imipramine	55-65	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	126-134
1494903-5	1992	Moreover, chronic administration of the antidepressant imipramine or tranylcypromine produced a similar increase in levels of DARPP-32 in frontal cortex, whereas other types of psychotropic drugs, including haloperidol, morphine, and cocaine, did not influence DARPP-32 levels.	Imipramine	55-65	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	261-269
1305956-4	1992	(+)-OXA, imipramine and mianserin produced similar effects on 5-HT1A binding parameters.	Imipramine	9-19	5-hydroxytryptamine receptor 1A	Rattus norvegicus	62-68
1379870-9	1992	In vitro study, imipramine dose-dependently inhibited specific [3H]SP binding in the spinal cord homogenate with IC50 value of 2.37 x 10(-4) M and this value corresponds to 8.6 mumol/g tissue concentration.	Imipramine	16-26	tachykinin 1	Mus musculus	67-69
1379870-0	1992	Imipramine inhibits intrathecal substance P-induced behavior and blocks spinal cord substance P receptors in mice.	Imipramine	0-10	tachykinin 1	Mus musculus	32-43
1438647-0	1992	A double-blind, placebo-controlled study of the effect of imipramine on TRH-induced urinary urgency in healthy men.	Imipramine	58-68	thyrotropin releasing hormone	Homo sapiens	72-75
1379870-0	1992	Imipramine inhibits intrathecal substance P-induced behavior and blocks spinal cord substance P receptors in mice.	Imipramine	0-10	tachykinin 1	Mus musculus	84-95
1379870-8	1992	In the SP-induced behavior, the antinociceptive effect of 31.6 nmol of imipramine was not antagonized by the alpha-adrenergic receptor antagonist phentolamine, the serotonergic receptor antagonist methysergide, or the opioid receptor antagonist naloxone.	Imipramine	71-81	tachykinin 1	Mus musculus	7-9
1589591-13	1992	It was observed that all the antidepressant drugs except for imipramine increased the number of high-affinity sites of the 5HT-1A receptors in the frontal cortex.	Imipramine	61-71	5-hydroxytryptamine receptor 1A	Rattus norvegicus	123-129
1438647-1	1992	We studied the effect of imipramine (IMI) on thyroid releasing hormone (TRH)-induced urinary urgency as a way of investigating the mechanism of the beneficial effect of IMI on enuresis.	Imipramine	25-35	thyrotropin releasing hormone	Homo sapiens	72-75
1438647-1	1992	We studied the effect of imipramine (IMI) on thyroid releasing hormone (TRH)-induced urinary urgency as a way of investigating the mechanism of the beneficial effect of IMI on enuresis.	Imipramine	37-40	thyrotropin releasing hormone	Homo sapiens	72-75
1345939-9	1992	Other treatments known to either increase (adrenalectomy) or decrease (chronic imipramine) levels of TH in the LC were also found to increase or decrease, respectively, levels of cAMP-dependent protein kinase activity in this brain region.	Imipramine	79-89	tyrosine hydroxylase	Rattus norvegicus	101-103
1372501-4	1992	Here we demonstrate for the first time that the imipramine-sensitive serotonin transport activity in either JAr choriocarcinoma or PC12 pheochromocytoma cell lines is subject to regulation by cAMP.	Imipramine	48-58	cathelicidin antimicrobial peptide	Rattus norvegicus	192-196
1313983-6	1992	These findings suggest that imipramine hydrochloride increases sensitivity to the hypoglycemic effects of insulin, but does not alter the counterregulatory response of ACTH and cortisol.	Imipramine	28-52	insulin	Homo sapiens	106-113
1346093-7	1992	Other psychotropic drugs and local anesthetics, namely, dibucaine, lidocaine, imipramine, tetracaine and procaine, also induced DnaK and GroEL proteins and the small molecular weight proteins.	Imipramine	78-88	GroEL	Escherichia coli	137-142
1508839-0	1992	Serotonin receptors in the brain of rats treated chronically with imipramine or RU24969: support for the 5-HT1B receptor being a 5-HT autoreceptor.	Imipramine	66-76	5-hydroxytryptamine receptor 1B	Rattus norvegicus	105-111
1508839-5	1992	The 5-HT1B receptor was found decreased both by the imipramine treatment (Bmax = 106 fmol/mg protein) and the treatment with RU24969 (Bmax = 105 fmol/mg protein), compared with control rats (Bmax = 130 fmol/mg protein).	Imipramine	52-62	5-hydroxytryptamine receptor 1B	Rattus norvegicus	4-10
1636501-2	1992	Preincubation of cortical synaptosomal membranes of rat brain with phospholipase A2 (PLA2) increases the number of [3H]imipramine ([3H]IMI) high affinity binding sites without altering Kd (Bmax control: 2.53 +/- 0.28 pmol/mg protein vs Bmax PLA2: 3.66 +/- 0.26 pmol/mg protein).	Imipramine	119-129	phospholipase A2 group IB	Rattus norvegicus	67-83
1636501-2	1992	Preincubation of cortical synaptosomal membranes of rat brain with phospholipase A2 (PLA2) increases the number of [3H]imipramine ([3H]IMI) high affinity binding sites without altering Kd (Bmax control: 2.53 +/- 0.28 pmol/mg protein vs Bmax PLA2: 3.66 +/- 0.26 pmol/mg protein).	Imipramine	119-129	phospholipase A2 group IB	Rattus norvegicus	85-89
1773822-0	1991	Evidence that imipramine activates 5-HT1C receptor function.	Imipramine	14-24	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	35-41
1357707-0	1992	Chronic imipramine treatment normalizes levels of tyrosine hydroxylase in the locus coeruleus of chronically stressed rats.	Imipramine	8-18	tyrosine hydroxylase	Rattus norvegicus	50-70
1357707-3	1992	It was found that chronic imipramine pretreatment (18 days) attenuated the induction of TH in response to cold stress, resulting in levels of TH immunoreactivity not different from control.	Imipramine	26-36	tyrosine hydroxylase	Rattus norvegicus	88-90
1357707-3	1992	It was found that chronic imipramine pretreatment (18 days) attenuated the induction of TH in response to cold stress, resulting in levels of TH immunoreactivity not different from control.	Imipramine	26-36	tyrosine hydroxylase	Rattus norvegicus	142-144
1762063-7	1991	Drug-appropriate responding occurred in pigeons trained at the lower dose of imipramine with the 5-HT1A compounds 8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide and gepirone; partial substitution occurred in pigeons trained with the higher dose of imipramine.	Imipramine	77-87	5-hydroxytryptamine receptor 1A	Homo sapiens	97-103
1839498-4	1991	The long-term treatments with imipramine and ECS, but not with paroxetine, increased the responsiveness of postsynaptic CA3 hippocampus pyramidal neurons to the microiontophoretic application of 5-HT and to that of the selective 5-HT1A receptor ligand 8-OH-DPAT.	Imipramine	30-40	carbonic anhydrase 3	Rattus norvegicus	120-123
1773822-1	1991	The anti-immobility effect of imipramine (15 mg/kg) in the forced swimming test in mice was antagonized by the non-selective 5-hydroxytryptamine (5-HT) antagonist, metitepine (0.5 mg/kg), by the 5-HT1C/5-HT2 antagonist, mesulergine (15 mg/kg), and by the dopamine D2 antagonist, d,l-sulpiride (50 mg/kg).	Imipramine	30-40	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	195-201
1773822-9	1991	Imipramine produced 50% inhibition of [3H]mesulergine binding to 5-HT1C receptors at 10 microM, a concentration below that obtained following i.p.	Imipramine	0-10	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	65-71
1773822-11	1991	The results suggest a contribution of 5-HT1C receptors in the mechanism of the imipramine effect in the forced swimming test.	Imipramine	79-89	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	38-44
1683700-5	1991	Chronic treatment with IMI significantly elevated the concentration of cytochrome P-450 in the liver and had a tendency to increase the concentration of cytochrome b-5.	Imipramine	23-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
1671867-7	1991	Imipramine also decreased proopiomelanocortin (POMC) mRNA levels by 38% and glucocorticoid receptor (GR, type II) mRNA levels by 51% in the anterior pituitary.	Imipramine	0-10	proopiomelanocortin	Rattus norvegicus	26-45
1859207-4	1991	Inhibitors of phospholipase A2, including a variety of phenothiazines, dibucaine, imipramine, and verapamil, inhibited in vitro microsomal lipid peroxidation in response to TCDD administration.	Imipramine	82-92	phospholipase A2 group IB	Rattus norvegicus	14-30
1671867-7	1991	Imipramine also decreased proopiomelanocortin (POMC) mRNA levels by 38% and glucocorticoid receptor (GR, type II) mRNA levels by 51% in the anterior pituitary.	Imipramine	0-10	proopiomelanocortin	Rattus norvegicus	47-51
1671867-7	1991	Imipramine also decreased proopiomelanocortin (POMC) mRNA levels by 38% and glucocorticoid receptor (GR, type II) mRNA levels by 51% in the anterior pituitary.	Imipramine	0-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	76-99
1671867-7	1991	Imipramine also decreased proopiomelanocortin (POMC) mRNA levels by 38% and glucocorticoid receptor (GR, type II) mRNA levels by 51% in the anterior pituitary.	Imipramine	0-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	101-103
1671867-9	1991	In the light of data that major depression is associated with an activation of brain CRH and LC-NE systems, the time-dependent effect of long-term imipramine administration on decreasing the gene expression of CRH in the hypothalamus and TH in the LC may be relevant to the therapeutic efficacy of this agent in depression.	Imipramine	147-157	corticotropin releasing hormone	Rattus norvegicus	85-88
1671867-9	1991	In the light of data that major depression is associated with an activation of brain CRH and LC-NE systems, the time-dependent effect of long-term imipramine administration on decreasing the gene expression of CRH in the hypothalamus and TH in the LC may be relevant to the therapeutic efficacy of this agent in depression.	Imipramine	147-157	corticotropin releasing hormone	Rattus norvegicus	210-213
1671867-9	1991	In the light of data that major depression is associated with an activation of brain CRH and LC-NE systems, the time-dependent effect of long-term imipramine administration on decreasing the gene expression of CRH in the hypothalamus and TH in the LC may be relevant to the therapeutic efficacy of this agent in depression.	Imipramine	147-157	tyrosine hydroxylase	Rattus norvegicus	238-240
1811246-6	1991	We conclude that desipramine, imipramine, ketanserin and lithium can modulate GR mRNA in regions of rat brain involved in the control of the HPA axis and may have a common mechanism of action at the level of the GR gene.	Imipramine	30-40	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	78-80
1672374-3	1991	Desipramine, imipramine, amitriptyline and iprindole inhibited thrombin-stimulated formation of [3H]IP2 and [3H]IP3 in human platelets but had no significant effect on [3H]IP1 formation.	Imipramine	13-23	coagulation factor II, thrombin	Homo sapiens	63-71
1672374-3	1991	Desipramine, imipramine, amitriptyline and iprindole inhibited thrombin-stimulated formation of [3H]IP2 and [3H]IP3 in human platelets but had no significant effect on [3H]IP1 formation.	Imipramine	13-23	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	100-103
1994003-4	1991	The 5-HT uptake characteristics of L-S1 and L-S2 are essentially comparable (in terms of Na+ dependence, temperature sensitivity, imipramine antagonizability, kinetic saturability and high affinities) and those of L-S1 have been reported previously.	Imipramine	130-140	serpin family D member 1	Homo sapiens	35-48
1711266-0	1991	Chronic imipramine treatment increases the affinity of [125I]galanin binding sites in the tel- and diencephalon of the rat and alters the 5-HT1A/galanin receptor interaction.	Imipramine	8-18	5-hydroxytryptamine receptor 1A	Rattus norvegicus	138-144
1811246-2	1991	Northern blot analysis of Type II GR mRNA showed that treatment of male rats with either desipramine or imipramine increased hypothalamic and hippocampal GR mRNA levels.	Imipramine	104-114	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	34-36
1811246-2	1991	Northern blot analysis of Type II GR mRNA showed that treatment of male rats with either desipramine or imipramine increased hypothalamic and hippocampal GR mRNA levels.	Imipramine	104-114	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	154-156
1811246-3	1991	Upregulation of GR mRNA following administration of imipramine was found in brain regions of female rats, while desipramine had no effect.	Imipramine	52-62	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	16-18
1829231-0	1991	Involvement of 5-HT1A activity in the discriminative stimulus effects of imipramine.	Imipramine	73-83	5-hydroxytryptamine receptor 1A	Homo sapiens	15-21
1829231-2	1991	The selective 5-HT1A agonist 8-OH-DPAT (0.03-1.0 mg/kg) resulted in dose-dependent increases in responding on the key correlated with imipramine administration.	Imipramine	134-144	5-hydroxytryptamine receptor 1A	Homo sapiens	14-20
1829231-5	1991	The discriminative stimulus effects of imipramine were also blocked by administration of the alpha 1-adrenoceptor antagonist prazosin, suggesting a dual mediation of imipramine through both 5-HT1A and alpha 1-adrenoreceptor systems.	Imipramine	39-49	5-hydroxytryptamine receptor 1A	Homo sapiens	190-196
1829231-5	1991	The discriminative stimulus effects of imipramine were also blocked by administration of the alpha 1-adrenoceptor antagonist prazosin, suggesting a dual mediation of imipramine through both 5-HT1A and alpha 1-adrenoreceptor systems.	Imipramine	166-176	5-hydroxytryptamine receptor 1A	Homo sapiens	190-196
1988236-3	1991	Imipramine demethylation clearance was 0.74 L.min-1 (mean; range, 0.31-1.24) in poor metabolizers of mephenytoin compared with 1.43 L.min-1 (mean; range, 0.61-3.81) in extensive metabolizers of mephenytoin (p = 0.01, Mann-Whitney U test).	Imipramine	0-10	CD59 molecule (CD59 blood group)	Homo sapiens	46-51
1988236-3	1991	Imipramine demethylation clearance was 0.74 L.min-1 (mean; range, 0.31-1.24) in poor metabolizers of mephenytoin compared with 1.43 L.min-1 (mean; range, 0.61-3.81) in extensive metabolizers of mephenytoin (p = 0.01, Mann-Whitney U test).	Imipramine	0-10	CD59 molecule (CD59 blood group)	Homo sapiens	134-139
1811246-6	1991	We conclude that desipramine, imipramine, ketanserin and lithium can modulate GR mRNA in regions of rat brain involved in the control of the HPA axis and may have a common mechanism of action at the level of the GR gene.	Imipramine	30-40	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	212-214
2234106-0	1990	Alteration of cytochrome P-450 by prolonged administration of imipramine and/or lithium to rats.	Imipramine	62-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
2017459-9	1991	However, both imipramine and lithium normalized the decreased level of AChE activity in striatum in rats exposed to shock stress.	Imipramine	14-24	acetylcholinesterase	Rattus norvegicus	71-75
1963597-3	1990	The same treatment schedule with GnRH produced an increase in the number of [3H]imipramine Bmax in cortical membranes that was statistically significant at the dose of 2 micrograms/kg.	Imipramine	80-90	gonadotropin releasing hormone 1	Mus musculus	33-37
2234106-1	1990	The aim of this study was to investigate imipramine-induced alterations of cytochrome P-450 and to determine whether prolonged concomitant administration of imipramine and lithium results in a pharmacokinetic interaction.	Imipramine	41-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	75-91
2234106-4	1990	The long term treatment with imipramine produced a very complex alteration of cytochrome P-450: imipramine increased the level of the cytochrome, but it decreased the rate of its own aromatic hydroxylation in position 2.	Imipramine	29-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
2234106-4	1990	The long term treatment with imipramine produced a very complex alteration of cytochrome P-450: imipramine increased the level of the cytochrome, but it decreased the rate of its own aromatic hydroxylation in position 2.	Imipramine	96-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
2234106-10	1990	The preliminary SDS-PAGE analysis of cytochrome P-450 isoenzymes of control and imipramine treated rats showed that the investigated antidepressant markedly intensified a protein band at 50.11 kD while bands at 51.28 kD, 56.20 kD and 56.88 kD were less intensive.	Imipramine	80-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
2234106-11	1990	These results indicate that the alteration of cytochrome P-450 by imipramine treatment is not only of quantitative but also of qualitative character.	Imipramine	66-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
2234106-13	1990	Lithium given jointly with imipramine reduced imipramine-induced elevation of cytochrome P-450.	Imipramine	27-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
2234106-13	1990	Lithium given jointly with imipramine reduced imipramine-induced elevation of cytochrome P-450.	Imipramine	46-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
2159606-0	1990	Imipramine prevents gastric lesions induced by centrally administered thyrotropin-releasing hormone (TRH) in rats.	Imipramine	0-10	thyrotropin releasing hormone	Rattus norvegicus	70-99
2353937-7	1990	SK-N-SH cells were depleted from stored MIBG by the Uptake-1 inhibitor imipramine but poorly so by the granule-depleting drug reserpine.	Imipramine	71-81	hedgehog acyltransferase	Homo sapiens	0-4
2159606-0	1990	Imipramine prevents gastric lesions induced by centrally administered thyrotropin-releasing hormone (TRH) in rats.	Imipramine	0-10	thyrotropin releasing hormone	Rattus norvegicus	101-104
2159606-2	1990	Potential interactions between TRH and imipramine (a typical tricyclic antidepressant (TCA] on the development of TRH-induced gastric lesions have not been investigated.	Imipramine	39-49	thyrotropin releasing hormone	Rattus norvegicus	114-117
2181052-10	1990	Imipramine stimulation is greatly decreased in cat-1 and cat-4 mutants, which have low levels of serotonin.	Imipramine	0-10	MFS domain-containing protein	Caenorhabditis elegans	47-52
2181052-10	1990	Imipramine stimulation is greatly decreased in cat-1 and cat-4 mutants, which have low levels of serotonin.	Imipramine	0-10	GTP cyclohydrolase 1	Caenorhabditis elegans	57-62
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Imipramine	0-10	interleukin 1 alpha	Homo sapiens	67-75
2398522-1	1990	The ADx total serum tricyclic antidepressant (TCA) fluorescence polarization immunoassay (Abbott Diagnostics) for the semi-quantitation of imipramine or amitriptyline and their respective N-demethylated metabolites in cases of TCA overdose was evaluated.	Imipramine	139-149	ferredoxin 1	Homo sapiens	4-7
2398522-4	1990	A good correlation between the results of patient serum containing imipramine and desipramine simultaneously analyzed by ADx and gas liquid chromatography (GC) was observed, r2 = 0.964, n = 32.	Imipramine	67-77	ferredoxin 1	Homo sapiens	121-124
2113675-1	1990	The present study investigated the effect of repeated treatment with the antidepressant drugs imipramine, amitryptyline, citalopram and mianserin (10 mg/kg PO, twice daily for 14 days) on levels of thyrotropin-releasing hormone (TRH) in several brain structures (cerebral cortex, amygdala + pyriform cortex, hippocampus, nucleus accumbens, striatum and hypothalamus) of the rat.	Imipramine	94-104	thyrotropin releasing hormone	Rattus norvegicus	198-227
33798597-8	2021	In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling.	Imipramine	64-74	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	183-192
33798597-8	2021	In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling.	Imipramine	64-74	X-box binding protein 1	Homo sapiens	193-197
33798597-9	2021	Despite potentiation of ER stress-induced XBP1 splicing, imipramine suppresses both thapsigargin- and tunicamycin-induced expression of Hrd1.	Imipramine	57-67	synoviolin 1	Homo sapiens	136-140
2129312-0	1990	Thyrotropin and prolactin responses to protirelin (TRH) prior to and during chronic imipramine treatment in patients with panic disorder.	Imipramine	84-94	prolactin	Homo sapiens	16-25
2129312-2	1990	During imipramine treatment, the patients exhibited an increase in their TSH response to TRH (delta delta max TSH = 3.65 +/- 6.02 mu IU/ml, p less than 0.05) and in their PRL response to TRH (delta AUCPRL = 734 +/- 965 ng/ml/45 min, p less than 0.005).	Imipramine	7-17	thyrotropin releasing hormone	Homo sapiens	89-92
2129312-2	1990	During imipramine treatment, the patients exhibited an increase in their TSH response to TRH (delta delta max TSH = 3.65 +/- 6.02 mu IU/ml, p less than 0.05) and in their PRL response to TRH (delta AUCPRL = 734 +/- 965 ng/ml/45 min, p less than 0.005).	Imipramine	7-17	thyrotropin releasing hormone	Homo sapiens	187-190
33775777-11	2021	Results showed that imipramine prevents memory impairment in STZ induced rats and this improvement was accompanied with an increase in ERK activity, reduction of caspase-3 and JNK activity, as well as partial restoration of P38 and IRS-1 activity.	Imipramine	20-30	Eph receptor B1	Rattus norvegicus	135-138
33775777-11	2021	Results showed that imipramine prevents memory impairment in STZ induced rats and this improvement was accompanied with an increase in ERK activity, reduction of caspase-3 and JNK activity, as well as partial restoration of P38 and IRS-1 activity.	Imipramine	20-30	caspase 3	Rattus norvegicus	162-171
33775777-11	2021	Results showed that imipramine prevents memory impairment in STZ induced rats and this improvement was accompanied with an increase in ERK activity, reduction of caspase-3 and JNK activity, as well as partial restoration of P38 and IRS-1 activity.	Imipramine	20-30	mitogen-activated protein kinase 8	Rattus norvegicus	176-179
33775777-11	2021	Results showed that imipramine prevents memory impairment in STZ induced rats and this improvement was accompanied with an increase in ERK activity, reduction of caspase-3 and JNK activity, as well as partial restoration of P38 and IRS-1 activity.	Imipramine	20-30	mitogen activated protein kinase 14	Rattus norvegicus	224-227
33775777-11	2021	Results showed that imipramine prevents memory impairment in STZ induced rats and this improvement was accompanied with an increase in ERK activity, reduction of caspase-3 and JNK activity, as well as partial restoration of P38 and IRS-1 activity.	Imipramine	20-30	insulin receptor substrate 1	Rattus norvegicus	232-237
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Imipramine	0-10	C-C motif chemokine ligand 2	Homo sapiens	77-81
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Imipramine	0-10	intercellular adhesion molecule 1	Homo sapiens	112-118
33814004-6	2021	These biochemical and behavioural changes were significantly alleviated by CAF and IMI chronic treatment.Conclusion: The results of this study implicate that mild-moderate consumption of CAF could impart anti-inflammatory properties under neuroinflammatory conditions by modulating the cytokine and neurotrophic mechanisms.	Imipramine	83-86	caffeine susceptibility	Mus musculus	187-190
19892699-2	2010	SERT is the target for widely used antidepressant drugs, including imipramine, fluoxetine, and (S)-citalopram, which are competitive inhibitors of the transport function.	Imipramine	67-77	solute carrier family 6 member 4	Homo sapiens	0-4
22423384-9	2012	Diabetic rats injected with saline did not show altered BDNF levels in the prefrontal cortex, hippocampus or amygdala, but interestingly, the treatment with imipramine in diabetic animals increased BDNF levels in the prefrontal cortex.	Imipramine	157-167	brain-derived neurotrophic factor	Rattus norvegicus	56-60
22423384-9	2012	Diabetic rats injected with saline did not show altered BDNF levels in the prefrontal cortex, hippocampus or amygdala, but interestingly, the treatment with imipramine in diabetic animals increased BDNF levels in the prefrontal cortex.	Imipramine	157-167	brain-derived neurotrophic factor	Rattus norvegicus	198-202
34729805-3	2022	In this study, we investigate the effect of imipramine on Eag1 channel expression in DU145 prostate cancer cells.	Imipramine	44-54	potassium voltage-gated channel subfamily H member 1	Homo sapiens	58-62
34729805-7	2022	It was observed that all three doses of imipramine significantly reduced Eag1 currents and conductivity compared with the control.	Imipramine	40-50	potassium voltage-gated channel subfamily H member 1	Homo sapiens	73-77
34729805-9	2022	Similarly, Eag1 channel protein expression was found to be significantly reduced for all three doses of imipramine compared with the control group, but there was no significant difference in gene expression between dose groups.	Imipramine	104-114	potassium voltage-gated channel subfamily H member 1	Homo sapiens	11-15
34729805-10	2022	Obtained results suggested that imipramine has the potential to be used as a pharmacological agent targeting the Eag1 channel in the treatment of prostate cancer.	Imipramine	32-42	potassium voltage-gated channel subfamily H member 1	Homo sapiens	113-117
34748647-0	2022	Inhibition of acid sphingomyelinase by imipramine abolishes the synergy between metabolic syndrome and periodontitis on alveolar bone loss.	Imipramine	39-49	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	14-35
34748647-5	2022	MATERIAL AND METHODS: We induced MetS and periodontitis in C57BL/6 mice by feeding high-fat diet (HFD) and periodontal injection of A. actinomycetemcomitans LPS, respectively, and treated mice with imipramine, a well-established inhibitor of aSMase.	Imipramine	198-208	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	242-248
34748647-11	2022	To elucidate the mechanisms by which imipramine attenuates MetS-exacerbated periodontitis, we showed that imipramine inhibited the upregulation of pro-inflammatory cytokines and transcription factor c-FOS as well as ceramide production by LPS plus PA in macrophages.	Imipramine	37-47	FBJ osteosarcoma oncogene	Mus musculus	199-204
34748647-11	2022	To elucidate the mechanisms by which imipramine attenuates MetS-exacerbated periodontitis, we showed that imipramine inhibited the upregulation of pro-inflammatory cytokines and transcription factor c-FOS as well as ceramide production by LPS plus PA in macrophages.	Imipramine	106-116	FBJ osteosarcoma oncogene	Mus musculus	199-204
34748647-12	2022	CONCLUSION: This study has shown that imipramine as an inhibitor of aSMase abolishes the synergy between MetS and periodontitis on alveolar bone loss in animal model and inhibits pro-inflammatory and pro-osteoclastogenic gene expression in macrophages in vitro.	Imipramine	38-48	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	68-74
34469035-0	2021	Imipramine impedes glioma progression by inhibiting YAP as a Hippo pathway independent manner and synergizes with temozolomide.	Imipramine	0-10	Yes1 associated transcriptional regulator	Homo sapiens	52-55
34251544-8	2021	shRNA and imipramine were used to regulate the expression and activity of ASMase.	Imipramine	10-20	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	74-80
34832986-0	2021	Combinatorial Regimen of Carbamazepine and Imipramine Exhibits Synergism against Grandmal Epilepsy in Rats: Inhibition of Pro-Inflammatory Cytokines and PI3K/Akt/mTOR Signaling Pathway.	Imipramine	43-53	AKT serine/threonine kinase 1	Rattus norvegicus	158-161
34832986-0	2021	Combinatorial Regimen of Carbamazepine and Imipramine Exhibits Synergism against Grandmal Epilepsy in Rats: Inhibition of Pro-Inflammatory Cytokines and PI3K/Akt/mTOR Signaling Pathway.	Imipramine	43-53	mechanistic target of rapamycin kinase	Rattus norvegicus	162-166
34832986-8	2021	We found that the low dose combinatorial therapy of CBZ (20 mg/kg) + IMI (10 mg/kg) exhibits synergism (p < 0.001) in abrogation of maximal electroshock (MES) induced convulsions/tonic hind limb extension (THLE), by reducing levels of pro-inflammatory cytokines, and weakening of the PI3K/Akt/mTOR signal.	Imipramine	69-72	AKT serine/threonine kinase 1	Rattus norvegicus	289-292
34832986-8	2021	We found that the low dose combinatorial therapy of CBZ (20 mg/kg) + IMI (10 mg/kg) exhibits synergism (p < 0.001) in abrogation of maximal electroshock (MES) induced convulsions/tonic hind limb extension (THLE), by reducing levels of pro-inflammatory cytokines, and weakening of the PI3K/Akt/mTOR signal.	Imipramine	69-72	mechanistic target of rapamycin kinase	Rattus norvegicus	293-297
34571049-0	2021	Upregulation of the mGlu5 receptor and COX-2 protein in the mouse brain after imipramine and NS398, searching for mechanisms of regulation.	Imipramine	78-88	prostaglandin-endoperoxide synthase 2	Mus musculus	39-44
34571049-5	2021	Our previous study revealed that manipulation of the AA pathway via inhibition of cyclooxygenase-2 (COX-2) by selective COX-2 inhibitor (NS398) could effectively modulate the behavior of mice treated with imipramine.	Imipramine	205-215	prostaglandin-endoperoxide synthase 2	Mus musculus	82-98
34571049-5	2021	Our previous study revealed that manipulation of the AA pathway via inhibition of cyclooxygenase-2 (COX-2) by selective COX-2 inhibitor (NS398) could effectively modulate the behavior of mice treated with imipramine.	Imipramine	205-215	prostaglandin-endoperoxide synthase 2	Mus musculus	100-105
34571049-5	2021	Our previous study revealed that manipulation of the AA pathway via inhibition of cyclooxygenase-2 (COX-2) by selective COX-2 inhibitor (NS398) could effectively modulate the behavior of mice treated with imipramine.	Imipramine	205-215	prostaglandin-endoperoxide synthase 2	Mus musculus	120-125
34571049-6	2021	Here, we hypothesized that COX-2 inhibition could similarly to imipramine influence mGlu5 receptor, and thus NS398 can modulate the effect of imipramine on Glu.	Imipramine	142-152	prostaglandin-endoperoxide synthase 2	Mus musculus	27-32
34571049-12	2021	A time-dependent change in mGlu5 receptor and COX-2 protein level, COX-2 expression, and 2-AG level in the PFC after imipramine administration was found.	Imipramine	117-127	prostaglandin-endoperoxide synthase 2	Mus musculus	46-51
34571049-12	2021	A time-dependent change in mGlu5 receptor and COX-2 protein level, COX-2 expression, and 2-AG level in the PFC after imipramine administration was found.	Imipramine	117-127	prostaglandin-endoperoxide synthase 2	Mus musculus	67-72
34765548-0	2021	Suppression of EGFR/PKC-delta/NF-kappaB Signaling Associated With Imipramine-Inhibited Progression of Non-Small Cell Lung Cancer.	Imipramine	66-76	epidermal growth factor receptor	Mus musculus	15-19
34765548-3	2021	Whether EGFR would be the target of imipramine for suppressing tumor signaling transduction and results in anti-tumor potential is remaining unclear.	Imipramine	36-46	epidermal growth factor receptor	Mus musculus	8-12
34765548-9	2021	The phosphorylation of EGFR/PKC-delta/NF-kappaB and their downstream proteins were all decreased by imipramine.	Imipramine	100-110	epidermal growth factor receptor	Mus musculus	23-27
34765548-9	2021	The phosphorylation of EGFR/PKC-delta/NF-kappaB and their downstream proteins were all decreased by imipramine.	Imipramine	100-110	protein kinase C, delta	Mus musculus	28-37
34765548-9	2021	The phosphorylation of EGFR/PKC-delta/NF-kappaB and their downstream proteins were all decreased by imipramine.	Imipramine	100-110	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-47
34765548-12	2021	Conclusion: Imipramine-triggered anti-NSCLC effects in both in vitro and in vivo model are at least partially attributed to its suppression of EGFR/PKC-delta/NF-kappaB pathway.	Imipramine	12-22	epidermal growth factor receptor	Mus musculus	143-147
34765548-12	2021	Conclusion: Imipramine-triggered anti-NSCLC effects in both in vitro and in vivo model are at least partially attributed to its suppression of EGFR/PKC-delta/NF-kappaB pathway.	Imipramine	12-22	protein kinase C, delta	Mus musculus	148-157
34765548-12	2021	Conclusion: Imipramine-triggered anti-NSCLC effects in both in vitro and in vivo model are at least partially attributed to its suppression of EGFR/PKC-delta/NF-kappaB pathway.	Imipramine	12-22	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	158-167
34390690-6	2021	Imipramine induced only a marginal reduction in the enhanced passive coping behaviour in GPR39KO mice, which was associated with attenuation of the hyperactive prefrontal cortex.	Imipramine	0-10	G protein-coupled receptor 39	Mus musculus	89-94
34390690-7	2021	Similarly, the aberrant activity within the amygdalar subregions was normalized following imipramine treatment in the GPR39KO mice, indicating that imipramine mediates these effects independently of GPR39 in the prefrontal cortex and amygdala.	Imipramine	90-100	G protein-coupled receptor 39	Mus musculus	118-123
34390690-10	2021	Taken together, our data suggest that monoamine-based antidepressants such as imipramine exert their action via GPR39-dependent and -independent pathways.	Imipramine	78-88	G protein-coupled receptor 39	Mus musculus	112-117
34469035-6	2021	Mechanistically, imipramine suppressed tumour proliferation by inhibiting yes-associated protein (YAP), a recognized oncogene in glioma, independent of Hippo pathway.	Imipramine	17-27	Yes1 associated transcriptional regulator	Homo sapiens	74-96
34469035-6	2021	Mechanistically, imipramine suppressed tumour proliferation by inhibiting yes-associated protein (YAP), a recognized oncogene in glioma, independent of Hippo pathway.	Imipramine	17-27	Yes1 associated transcriptional regulator	Homo sapiens	98-101
34469035-7	2021	In addition to inhibiting YAP transcription, imipramine also promoted the subcellular translocation of YAP from nucleus into cytoplasm.	Imipramine	45-55	Yes1 associated transcriptional regulator	Homo sapiens	26-29
34469035-7	2021	In addition to inhibiting YAP transcription, imipramine also promoted the subcellular translocation of YAP from nucleus into cytoplasm.	Imipramine	45-55	Yes1 associated transcriptional regulator	Homo sapiens	103-106
34469035-9	2021	Moreover, exogenous overexpression of YAP partially restored the inhibitory effect of imipramine on glioma progression.	Imipramine	86-96	Yes1 associated transcriptional regulator	Homo sapiens	38-41
34469035-11	2021	In conclusion, we found that tricyclic antidepressant imipramine impedes glioma progression by inhibiting YAP.	Imipramine	54-64	Yes1 associated transcriptional regulator	Homo sapiens	106-109
34564583-5	2021	Furthermore, the obese mice that received imipramine treatment exhibited insulin resistance, worse glucose intolerance, decreased glucose transporter 4 expression and Akt phosphorylation levels, and increased chromium loss through urine.	Imipramine	42-52	thymoma viral proto-oncogene 1	Mus musculus	167-170
34527794-3	2021	Here, we show that tricyclic antidepressants (TCAs) with weight-gain side effects, such as imipramine and amitriptyline, directly increased FTO expression and activated its epigenetic function in the ventral tegmental area (VTA).	Imipramine	91-101	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	140-143
34527794-5	2021	Mechanistically, both transcriptome sequencing and quantitative PCR revealed that overexpression of FTO in the VTA decreased the transcription of stress-related neuropeptides, such as cocaine- and amphetamine-regulated transcript peptide and urocortin, in the social defeat model, which was mimicked by imipramine, suggesting an m6A-dependent transcription mechanism of stress-related neuropeptides may underlie the responses to antidepressant.	Imipramine	303-313	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	100-103
34527794-5	2021	Mechanistically, both transcriptome sequencing and quantitative PCR revealed that overexpression of FTO in the VTA decreased the transcription of stress-related neuropeptides, such as cocaine- and amphetamine-regulated transcript peptide and urocortin, in the social defeat model, which was mimicked by imipramine, suggesting an m6A-dependent transcription mechanism of stress-related neuropeptides may underlie the responses to antidepressant.	Imipramine	303-313	urocortin	Homo sapiens	242-251
34564583-7	2021	Retinal injury worsened in imipramine-treated mice; decreases in retinal cell layer organization and retinal thickness and increases in nuclear factor kappaB and inducible nitric oxide synthase levels were observed.	Imipramine	27-37	nitric oxide synthase 2, inducible	Mus musculus	162-193
34421682-7	2021	GUO and IMI reversed the OBX-induced hyperlocomotion and recognition memory impairment, hippocampal BDNF increase, and redox imbalance (ROS, NO, and GSH levels).	Imipramine	8-11	brain derived neurotrophic factor	Mus musculus	100-104
34417466-8	2021	Our SERT structure with bound imipramine and vilazodone reveals a unique binding pocket for vilazodone, expanding the boundaries of the extracellular vestibule.	Imipramine	30-40	solute carrier family 6 member 4	Homo sapiens	4-8
34421605-5	2021	Imipramine inhibited neutrophil adhesion and concomitant secretion of proteins, including matrix metalloproteinase 9 (MMP-9) and neutrophil gelatinase-associated lipocalin (NGAL), which modify the extracellular matrix and basement membranes required for cell migration.	Imipramine	0-10	matrix metallopeptidase 9	Homo sapiens	90-116
34421605-5	2021	Imipramine inhibited neutrophil adhesion and concomitant secretion of proteins, including matrix metalloproteinase 9 (MMP-9) and neutrophil gelatinase-associated lipocalin (NGAL), which modify the extracellular matrix and basement membranes required for cell migration.	Imipramine	0-10	matrix metallopeptidase 9	Homo sapiens	118-123
34421605-5	2021	Imipramine inhibited neutrophil adhesion and concomitant secretion of proteins, including matrix metalloproteinase 9 (MMP-9) and neutrophil gelatinase-associated lipocalin (NGAL), which modify the extracellular matrix and basement membranes required for cell migration.	Imipramine	0-10	lipocalin 2	Homo sapiens	129-171
34421605-5	2021	Imipramine inhibited neutrophil adhesion and concomitant secretion of proteins, including matrix metalloproteinase 9 (MMP-9) and neutrophil gelatinase-associated lipocalin (NGAL), which modify the extracellular matrix and basement membranes required for cell migration.	Imipramine	0-10	lipocalin 2	Homo sapiens	173-177
34421605-7	2021	In contrast, imipramine enhanced the release of ROS by neutrophils during adhesion to fibronectin and stimulated apoptosis.	Imipramine	13-23	fibronectin 1	Homo sapiens	86-97
35597327-0	2022	Pro-cognitive effect of acute imipramine administration correlates with direct interaction of BDNF with its receptor, Trkbeta.	Imipramine	30-40	brain-derived neurotrophic factor	Rattus norvegicus	94-98
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	163-192
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	194-199
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	243-247
35597327-0	2022	Pro-cognitive effect of acute imipramine administration correlates with direct interaction of BDNF with its receptor, Trkbeta.	Imipramine	30-40	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	118-125
35568265-0	2022	The antidepressant imipramine inhibits breast cancer growth by targeting estrogen receptor signaling and DNA repair events.	Imipramine	19-29	estrogen receptor 1	Homo sapiens	73-90
35568265-2	2022	Here, we demonstrate that the anti-depressant imipramine blocks growth of triple-negative (TNBC) and estrogen receptor-positive (ER+) breast cancers by inducing cell cycle arrest and by blocking heightened homologous recombination (HR) and non-homologous end joining-mediated (NHEJ) DNA repair activities.	Imipramine	46-56	estrogen receptor 1	Homo sapiens	101-118
35568265-4	2022	In addition, we show that imipramine inhibits the growth of ER + breast cancers by inhibiting the estrogen receptor- alpha (ER-alpha) signaling.	Imipramine	26-36	estrogen receptor 1	Homo sapiens	98-122
35568265-2	2022	Here, we demonstrate that the anti-depressant imipramine blocks growth of triple-negative (TNBC) and estrogen receptor-positive (ER+) breast cancers by inducing cell cycle arrest and by blocking heightened homologous recombination (HR) and non-homologous end joining-mediated (NHEJ) DNA repair activities.	Imipramine	46-56	epiregulin	Homo sapiens	129-131
35568265-4	2022	In addition, we show that imipramine inhibits the growth of ER + breast cancers by inhibiting the estrogen receptor- alpha (ER-alpha) signaling.	Imipramine	26-36	estrogen receptor 1	Homo sapiens	124-132
35568265-5	2022	Our studies in preclinical mouse models and ex vivo explants from breast cancer patients show that imipramine sensitizes TNBC to the PARP inhibitor olaparib and endocrine resistant ER + breast cancer to anti-estrogens.	Imipramine	99-109	collagen type XI alpha 2 chain	Homo sapiens	133-137
35568265-7	2022	Based on these results, we designed an ongoing clinical trial, where we are testing the efficacy of imipramine for treating patients with triple-negative and estrogen receptor-positive breast cancer.	Imipramine	100-110	estrogen receptor 1	Homo sapiens	158-175
35568265-3	2022	Our results reveal that imipramine inhibits the expression of several cell cycle- and DNA repair-associated proteins including E2F1, CDK1, Cyclin D1, and RAD51.	Imipramine	24-34	E2F transcription factor 1	Homo sapiens	127-131
35568265-3	2022	Our results reveal that imipramine inhibits the expression of several cell cycle- and DNA repair-associated proteins including E2F1, CDK1, Cyclin D1, and RAD51.	Imipramine	24-34	cyclin dependent kinase 1	Homo sapiens	133-137
35568265-3	2022	Our results reveal that imipramine inhibits the expression of several cell cycle- and DNA repair-associated proteins including E2F1, CDK1, Cyclin D1, and RAD51.	Imipramine	24-34	cyclin D1	Homo sapiens	139-148
35568265-3	2022	Our results reveal that imipramine inhibits the expression of several cell cycle- and DNA repair-associated proteins including E2F1, CDK1, Cyclin D1, and RAD51.	Imipramine	24-34	RAD51 recombinase	Homo sapiens	154-159
35568265-4	2022	In addition, we show that imipramine inhibits the growth of ER + breast cancers by inhibiting the estrogen receptor- alpha (ER-alpha) signaling.	Imipramine	26-36	epiregulin	Homo sapiens	60-62
2613103-4	1989	3) In imipramine treated heart, isoproterenol-induced stimulation of ornithine decarboxylase activity was significantly decreased compared with that in the vehicle control.	Imipramine	6-16	ornithine decarboxylase 1	Rattus norvegicus	69-92
35203316-7	2022	Imipramine is mainly used in the treatment of depression and certain anxiety disorders, and it is particularly known as an ASMase inhibitor.	Imipramine	0-10	sphingomyelin phosphodiesterase 1	Homo sapiens	123-129
35203316-8	2022	We hypothesized that imipramine could decrease hippocampal neuronal death by reducing ceramide via the inhibition of ASMase after hypoglycemia.	Imipramine	21-31	sphingomyelin phosphodiesterase 1	Homo sapiens	117-123
35370268-6	2022	Imipramine N-glucuronidation, which is formed mainly by UGT1A4, was also decreased by SWCNTs.	Imipramine	0-10	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	56-62
2557127-3	1989	This study investigated acute and chronic effects of imipramine on intracellularly-recorded responses mediated by 5-HT and beta-adrenergic receptors on pyramidal cells from area CA1 of rat hippocampal slices maintained in vitro.	Imipramine	53-63	carbonic anhydrase 1	Rattus norvegicus	178-181
2557127-4	1989	Addition of 10 microM imipramine in the perfusion medium sinistrally shifted the 5-HT1A concentration-response curve for membrane hyperpolarization and the 5-HT concentration-response curve for the reduction in the amplitude of the slow afterhyperpolarization (AHP) elicited by a train of action potentials.	Imipramine	22-32	5-hydroxytryptamine receptor 1A	Rattus norvegicus	81-87
35631123-5	2022	This finding prompted us to investigate the possibility of testing imipramine, an antidepressant drug known to inhibit NPC1 function by interfering with intracellular cholesterol trafficking.	Imipramine	67-77	NPC intracellular cholesterol transporter 1	Homo sapiens	119-123
2576687-0	1989	Does chronic imipramine facilitate neurotransmission at dopamine-D1 receptor level?	Imipramine	13-23	dopamine receptor D1	Homo sapiens	56-76
2811859-2	1989	Iodoimipramine competitively inhibits [3H]imipramine binding with a KI of 0.52 nM and also inhibits [3H]serotonin transport competitively, suggesting that serotonin, imipramine, and iodoimipramine all bind to the same site on the serotonin transporter.	Imipramine	4-14	solute carrier family 6 member 4	Homo sapiens	230-251
2573711-3	1989	Both imipramine and amitriptyline, given repeatedly, potentiated the TRH response, though the effect was observed 2 but not 72 h after the last dose of those drugs.	Imipramine	5-15	thyrotropin releasing hormone	Mus musculus	69-72
2541855-16	1989	These data indicate that TRH is able to potentiate the effect not only of imipramine but of other antidepressants in the mouse forced-swimming test, although these other antidepressants act in various ways on cerebral amines.	Imipramine	74-84	thyrotropin releasing hormone	Mus musculus	25-28
2775233-1	1989	The effects of the local anaesthetics procaine, tetracaine and lidocaine and of the antidepressant imipramine on human erythrocyte acetylcholinesterase were investigated.	Imipramine	99-109	acetylcholinesterase (Cartwright blood group)	Homo sapiens	131-151
2761132-3	1989	administration of imipramine (20 mg/kg/day for 21 days) decreased the densities of 5-HT1, 5-HT1A, 5-HT1C and 5-HT2 sites in the frontal cortex, hippocampus and choroid plexus.	Imipramine	18-28	5-hydroxytryptamine receptor 1A	Rattus norvegicus	90-96
2761132-3	1989	administration of imipramine (20 mg/kg/day for 21 days) decreased the densities of 5-HT1, 5-HT1A, 5-HT1C and 5-HT2 sites in the frontal cortex, hippocampus and choroid plexus.	Imipramine	18-28	5-hydroxytryptamine receptor 2C	Rattus norvegicus	98-104
2761132-5	1989	Imipramine and lithium very markedly decreased the density of 5-HT1C sites in the choroid plexus.	Imipramine	0-10	5-hydroxytryptamine receptor 2C	Rattus norvegicus	62-68
2541855-2	1989	It has been shown that thyrotropin releasing hormone (TRH) can potentiate the effects of the antidepressant, imipramine, as measured by the mouse forced-swimming test.	Imipramine	109-119	thyrotropin releasing hormone	Mus musculus	23-52
2541855-2	1989	It has been shown that thyrotropin releasing hormone (TRH) can potentiate the effects of the antidepressant, imipramine, as measured by the mouse forced-swimming test.	Imipramine	109-119	thyrotropin releasing hormone	Mus musculus	54-57
2473464-3	1989	Moreover, treatment of rats with amitriptyline or imipramine, tricyclic antidepressants in wide therapeutic use for depression, markedly increases the amount of RNA species hybridizing with P-450b cDNA probe in comparison to untreated controls.	Imipramine	50-60	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	190-196
2553044-1	1989	We examined the effects of chronic treatment with antidepressants (imipramine or desipramine) or benzodiazepines (diazepam, alprazolam, or adinazolam) on modulation of corticotropin-releasing-factor (CRF) receptors in discrete areas of rat brain and in anterior pituitary.	Imipramine	67-77	corticotropin releasing hormone	Rattus norvegicus	168-198
2521644-0	1989	Effect of imipramine treatment on the prolactin response to fenfluramine and placebo challenge in depressed patients.	Imipramine	10-20	prolactin	Homo sapiens	38-47
2734349-0	1989	Long-term imipramine treatment potentiates m-chlorophenylpiperazine-induced changes in prolactin but not corticosterone or growth hormone levels in rats.	Imipramine	10-20	prolactin	Rattus norvegicus	87-96
2642913-8	1989	The configurational change was blocked by agents that inhibited 5-HT uptake, such as imipramine, verapamil, ketanserin, and methiothepin; it was unaffected by inhibitors of protein kinase C, phospholipase C, and calmodulin or absence of Ca2+ from the medium.	Imipramine	85-95	calmodulin	Bos taurus	212-222
2565359-0	1989	The influence of repeated treatment with imipramine, (+)- and (-)-oxaprotiline on behavioural effects of dopamine D-1 and D-2 agonists.	Imipramine	41-51	solute carrier family 3 member 1	Rattus norvegicus	105-125
2565359-1	1989	The paper examined the action of imipramine, (+)- and (-)-oxaprotiline, administered repeatedly to rats, on the behavioural effects of the dopamine D-1 and D-2 agonists, SKF 38393 and quinpirole, respectively.	Imipramine	33-43	solute carrier family 3 member 1	Rattus norvegicus	139-159
3225754-7	1988	These data strongly suggest that the hydroxylation pathways of imipramine and desipramine and the demethylation pathways of imipramine and 2-hydroxyimipramine are each sharing the same species of cytochrome P-450.	Imipramine	63-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	196-212
3225754-7	1988	These data strongly suggest that the hydroxylation pathways of imipramine and desipramine and the demethylation pathways of imipramine and 2-hydroxyimipramine are each sharing the same species of cytochrome P-450.	Imipramine	124-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	196-212
2967771-3	1988	Imipramine increased the concentration of NPY-LI in the hypothalamus by 65% while zimeldine was without effect.	Imipramine	0-10	neuropeptide Y	Rattus norvegicus	42-45
3167143-4	1988	This study shows that an oral dose of 50 mg imipramine given at bedtime to depressed patients has little effect on the secretion of prolactin and melatonin, but acutely advances the secretion of growth hormone and cortisol.	Imipramine	44-54	growth hormone 1	Homo sapiens	195-209
2854066-1	1988	The activity of various calcium channel blockers at the serotonin transporter, as determined by their effects on imipramine binding and serotonin uptake, was investigated in rat brain and human platelets.	Imipramine	113-123	solute carrier family 6 member 4	Rattus norvegicus	56-77
3392536-3	1988	Equilibrium dialysis showed that imipramine is highly bound to human serum albumin (HSA), alpha 1-acid glycoprotein (AAG), lipoproteins, and erythrocytes.	Imipramine	33-43	albumin	Rattus norvegicus	69-82
3392536-3	1988	Equilibrium dialysis showed that imipramine is highly bound to human serum albumin (HSA), alpha 1-acid glycoprotein (AAG), lipoproteins, and erythrocytes.	Imipramine	33-43	orosomucoid 1	Rattus norvegicus	90-115
3392536-3	1988	Equilibrium dialysis showed that imipramine is highly bound to human serum albumin (HSA), alpha 1-acid glycoprotein (AAG), lipoproteins, and erythrocytes.	Imipramine	33-43	orosomucoid 1	Rattus norvegicus	117-120
3199589-0	1988	Chronic effects of imipramine and lithium on postsynaptic 5-HT1A and 5-HT1B sites and on presynaptic 5-HT3 sites in rat brain.	Imipramine	19-29	5-hydroxytryptamine receptor 1A	Rattus norvegicus	58-64
3199589-0	1988	Chronic effects of imipramine and lithium on postsynaptic 5-HT1A and 5-HT1B sites and on presynaptic 5-HT3 sites in rat brain.	Imipramine	19-29	5-hydroxytryptamine receptor 1B	Rattus norvegicus	69-75
3199589-1	1988	The effects of chronic treatment with imipramine, a tricyclic antidepressant, or lithium, an antimanic-depressive illness drug, on postsynaptic serotonin-1A (5-HT1A) and 5-HT1B sites and on presynaptic 5-HT3 sites in the frontal cortex and hippocampus from rat brains were studied.	Imipramine	38-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	158-164
3199589-1	1988	The effects of chronic treatment with imipramine, a tricyclic antidepressant, or lithium, an antimanic-depressive illness drug, on postsynaptic serotonin-1A (5-HT1A) and 5-HT1B sites and on presynaptic 5-HT3 sites in the frontal cortex and hippocampus from rat brains were studied.	Imipramine	38-48	5-hydroxytryptamine receptor 1B	Rattus norvegicus	170-176
3199589-3	1988	administration (21 days) of imipramine reduced the maximum number of binding sites (Bmax) for postsynaptic 5-HT1A as monitored by the radioligands 3H-5-HT or 3H-8-hydroxy-2-(di-n-propylamino)tetralin (3H-8-OH-DPAT), but did not change the Bmax for postsynaptic 5-HT1B and presynaptic 5-HT3 in either the frontal cortex or the hippocampus.	Imipramine	28-38	5-hydroxytryptamine receptor 1A	Rattus norvegicus	107-113
3199589-3	1988	administration (21 days) of imipramine reduced the maximum number of binding sites (Bmax) for postsynaptic 5-HT1A as monitored by the radioligands 3H-5-HT or 3H-8-hydroxy-2-(di-n-propylamino)tetralin (3H-8-OH-DPAT), but did not change the Bmax for postsynaptic 5-HT1B and presynaptic 5-HT3 in either the frontal cortex or the hippocampus.	Imipramine	28-38	5-hydroxytryptamine receptor 1B	Rattus norvegicus	261-267
3199589-6	1988	There was a specific difference between imipramine and lithium regarding the inhibitory effect on postsynaptic 5-HT1A sites in the frontal cortex.	Imipramine	40-50	5-hydroxytryptamine receptor 1A	Rattus norvegicus	111-117
3199589-9	1988	It is concluded that enhanced 5-HT neurotransmission which develops during chronic treatment with imipramine or lithium seems tob e related to the down-regulation of postsynaptic 5-HT1A receptors in addition to postsynaptic 5-HT2 receptors, which may also have an important role in the antidepressant effects of these drugs.	Imipramine	98-108	5-hydroxytryptamine receptor 1A	Rattus norvegicus	179-185
2898799-4	1988	The association of high affinity [3H]imipramine binding with the serotonin transporter in brain and platelets is well established.	Imipramine	37-47	solute carrier family 6 member 4	Homo sapiens	65-86
3348672-1	1988	An 11 year old girl who was being treated for enuresis with imipramine developed acrocyanosis of the hands and feet.	Imipramine	60-70	DDB1 and CUL4 associated factor 7	Homo sapiens	0-5
3210008-0	1988	Effects of chronic imipramine treatment on glucocorticoid receptor immunoreactivity in various regions of the rat brain.	Imipramine	19-29	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	43-66
3210008-2	1988	Glucocorticoid receptor (GR) immunoreactivity (IR) was analyzed semi-automatically in the forebrain and in the lower brain stem of male rats treated for two weeks with imipramine (10 mumol/kg).	Imipramine	168-178	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	0-23
3210008-9	1988	The present results open up the possibility that chronic imipramine treatment may help to maintain the glucocorticoid receptor function in the locus coeruleus and in the 5-HT cell groups of the rostral ventromedial medulla of depressed patients.	Imipramine	57-67	nuclear receptor subfamily 3 group C member 1	Homo sapiens	103-126
3368009-4	1988	On the basis of studies in vitro it is concluded that the observed metabolic interaction between carbamazepine and imipramine is due to the competition of the drugs for the active centre of cytochrome P 450 and to a certain qualitative alteration of the enzyme by imipramine as can be deducted from the decrease of carbamazepine binding to the cytochrome.	Imipramine	115-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	190-206
2961332-2	1987	These results support the hypotheses that 1) treatment of psychotic Hex A deficient patients with amphiphilic antidepressants (such as imipramine) aggravates the patients" disease through depletion of their residual cellular Hex A, and 2) concomitant medication with dexamethasone may mitigate this drug-induced deleterious effect.	Imipramine	135-145	hexosaminidase subunit alpha	Homo sapiens	225-237
2963971-1	1987	The effect of imipramine on the responsiveness of CA1 pyramidal neurons to dopamine was studied in hippocampal slices, obtained from rats treated acutely or repeatedly with imipramine (10 mg/kg, 14 days, twice a day p.o.).	Imipramine	14-24	carbonic anhydrase 1	Rattus norvegicus	50-53
2885761-3	1987	Imipramine (4 days) resulted in a marked inhibition of the ability of [D-Ala2, D-Leu5] enkephalin to decrease electrically evoked contractions of the vas deferens (presynaptic opioid receptor response) but did not significantly affect the carbachol-induced increase in electrically evoked contractions (muscarinic receptor response).	Imipramine	0-10	proenkephalin	Rattus norvegicus	87-97
2961332-0	1987	Depletion of cellular beta-hexosaminidase by imipramine is prevented by dexamethasone; implications for treating psychotic hexosaminidase-A deficient patients.	Imipramine	45-55	O-GlcNAcase	Homo sapiens	22-41
3039914-9	1987	A variety of structurally diverse calmodulin antagonists examined were also found to effectively protect P-450Ch7 alpha from deactivation; these include calmidazolium and tamoxifen (IC50 = 25 to 50 microM), chlorpromazine, thioridazine, amitriptyline, imipramine, and the naphthalene sulfonamide compound W-7 (IC50 = 50 to 300 microM).	Imipramine	252-262	calmodulin 1	Rattus norvegicus	34-44
3598027-1	1987	Adverse reactions to the tricyclic antidepressant drugs imipramine and desipramine have been described and include eosinophilia, pulmonary infiltrates with eosinophilia, and elevated total serum IgE levels.	Imipramine	56-66	immunoglobulin heavy constant epsilon	Homo sapiens	195-198
2439937-9	1987	In the frontal cortex, in which separate monoaminergic and tachykinin-containing neurones interact, treatment with imipramine reduced the levels of SP-LI and NKA/NKB-LI, while treatment with alaproclate had the opposite effect.	Imipramine	115-125	Natural killer alloreactivity QTL 1	Rattus norvegicus	158-161
2439937-10	1987	In the periaqueductal grey matter, treatment with zimelidine and alaproclate increased the levels of SP-LI and NKA/NKB-LI, while treatment with imipramine increased only the level of NKA/NKB-LI.	Imipramine	144-154	Natural killer alloreactivity QTL 1	Rattus norvegicus	183-186
2882523-4	1987	After chronic administration of tricyclic antidepressants (imipramine and desipramine) the number of cortical beta 1 adrenergic receptors decreased without impairing the clenbuterol-induced decrease in spontaneous motor activity.	Imipramine	59-69	hemoglobin, beta adult major chain	Mus musculus	110-116
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	155-165	solute carrier family 6 member 4	Homo sapiens	174-190
2947974-2	1987	As this apparent discrepancy could be related to the assay temperature, we studied the thermodynamics of drug interaction with the 5-HT transporter at assay temperatures between 0 degrees C and 37 degrees C, using as radioligands [3H]imipramine (0 degrees C and 20 degrees C) and [3H]paroxetine (20 degrees C and 37 degrees C), a newly available probe for the 5-HT transporter.	Imipramine	234-244	solute carrier family 6 member 4	Homo sapiens	131-147
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	16-26	solute carrier family 6 member 4	Homo sapiens	35-51
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	16-26	solute carrier family 6 member 4	Homo sapiens	174-190
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	155-165	solute carrier family 6 member 4	Homo sapiens	35-51
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	155-165	solute carrier family 6 member 4	Homo sapiens	174-190
2947974-4	1987	The affinity of imipramine for the 5-HT transporter is progressively enhanced with decreasing incubation temperature, thus favoring the selectivity of [3H]imipramine for the 5-HT transporter at 0 degrees C. At 37 degrees C, the Ki of imipramine for inhibition of [3H]paroxetine binding is 32 nM, and equals its Ki value for inhibition of 5-HT uptake into human platelets.	Imipramine	155-165	solute carrier family 6 member 4	Homo sapiens	35-51
3019941-1	1986	A new rapid high yield synthesis of radiolabeled N"-(4-11C-methyl)imipramine has been developed using a reductive-carboxylation approach, in which 11CO2 is reacted with either N"-trimethylsilyldesimipramine or N"-lithium derivative of desimipramine, followed by lithium aluminum hydride reduction, to give no carrier added or carrier added 11C-labeled imipramine respectively.	Imipramine	66-76	complement C2	Homo sapiens	149-152
3027154-4	1986	When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression.	Imipramine	5-15	C-C motif chemokine ligand 4	Rattus norvegicus	39-43
3027154-4	1986	When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression.	Imipramine	5-15	C-C motif chemokine ligand 4	Rattus norvegicus	69-73
3027154-4	1986	When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression.	Imipramine	5-15	C-C motif chemokine ligand 4	Rattus norvegicus	69-73
3027154-4	1986	When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression.	Imipramine	5-15	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-242
3027154-4	1986	When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression.	Imipramine	5-15	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	264-285
3027154-6	1986	Early preventive effects of imipramine on cytochrome P-450, might be attributed to inhibition of covalent interactions of reactive metabolites.	Imipramine	28-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
3518138-1	1986	A therapeutic trial with a vasopressin analog: desmopressin and imipramine].	Imipramine	64-74	arginine vasopressin	Homo sapiens	27-38
3816412-1	1986	[3H]Imipramine and [3H]paroxetine label with high affinity a site associated with the serotonin transporter in brain and platelets.	Imipramine	4-14	solute carrier family 6 member 4	Homo sapiens	86-107
3572714-1	1986	The binding property of some tertiary amines (chlorpromazine, promethazine and imipramine) and quaternary ammonium compounds (propantheline, mepenzolate and butylscopolamine) for gastric mucin was investigated.	Imipramine	79-89	solute carrier family 13 member 2	Rattus norvegicus	187-192
2992664-0	1985	Potentiation by TRH of the effect of imipramine on the forced-swimming test.	Imipramine	37-47	thyrotropin releasing hormone	Mus musculus	16-19
2992664-6	1985	TRH made effective a completely inactive dose of imipramine as small as 2 mg kg-1 (i.p.)	Imipramine	49-59	thyrotropin releasing hormone	Mus musculus	0-3
2863142-14	1985	Two reversible inhibitors of pseudocholinesterase, namely ethopropazine and imipramine, were used as protectors during modification.	Imipramine	76-86	butyrylcholinesterase	Homo sapiens	29-49
2864085-4	1985	Neuroleptics of the butyrophenone group as well as imipramine and diphenehydramine having a low efficiency interact only with calmodulin.	Imipramine	51-61	calmodulin 1	Homo sapiens	126-136
2992664-3	1985	The effects of imipramine were potentiated by TRH.	Imipramine	15-25	thyrotropin releasing hormone	Mus musculus	46-49
2992664-14	1985	The imipramine potentiation by TRH was blocked by pretreatment with an opiate antagonist (naloxone, 1 mg kg-1 i.p.)	Imipramine	4-14	thyrotropin releasing hormone	Mus musculus	31-34
6548381-4	1984	Little displacement by AHR-9377 at beta, alpha 1 and alpha 2 adrenergic, histaminergic, muscarinic, GABA-ergic, benzodiazepine of imipramine sites was observed.	Imipramine	130-140	aryl hydrocarbon receptor	Rattus norvegicus	23-26
3871227-0	1985	Tryptamine, a substrate for the serotonin transporter in human platelets, modifies the dissociation kinetics of [3H]imipramine binding: possible allosteric interaction.	Imipramine	116-126	solute carrier family 6 member 4	Homo sapiens	32-53
2983787-4	1985	Imipramine-like activity of the extract was markedly degraded by carboxypeptidase B and leucine aminopeptidase, but was resistant to neurominidase and phospholipases A2, C, and D. The elution profile of the extract after gel chromatography on Bio-Gel P-2 showed two major peaks of serotonin uptake and imipramine binding inhibition and three additional peaks of serotonin uptake inhibitory activity that did not have a significant effect on imipramine binding.	Imipramine	0-10	carboxypeptidase B1	Homo sapiens	65-83
2983787-4	1985	Imipramine-like activity of the extract was markedly degraded by carboxypeptidase B and leucine aminopeptidase, but was resistant to neurominidase and phospholipases A2, C, and D. The elution profile of the extract after gel chromatography on Bio-Gel P-2 showed two major peaks of serotonin uptake and imipramine binding inhibition and three additional peaks of serotonin uptake inhibitory activity that did not have a significant effect on imipramine binding.	Imipramine	0-10	carboxypeptidase Q	Homo sapiens	96-110
6735152-3	1984	Similarly inhibition of NE reuptake by imipramine or desmethylimipramine were followed by reduced GH secretion.	Imipramine	39-49	growth hormone 1	Homo sapiens	98-100
6873187-3	1983	In vitro studies on the inhibition of [ 3H ]imipramine binding to membranes from human and rat platelets and hypothalamus by CdCl2 corroborate the in vivo results which imply that the imipramine binding protein contains Cd2+-sensitive groups.	Imipramine	44-54	Cd2 molecule	Rattus norvegicus	220-223
6732837-2	1984	Numerous cationic amphiphilic drugs including imipramine, propranolol, 4,4"-bis(diethylaminoethoxy)-alpha, beta- diethyldiphenylethane and chloropromazine inhibit phospholipase A.	Imipramine	46-56	phospholipase A and acyltransferase 1	Rattus norvegicus	163-178
6137344-4	1983	During the drug-free perfusion, the previously accumulated imipramine was released from two distinct pools (E1 and E2).	Imipramine	59-69	carboxylesterase 1C	Rattus norvegicus	108-117
6227192-5	1983	The in vitro responsiveness of the pituitary gland to hypothalamic stimuli eliciting prolactin secretion was increased by in vivo pargyline and combined tryptophan: imipramine treatment but reduced by PCPA administration.	Imipramine	165-175	prolactin	Gallus gallus	85-94
6227192-6	1983	The in vitro GH response to hypothalamic stimulation was reduced after the in vivo injection of pargyline, clorgyline and tryptophan: imipramine.	Imipramine	134-144	growth hormone	Gallus gallus	13-15
6227192-7	1983	The hypothalami from clorgyline and tryptophan: imipramine treated birds induced a greater stimulation of in vitro prolactin secretion from control pituitary glands than hypothalami from controls birds, whereas the GH releasing activity was reduced.	Imipramine	48-58	prolactin	Gallus gallus	115-124
6853461-0	1983	Imipramine-induced tremor: effects of a beta-adrenergic blocking agent.	Imipramine	0-10	amyloid beta precursor protein	Homo sapiens	38-44
6853461-1	1983	Assessment of an elderly depressed patient with an imipramine-induced tremor led to the conclusions that imipramine tremor (1) can be severe and incapacitating, (2) is most pronounced early in the treatment, (3) does not seem to be dose-related, and (4) is readily reversible with a beta-adrenergic blocking agent.	Imipramine	51-61	amyloid beta precursor protein	Homo sapiens	281-287
6853461-1	1983	Assessment of an elderly depressed patient with an imipramine-induced tremor led to the conclusions that imipramine tremor (1) can be severe and incapacitating, (2) is most pronounced early in the treatment, (3) does not seem to be dose-related, and (4) is readily reversible with a beta-adrenergic blocking agent.	Imipramine	105-115	amyloid beta precursor protein	Homo sapiens	281-287
6835029-0	1983	[3H]2-Nitroimipramine: a selective "slowly-dissociating" probe of the imipramine binding site ("serotonin transporter") in platelets and brain.	Imipramine	11-21	solute carrier family 6 member 4	Homo sapiens	96-118
6305362-4	1983	Correspondingly, ornithine decarboxylase activity was 5.5 times higher than the control value and S-adenosylmethionine decarboxylase activity about 40% from that after imipramine injection (80 mg/kg).	Imipramine	168-178	ornithine decarboxylase, structural 1	Mus musculus	17-40
6305362-2	1983	Intraperitoneal injection of chlorpromazine and imipramine increases mouse brain ornithine decarboxylase but decreases S-adenosyl-L-methionine decarboxylase activity.	Imipramine	48-58	ornithine decarboxylase, structural 1	Mus musculus	81-104
6835029-3	1983	Our results support the relative utility of this ligand for studying the impramine binding site (serotonin transporter) since this analogue has both a higher affinity and specific activity than [3H]imipramine.	Imipramine	73-82	solute carrier family 6 member 4	Homo sapiens	97-118
6317800-5	1983	Lesioning of the dorsal noradrenergic bundle blocks the decline in beta-receptor number and activity produced by the ACTH-imipramine treatment.	Imipramine	122-132	proopiomelanocortin	Homo sapiens	117-121
6139243-3	1983	Injection of the serotonin precursor tryptophan and the serotonin re-uptake blocker imipramine resulted in elevated prolactin and reduced growth hormone levels.	Imipramine	84-94	growth hormone 1	Homo sapiens	138-152
6840904-5	1983	There was a difference between the drug-free period and desmethylimipramine or imipramine on the PEPc (P less than 0.05) and the PEP/LVET ratio (P less than 0.05); on the R-R (P less than 0.05), PR (P less than 0.05), QRS (P less than 0.05), and QTc (P less than 0.05) intervals; but no difference on the LVETc or shortening fraction or the mean velocity of circumferential shortening.	Imipramine	65-75	peptidase C	Homo sapiens	97-101
6840904-5	1983	There was a difference between the drug-free period and desmethylimipramine or imipramine on the PEPc (P less than 0.05) and the PEP/LVET ratio (P less than 0.05); on the R-R (P less than 0.05), PR (P less than 0.05), QRS (P less than 0.05), and QTc (P less than 0.05) intervals; but no difference on the LVETc or shortening fraction or the mean velocity of circumferential shortening.	Imipramine	65-75	progestagen associated endometrial protein	Homo sapiens	97-100
6840904-6	1983	Drugs such as desmethylimipramine and imipramine which prolong intraventricular conduction can probably be expected to prolong the PEP and PEP/LVET.	Imipramine	23-33	progestagen associated endometrial protein	Homo sapiens	131-134
6840904-6	1983	Drugs such as desmethylimipramine and imipramine which prolong intraventricular conduction can probably be expected to prolong the PEP and PEP/LVET.	Imipramine	23-33	progestagen associated endometrial protein	Homo sapiens	139-142
6297962-1	1983	It has been shown in experiments on rat vas deferens that melipramine, harmane and 3-methylharman in low concentrations of the order of 10(-8)--10(-6) M increase the contraction of the vas deference induced by noradrenaline and transmural stimulation.	Imipramine	58-69	arginine vasopressin	Rattus norvegicus	40-43
6297962-1	1983	It has been shown in experiments on rat vas deferens that melipramine, harmane and 3-methylharman in low concentrations of the order of 10(-8)--10(-6) M increase the contraction of the vas deference induced by noradrenaline and transmural stimulation.	Imipramine	58-69	arginine vasopressin	Rattus norvegicus	185-188
6289837-0	1982	Vinculin phosphorylation by the src kinase: inhibition by chlorpromazine, imipramine and local anesthetics.	Imipramine	74-84	vinculin	Homo sapiens	0-8
7151856-1	1982	The effects of constant darkness, chronic lithium, clorgyline, imipramine and fluphenazine treatment on the content and diurnal rhythm of alpha-MSH in rat forebrain were investigated.	Imipramine	63-73	proopiomelanocortin	Rattus norvegicus	138-147
7151856-4	1982	In addition, imipramine and clorgyline delayed the phase of the alpha-MSH circadian rhythm while lithium advanced it.	Imipramine	13-23	proopiomelanocortin	Rattus norvegicus	64-73
7056352-2	1982	L-Aspartic acid was found to be as effective as imipramine in reducing the effects of forced swimming, presumable by normalizing the decreased level of endogenous L-aspartic acid, due to the inhibition of L-asparaginase activity and/or by stimulating the inhibited enzyme.	Imipramine	48-58	asparaginase and isoaspartyl peptidase 1	Rattus norvegicus	205-219
7056713-3	1982	This process requires Na+ and is blocked by imipramine, indicating that it is mediated by the serotonin transporter.	Imipramine	44-54	solute carrier family 6 member 4	Homo sapiens	94-115
6280730-2	1982	Activation was measured over a range of calmodulin concentrations, and is antagonised by several tricyclic psychotropic drugs including trifluoperazine, imipramine, chlorpromazine and amitriptyline.	Imipramine	153-163	calmodulin-3	Cavia porcellus	40-50
6178817-2	1982	A series of neuroleptic drugs (five phenothiazines, imipramine, and pimozide) and the smooth muscle relaxant W-7, which all inhibit calcium-calmodulin-activated processes inhibited rat mast cell secretion elicited by antigen, by 48/80, and by the calcium ionophore A23187.	Imipramine	52-62	calmodulin 1	Rattus norvegicus	140-150
6971560-2	1981	Chlorimipramine, citalopram, fluoxetine, imipramine and zimelidine potentiated the low dose 5-hydroxytryptophan (5-HTP)-induced increase in prolactin secretion, suggesting inhibition of serotonin (5-HT) uptake by these drugs.	Imipramine	5-15	prolactin	Rattus norvegicus	140-149
7202372-0	1982	In vitro effect of haloperidol, chlorpromazine, imipramine and lithium on the erythrocyte catechol-O-methyltransferase.	Imipramine	48-58	catechol-O-methyltransferase	Homo sapiens	90-118
6170395-3	1981	When TRH was administered concurrently with imipramine (10 mg/kg), this neuropeptide significantly potentiated the effects of imipramine on lowering of endogenous levels of 5-hydroxytryptamine (striatum, hypothalamus) and 5-hydroxyindoleacetic acid (striatum, midbrain, pons-medulla).	Imipramine	126-136	thyrotropin releasing hormone	Homo sapiens	5-8
6912385-4	1981	The initial thrombin-induced decrease of 14C-5HT, in contrast to that of 3H-catecholamines, showed a partial recovery after 30 min which was abolished by imipramine.	Imipramine	154-164	coagulation factor II, thrombin	Homo sapiens	12-20
6291085-9	1982	Chronic pretreatment with CLON or imipramine, either of which can be expected to produce a reduced sensitivity of central alpha 2 receptors, resulted in reduced GH responses to CLON.	Imipramine	34-44	gonadotropin releasing hormone receptor	Rattus norvegicus	161-163
7323121-5	1981	Furthermore, inactivation of imipramine binding was achieved by very low concentrations (IC50 = 5 microgram/ml) of phospholipase A2.	Imipramine	29-39	phospholipase A2 group IB	Homo sapiens	115-131
7018438-0	1981	The effect of amoxapine and imipramine on serum prolactin levels.	Imipramine	28-38	prolactin	Homo sapiens	48-57
6272818-10	1981	At even higher concentrations of amitriptyline, nortriptyline or imipramine with spin label 616, however, no significant change of order parameter was observed indicating that perturbation of the hydrophobic membrane interior is not sensed.	Imipramine	65-75	spindlin 1	Homo sapiens	81-85
6796626-3	1981	In two patients taking medications (imipramine and dogmatil), prolactin levels were high.	Imipramine	36-46	prolactin	Homo sapiens	62-71
6254586-1	1980	Thyrotropin releasing hormone (TRH) causes hyperthermia in mice which is potentiated by tricyclic antidepressants (nortriptyline, imipramine, clomipramine, amitriptyline), the monoamine oxidase inhibitor, tranylcypromine, and various other antidepressants (maprotiline, nomifensin, viloxazine).	Imipramine	130-140	thyrotropin releasing hormone	Mus musculus	0-29
6110219-0	1980	Thyrotropin releasing hormone: neurochemical evidence for the potentiation of imipramine effects on the metabolism and uptake of brain catecholamines.	Imipramine	78-88	thyrotropin releasing hormone	Homo sapiens	0-29
7263149-5	1980	The antiaggregating action of CPZ and IMP was thought to be due to their inhibitory effects on AA liberation from platelet membranes, suggesting that they might inhibit participating enzymes (phospholipase A2, C or lipase) or the process of the activation of the enzymes.	Imipramine	38-41	phospholipase A2 group IB	Homo sapiens	192-221
476283-1	1979	A procedure is described which permits the simultaneous determination of imipramine and desipramine or clomipramine and N-desmethylclomipramine in serum or plasma for concentrations in the range of 1-200 ng ml-1.	Imipramine	73-83	interleukin 17F	Homo sapiens	207-211
386715-6	1979	The present study has shown that, after 3 weeks" treatment, imipramine and L-tryptophan has decreased the mean score on individual items of HRS in about the same degree.	Imipramine	60-70	hepatocyte growth factor-regulated tyrosine kinase substrate	Homo sapiens	140-143
476283-2	1979	Detection limits of 0.2 ng ml-1 for imipramine and 0.1 ng ml-1 for desipramine were demonstrated with a signal-to-noise ratio maintained at 2:1 or better.	Imipramine	36-46	interleukin 17F	Homo sapiens	27-31
461967-3	1979	Occupancy of active sites on mitochondrial MAO by imipramine probably does not occur at doses of imipramine adequate to inhibit monoamine uptake.	Imipramine	50-60	monoamine oxidase A	Rattus norvegicus	43-46
426143-2	1979	The superiority of ECT was evident among patients with endogenous depression, and especially evident among those with delusional depression (83% improved with ECT versus 40% with imipramine) and depressions defined as severe (83% versus 35%).	Imipramine	179-189	ECT	Homo sapiens	19-22
365126-3	1978	The levels of both drugs were approximately equal in plasma, but desipramine predominated in CSF (imipramine/desipramine ratio of 0.8).	Imipramine	98-108	colony stimulating factor 2	Homo sapiens	93-96
365126-4	1978	The imipramine-induced alteration in CSF levels of the serotonin metabolite (5-hydroxy-indoleacetic acid [5HIAA]) correlated with imipramine levels but not with desipramine.	Imipramine	4-14	colony stimulating factor 2	Homo sapiens	37-40
365126-4	1978	The imipramine-induced alteration in CSF levels of the serotonin metabolite (5-hydroxy-indoleacetic acid [5HIAA]) correlated with imipramine levels but not with desipramine.	Imipramine	130-140	colony stimulating factor 2	Homo sapiens	37-40
580997-3	1978	The serotonin-induced ODC activity is significantly blocked by imipramine (10(-5) M) or Lilly 110140 (10(-6) M).	Imipramine	63-73	ornithine decarboxylase	Bos taurus	22-25
277090-2	1978	Ad 1) Few drugs give a reproducible, dose dependent, hepatic reaction (e.g. acetaminophen), a greater problem is the unpredictable, dose independent reactions caused by "indirect" hepatotoxic drugs (e.g. imipramin).	Imipramine	204-213	amyloid beta precursor protein	Homo sapiens	0-4
25425-1	1978	Choline acetyltransferase (Ach-T) and acetylcholinesterase (Ach-E) activities in mice brain during the reverse action by imipramine, pheniprazine and pargyline to the syndrome elicited by intraperitoneal administration of Ro 4--1284 were investigated.	Imipramine	121-131	choline acetyltransferase	Mus musculus	0-25
25425-1	1978	Choline acetyltransferase (Ach-T) and acetylcholinesterase (Ach-E) activities in mice brain during the reverse action by imipramine, pheniprazine and pargyline to the syndrome elicited by intraperitoneal administration of Ro 4--1284 were investigated.	Imipramine	121-131	acetylcholinesterase	Mus musculus	38-58
25425-1	1978	Choline acetyltransferase (Ach-T) and acetylcholinesterase (Ach-E) activities in mice brain during the reverse action by imipramine, pheniprazine and pargyline to the syndrome elicited by intraperitoneal administration of Ro 4--1284 were investigated.	Imipramine	121-131	acetylcholinesterase	Mus musculus	60-65
25425-2	1978	A single dose of imipramine did not reverse reserpine-like syndrome whereas inhibited Ach-E activity and increased Ach-T activity at the same time.	Imipramine	17-27	acetylcholinesterase	Mus musculus	86-91
402671-1	1977	A previous report indicated that the tricyclic antidepressants imipramine and amitriptyline markedly increased plasma prolactin levels in man.	Imipramine	63-73	prolactin	Homo sapiens	118-127
144573-8	1977	The activities of sarcolemmal adenosinetriphosphatase and acetylcholinesterase were inhibited in vitro by imipramine and serotonin.	Imipramine	106-116	acetylcholinesterase	Rattus norvegicus	58-78
407903-6	1977	The enzyme lacks NADPH dehydrogenase activity and is insensitive to treatment with 2-bromo-4"-nitroacetophenone and steapsin: it catalyses N-oxidation of imipramine, trimethylamine and NN-dimethylaniline in molar proportions considerably different from those of the cytochrome P-450-supported reactions.	Imipramine	154-164	cytochrome P-450	Oryctolagus cuniculus	266-282
186834-6	1976	By that time the MUA changes of PH and MRF showed similar characteristics in response to TRH administration which was observed following the injection of desipramine and imipramine.	Imipramine	170-180	thyrotropin releasing hormone	Felis catus	89-92
589954-1	1977	Subtoxic doses of physostigmine have been found to potentiate the convulsive toxicity and lethality of amitriptyline and imipramine in CD1 and B6A mice.	Imipramine	121-131	CD1 antigen complex	Mus musculus	135-138
177012-0	1976	Regulation of prostaglandin metabolism: activation of 15-hydroxyprostaglandin dehydrogenase by chlorpromazine and imipramine related drugs.	Imipramine	114-124	carbonyl reductase 1	Homo sapiens	54-91
942009-1	1976	When baseline red blood cell catechol O-methyltransferase (COMT) was measured in 15 unipolar depressive women, the authors found a linear correlation between COMT and response to imipramine (best outcome occurring at low COMT).	Imipramine	179-189	catechol-O-methyltransferase	Homo sapiens	29-57
942009-1	1976	When baseline red blood cell catechol O-methyltransferase (COMT) was measured in 15 unipolar depressive women, the authors found a linear correlation between COMT and response to imipramine (best outcome occurring at low COMT).	Imipramine	179-189	catechol-O-methyltransferase	Homo sapiens	59-63
942009-1	1976	When baseline red blood cell catechol O-methyltransferase (COMT) was measured in 15 unipolar depressive women, the authors found a linear correlation between COMT and response to imipramine (best outcome occurring at low COMT).	Imipramine	179-189	catechol-O-methyltransferase	Homo sapiens	158-162
942009-1	1976	When baseline red blood cell catechol O-methyltransferase (COMT) was measured in 15 unipolar depressive women, the authors found a linear correlation between COMT and response to imipramine (best outcome occurring at low COMT).	Imipramine	179-189	catechol-O-methyltransferase	Homo sapiens	158-162
187035-1	1976	15-Hydroxyprostaglandin dehydrogenase was inhibited by xylocaine, furosemide, and ethacrynic acid, but was activated by imipramine and other related drugs.	Imipramine	120-130	carbonyl reductase 1	Homo sapiens	0-37
1105628-2	1975	The average increase of the two metabolites in the CSF after probenecid was similar in the untreated depressed patients and in the same patients improved after both imipramine or ECT treatment.	Imipramine	165-175	colony stimulating factor 2	Homo sapiens	51-54
5726781-7	1968	Imipramine inhibited the in vitro uptake of noradrenaline-(3)H in rat vas deferens as did cocaine, desmethylimipramine and dexchlorpheniramine.	Imipramine	0-10	arginine vasopressin	Rattus norvegicus	70-73
2494-3	1975	Phthoracizine, impramine and spasmolytin were found to capable of inhibiting accumulation of the exogenous NE in the tissue and in the adrenergic nerves of Vas deferens, provided the mediator is present in the extraneuronal medium in a concentration of 0.5 gamma/ml.	Imipramine	15-24	arginine vasopressin	Rattus norvegicus	156-159
4707505-0	1973	[Inhibition of tryptophan pyrrolase activity in rat liver by the administration of imipramine and other antidepressants].	Imipramine	83-93	tryptophan 2,3-dioxygenase	Rattus norvegicus	15-35
810812-5	1975	TRH was found to potentiate the effects of imipramine.	Imipramine	43-53	thyrotropin releasing hormone	Mus musculus	0-3
169190-3	1975	IMP 25 mg produced moderate decrease in %REMP in the three drug nights, whereas REM density decreased only in the first drug night.	Imipramine	0-3	solute carrier family 16 member 8	Homo sapiens	41-45
5015032-15	1972	Methysergide was a weak inhibitor of 5-HT uptake (K(i) approximately 125 muM) whereas imipramine was very effective (K(i) approximately 0.3 muM).10.	Imipramine	86-96	latexin	Homo sapiens	140-143
5768130-0	1969	The effect of cocaine and imipramine on tyramine-induced release of noradrenaline-3H from the rat vas deferens in vitro.	Imipramine	26-36	arginine vasopressin	Rattus norvegicus	98-101
5392263-0	1969	[Effect of imipramine on cholinesterase activity in dog brain].	Imipramine	11-21	butyrylcholinesterase	Canis lupus familiaris	25-39
5947700-0	1966	[Studies on the influence of imipramine on the serum insulin content in depressive schizophrenics].	Imipramine	29-39	insulin	Homo sapiens	53-60
5586714-0	1967	[Glutamine-pyruvic acid-transaminase (GPT) in treatment with amitriptylone and imipramine].	Imipramine	79-89	glutamic--pyruvic transaminase	Homo sapiens	38-41
4225396-2	1967	Effects of imipramine and ouabain on the (Na+ plus K+)activated ATPase from brain microsomes and cooperative interactions with the enzyme.	Imipramine	11-21	dynein axonemal heavy chain 8	Homo sapiens	64-70
13868140-0	1962	[Activity of expired carbon dioxide, CNS and other organs after the administration of C14-labelled N-(gamma-dimethyl-aminopropyl)-iminodibenzyl (psychopharmacological drug Tofranil) to rats and dogs].	Imipramine	99-143	anti-Mullerian hormone receptor type 2	Rattus norvegicus	86-89
13868140-0	1962	[Activity of expired carbon dioxide, CNS and other organs after the administration of C14-labelled N-(gamma-dimethyl-aminopropyl)-iminodibenzyl (psychopharmacological drug Tofranil) to rats and dogs].	Imipramine	172-180	anti-Mullerian hormone receptor type 2	Rattus norvegicus	86-89
14486949-0	1962	CPT and VCRT performances as functions of imipramine and nialamide.	Imipramine	42-52	choline phosphotransferase 1	Homo sapiens	0-3
34017503-6	2021	Imipramine was sensitive to MDR-PA, MDRAB, ESBL KP, and ESBL E. coli, and vancomycin was sensitive to MRSA.	Imipramine	0-10	EsbL	Escherichia coli	43-47
33839161-0	2021	Imipramine attenuates anxiety- and depressive-like effects of acute and prolonged ethanol-abstinence in male rats by modulating SERT and GR expression in the dorsal hippocampus.	Imipramine	0-10	solute carrier family 6 member 4	Rattus norvegicus	128-132
33839161-0	2021	Imipramine attenuates anxiety- and depressive-like effects of acute and prolonged ethanol-abstinence in male rats by modulating SERT and GR expression in the dorsal hippocampus.	Imipramine	0-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	137-139
33839161-12	2021	Imipramine prevented protracted abstinence -induced decrease in glucocorticoid receptor (GR) and serotonin transporter (SERT) expression in the dorsal hippocampus.	Imipramine	0-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	64-87
33839161-12	2021	Imipramine prevented protracted abstinence -induced decrease in glucocorticoid receptor (GR) and serotonin transporter (SERT) expression in the dorsal hippocampus.	Imipramine	0-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	89-91
33839161-12	2021	Imipramine prevented protracted abstinence -induced decrease in glucocorticoid receptor (GR) and serotonin transporter (SERT) expression in the dorsal hippocampus.	Imipramine	0-10	solute carrier family 6 member 4	Rattus norvegicus	97-118
33839161-12	2021	Imipramine prevented protracted abstinence -induced decrease in glucocorticoid receptor (GR) and serotonin transporter (SERT) expression in the dorsal hippocampus.	Imipramine	0-10	solute carrier family 6 member 4	Rattus norvegicus	120-124
33181580-10	2021	Median score for total pain on imipramine changed from NRS 6.6 to 4.8 with an average effect as compared to placebo of -1.17 (95% CI -1.42; -0.92, p < 0.001).	Imipramine	31-41	sphingolipid transporter 1 (putative)	Homo sapiens	55-58
33611821-6	2021	MV signaling was implicated in this response as reduction of MV secretion by imipramine blocked pro-inflammatory TNF-alpha and IL-1beta induction by ethanol, and ethanol-conditioned MVs (EtOH-MVs) reproduced the ethanol-associated immune gene signature in naive OBSC slices.	Imipramine	77-87	tumor necrosis factor	Homo sapiens	113-122
33556704-7	2021	Imipramine was used as a reference drug having a documented interaction with the mGluR5 receptors.	Imipramine	0-10	glutamate receptor, ionotropic, kainate 1	Mus musculus	81-87
33612104-7	2021	Additionally, imipramine suppressed the LPS/ATP-induced expression of thioredoxin interacting protein (TXNIP), NLRP3, caspase-1, IL-1beta, and IL-18 at the protein and mRNA level.	Imipramine	14-24	thioredoxin interacting protein	Mus musculus	103-108
33612104-7	2021	Additionally, imipramine suppressed the LPS/ATP-induced expression of thioredoxin interacting protein (TXNIP), NLRP3, caspase-1, IL-1beta, and IL-18 at the protein and mRNA level.	Imipramine	14-24	NLR family, pyrin domain containing 3	Mus musculus	111-116
33611821-6	2021	MV signaling was implicated in this response as reduction of MV secretion by imipramine blocked pro-inflammatory TNF-alpha and IL-1beta induction by ethanol, and ethanol-conditioned MVs (EtOH-MVs) reproduced the ethanol-associated immune gene signature in naive OBSC slices.	Imipramine	77-87	interleukin 1 alpha	Homo sapiens	127-135
32048914-5	2020	At the end of the 3-week experimental period, biochemical and behavioral parameters were examined.Results: The results showed that treatment with GOEE or imipramine significantly improved rats" sucrose consumption which was diminished by chronic mild stress, restored serum levels of corticosterone and proinflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)), prevented the increase of liver index of rats.	Imipramine	154-164	interleukin 6	Rattus norvegicus	330-343
33328497-5	2020	Chronic infusion of ANGII into mice induced depressive-like behaviors, including the tail suspension test and forced swimming test, which were reversed by imipramine.	Imipramine	155-165	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	20-25
32975484-4	2020	We find that fluoxetine, a widely used antidepressant and a functional inhibitor of acid sphingomyelinase (FIASMA), efficiently inhibited the entry and propagation of SARS-CoV-2 in the cell culture model without cytotoxic effects and also exerted potent antiviral activity against two currently circulating influenza A virus subtypes, an effect which was also observed upon treatment with the FIASMAs amiodarone and imipramine.	Imipramine	416-426	sphingomyelin phosphodiesterase 1	Homo sapiens	84-105
32048914-5	2020	At the end of the 3-week experimental period, biochemical and behavioral parameters were examined.Results: The results showed that treatment with GOEE or imipramine significantly improved rats" sucrose consumption which was diminished by chronic mild stress, restored serum levels of corticosterone and proinflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)), prevented the increase of liver index of rats.	Imipramine	154-164	interleukin 6	Rattus norvegicus	345-349
32048914-5	2020	At the end of the 3-week experimental period, biochemical and behavioral parameters were examined.Results: The results showed that treatment with GOEE or imipramine significantly improved rats" sucrose consumption which was diminished by chronic mild stress, restored serum levels of corticosterone and proinflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)), prevented the increase of liver index of rats.	Imipramine	154-164	tumor necrosis factor	Rattus norvegicus	352-379
32048914-5	2020	At the end of the 3-week experimental period, biochemical and behavioral parameters were examined.Results: The results showed that treatment with GOEE or imipramine significantly improved rats" sucrose consumption which was diminished by chronic mild stress, restored serum levels of corticosterone and proinflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)), prevented the increase of liver index of rats.	Imipramine	154-164	tumor necrosis factor	Rattus norvegicus	381-390
33050597-0	2020	Imipramine Inhibits Migration and Invasion in Metastatic Castration-Resistant Prostate Cancer PC-3 Cells via AKT-Mediated NF-kappaB Signaling Pathway.	Imipramine	0-10	AKT serine/threonine kinase 1	Homo sapiens	109-112
33163980-2	2020	Here we report that either pharmacological inhibition of acid sphingomyelinase with amitriptyline, imipramine, fluoxetine, sertraline, escitalopram, or maprotiline, or genetic downregulation of the enzyme prevents infection of cultured cells or freshy isolated human nasal epithelial cells with SARS-CoV-2 or pseudoviral pp-VSV-SARS-CoV-2 particles expressing spike, a bona fide system mimicking SARS-CoV-2 infection.	Imipramine	99-109	sphingomyelin phosphodiesterase 1	Homo sapiens	57-78
33010168-10	2020	The imipramine-mediated inhibition of Kv channels was associated with the Kv1.5 channel, not the Kv2.1 or Kv7 channel.	Imipramine	4-14	potassium voltage-gated channel subfamily A member 5	Homo sapiens	74-79
32905805-0	2020	Imipramine exerts antidepressant-like effects in chronic stress models of depression by promoting CRTC1 expression in the mPFC.	Imipramine	0-10	CREB regulated transcription coactivator 1	Mus musculus	98-103
32905805-0	2020	Imipramine exerts antidepressant-like effects in chronic stress models of depression by promoting CRTC1 expression in the mPFC.	Imipramine	0-10	complement factor properdin	Mus musculus	122-126
32905805-3	2020	In this study, the effects of imipramine on CRTC1 were studied in several models of depression, including the chronic restraint stress (CRS), chronic unpredictable mild stress (CUMS) and chronic social defeat stress (CSDS) models.	Imipramine	30-40	CREB regulated transcription coactivator 1	Mus musculus	44-49
32905805-4	2020	We examined whether repeated imipramine administration can reverse the effects of CRS, CUMS and CSDS on CRTC1 expression in both the hippocampus and medial prefrontal cortex (mPFC).	Imipramine	29-39	CREB regulated transcription coactivator 1	Mus musculus	104-109
32905805-4	2020	We examined whether repeated imipramine administration can reverse the effects of CRS, CUMS and CSDS on CRTC1 expression in both the hippocampus and medial prefrontal cortex (mPFC).	Imipramine	29-39	complement factor properdin	Mus musculus	175-179
32905805-6	2020	Our results showed that imipramine reversed the down-regulating effects of CRS, CUMS and CSDS on CRTC1 expression in the mPFC but not the hippocampus, and that CRTC1-shRNA fully abolished the antidepressant-like actions of imipramine in mice.	Imipramine	24-34	CREB regulated transcription coactivator 1	Mus musculus	97-102
32905805-6	2020	Our results showed that imipramine reversed the down-regulating effects of CRS, CUMS and CSDS on CRTC1 expression in the mPFC but not the hippocampus, and that CRTC1-shRNA fully abolished the antidepressant-like actions of imipramine in mice.	Imipramine	24-34	complement factor properdin	Mus musculus	121-125
32905805-6	2020	Our results showed that imipramine reversed the down-regulating effects of CRS, CUMS and CSDS on CRTC1 expression in the mPFC but not the hippocampus, and that CRTC1-shRNA fully abolished the antidepressant-like actions of imipramine in mice.	Imipramine	223-233	CREB regulated transcription coactivator 1	Mus musculus	160-165
32905805-7	2020	In conclusion, CRTC1 in the mPFC is involved in the antidepressant mechanism of imipramine.	Imipramine	80-90	CREB regulated transcription coactivator 1	Mus musculus	15-20
32905805-7	2020	In conclusion, CRTC1 in the mPFC is involved in the antidepressant mechanism of imipramine.	Imipramine	80-90	complement factor properdin	Mus musculus	28-32
33050597-0	2020	Imipramine Inhibits Migration and Invasion in Metastatic Castration-Resistant Prostate Cancer PC-3 Cells via AKT-Mediated NF-kappaB Signaling Pathway.	Imipramine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	122-131
33050597-7	2020	Furthermore, IMI treatment resulted in decreased AKT-mediated downstream signaling, including p-inhibitor of kappaB kinase (IKK)alpha/beta, p-inhibitor of kappaB (IkappaBalpha), and p-p65.	Imipramine	13-16	AKT serine/threonine kinase 1	Homo sapiens	49-52
33050597-7	2020	Furthermore, IMI treatment resulted in decreased AKT-mediated downstream signaling, including p-inhibitor of kappaB kinase (IKK)alpha/beta, p-inhibitor of kappaB (IkappaBalpha), and p-p65.	Imipramine	13-16	NFKB inhibitor alpha	Homo sapiens	163-175
33050597-7	2020	Furthermore, IMI treatment resulted in decreased AKT-mediated downstream signaling, including p-inhibitor of kappaB kinase (IKK)alpha/beta, p-inhibitor of kappaB (IkappaBalpha), and p-p65.	Imipramine	13-16	RELA proto-oncogene, NF-kB subunit	Homo sapiens	184-187
32446929-9	2020	RESULTS: The results showed that chronic administration of ZM (150, 300, and 600 mg/kg, p.o., 30 days) and imipramine treatment (20 mg/kg, p.o, 30 days) remarkably (P < 0.05) reversed the UCMS-induced behavioral changes observed in stress vehicle treated rats by reducing sucrose preference, decreased the immobility period in the FST and latency in NSF.	Imipramine	107-117	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Rattus norvegicus	350-353
32679212-1	2020	Single-crystal X-ray diffraction and DFT calculation have been carried out for an atomic-level understanding of beta-cyclodextrin (beta-CD) inclusion complexation with two tricyclic antidepressants (TCAs), desipramine and imipramine.	Imipramine	222-232	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	131-138
32748256-1	2020	BACKGROUND: The aim of our research was to determine the effects of chronic treatment with the atypical antidepressant agomelatine on the expression and activity of liver cytochrome P450 (CYP) in the chronic mild stress (CMS) model of depression, and to compare the results with those obtained for the first-generation antidepressant imipramine.	Imipramine	334-344	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	171-186
32748256-1	2020	BACKGROUND: The aim of our research was to determine the effects of chronic treatment with the atypical antidepressant agomelatine on the expression and activity of liver cytochrome P450 (CYP) in the chronic mild stress (CMS) model of depression, and to compare the results with those obtained for the first-generation antidepressant imipramine.	Imipramine	334-344	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	188-191
32748256-5	2020	RESULTS: Agomelatine and imipramine produced different broad-spectrum effects on cytochrome P450.	Imipramine	25-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-96
32748256-6	2020	Like imipramine, agomelatine increased the expression/activity of CYP2B and CYP2C6, and decreased the CYP2D activity.	Imipramine	5-15	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	76-82
32748256-10	2020	CONCLUSION: We conclude the following: (1) the effects of agomelatine and imipramine on cytochrome P450 are different and involve both central and peripheral regulatory mechanisms, which implicates the possibility of drug-drug interactions; (2) CMS influences the effects of antidepressants on cytochrome P450 expression, but does not change appreciably their effects on the enzyme activity.	Imipramine	74-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	88-103
32748256-10	2020	CONCLUSION: We conclude the following: (1) the effects of agomelatine and imipramine on cytochrome P450 are different and involve both central and peripheral regulatory mechanisms, which implicates the possibility of drug-drug interactions; (2) CMS influences the effects of antidepressants on cytochrome P450 expression, but does not change appreciably their effects on the enzyme activity.	Imipramine	74-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	294-309
32240535-5	2020	METHODS: SH-SY5Y cells were preincubated with mirtazapine and imipramine (1-20 muM) for 24 h, then hydrogen peroxide (H2O2) was added into the medium containing the antidepressants for additional 24 h, and MTT assay was carried out subsequently.	Imipramine	62-72	latexin	Homo sapiens	79-82
32240535-6	2020	Also, to elucidate the molecular mechanism underlying the neuroprotective properties of antidepressants, we investigated the effects of mirtazapine and imipramine (2 muM) in pro- and anti-apoptotic proteins gene expression in SH-SY5Y cells.	Imipramine	152-162	latexin	Homo sapiens	166-169
32240535-8	2020	Most importantly, both compounds reduced p53 mRNA expression, but only imipramine enhanced the Bcl-2/Bax ratio.	Imipramine	71-81	BCL2 apoptosis regulator	Homo sapiens	95-100
32240535-8	2020	Most importantly, both compounds reduced p53 mRNA expression, but only imipramine enhanced the Bcl-2/Bax ratio.	Imipramine	71-81	BCL2 associated X, apoptosis regulator	Homo sapiens	101-104
32240535-10	2020	Although both antidepressants reduced Bax and p53 mRNA expression, only the protection mediated by imipramine might be due to its ability to enhance Bcl-2/Bax ratio.	Imipramine	99-109	BCL2 apoptosis regulator	Homo sapiens	149-154
32240535-10	2020	Although both antidepressants reduced Bax and p53 mRNA expression, only the protection mediated by imipramine might be due to its ability to enhance Bcl-2/Bax ratio.	Imipramine	99-109	BCL2 associated X, apoptosis regulator	Homo sapiens	155-158
32132240-8	2020	While the functional importance of CHIKV nsP1 preference for cholesterol-rich membrane domains remains to be determined, we observed that U18666A- and imipramine-induced sequestration of cholesterol in late endosomes redirected nsP1 to these compartments and simultaneously dramatically decreased CHIKV genome replication.	Imipramine	151-161	SH2 domain containing 3A	Homo sapiens	41-45
32132240-8	2020	While the functional importance of CHIKV nsP1 preference for cholesterol-rich membrane domains remains to be determined, we observed that U18666A- and imipramine-induced sequestration of cholesterol in late endosomes redirected nsP1 to these compartments and simultaneously dramatically decreased CHIKV genome replication.	Imipramine	151-161	SH2 domain containing 3A	Homo sapiens	228-232
32088181-0	2020	NS398, a cyclooxygenase-2 inhibitor, reverses memory performance disrupted by imipramine in C57Bl/6J mice.	Imipramine	78-88	prostaglandin-endoperoxide synthase 2	Mus musculus	9-25
31848475-6	2020	We found that these indicators of leptin resistance were reversed by knockdown of ASM or by the selective ASM inhibitors amitriptyline (AMI) and imipramine (IMI).	Imipramine	145-155	leptin	Rattus norvegicus	34-40
31848475-6	2020	We found that these indicators of leptin resistance were reversed by knockdown of ASM or by the selective ASM inhibitors amitriptyline (AMI) and imipramine (IMI).	Imipramine	157-160	leptin	Rattus norvegicus	34-40
31848475-9	2020	High-fat diet (HFD) feeding-induced leptin resistance in rats in vivo; administration of AMI and IMI (10 mg  kg-1 per day, intraperitoneally, for 2 weeks) increased the release of endothelial NO to relieve the vasodilatory response and improved the endothelial leptin resistance in the aorta of HFD-fed rats.	Imipramine	97-100	leptin	Rattus norvegicus	36-42
31848475-9	2020	High-fat diet (HFD) feeding-induced leptin resistance in rats in vivo; administration of AMI and IMI (10 mg  kg-1 per day, intraperitoneally, for 2 weeks) increased the release of endothelial NO to relieve the vasodilatory response and improved the endothelial leptin resistance in the aorta of HFD-fed rats.	Imipramine	97-100	leptin	Rattus norvegicus	261-267
32028757-10	2020	In addition, structural changes caused by stress and blocking the changes by imipramine were corelated well with altered activation and expression of synaptic plasticity-promoting molecules such as phospho-CREB, phospho-CAMKII, and PSD-95.	Imipramine	77-87	cAMP responsive element binding protein 1	Mus musculus	206-210
32028757-10	2020	In addition, structural changes caused by stress and blocking the changes by imipramine were corelated well with altered activation and expression of synaptic plasticity-promoting molecules such as phospho-CREB, phospho-CAMKII, and PSD-95.	Imipramine	77-87	discs large MAGUK scaffold protein 4	Mus musculus	232-238
32088181-5	2020	Because chronic administration of imipramine has been shown to affect mGluR5, the purpose of this study was to verify the hypothesis of COX-2 pathway engagement in disrupting effects of imipramine.	Imipramine	34-44	glutamate receptor, ionotropic, kainate 1	Mus musculus	70-76
32088181-5	2020	Because chronic administration of imipramine has been shown to affect mGluR5, the purpose of this study was to verify the hypothesis of COX-2 pathway engagement in disrupting effects of imipramine.	Imipramine	34-44	prostaglandin-endoperoxide synthase 2	Mus musculus	136-141
32088181-5	2020	Because chronic administration of imipramine has been shown to affect mGluR5, the purpose of this study was to verify the hypothesis of COX-2 pathway engagement in disrupting effects of imipramine.	Imipramine	186-196	prostaglandin-endoperoxide synthase 2	Mus musculus	136-141
32088181-12	2020	In conclusion, our data show the involvement of the COX-2 pathway in changes in the long-term memory, and procedural memory of C57Bl/6J mice after chronic imipramine treatment.	Imipramine	155-165	prostaglandin-endoperoxide synthase 2	Mus musculus	52-57
32188962-2	2020	The hybrid nature of this material is founded on two key elements: the presence of the DAT backbone induced the formation of hydrophobic regions that allowed efficient loading of a series of drugs of increasing hydrophobicity (Metronidazole, Benzocaine, Ibuprofen, Naproxen and Imipramine), while simultaneously endowing swelling-induced pH-responsiveness to the hydrogel.	Imipramine	278-288	solute carrier family 6 member 3	Homo sapiens	87-90