Abstract:
:Clinically effective antidepressants are thought to exert their therapeutic effects by facilitating central monoamine neurotransmission. However, recent data showing that neurokinin-1 receptor (NK1R) antagonists have antidepressant properties in both animal and clinical studies raise the possibility that classical antidepressants may also influence NK1R expression in the brain. To test this hypothesis, rats were treated with desipramine, paroxetine, venlafaxine, tranylcypromine or vehicle for 14-42 days. NK1R binding sites and mRNA were determined in a wide variety of brain areas using in situ hybridization and quantitative receptor autoradiography. In all areas examined, the abundance of NK1R binding sites was unchanged after 14 days of treatment. None of the treatments altered the number of NK1R binding sites following 42 days treatment with the exception that an increase was found in the locus coeruleus with tranylcypromine. Taken together, we report that repeated treatment with antidepressants of different classes does not cause significant changes in NK1R expression.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Sartori SB,Burnet PWJ,Sharp T,Singewald Ndoi
10.1016/j.neuropharm.2004.02.013subject
Has Abstractpub_date
2004-06-01 00:00:00pages
1177-1183issue
8eissn
0028-3908issn
1873-7064pii
S0028-3908(04)00051-6journal_volume
46pub_type
杂志文章abstract::The nomenclature system used to characterize 5-hydroxytryptamine receptor subtypes remains controversial. To date, the majority of nomenclature systems have been on the differential pharmacological properties of the receptors. However, the availability of molecular biological data allows for a nomenclature system base...
journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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abstract::The United States is in the midst of an opiate epidemic, with abuse of prescription and illegal opioids increasing steadily over the past decade. While it is clear that there is a genetic component to opioid addiction, there is a significant portion of heritability that cannot be explained by genetics alone. The curre...
journal_title:Neuropharmacology
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doi:10.1016/j.neuropharm.2016.10.006
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更新日期:2014-04-01 00:00:00
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/j.neuropharm.2006.06.020
更新日期:2007-01-01 00:00:00
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/j.neuropharm.2016.09.001
更新日期:2016-12-01 00:00:00
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journal_title:Neuropharmacology
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pub_type: 杂志文章
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/0028-3908(83)90242-3
更新日期:1983-03-01 00:00:00
abstract::The role in ligand recognition and receptor activation of two adjacent charged residues (lysine 195 and aspartate 196) in the first extracellular loop of the human VPAC(1) receptor was investigated in stably transfected CHO cells expressing the wild type or point mutated receptors.Replacement of lysine 195 by glutamin...
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pub_type: 杂志文章
doi:10.1016/s0028-3908(02)00233-2
更新日期:2003-01-01 00:00:00
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/0028-3908(86)90028-6
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章,评审
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更新日期:1996-01-01 00:00:00
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journal_title:Neuropharmacology
pub_type: 杂志文章
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更新日期:2004-05-01 00:00:00
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journal_title:Neuropharmacology
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更新日期:1986-08-01 00:00:00
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
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更新日期:1987-11-01 00:00:00
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journal_title:Neuropharmacology
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更新日期:1984-11-01 00:00:00
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
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更新日期:2015-01-01 00:00:00
abstract::In low cerveau isolé transected rats, the effects of microiontophoretic application of putative serotonin 5-HT1A and 5-HT1B agonists on the spontaneous firing rate of CA1 pyramidal cells were compared to those of 5-HT. In contrast to the large current-dependent suppression of unit activity observed with 5-HT, the 5-HT...
journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/0028-3908(88)90079-2
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更新日期:1998-09-01 00:00:00