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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.

Original publication

DOI

10.1016/j.neuropharm.2004.02.013

Type

Journal article

Journal

Neuropharmacology

Publication Date

06/2004

Volume

46

Pages

1177 - 1183

Keywords

Animals, Antidepressive Agents, Binding Sites, Brain, Drug Evaluation, Preclinical, Gene Expression Regulation, Male, Neurokinin-1 Receptor Antagonists, Rats, Rats, Sprague-Dawley, Receptors, Neurokinin-1