Downregulation of human platelet tritiated imipramine binding sites is associated with the antidepressant response to etoperidone hydrochloride

J. R. Magliozzi, D. W. Gietzen, S. Wimberg, Richard J Maddock

Research output: Contribution to journalArticle

Abstract

Despite similarities between conventional dibenzazepine antidepressants and newer triazolopyridine antidepressants the mechanism of the latter class of agents is still not well understood. In addition to possessing monoamine reuptake blocking ability, these agents appear to have antagonist effects at 5HT2 receptors and to be metabolized to a psychoactive agent meta-chlorophenylpiperizene. In an effort to clarify the mechanism of action of these agents, platelet 3H-imipramine receptor binding was measured at baseline, six weeks, and 14 weeks after initiation of treatment with etoperidone hydrochloride or placebo. 3H-imipramine receptor density (B(max)) declined throughout the treatment period in both the drug-treated and placebo-treated group. However, a statistically significant (P = 0.01) difference between etoperidone hydrochloride treatment and placebo treatment was found, with patients receiving etoperidone demonstrating a longer decrease in imipramine receptor density than placebo-treated patients. A trend toward a correlation between Hamilton Depression Scale scores and imipramine receptor B(max) values was noted in the drug-treated group. We interpret these results to be evidence of common mechanisms of antidepressant action between triazolopyridine agents and serotonin reuptake blocking agents. These data also raise the possibility that nondrug responses in depression may also be associated with changes in imipramine receptor B(max).

Original languageEnglish (US)
Pages (from-to)299-308
Number of pages10
JournalCurrent Therapeutic Research - Clinical and Experimental
Volume51
Issue number3
StatePublished - 1992

ASJC Scopus subject areas

  • Medicine(all)

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