Effects of antidepressant treatment on inhibitory avoidance behavior and amygdaloid β-Adrenoceptors in rats

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Abstract

Chronic treatment of rats with a variety of antidepressants results in the down-regulation of β1-adrenoceptors in the amygdaloid nuclei. The present study sought to determine if this specific neurochemical effect caused an alteration in inhibitory avoidance conditioning, a behavior considered to be mediated by β-adrenoceptors in the amygdala. Rats treated chronically with either desipramine (DMI) or phenelzine (PHEN), which down-regulate β1-adrenoceptors in the amygdala, or fluoxetine (FLUOX), which does not do this, did not exhibit a deficit in the retention of the inhibitory avoidance task. However, when scopolamine was given prior to acquisition of the task in a dose that, by itself, did not affect retention, DMI- and PHEN-treated rats showed a marked deficit in retention. This effect was also observed after acute administration of these drugs, although they did not down-regulate amygdaloid β1-adrenoceptors at this time. It seems that the ability of these antidepressants to potentiate the amnesic effect of scopolamine is unrelated to their effect on β1-adrenoceptor number in the amygdala and that the extent of antidepressant-induced amygdaloid β1-adrenoceptor down-regulation is not sufficient, by itself, to cause a deficit in an inhibitory avoidance task. Copyright (C) 1998 American College of Neuropsychopharmacology.

Original languageEnglish (US)
Pages (from-to)300-313
Number of pages14
JournalNeuropsychopharmacology
Volume19
Issue number4
DOIs
StatePublished - Oct 1 1998

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Keywords

  • Amygdala
  • Desipramine
  • Fluoxetine
  • Inhibitory avoidance
  • Phenelzine
  • β-Adrenoceptors

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health

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