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

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.