CHRONIC TREATMENT WITH DESIPRAMINE - EFFECT ON ENDOCRINE AND BEHAVIORAL-RESPONSES INDUCED BY INESCAPABLE STRESS

Inescapable shock (IS) exposure induces behavioral inactivity, related to behavioral alterations in subsequent tests (i.e. escape failure du ring shuttle box task). Previous studies have demonstrated that variou s antidepressant treatments administered either before or after IS exp osure reversed these behavioral deficits. Recently, we demonstrated co rticosterone (CS) involvement both in inactivity performance during IS and in the number of escape failures in a shuttle box task. In the pr esent study, we analyzed the effects of chronic desipramine (DMI) trea tment administered before or after IS exposure on the dynamics of chan ges in serum CS concentration after both IS and shuttle box task, to e xplore a possible relationship between the hormonal response and the r eversion of the behavioral deficits induced by DMI. DMI (10 mg/kg intr aperitoneally i.p.) administered during 6 consecutive days before IS r educed CS release and inactivity induced by this aversive experience. Two days later, when these DMI-treated rats were submitted to a shuttl e box task, a reduction in CS release and IS-induced escape failures w as observed as compared with saline-treated rats. Besides, in animals without IS experience, the pretreatment with DMI did not modify either the pattern of CS secretion or the percentage of escape failures as c ompared with saline injected mts. On the other hand, CS values of rats treated with DMI during 6 consecutive days after IS exposure recovere d to resting controls levels within 60 min post-shuttle box task, exhi biting fewer escape failures; unlike saline-treated, IS-exposed rats, which retained persistently elevated levels of CS (during the post-tas k sampling interval) and showed a high percentage of escape failures. Thus, chronic DMI administration before IS attenuated CS secretion and prevented the onset and expression of behavioral deficits induced by uncontrollable stressor. However, when it was administered after IS, i t induced an increased negative feedback sensitivity in coincidence wi th the reversion of the IS-induced behavioral deficits. (C) 1997 Elsev ier Science Inc.