Centeno V A, Volosin M
Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
Physiol Behav. 1997 Oct;62(4):939-44. doi: 10.1016/s0031-9384(97)00255-2.
Inescapable shock (IS) exposure induces behavioral inactivity, related to behavioral alterations in subsequent tests (i.e. escape failure during shuttle box task). Previous studies have demonstrated that various antidepressant treatments administered either before or after IS exposure reversed these behavioral deficits. Recently, we demonstrated corticosterone (CS) involvement both in inactivity performance during IS and in the number of escape failures in a shuttle box task. In the present study, we analyzed the effects of chronic desipramine (DMI) treatment administered before or after IS exposure on the dynamics of changes in serum CS concentration after both IS and shuttle box task, to explore a possible relationship between the hormonal response and the reversion of the behavioral induced by DMI. DMI (10 mg/kg intraperitoneally i.p.) administered during 6 consecutive days before IS reduced release and inactivity induced by this aversive experience. Two days later, when these DMI-treated rats were submitted to a shuttle box task, a reduction in CS release and IS-induced escape failures were 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 compared with saline-injected rats. On the other hand, CS values of rats treated with DMI during 6 consecutive days after IS exposure recovered to resting controls levels within 60 min post-shuttle box task, exhibiting fewer escape failures; unlike saline-treated, IS-exposed rats, which retained persistently elevated levels of CS (during the post-task sampling interval) a 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 stressors. However, when it was administered after IS, it induced an increased negative feedback sensitivity in coincidence with the reversion of the IS-induced behavioral deficits.
不可逃避电击（IS）暴露会导致行为活动减少，这与后续测试中的行为改变有关（例如穿梭箱任务中的逃避失败）。先前的研究表明，在IS暴露之前或之后给予各种抗抑郁治疗可逆转这些行为缺陷。最近，我们证明了皮质酮（CS）既参与了IS期间的静止行为表现，也参与了穿梭箱任务中的逃避失败次数。在本研究中，我们分析了在IS暴露之前或之后给予慢性地昔帕明（DMI）治疗对IS和穿梭箱任务后血清CS浓度变化动态的影响，以探讨激素反应与DMI诱导的行为逆转之间的可能关系。在IS之前连续6天腹腔注射（i.p.）10 mg/kg的DMI可减少这种厌恶经历诱导的释放和静止行为。两天后，当这些接受DMI治疗的大鼠进行穿梭箱任务时，与生理盐水处理的大鼠相比，观察到CS释放减少以及IS诱导的逃避失败减少。此外，在没有IS经历的动物中，与注射生理盐水的大鼠相比，DMI预处理既没有改变CS分泌模式，也没有改变逃避失败的百分比。另一方面，在IS暴露后连续6天接受DMI治疗的大鼠，在穿梭箱任务后60分钟内CS值恢复到静息对照水平，逃避失败次数减少；与生理盐水处理的、暴露于IS的大鼠不同，后者（在任务后采样间隔期间）CS水平持续升高，逃避失败的百分比很高。因此，在IS之前给予慢性DMI可减弱CS分泌，并防止由不可控应激源诱导的行为缺陷的发生和表现。然而，当在IS之后给予时，它会诱导负反馈敏感性增加，同时IS诱导的行为缺陷得到逆转。
