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抑郁症动物模型:享乐缺失的药理学敏感性

Animal model of depression: pharmacological sensitivity of a hedonic deficit.

作者信息

Katz R J

出版信息

Pharmacol Biochem Behav. 1982 Jun;16(6):965-8. doi: 10.1016/0091-3057(82)90053-3.

DOI:10.1016/0091-3057(82)90053-3
PMID:7202217
Abstract

A reduction in sucrose and saccharine consumption following chronic stress is reported for the rat. This deficit may be related to consummatory deficits seen in endogenous depression. To further examine this state pharmacologically, stressed rats were treated with the antidepressant imipramine. Despite a general absence of appetitive effects (or in some cases mild anorexia) imipramine significantly restored saccharine consumption in a variety of tests. The pharmacological similarity of the deficit to the changes accompanying affective disorders further supports the potential applicability of the chronic stress model.

摘要

据报道,大鼠在长期应激后蔗糖和糖精的消耗量会减少。这种缺陷可能与内源性抑郁症中出现的进食缺陷有关。为了从药理学角度进一步研究这种状态,给应激大鼠服用抗抑郁药丙咪嗪。尽管丙咪嗪通常没有食欲增强作用(或在某些情况下有轻微厌食),但在各种测试中它能显著恢复糖精的消耗量。这种缺陷与情感障碍伴随变化在药理学上的相似性进一步支持了慢性应激模型的潜在适用性。

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