ANIMAL-MODEL OF DEPRESSION - PHARMACOLOGICAL SENSITIVITY OF A HEDONIC DEFICIT
ANIMAL-MODEL OF DEPRESSION - PHARMACOLOGICAL SENSITIVITY OF A HEDONIC DEFICIT
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DOI：
10.1016/0091-3057(82)90053-3
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发表时间：
1982-01-01
影响因子：
3.6
通讯作者：
KATZ, RJ
中科院分区：
文献类型：
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作者：
KATZ, RJ
据报道，慢性应激后大鼠的蔗糖和糖精消耗量减少。这种缺陷可能与内源性抑郁症中的完善缺陷有关。为了进一步从药理学上检查这种状态，我们用抗抑郁药丙咪嗪治疗应激大鼠。尽管总体上没有食欲作用（或在某些情况下轻度厌食症），丙咪嗪在各种试验中显著恢复了糖精的消耗。这种缺陷与伴随疾病的变化的药理学相似性进一步支持了慢性应激模型的潜在适用性。
A reduction in sucrose and saccharin 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 saccharin consumption in a variety of tests. The pharmacological similarity of the deficit to the changes accompanying disorders further supports the potential applicability of the chronic stress model.