Sampson D, Willner P, Muscat R
Psychology Department, City of London Polytechnic, UK.
Psychopharmacology (Berl). 1991;104(4):491-5. doi: 10.1007/BF02245655.
Rats subjected chronically (12 weeks) to a variety of mild, unpredictable stressors showed a reduced consumption of sucrose or a sucrose/saccharin mixture in two-bottle consumption tests (sweet solution versus water). The deficit was apparent within 2 weeks of stress; normal behaviour was restored by chronic (7 weeks) treatment with the tricyclic antidepressants desmethylimipramine (DMI) or amitriptyline (AMI). Acute administration of the dopamine D1 receptor antagonist SCH-23390 1 week after withdrawal, or the dopamine D2 receptor antagonist sulpiride 2 weeks after withdrawal, were without effect in vehicle-treated stressed animals, and in non-stressed animals. However, the DA antagonists selectively reversed the improvement of performance in DMI- or AMI-treated stressed animals. This suggests that an increase in functional activity at DA synapses is the mechanism of action of DMI and AMI in this model.
长期（12周）遭受各种轻度、不可预测应激源的大鼠，在双瓶消耗试验（甜味溶液与水）中，蔗糖或蔗糖/糖精混合物的消耗量减少。应激2周内这种缺陷就很明显；用三环类抗抑郁药去甲丙咪嗪（DMI）或阿米替林（AMI）进行长期（7周）治疗可恢复正常行为。撤药1周后急性给予多巴胺D1受体拮抗剂SCH - 23390，或撤药2周后给予多巴胺D2受体拮抗剂舒必利，对接受载体处理的应激动物和非应激动物均无影响。然而，多巴胺拮抗剂选择性地逆转了DMI或AMI治疗的应激动物的行为改善。这表明多巴胺突触功能活性的增加是DMI和AMI在此模型中的作用机制。
