Tejedor-Real P, Mico J A, Maldonado R, Roques B P, Gibert-Rahola J
Department of Neurosciences, School of Medicine, Cádiz, Spain.
Pharmacol Biochem Behav. 1995 Sep;52(1):145-52. doi: 10.1016/0091-3057(95)00067-7.
The involvement of opioid system on the learned helplessness model of depression was investigated. Animals preexposed to inescapable shocks were treated with either Met-enkephalin, Leu-enkephalin, morphine, imipramine, naloxone, RB 38A (a mixed inhibitor of enkephalin degrading enzymes), or RB 38B (a selective inhibitor of neutral endopeptidase EC 3.4.24.11). Stimulation of opioid system by either opioid agonists or enkephalin catabolism inhibitors reversed the escape deficit induced by shock pretreatment. In contrast, administration of naloxone potentiated the effect of inescapable shocks. Imipramine reduced the number of escape failures in this test, and this effect was antagonized by naloxone. These results point to the involvement of the endogenous opioid system in this model of depression.
研究了阿片系统在抑郁症习得性无助模型中的作用。预先暴露于不可逃避电击的动物分别用甲硫氨酸脑啡肽、亮氨酸脑啡肽、吗啡、丙咪嗪、纳洛酮、RB 38A（脑啡肽降解酶的混合抑制剂）或RB 38B（中性内肽酶EC 3.4.24.11的选择性抑制剂）进行处理。阿片类激动剂或脑啡肽分解代谢抑制剂对阿片系统的刺激可逆转电击预处理诱导的逃避缺陷。相反，给予纳洛酮可增强不可逃避电击的作用。丙咪嗪减少了该试验中的逃避失败次数，且这种作用被纳洛酮拮抗。这些结果表明内源性阿片系统参与了该抑郁症模型。
