Rockman G E, Amit Z, Carr G, Ogren S O
Arch Int Pharmacodyn Ther. 1979 Oct;241(2):260-5.
This experiment was undertaken to examine whether the attenuation of ethanol consumption following treatment with zimelidine (H102/09) could be due to an invasion of surplus serotonin into norepinephrine neurons. In an attempt to prevent this proposed invasion by serotonin, ethanol preferring animals were pre-treated with desmethylimipramine (DMI), a norepinephrine reuptake inhibitor, prior to treatment with zimelidine. The results demonstrated that those animals treated in such a manner consumed significantly more ethanol than those animals treated with zimelidine alone. Based on these results it is suggested that the observed attenuation of ethanol consumption following zimelidine treatment, could be partially due to a serotonin-induced functional depletion of norepinephrine.
进行本实验是为了研究用齐美利定(H102/09)治疗后乙醇摄入量的减少是否可能是由于过量的5-羟色胺侵入去甲肾上腺素能神经元所致。为了防止5-羟色胺的这种侵入,在给予齐美利定之前,先给偏好乙醇的动物用去甲丙咪嗪(DMI)进行预处理,DMI是一种去甲肾上腺素再摄取抑制剂。结果表明,以这种方式处理的动物比单独用齐美利定处理的动物消耗的乙醇明显更多。基于这些结果,有人提出,齐美利定治疗后观察到的乙醇摄入量的减少,可能部分是由于5-羟色胺诱导的去甲肾上腺素功能耗竭所致。