Towell A, Muscat R, Willner P
Psychology Department, City of London Polytechnic, London.
Pharmacol Biochem Behav. 1988 Jul;30(3):641-8. doi: 10.1016/0091-3057(88)90077-9.
A microstructural analysis paradigm was used to study amphetamine anorexia. Doses above 0.40 mg/kg significantly reduced food intake by reducing eating time; in contrast, eating rate was increased at these doses. Examination of the frequency distribution of interresponse times (IRTs) revealed a significant shift to shorter IRTs at doses as low as 0.125 mg/kg. Pimozide blocked amphetamine anorexia at 0.5 and 1.0 mg/kg, suggesting that at both doses amphetamine anorexia has a dopaminergic substrate. However, the atypical neuroleptic thioridazine did not antagonize amphetamine. Furthermore, effects of amphetamine were additive with those of apomorphine, administered at a dose known to suppress feeding by inhibiting mesolimbic DA neurons. These results provide evidence against an involvement of the mesolimbic DA system in amphetamine anorexia.
采用微观结构分析范式研究苯丙胺性厌食症。剂量高于0.40mg/kg时,通过减少进食时间显著降低食物摄入量;相反,在这些剂量下进食速率增加。对反应间隔时间(IRT)的频率分布进行检查发现,低至0.125mg/kg的剂量就能使IRT显著缩短。匹莫齐特在0.5和1.0mg/kg时可阻断苯丙胺性厌食症,这表明在这两种剂量下苯丙胺性厌食症都有一个多巴胺能底物。然而,非典型抗精神病药物硫利达嗪并不拮抗苯丙胺。此外,苯丙胺的作用与阿扑吗啡的作用具有相加性,阿扑吗啡的给药剂量已知可通过抑制中脑边缘多巴胺能神经元来抑制进食。这些结果提供了证据,证明中脑边缘多巴胺能系统不参与苯丙胺性厌食症。