Andén N E, Grenhoff J, Svensson T H
Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
Psychopharmacology (Berl). 1988;96(4):558-60. doi: 10.1007/BF02180041.
Treatment of rats with haloperidol, 0.5 mg/kg SC daily for 3 weeks, did not increase the concentration of dopamine in the dopamine-rich nuclei of the forebrain apart from a small effect in the olfactory tubercle. Cessation of the nerve impulse flow in the ascending dopamine neurons induced by gamma-butyrolactone caused an approximately twofold increase in the dopamine levels of both haloperidol-treated and control rats. The results are hard to reconcile with the notion of haloperidol-induced depolarization block, i.e., cessation of impulse flow in the majority of midbrain dopamine neurons of unanaesthetized rats.
用氟哌啶醇（每天皮下注射0.5毫克/千克，持续3周）治疗大鼠，除了对嗅结节有轻微影响外，并未增加前脑富含多巴胺的核团中的多巴胺浓度。由γ-丁内酯诱导的升支多巴胺神经元神经冲动流的停止，导致氟哌啶醇治疗组和对照组大鼠的多巴胺水平均增加了约两倍。这些结果很难与氟哌啶醇诱导的去极化阻滞概念相协调，即未麻醉大鼠的大多数中脑多巴胺神经元冲动流的停止。
