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用氟哌啶醇治疗3周会在未麻醉大鼠的中脑多巴胺神经元中产生去极化阻滞吗?

Does treatment with haloperidol for 3 weeks produce depolarization block in midbrain dopamine neurons of unanaesthetized rats?

作者信息

Andén N E, Grenhoff J, Svensson T H

机构信息

Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.

出版信息

Psychopharmacology (Berl). 1988;96(4):558-60. doi: 10.1007/BF02180041.

Abstract

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.

摘要

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。

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