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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Enhancement of haloperidol-induced catalepsy by nicotine: an investigation of possible mechanisms.
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Enhancement of haloperidol-induced catalepsy by nicotine: an investigation of possible mechanisms.

机译：尼古丁增强氟哌啶醇诱导的僵直症的可能机制研究。

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摘要

Nicotine has been reported to potentiate the cataleptic effect of the dopamine receptor antagonist haloperidol in rats. This effect is paradoxical, since nicotine alone tends to increase nigrostriatal dopamine release. In the present experiments, a pro-cataleptic effect of nicotine was confirmed statistically but was small and variable. Three potential mechanisms underlying this effect were investigated. (i) Desensitization of brain nicotinic receptors appears to make little if any contribution to the pro-cataleptic effect of nicotine, insofar as the latter was not mimicked by two centrally active nicotinic antagonists (mecamylamine and chlorisondamine). (ii) Depolarization inactivation resulting from combined treatment with haloperidol and nicotine does not appear to be critical, since the pro-cataleptic effect of nicotine was not enhanced by chronic haloperidol administration, a treatment designed to enhance depolarization inactivation. (iii) The slow emergence and persistence of the acute pro-cataleptic effect of nicotine suggested possible mediation by a nicotine metabolite. However, neither cotinine nor nornicotine, the principal pharmacologically-active metabolites of nicotine, exerted a significant pro-cataleptic effect. In conclusion, the pro-cataleptic effect of nicotine was weak and variable in the present study, and its mechanism remains obscure.
机译：据报导，尼古丁可增强多巴胺受体拮抗剂氟哌啶醇对大鼠的镇静作用。这种效果是自相矛盾的，因为单独使用尼古丁会增加黑质纹状体多巴胺的释放。在本实验中，尼古丁的促感激作用在统计学上得到证实，但很小且变化很大。研究了这种作用的三种潜在机制。 （i）脑尼古丁受体的脱敏似乎对尼古丁的抗感激作用几乎没有任何贡献，只要后者没有被两种中枢活性尼古丁拮抗剂（美卡敏和毒死d）模仿即可。 （ii）由氟哌啶醇和尼古丁联合治疗导致的去极化失活似乎不是关键的，因为通过长期施用氟哌啶醇（一种旨在增强去极化失活的治疗）不能增强尼古丁的前感性作用。 （iii）尼古丁的急性前感官作用缓慢出现并持续存在，提示可能由尼古丁代谢物介导。然而，尼古丁的主要药理活性代谢产物可替宁和去甲烟碱均未发挥明显的促感激作用。总之，在本研究中，尼古丁的促感激作用微弱且变化不定，其机制仍不清楚。

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