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尼古丁增强氟哌啶醇诱导的僵住症:纹状体机制

Nicotine potentiation of haloperidol-induced catalepsy: striatal mechanisms.

作者信息

Sanberg P R, Emerich D F, el-Etri M M, Shipley M T, Zanol M D, Cahill D W, Norman A B

机构信息

Department of Surgery, University of South Florida College of Medicine, Tampa 33612.

出版信息

Pharmacol Biochem Behav. 1993 Oct;46(2):303-7. doi: 10.1016/0091-3057(93)90357-y.

DOI:10.1016/0091-3057(93)90357-y
PMID:8265684
Abstract

Nicotine potentiated the catalepsy produced by haloperidol. The excitotoxin quinolinic acid (QA) selectively destroys striatal neurons when injected directly into the striatum. Bilateral QA lesions of the rat striatum (150 nmol) significantly reduced the catalepsy produced by haloperidol as well as the ability of nicotine to potentiate haloperidol-induced catalepsy. A second experiment examined whether the ability of nicotine to potentiate haloperidol-induced catalepsy was associated with a potentiation of dopamine turnover following haloperidol. Nicotine alone produced a mild increase in dopamine turnover relative to saline treated controls while haloperidol produced a marked increase in dopamine turnover relative to saline- and nicotine-treated controls. However, the combined administration of haloperidol and nicotine did not further elevate dopamine turnover over that observed following haloperidol alone. The results indicated that: 1) nicotine could not potentiate haloperidol-induced catalepsy without an intact striatum and 2) the behavioral effect of nicotine and haloperidol cotreatment was not due to any change in dopamine turnover.

摘要

尼古丁增强了氟哌啶醇引起的僵住症。兴奋性毒素喹啉酸(QA)直接注射到纹状体时会选择性地破坏纹状体神经元。大鼠纹状体双侧QA损伤(150纳摩尔)显著降低了氟哌啶醇引起的僵住症以及尼古丁增强氟哌啶醇诱导僵住症的能力。第二个实验研究了尼古丁增强氟哌啶醇诱导僵住症的能力是否与氟哌啶醇给药后多巴胺周转的增强有关。相对于生理盐水处理的对照组,单独使用尼古丁使多巴胺周转略有增加,而相对于生理盐水和尼古丁处理的对照组,氟哌啶醇使多巴胺周转显著增加。然而,氟哌啶醇和尼古丁联合给药并没有比单独使用氟哌啶醇后观察到的多巴胺周转进一步升高。结果表明:1)没有完整的纹状体,尼古丁就不能增强氟哌啶醇诱导的僵住症;2)尼古丁和氟哌啶醇联合治疗的行为效应不是由于多巴胺周转的任何变化。

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