伊拉地平可减轻大鼠纹状体中缺血诱导的多巴胺释放。

Isradipine attenuates the ischemia-induced release of dopamine in the striatum of the rat.

作者信息

Ooboshi H, Sadoshima S, Ibayashi S, Yao H, Uchimura H, Fujishima M

机构信息

Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Eur J Pharmacol. 1993 Mar 16;233(1):165-8. doi: 10.1016/0014-2999(93)90363-m.

DOI:10.1016/0014-2999(93)90363-m

PMID:8472744

Abstract

We examined the effect of isradipine, a blocker of L-type voltage-sensitive Ca2+ channels (VSCCs), on the ischemia-induced release of dopamine in the rat striatum. Perfusion of 200 micrograms/ml isradipine in the striatum did not alter extracellular dopamine concentrations monitored by microdialysis. However, a marked increase (145-fold) in dopamine level during forebrain ischemia, developed by bilateral carotid artery occlusion, was attenuated significantly by 37% by isradipine whereas the intensity of ischemia, monitored by striatal blood flow, was unchanged. These results suggest that isradipine attenuates the ischemia-induced release of dopamine via blockade of L-type VSCCs on dopaminergic neurons.

摘要

我们研究了L型电压敏感性钙通道（VSCCs）阻滞剂伊拉地平对大鼠纹状体中缺血诱导的多巴胺释放的影响。在纹状体中灌注200微克/毫升的伊拉地平并不会改变通过微透析监测到的细胞外多巴胺浓度。然而，双侧颈动脉闭塞导致的前脑缺血期间多巴胺水平显著升高（145倍），伊拉地平可使其显著降低37%，而通过纹状体血流量监测的缺血强度并未改变。这些结果表明，伊拉地平通过阻断多巴胺能神经元上的L型VSCCs来减弱缺血诱导的多巴胺释放。