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短暂性前脑缺血会使大鼠外侧新纹状体中的多巴胺D1传递产生多种缺陷。

Transient forebrain ischemia produces multiple deficits in dopamine D1 transmission in the lateral neostriatum of the rat.

作者信息

Benfenati F, Pich E M, Grimaldi R, Zoli M, Fuxe K, Toffano G, Agnati L F

机构信息

Institute of Human Physiology, University of Modena, Italy.

出版信息

Brain Res. 1989 Oct 2;498(2):376-80. doi: 10.1016/0006-8993(89)91120-7.

Abstract

Striatal dopamine D1 transmission was studied in rats 7 days after transient (30 min) forebrain ischemia using the 4-vessel occlusion model. The striatal distribution of dopamine D1 ([3H]SCH 23390 binding sites) and D2 ([3H]sulpiride binding sites) receptors as well as the distribution of adenylate cyclase ( [3H]forskolin binding sites) and of the intracytoplasmic dopamine and cAMP-regulated phosphoprotein DARPP-32 related to D1 transmission were analyzed. While the distribution of D2 receptors was unaffected 7 days after the ischemic insult, all the other markers showed a patchy disappearance in the dorsolateral part of the neostriatum. These findings underline the existence of selective multiple deficits in D1 transmission after transient forebrain ischemia in rat striatum.

摘要

使用四血管闭塞模型,在短暂性(30分钟)前脑缺血7天后的大鼠中研究纹状体多巴胺D1传递。分析了多巴胺D1([3H] SCH 23390结合位点)和D2([3H]舒必利结合位点)受体在纹状体中的分布,以及腺苷酸环化酶([3H]福司柯林结合位点)和与D1传递相关的胞质内多巴胺和cAMP调节磷蛋白DARPP-32的分布。缺血性损伤7天后,D2受体的分布未受影响,而所有其他标志物在新纹状体的背外侧部分均呈现斑片状消失。这些发现强调了大鼠纹状体短暂性前脑缺血后D1传递中存在选择性多重缺陷。

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