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MPTP诱导的小鼠黑质纹状体损伤后的多巴胺受体可塑性

Dopamine receptor plasticity following MPTP-induced nigrostriatal lesions in the mouse.

作者信息

Weihmuller F B, Bruno J P, Neff N H, Hadjiconstantinou M

机构信息

Department of Psychology, College of Social and Behavioral Studies, Ohio State University, Columbus 43210.

出版信息

Eur J Pharmacol. 1990 May 16;180(2-3):369-72. doi: 10.1016/0014-2999(90)90324-y.

DOI:10.1016/0014-2999(90)90324-y
PMID:2365010
Abstract

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) destroys dopamine-containing nigrostriatal neurons and increases the apparent Bmax of both D1 and D2 binding sites in the striatum. However, the changes of Bmax occur at different intervals after the lesion. Up-regulation of D2 sites becomes evident about 3 weeks after the lesion and lasts for about 3 months. In contrast, about 3 months are required for the up-regulation of D1 sites and increased binding is still evident after 5 months.

摘要

MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)会破坏含多巴胺的黑质纹状体神经元,并增加纹状体中D1和D2结合位点的表观最大结合容量(Bmax)。然而,损伤后Bmax的变化发生在不同的时间间隔。D2位点的上调在损伤后约3周变得明显,并持续约3个月。相比之下,D1位点的上调需要约3个月,并且在5个月后结合增加仍然明显。

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