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中脑边缘多巴胺系统受损后,伏隔核中的苯环利定结合位点及苯环利定诱发的多动会减少。

Phencyclidine binding sites in the nucleus accumbens and phencyclidine-induced hyperactivity are decreased following lesions of the mesolimbic dopamine system.

作者信息

French E D, Pilapil C, Quirion R

出版信息

Eur J Pharmacol. 1985 Oct 8;116(1-2):1-9. doi: 10.1016/0014-2999(85)90178-5.

DOI:10.1016/0014-2999(85)90178-5
PMID:2996909
Abstract

[3H]Phencyclidine [( 3H]PCP) binding to rat nucleus accumbens, hippocampal and striatal membranes, and PCP-induced locomotor hyperactivity were assessed following selective lesions of the mesolimbic dopaminergic system. 6-Hydroxydopamine (6-OHDA) injections into the A10 region of the ventral tegmental area or into the accumbens itself resulted in a blockade of PCP's stimulatory effects and a highly significant reduction in the number of [3H]PCP binding sites and dopamine content of the nucleus accumbens. However, destruction of the dopaminergic mesolimbic fibers did not significantly alter hippocampal or striatal [3H]PCP binding. The data suggest that PCP elicits its locomotor stimulating effects via an interaction with PCP binding sites located mostly on mesolimbic dopaminergic terminals within the nucleus accumbens.

摘要

在对中脑边缘多巴胺能系统进行选择性损伤后,评估了[3H]苯环利定([3H]PCP)与大鼠伏隔核、海马和纹状体膜的结合情况以及PCP诱导的运动性活动亢进。向腹侧被盖区的A10区域或伏隔核本身注射6-羟基多巴胺(6-OHDA),导致PCP的刺激作用被阻断,伏隔核中[3H]PCP结合位点的数量和多巴胺含量显著降低。然而,多巴胺能中脑边缘纤维的破坏并没有显著改变海马或纹状体的[3H]PCP结合。数据表明,PCP通过与主要位于伏隔核内中脑边缘多巴胺能终末上的PCP结合位点相互作用,引发其运动刺激作用。

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