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胆囊收缩素通过两种不同机制调节伏隔核前后部多巴胺的释放。

Cholecystokinin modulates the release of dopamine from the anterior and posterior nucleus accumbens by two different mechanisms.

作者信息

Marshall F H, Barnes S, Hughes J, Woodruff G N, Hunter J C

机构信息

Parke-Davis Research Unit, Addenbrookes Hospital, Cambridge, England.

出版信息

J Neurochem. 1991 Mar;56(3):917-22. doi: 10.1111/j.1471-4159.1991.tb02009.x.

Abstract

The effects of various cholecystokinin (CCK)-related peptides were investigated on 35 mM K(+)-stimulated endogenous dopamine release from slices of either anterior or posterior nucleus accumbens of the rat. CCK sulphated octapeptide (1-10 microM), but not pentagastrin or CCK unsulphated octapeptide, was found to cause a dose-dependent increase in the release from the posterior nucleus accumbens. This effect was blocked by low doses of the CCKA receptor antagonist L364,718 (10 nM) but not the CCKB receptor antagonist L365,260. In the anterior nucleus accumbens CCK sulphated octapeptide (1 microM) and CCK unsulphated octapeptide (0.1-1 microM) inhibited the dopamine release, and this effect was blocked by L365,260 (10-100 nM) but not by L364,718. These results suggest that CCK has a different effect on dopamine release from the anterior and posterior nucleus accumbens and that these effects are mediated by two different types of CCK receptor.

摘要

研究了各种胆囊收缩素(CCK)相关肽对35 mM K⁺刺激大鼠伏隔核前部或后部切片内源性多巴胺释放的影响。发现CCK硫酸化八肽(1 - 10 μM)能使伏隔核后部的多巴胺释放呈剂量依赖性增加,而五肽胃泌素或CCK非硫酸化八肽则无此作用。低剂量的CCKA受体拮抗剂L3,64,718(10 nM)可阻断此效应,而CCKB受体拮抗剂L3,65,260则不能。在伏隔核前部,CCK硫酸化八肽(1 μM)和CCK非硫酸化八肽(0.1 - 1 μM)抑制多巴胺释放,此效应可被L3,65,260(10 - 100 nM)阻断,而L3,64,718则不能。这些结果表明,CCK对伏隔核前部和后部的多巴胺释放有不同影响,且这些影响由两种不同类型的CCK受体介导。

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