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D2多巴胺能受体参与大鼠伏隔核后部注射胆囊收缩素八肽(CCK-8)所诱导的情绪和动机反应。

Involvement of D2 dopaminergic receptors in the emotional and motivational responses induced by injection of CCK-8 in the posterior part of the rat nucleus accumbens.

作者信息

Derrien M, Durieux C, Daugé V, Roques B P

机构信息

Unité de Pharmacochimie Moléculaire et Structurale U266 INSERM, URA D1500 CNRS, Université René Descartes, Paris, France.

出版信息

Brain Res. 1993 Jul 23;617(2):181-8. doi: 10.1016/0006-8993(93)91084-6.

Abstract

When CCK-8 was injected in the rat posterior nucleus accumbens, where it is in part co-localized with dopamine, a decrease in exploration of the four hole box and the elevated plus maze was observed. In this study, a selective destruction of the dopaminergic mesoaccumbens pathway induced by local injection of 6-hydroxydopamine (6-OHDA) in the nucleus accumbens was found to suppress the CCK-8-evoked behavioral effects. Moreover, an ex vivo measurement of the dopaminergic metabolism has been performed after injection of CCK-8 in the posterior nucleus accumbens by electrochemical detection of dopamine and its metabolites extracted from punches of brain tissue. The results showed that CCK-8 decreased the turnover of dopamine in the posterior part but not in the anterior part of the nucleus accumbens or in the ventral tegmental area. Furthermore, sulpiride, a selective antagonist for D2 dopamine receptors, but not SCH 23390, a selective antagonist for D1 dopamine receptors, prevented CCK-8-induced behavioral responses. Taken together, these results suggest that CCK-8 could be involved in behavioral adaptation to situations producing change in emotional and/or motivational states through modulation of presynaptic D2 receptor functioning.

摘要

当向大鼠伏隔核后部注射CCK-8时(CCK-8在该部位部分与多巴胺共定位),观察到在四孔箱和高架十字迷宫中的探索行为减少。在本研究中,发现通过向伏隔核局部注射6-羟基多巴胺(6-OHDA)诱导的多巴胺能中脑伏隔核通路的选择性破坏可抑制CCK-8诱发的行为效应。此外,在向伏隔核后部注射CCK-8后,通过电化学检测从脑组织切片中提取的多巴胺及其代谢产物,对多巴胺能代谢进行了离体测量。结果表明,CCK-8降低了伏隔核后部而非前部或腹侧被盖区的多巴胺周转率。此外,D2多巴胺受体的选择性拮抗剂舒必利可阻止CCK-8诱导的行为反应,但D1多巴胺受体的选择性拮抗剂SCH 23390则不能。综上所述,这些结果表明CCK-8可能通过调节突触前D2受体功能参与对产生情绪和/或动机状态变化的情况的行为适应。

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