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β-arrestin2是G蛋白偶联受体的负反馈调控蛋白,介导受体的脱敏,此外β-arrestin2还可以通过招募信号分子,介导G蛋白非依赖的信号传导过程。β-arrestin2广泛分布于各重要脑区,参与神经环路的信号传递。本文旨在研究β-arrestin2在可卡因诱导的小鼠奖赏行为中的作用。采用β-arrestin2基因敲除小鼠(Arrb2/),检测了β-arrestin2在不同剂量可卡因诱导的条件性位置偏爱(conditioned place preference,CPP)形成中的作用,还检测了其在可卡因诱导的自主活动性变化中的作用。结果显示,在中等剂量(20mg/kg)和高剂量(30mg/kg)可卡因诱导的CPP实验中,Arrb2/小鼠比野生型小鼠(Arrb2+/+)表现出更强的可卡因诱导的位置偏爱,而在低剂量(10mg/kg)可卡因实验中两者无显著性差异。可卡因诱导的Arrb2/小鼠的自主活动性显著低于Arrb2+/+小鼠。以上结果提示,β-arresstin2在可卡因诱导的奖赏行为中起重要作用。
β-arrestin2 is a negative feedback regulatory protein of G-protein coupled receptors, which mediates receptor desensitization. In addition, β-arrestin2 can mediate G-protein independent signal transduction through recruitment of signaling molecules. β-arrestin2 is widely distributed in various brain regions and participates in the signal transmission of the neural circuit. This article aims to investigate the role of beta-arrestin2 in cocaine-induced mouse reward. Β-arrestin2 knockout mice (Arrb2 /) were used to test the role of β-arrestin2 in cocaine-induced conditioned place preference (CPP) formation. Cocaine-induced autonomic The role of changes in activity. The results showed that Arrb2 / mice showed stronger cocaine-induced position preference than wild type mice (Arrb2 + / +) in moderate doses (20 mg / kg) and high doses (30 mg / kg) of CPP experiments induced by cocaine , While there was no significant difference between low dose (10mg / kg) cocaine experiments. Cocaine-induced Arrb2 / mice had significantly less autonomic activity than Arrb2 + / + mice. The above results suggest that β-arresstin2 plays an important role in cocaine-induced reward.