学习记忆在成瘾行为的形成和保持中发挥着重要的作用，成瘾性药物导致的异常记忆的长期存在是产生精神依赖的重要原因。Beta-arrestin2在药物成瘾中起重要作用，但Beta-arrestin2在药物成瘾记忆消退中的作用及机制并不清楚。本项目采用Beta-arrestin基因敲除以及条件性敲除小鼠，结合条件位置偏爱模型，综合分子、组化以及电生理记录等多种实验方法，系统地研究Beta-arrestin2在药物成瘾记忆消退中的作用及机制，探讨Beta-arrestin在特异性神经核团和神经元中的调控作用，阐述Beta-arrestin在成瘾药物作用下的信号转导、神经突触重塑中的作用机制。这些研究将加深对药物成瘾形成中的分子和信号网络基础以及成瘾的神经生物学机制的理解，为探索药物成瘾新的治疗手段提供科学理论依据，为药物成瘾的治疗提供新的靶点

Learning and memory play an important role in shaping and maintaining of addiction behavior, the long-term abnormal memory caused by addictive drugs is an important reason of psychological dependence. Beta-arrestin2 can regulate drug addiction by multiple cell signaling pathway, but the role of Beta-arrestin2 in extinction behavior of drug addiction and the underlying mechanism is unclear. Here, using Beta-arrestin2 knock-out and conditional knock-out mice, behavior model of conditional place preference and techniques of molecular and biochemistry, tissue chemistry and electrophysiological recording, we will focus on the role of Beta-arrestin2 in extinction memory of drug addiction in order to determine the specific nucleus and neuron type and describe the underlying mechanisms of signal transduction and synaptic plasticity. Our research will help us understand the molecular and signal net and neurobiology mechanism of drug addiction extinction. Furthermore, our research will provide the theory basis for novel therapy strategies and novel pharmaceutical targets of drug addiction.