突触骨架重塑调控吗啡戒断负性记忆的分子机制进展简

成瘾性药物戒断所产生的负性情绪记忆被认为是导致强迫性用药的主要原因. 戒断会引起相关脑区发生诸如突触传递和神经结构可塑性等适应性变化，这种适应性变化最终会引起病理性记忆的形成. 研究表明，肌动蛋白actin骨架重塑与突触可塑性以及记忆的形成关系密切，然而对其调控记忆的分子机制知之甚少. 最近，本研究小组围绕吗啡戒断负性情绪记忆的形成机制展开研究，在整体水平上阐述了突触骨架actin及其一系列下游信号参与调控吗啡戒断负性记忆的分子机制. 本文将讨论近年来突触结构可塑性参与调控成瘾性药物负性记忆形成的最新进展，着重探讨阿片类物质成瘾负性动机的形成机制，有助于深入了解成瘾形成的分子机制，为成瘾的研究和治疗提供新思路.

Progress on the molecular mechanisms of synaptic actin rearrangements in regulating morphine withdrawal induced aversive memory formation

The formation of aversive learning and memory attributes to the abnormal addictive behaviors, which leads to long-term adaptations such as synaptic transmission and neuronal architectural plasticity in addiction-related brain regions, and finally causes pathological memory formation. Researches show that the cytoskeletal actin rearrangements play a critical role in synaptic plasticity and memory formation. However, little is known about the molecular mechanisms of actin rearrangements regulated memory. Recently, our research group focused on the study of mechanisms of morphine withdrawal induced aversive memory formation, manifesting the involvement of cytoskeletal actin and its downstream effectors in regulation memory in vivo. This article will discuss the latest progress on the involvement of synaptic structural plasticity in regulating addictive drugs, especially opioid withdrawal induced aversive motivation formation, which would contribute to a better understanding of the molecular foundation of addictive behaviors, and provides us new ideas for addiction research and therapy.