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摘要 : 瑞士日内瓦大学和法国INSERM的研究人员揭示伏核上信息集成的可塑性机制,显示了可卡因何以能够改变这种可塑性以让毒瘾复发。相关无章发表于2014年5月21日的《Nature》杂志上。


在这项研究中,Christian Lüscher 及同事在来自前额皮质或背侧海马体的投射中,识别出了与小鼠伏核中的不同多巴胺能类群发生相互作用的特定神经通道所发生的由可卡因激发的改变。对这两个通道内由药物诱导的可塑性的操纵会消除寻找药物的行为,而仅仅破坏其中一个通道的可塑性则会降低对药物反应的分辨能力或对提示信息的反应强度。



Contrasting forms of cocaine-evoked plasticity control components of relapse

Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin Cornelius O’Connor & Christian Lüscher

Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivoelectrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-D-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, wheras selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders.


对应Nature杂志: 2014年5月22日Nature杂志精选

来源: Nature中文 浏览次数:51


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