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Rabies screen reveals GPe control of cocaine-triggered plasticity
Nature ( IF 64.8 ) Pub Date : 2017-09-01 , DOI: 10.1038/nature23888
Kevin T. Beier , Christina K. Kim , Paul Hoerbelt , Lin Wai Hung , Boris D. Heifets , Katherine E. DeLoach , Timothy J. Mosca , Sophie Neuner , Karl Deisseroth , Liqun Luo , Robert C. Malenka

Identification of neural circuit changes that contribute to behavioural plasticity has routinely been conducted on candidate circuits that were preselected on the basis of previous results. Here we present an unbiased method for identifying experience-triggered circuit-level changes in neuronal ensembles in mice. Using rabies virus monosynaptic tracing, we mapped cocaine-induced global changes in inputs onto neurons in the ventral tegmental area. Cocaine increased rabies-labelled inputs from the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to participate in behavioural plasticity triggered by drugs of abuse. We demonstrated that cocaine increased GPe neuron activity, which accounted for the increase in GPe labelling. Inhibition of GPe activity revealed that it contributes to two forms of cocaine-triggered behavioural plasticity, at least in part by disinhibiting dopamine neurons in the ventral tegmental area. These results suggest that rabies-based unbiased screening of changes in input populations can identify previously unappreciated circuit elements that critically support behavioural adaptations.

中文翻译:

狂犬病筛查显示 GPe 控制可卡因触发的可塑性

有助于行为可塑性的神经回路变化的识别通常在根据先前结果预先选择的候选回路上进行。在这里,我们提出了一种无偏见的方法,用于识别小鼠神经元集合中由经验触发的电路级变化。使用狂犬病病毒单突触追踪,我们将可卡因诱导的全局输入变化映射到腹侧被盖区的神经元上。可卡因增加了来自苍白球外部 (GPe) 的狂犬病标记输入,GPe 是一种基底神经节核,以前不知道参与由滥用药物引发的行为可塑性。我们证明可卡因增加了 GPe 神经元活动,这是 GPe 标记增加的原因。GPe 活动的抑制表明它有助于两种形​​式的可卡因触发的行为可塑性,至少部分是通过解除腹侧被盖区的多巴胺神经元。这些结果表明,基于狂犬病的对输入人群变化的无偏见筛查可以识别以前未被重视的电路元件,这些元件关键地支持行为适应。
更新日期:2017-09-01
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