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小鼠传染性瘙痒行为的分子与神经基础

Molecular and neural basis of contagious itch behavior in mice.

作者信息

Yu Yao-Qing, Barry Devin M, Hao Yan, Liu Xue-Ting, Chen Zhou-Feng

机构信息

Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO 63110, USA.

Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

Science. 2017 Mar 10;355(6329):1072-1076. doi: 10.1126/science.aak9748.

Abstract

Socially contagious itch is ubiquitous in human society, but whether it exists in rodents is unclear. Using a behavioral paradigm that does not entail prior training or reward, we found that mice scratched after observing a conspecific scratching. Molecular mapping showed increased neuronal activity in the suprachiasmatic nucleus (SCN) of the hypothalamus of mice that displayed contagious scratching. Ablation of gastrin-releasing peptide receptor (GRPR) or GRPR neurons in the SCN abolished contagious scratching behavior, which was recapitulated by chemogenetic inhibition of SCN GRP neurons. Activation of SCN GRP/GRPR neurons evoked scratching behavior. These data demonstrate that GRP-GRPR signaling is necessary and sufficient for transmitting contagious itch information in the SCN. The findings may have implications for our understanding of neural circuits that control socially contagious behaviors.

摘要

社会传染性瘙痒在人类社会中普遍存在,但在啮齿动物中是否存在尚不清楚。我们采用一种无需预先训练或奖励的行为范式,发现小鼠在观察到同种个体抓挠后也会抓挠。分子图谱显示,表现出传染性抓挠行为的小鼠下丘脑视交叉上核(SCN)中的神经元活动增强。胃泌素释放肽受体(GRPR)或SCN中的GRPR神经元被切除后,传染性抓挠行为消失,而通过化学遗传学抑制SCN中的GRP神经元也可重现这一现象。激活SCN中的GRP/GRPR神经元会引发抓挠行为。这些数据表明,GRP-GRPR信号传导对于在SCN中传递传染性瘙痒信息是必要且充分的。这些发现可能有助于我们理解控制社会传染性行为的神经回路。

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