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乙醇通过招募痛敏前扣带皮层神经元促进小鼠的社交诱发记忆回忆。

Ethanol facilitates socially evoked memory recall in mice by recruiting pain-sensitive anterior cingulate cortical neurons.

机构信息

Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan.

Center for Information and Neural Networks, National Institute of Information and Communications Technology, Suita City, Osaka, 565-0871, Japan.

出版信息

Nat Commun. 2018 Aug 30;9(1):3526. doi: 10.1038/s41467-018-05894-y.

Abstract

Alcohol is a traditional social-bonding reinforcer; however, the neural mechanism underlying ethanol-driven social behaviors remains elusive. Here, we report that ethanol facilitates observational fear response. Observer mice exhibited stronger defensive immobility while observing cagemates that received repetitive foot shocks if the observer mice had experienced a brief priming foot shock. This enhancement was associated with an observation-induced recruitment of subsets of anterior cingulate cortex (ACC) neurons in the observer mouse that were responsive to its own pain. The vicariously activated ACC neurons projected their axons preferentially to the basolateral amygdala. Ethanol shifted the ACC neuronal balance toward inhibition, facilitated the preferential ACC neuronal recruitment during observation, and enhanced observational fear response, independent of an oxytocin signaling pathway. Furthermore, ethanol enhanced socially evoked fear response in autism model mice.

摘要

酒精是一种传统的社交强化物;然而,乙醇驱动的社会行为的神经机制仍难以捉摸。在这里,我们报告说乙醇促进了观察性恐惧反应。如果观察者小鼠经历了短暂的引发足电击,那么观察者小鼠在观察到接受重复足部电击的同笼小鼠时,表现出更强的防御性不动。这种增强与观察诱导的观察者小鼠前扣带皮层 (ACC) 神经元亚群的募集有关,这些神经元对其自身的疼痛有反应。替代性激活的 ACC 神经元将其轴突优先投射到基底外侧杏仁核。乙醇使 ACC 神经元的平衡向抑制倾斜,促进观察期间 ACC 神经元的优先募集,并增强观察性恐惧反应,而不依赖于催产素信号通路。此外,乙醇增强了自闭症模型小鼠的社交诱发的恐惧反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d251/6117351/fb4d9f57f63e/41467_2018_5894_Fig1_HTML.jpg

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