小柯机器人

美国哈佛医学院Ziv M. Williams小组发现调控自闭症与社交行为的神经元。这一研究成果发表在2021年7月12日出版的国际学术期刊《自然—神经科学》上。

在成年雄性小鼠中，研究人员打乱并恢复了自闭症谱系障碍（ASD）相关基因Shank3的表达，同时在几周内跟踪内侧前额定皮层（MPFC）中神经元的编码动态。研究人员发现，Shank3中断导致编码其他小鼠经验神经元的减少以及编码动物自我经验神经元的增加。这种转变与神经元区分自我的能力丧失有关，因此，无法编码社会行动。在MPFC中恢复Shank3表达逆转了这一编码不平衡并增加了5-8周的社交性。这些调查结果揭示了社会行为所必需的神经元编码过程，并且可能在ASD中扰乱。

据了解，尽管对ASD的分子和发育基础越来越了解，但社会信息的神经元编码如何扰乱ASD，以及是否有助于异常的社会行为仍然不明确。

附：英文原文

Title: Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time

Author: Daniel K. Lee, S. William Li, Firas Bounni, Gabriel Friedman, Mohsen Jamali, Leah Strahs, Omer Zeliger, Pauline Gabrieli, Michael A. Stankovich, Jack Demaree, Ziv M. Williams

Issue&Volume: 2021-07-12

Abstract: Despite a growing understanding of the molecular and developmental basis of autism spectrum disorder (ASD), how the neuronal encoding of social information is disrupted in ASD and whether it contributes to abnormal social behavior remains unclear. Here, we disrupted and then restored expression of the ASD-associated gene Shank3 in adult male mice while tracking the encoding dynamics of neurons in the medial prefrontal cortex (mPFC) over weeks. We find that Shank3 disruption led to a reduction of neurons encoding the experience of other mice and an increase in neurons encoding the animal’s own experience. This shift was associated with a loss of ability by neurons to distinguish other from self and, therefore, the inability to encode social agency. Restoration of Shank3 expression in the mPFC reversed this encoding imbalance and increased sociability over 5–8 weeks. These findings reveal a neuronal-encoding process that is necessary for social behavior and that may be disrupted in ASD.

DOI: 10.1038/s41593-021-00888-4

Source: https://www.nature.com/articles/s41593-021-00888-4

Nature Neuroscience：《自然—神经科学》，创刊于1998年。隶属于施普林格·自然出版集团，最新IF：28.771
官方网址：https://www.nature.com/neuro/
投稿链接：https://mts-nn.nature.com/cgi-bin/main.plex