支持感知的感觉运动整合需要Syngap1在皮层中的表达。

Thomas Vaissiere, Sheldon D Michaelson, Thomas Creson, Jessie Goins, Daniel Fürth, Diana Balazsfi, Camilo Rojas, Randall Golovin, Konstantinos Meletis, Courtney A Miller, Daniel O'Connor, Lorenzo Fontolan, Gavin Rumbaugh
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摘要

感知是一种认知结构,通过感觉运动整合(SMI)产生。在促进认知的电路中形成SMI的分子和细胞机制尚不清楚。在这里,我们证明了自闭症/智力残疾基因Syngap1在小鼠皮层兴奋性神经元中的表达促进了引发感知行为所需的触摸敏感性。皮层突触间隙1的表达通过组装支持触觉敏感性的电路,在感觉运动回路中实现触摸诱导的反馈信号。这些回路还编码了注意力的相关性,这些相关性促进了有目的和持续的物体探索背后的自我生成的胡须运动。当Syngap1缺陷动物探索有胡须的物体时,相对较弱的触摸信号与相对较强的运动信号相结合。这产生了与触觉敏感性受损、触觉探索减少和触觉学习薄弱一致的信噪比缺陷。因此,皮层中Syngap1的表达通过组装整合触摸和胡须运动信号的电路来促进触觉感知。Syngap1表达不足可能通过自上而下的异常SMI导致认知障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Syngap1 Promotes Cognitive Function through Regulation of Cortical Sensorimotor Dynamics.

Perception, a cognitive construct, emerges through sensorimotor integration (SMI). The genetic mechanisms that shape SMI required for perception are unknown. Here, we demonstrate in mice that expression of the autism/intellectual disability gene, Syngap1, in cortical excitatory neurons is required for formation of somatomotor networks that promote SMI-mediated perception. Cortical Syngap1 expression was necessary and sufficient for setting tactile sensitivity, sustaining tactile object exploration, and promoting tactile learning. Mice with deficient Syngap1 expression exhibited impaired neural dynamics induced by exploratory touches within a cortical-thalamic network known to promote attention and perception. Disrupted neuronal dynamics were associated with circuit-specific long-range synaptic connectivity abnormalities. Our data support a model where autonomous Syngap1 expression in cortical excitatory neurons promotes cognitive abilities through assembly of circuits that integrate temporally-overlapping sensory and motor signals, a process that promotes perception and attention. These data provide systems-level insights into the robust association between Syngap1 expression and cognitive ability.

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