Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction
Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction
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DOI：
10.1038/s41598-020-60662-7
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发表时间：
2020-02-28
影响因子：
4.6
通讯作者：
Miyata, Mariko
中科院分区：
文献类型：
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作者：
Fukui, Atsushi;Osaki, Hironobu;Miyata, Mariko
原发性运动皮质（M1）梗死有时会引起感觉障碍。由于感觉信号在运动控制中起着至关重要的作用，感觉障碍损害了运动障碍的恢复和康复。然而，感觉障碍的神经机制尚不清楚。我们发现小鼠初级体感觉皮层（S1）的感觉加工在M1梗死急性期受损，并在亚急性期以层特异性方式恢复。这种层依赖的恢复过程和M1到S1的解剖连接模式表明，M1到S1的功能连接在感觉加工损伤中起关键作用。模拟研究表明，M1梗死急性期M1对S1的抑制丧失会损害S1的感觉加工，对抑制的补偿可以恢复时间编码。与此一致的是，光遗传激活M1抑制了S1的持续反应。综上所述，我们揭示了M1的局灶性中风如何改变感觉加工的皮质网络活动，其中可能涉及M1到S1的抑制性输入。
Primary motor cortex (M1) infarctions sometimes cause sensory impairment. Because sensory signals play a vital role in motor control, sensory impairment compromises the recovery and rehabilitation of motor disability. However, the neural mechanism of the sensory impairment is poorly understood. We show that sensory processing in mouse primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarctions and recovered in a layer-specific manner in the subacute phase. This layer-dependent recovery process and the anatomical connection pattern from M1 to S1 suggested that functional connectivity from M1 to S1 plays a key role in the sensory processing impairment. A simulation study demonstrated that the loss of inhibition from M1 to S1 in the acute phase of M1 infarctions could impair sensory processing in S1, and compensation for the inhibition could recover the temporal coding. Consistently, the optogenetic activation of M1 suppressed the sustained response in S1. Taken together, we revealed how focal stroke in M1 alters the cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.