Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

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 s...

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Bibliographic Details
Published in:Scientific reports 2020-02, Vol.10 (1), p.3771-3771, Article 3771
Main Authors: Fukui, Atsushi, Osaki, Hironobu, Ueta, Yoshifumi, Kobayashi, Kenta, Muragaki, Yoshihiro, Kawamata, Takakazu, Miyata, Mariko
Format: Article
Language:English
Subjects:
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Animals
Brain Infarction - pathology
Brain Infarction - physiopathology
Cerebral infarction
Cortex (motor)
Dreams
Humanities and Social Sciences
Information processing
Male
Mice
Motor task performance
multidisciplinary
Optogenetics
Rehabilitation
Science
Science (multidisciplinary)
Sensation
Sensory integration
Sensory perception
Somatosensory cortex
Somatosensory Cortex - pathology
Somatosensory Cortex - physiopathology
Stroke - pathology
Stroke - physiopathology
Temporal lobe
Temporal variations
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Description
Summary: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.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-020-60662-7