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Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction
Atsushi Fukui1,2,3, Hironobu Osaki4, Yoshifumi Ueta3
1Faculty of Advanced Techno-Surgery, Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, Tokyo, Japan.
Scientific Reports
|March 1, 2020
Summary
Primary motor cortex (M1) strokes impair sensory processing in the somatosensory cortex (S1). This impairment, linked to reduced M1-S1 inhibition, can be reversed, aiding motor rehabilitation.
Area of Science:
- Neuroscience
- Systems Neuroscience
- Stroke Research
Background:
- Primary motor cortex (M1) strokes can lead to sensory deficits, hindering motor recovery.
- The underlying neural mechanisms of sensory impairment post-M1 stroke are not well understood.
Purpose of the Study:
- To investigate the neural mechanisms of sensory processing impairment following M1 infarction.
- To elucidate the role of functional connectivity between M1 and S1 in sensory deficits.
Main Methods:
- Studied sensory processing in the primary somatosensory cortex (S1) of mice after M1 infarction.
- Utilized computational simulation and optogenetic activation of M1.
- Examined layer-specific changes in S1 during acute and subacute phases.
Main Results:
- Sensory processing in S1 was impaired acutely post-M1 infarction, with layer-specific recovery in the subacute phase.
- Functional connectivity from M1 to S1, particularly inhibitory input, was implicated in the impairment.
- Optogenetic activation of M1 suppressed sustained responses in S1, supporting the role of M1-S1 inhibition.
Conclusions:
- Focal M1 stroke alters cortical network activity in sensory processing areas.
- Inhibitory projections from M1 to S1 play a crucial role in modulating sensory processing and may be involved in stroke-induced deficits.
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