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Kawamata, T.

Publications and source records attributed to Kawamata, T..

2 recordsLinked to original sources

Encoding of social exploration by neural ensembles in the insular cortex

The insular cortex participates in diverse complex brain functions including sociality, yet little is known about their cellular bases. Using microendoscopic calcium imaging of the agranular insular cortex (AI) in mice interacting with freely-moving and restrained social targets, we identified two subsets of AI neurons -a larger fraction of Social-ON cells and a smaller fraction of Social-OFF cells- that change their activity in opposite directions during social exploration. Social-ON cells included those that represented social investigation independent of location and consisted of multiple subsets, each of which were preferentially active during exploration under particular behavioral state or with a particular target of physical contact. These results uncover a previously unknown function of AI neurons in encoding conjunctive information on social behavior and suggest that AI may act to monitor the ongoing status of social exploration while an animal interacts with unfamiliar conspecifics.

neuroscience

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

Primary motor cortex (M1) infarction occasionally causes sensory impairment. Because sensory signal plays an important role in motor control, sensory impairment compromises recovery and rehabilitation from motor disability. Despite the importance of sensory-motor integration for rehabilitation after M1 infarction, the neural mechanism of the sensory impairment is poorly understood. We show that the sensory processing in the primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarction 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 the functional connectivity from M1 to S1 plays a key role in the impairment of sensory processing in S1. The simulation study demonstrated that the loss of inhibition from M1 to S1 in the acute phase of M1 infarction could cause the sensory processing impairment in S1, and the complementation of inhibition could recover the temporal coding. Taken together, we revealed how focal stroke of M1 alters cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.

physiology