Loss of GABAB‐mediated interhemispheric synaptic inhibition in stroke periphery

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12890-list-0001">Recovery from the potentially devastating consequences of stroke depends largely upon plastic changes occurring in the lesion periphery and its inputs.In a focal model of stroke in mouse somatosensory cortex, we found that the recovery of sensory responsiveness occurs at the level of synaptic inputs, without gross changes of the intrinsic electrical excitability of neurons, and also that recovered responses had longer than normal latencies.Under normal conditions, one somatosensory cortex inhibits the responsiveness of the other located in the opposite hemisphere (interhemispheric inhibition) via activation of GABAB receptors.In stroke‐recovered animals, the powerful interhemispheric inhibition normally present in controls is lost in the lesion periphery.By contrast, contralateral hemisphere activation selective contributes to the recovery of sensory responsiveness after stroke.