Unilateral cerebral ischemia induces morphological changes in the layer V projection neurons of the contralateral hemisphere

Decreased blood flow to the brain causes stroke and damage to neuronal networks. Neuronal damage occurs not only in the infarct core but also in areas away from the infarcts. This study was aimed to assess alterations of the cortical projection neurons that were distantly connected with the infarcts. Unilateral cortical ischemia was generated by middle cerebral artery occlusion in the right somatosensory cortex. Pre-labeled thalamocortical neurons disappeared, whereas contralateral callosal projection neurons survived 48 h post-ischemia. The unilateral ischemia increased the total length, segment length and the spine volume of dendrites from layer V callosal neurons in the homotopic cortex of the contralateral hemisphere. The morphological remolding of the contralateral cortical neurons cannot be reproduced by the spinal cord hemisection that cuts axons of corticospinal projection neurons of layer V. The data suggest that the retrograde degeneration of axons may not account for the early morphological changes in the contralateral cortex. We hypothesize that the loss of innervations from the ischemic cortex may bring in adaptive changes to the connected neurons, and adult cortical neurons can adjust their morphology to meet the reduction of synaptic inputs. This study may improve our understanding of the re-organization of cortical circuits following focal cerebral ischemia and help the development of new treatments designed to minimize the disability associated with stroke. [Display omitted] •Unilateral cerebral ischemia leads to the loss of thalamocortical neurons.•Callosal neurons still survive after unilateral cerebral ischemia.•Dendrite growth is induced by cerebral ischemia but not spinal cord hemisection.•Dendritic spines of the layer V callosal neurons remodel after cerebral ischemia.