Postischemic voluntary running exercise promotes the survival of astrocytes born after cerebral ischemia and alters astrocytic gene expression

Abstract

Cerebral ischemia causes neuronal damage and functional impairment. Dendritic spine dynamics is involved in functional recovery. We have previously reported that voluntary running exercise after focal cerebral ischemia ameliorates the ischemia-induced dendritic spine loss in the peri-infarct motor cortex layer 5. Environmental change surrounding neurons affects the neuronal morphologic plasticity. The aim of this study is to reveal the effect of postischemic exercise on the glial phenotypes. We found that voluntary running exercise promoted the survival of astrocytes born after middle cerebral artery occlusion (MCAO) until postoperative day 15. Transcriptome analysis of astrocytes detected 10 upregulated genes and 70 downregulated genes in exercise group compared with non-exercise group. Gene ontology analysis showed that the downregulated genes were related to apoptosis and neuronal morphology. Exercise tended to decrease the expression of Lipocalin 2 known to reduce dendritic spines in astrocytes after MCAO. Our data suggest that voluntary running exercise after cerebral ischemia alters astrocytic gene expression, which contributes to the amelioration of the ischemia-induced dendritic spine loss.