Voluntary running exercise after focal cerebral ischemia ameliorates dendritic spine loss and promotes functional recovery

Cerebral infarction causes motor, sensory, and cognitive impairments. Although rehabilitation enhances recovery of activities of daily living after cerebral infarction, its mechanism remains elusive due to the lack of reproducibility and low survival rate of brain ischemic model animals. Here, to investigate the relationship between rehabilitative intervention, motor function, and pathophysiological remodeling of the tissue in the ipsilateral hemisphere after cerebral infarction, we took advantage of a highly reproducible model of cerebral infarction using C.B-17/Icr-+/+Jcl mice. In this model, we confirmed that voluntary running exercise improved functional recovery after ischemia. Exercise did not alter the volume of infarction or survived cortex, or the number of NeuN-labeled cells in the peri-infarct cortex. In mice who did not exercise, the number of basal dendritic spines of layer 5 pyramidal cells decreased in the peri-infarct motor cortex, whereas in mice who exercised it remained at the normal level. The voluntary exercise intervention maintained basal dendritic spine density within the periinfarct area, which may reflect an adaptive remodeling of the surviving neural circuitry that might contribute to promoting the recovery of activities of daily living.

Automated summary

Voluntary running exercise improves functional recovery after cerebral infarction by maintaining adaptive remodeling of surviving neural circuitry, contributing to promoting recovery of activities of daily living. The number of basal dendritic spines of layer 5 pyramidal cells in the peri-infarct motor cortex decreased in non-exercised mice but remained normal in exercised mice. This study provides insights into the relationship between rehabilitative intervention, motor function, and pathophysiological remodeling after cerebral infarction.