Axonal outgrowth and functional recovery after stroke

Abstract

Axonal remodeling is critical to reorganization of damaged brain tissue and associated with functional outgrowth after stroke. We analyzed the mechanisms of axonal outgrowth after stroke. In the peri-infarct area of rat brains, axonal outgrowth and myelination were induced from 7 to 56 days after middle cerebral artery occlusion. In primary cortical neurons, phosphatase tensin homolog deleted on chromosome 10/Akt/Glycogen synthase kinase 3β signaling was related to axonal outgrowth after ischemia. In rat cerebral hypoperfusion, L-carnitine regulated the phosphatase tensin homolog deleted on chromosome 10/Akt/ mammalian target of rapamycin signaling pathway, and enhanced axonal plasticity while concurrently ameliorating oxidative stress and increasing oligodendrocyte myelination of axons, thereby improving white matter lesions and cognitive impairment in rats. Thus, the diverse mechanisms that axons regrow after stroke, potential candidates for a novel therapeutic agent to enhance axonal outgrowth and improve functional outcome human stroke survivors are warranted.