Axonal Outgrowth and Dendritic Plasticity in the Cortical Peri-Infarct Area After Experimental Stroke

• DOI: 10.1161/strokeaha.111.646224
• Publication Date: 2012-05-24T00:58:26Z
• Authors: Yuji Ueno; Michael Chopp; Li Zhang; Benjamin Buller; Zhongwu Liu; Norman L. Lehman; Xian Shuang Liu; Yi Zhang; Cynthia Roberts; Zheng Gang Zhang
• Keywords: GSK3B; Axoplasmic transport

Background and Purpose— Axonal remodeling is critical to brain repair after stroke. The present study investigated axonal outgrowth stroke the signaling pathways mediating in cortical neurons. Methods— Using a rodent model of middle cerebral artery occlusion, we examined high-molecular weight neurofilament (NFH) immunoreactive axons myelin basic protein-positive oligodendrocytes peri-infarct area. In vitro, using cultured neurons microfluidic chamber challenged by oxygen-glucose deprivation (OGD), mechanisms selectively regulating OGD. Results— NFH + MBP substantially increased area during recovery, concomitantly with an increase dendrites spines identified Golgi-Cox staining. subjected OGD exhibited significant increases phosphorylated protein levels, concurrently downregulation phosphatase tensin homolog deleted on chromosome 10, activation Akt, inactivation glycogen synthase kinase-3β regenerated axons. Blockage phosphoinositide 3-kinase pharmacological inhibitors suppressed Akt attenuated phosphorylation kinase-3β, which resulted suppression OGD; whereas GSK-3 augmented regeneration elevated levels Conclusions— Stroke induces myelination ischemic 3-kinase/Akt/glycogen pathway mediates