Protein kinase C activator, bryostatin-1, promotes exercise-dependent functional recovery in rats with cerebral infarction.

Recently, it has become widely known that neuronal reorganization in the perilesional cortex contributes to some improvement of hemiparesis after stroke. Here, the authors examined in vivo the effects of administration of bryostatin-1, an activator of protein kinase C, combined with voluntary exercise on functional recovery and on cortical phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluR1 after infarction.In behavioral evaluation, the mean latency until falling from a rotating rod in the group with exercise and administered agent at 8 days after infarction was significantly longer than that in the other groups. Although there were no significant changes in GluR1 phosphorylation between bryostatin-1 administration alone and the untreated groups, exercise induced an increase in phosphorylated-Ser845-GluR1. Moreover, combining exercise with administration led to increased phosphorylated-Ser831-GluR1.These results suggest that bryostatin-1 facilitated exercise-induced paralysis recovery, which is possibly mediated by synaptic plasticity related to an increase in synaptic transmission efficiency.