Electroconvulsive shock increases the phosphorylation of amphiphysin II in the rat cerebellum

Amphiphysin II (Amph2) is known to undergo rapid dephosphorylation and phosphorylation at nerve terminals. After in vivo electroconvulsive shock (ECS) in the rat cerebellum, we found an electrophoretic mobility retardation of Amph2, which suggested an increased degree of phosphorylation above the non-stimulated level. This shifted signal was observed from 1 min, reached the maximum level at 5 min and extended beyond 2 h after ECS. The shifted band was markedly decreased by the phosphatase treatment. Pretreatment with cyclosporin A augmented the mobility retardation of Amph2 after ECS. Our results indicate that ECS induces the phosphorylation of Amph2 in the rat cerebellum.