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.
Koo
Young Jin
YJ
Department of Psychiatry and Behavioral Science, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital and Institute for Neuroscience, Seoul National University, Seoul, South Korea.
Kim
Su-Jin
SJ
Jeon
Song Hee
SH
Kim
Seung Ryul
SR
Kang
Ung Gu
UG
Park
Joo-Bae
JB
Kim
Yong Sik
YS
D000818:Animals; D015153:Blotting, Western; D002531:Cerebellum / Q000378:metabolism*; D016572:Cyclosporine / Q000494:pharmacology; D024202:Electrophoretic Mobility Shift Assay / Q000379:methods; D004597:Electroshock; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D010744:Phosphoric Monoester Hydrolases / Q000187:drug effects / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley
D004791:Enzyme Inhibitors; D009419:Nerve Tissue Proteins; C075637:amphiphysin; D016572:Cyclosporine; D010744:Phosphoric Monoester Hydrolases