Brief seizure activity alters Ca2+/calmodulin dependent protein kinase II dephosphorylation and subcellular distribution in rat brain for several hours.
The effect of a brief pentylenetetrazol (PTZ) convulsive seizure on rat cerebral cortical Ca2+/calmodulin dependent protein kinase II (CaMKII) was investigated. By immunoblot, it was found that a single PTZ seizure, lasting less than a minute, caused translocation of CaMKII alpha-subunit (alpha-CaMKII) from the particulate to the soluble fraction for several hours, paralleled by a dramatic loss of alpha-CaMKII Thr286 phosphorylation. The reduced alpha-CaMKII Thr286 phosphorylation apparently resulted from enhanced phosphatase activity following PTZ seizure, especially in the particulate fraction. CaMKII translocation and phosphatase activation following a brief seizure episode can both contribute to long-lasting CaMKII regulation far outlasting the immediate effects of the seizure on neuronal function.
Dong
Yu
Y
Department of Pharmacology and Therapeutics, Medical College of Ohio, 3035 Arlington Avenue, Toledo, OH 43614-5804, USA.
Rosenberg
Howard C
HC
D000818:Animals; D001921:Brain / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000201:enzymology*; D013347:Subcellular Fractions / Q000187:drug effects / Q000201:enzymology; D013997:Time Factors
D004791:Enzyme Inhibitors; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases