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 -subunit (-CaMKII) from the particulate to the soluble fraction for several hours, paralleled by a dramatic loss of -CaMKII Thr286 phosphorylation. The reduced -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.
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