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.