We studied levels of mRNA for the alpha- and beta-subunits of calmodulin (CaM) kinase II using the amygdaloid kindling model of epilepsy. There were significant increases in mRNA for the beta-subunit of CaM kinase II in the hippocampus 4-24 h after stage 5-kindled seizures. Moreover, this mRNA was significantly increased by 20.0-26.5% in the bilateral dentate gyrus 8 to 24 h after kindled seizures. The beta-subunit mRNA was also significantly increased by 13.5-19.0% in the CA3 on the side ipsilateral to the stimulation, 4 to 8 h after kindled seizures. mRNA for the alpha-subunit of CaM kinase II was not significantly changed in the regions examined for up to 24 h after the kindled seizures. These results suggest that CaM kinase II mediates the molecular processes that follow kindled seizures. It is possible that increases in CaM kinase II-dependent protein phosphorylation are associated with the plastic changes in kindling.
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