|View Full Text||PubReader|
|Abstract||Print this Article|
|PMC||Export to Citation|
|Article as PDF||Open Access|
Exp Neurobiol 2006; 15(1): 15-21
Published online November 30, -0001
© The Korean Society for Brain and Neural Sciences
Department of Physiology, Cheju National University, College of Medicine, Jeju 690-756, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-64-754-3831, FAX: 82-64-702-2687
Different subtypes of protein kinase C (PKC) have been reported to play different roles in excitotoxicity and epileptogenesis. However, the exact role of each PKC subtype in cellular functions is unknown. The previous studies by Western blot analysis did not distinguish hippocampal laminae or cell types in which the changes in PKC expression occurred. The significance of studies by in situ hybridization is also limited, since mRNA changes do not always parallel or match with protein expression. Therefore, using immunohistochemistry, we investigated temporal alterations of cellular distribution of PKCՆ and PKCՅ in the hippocampus following kainic acid (KA)-induced seizure. KA (25 mg/kg, i.p.) was administered to eight to nine week-old C57BL/6 mice. Behavioral seizure activity was observed for 2 hours after the onset of seizure and was terminated with diazepam (8 mg/kg, i.p.). The animals were sacrificed and analyzed at various points in time after the initiation of seizure activity. We demonstrated here that expression of PKCՆ and PKCՅ was exclusively limited in the hippocampal neurons and they were not regulated in glial cells. PKCՆ expression was slightly increased 6 hour after seizure in CA3 pyramidal neurons. Dramatic upregulation was induced 1 day after seizure and persisted until 4 days after seizure, but the magnitude was slightly decreased. The alteration was reduced to basal level at the time point of 1 month after seizure. However, PKCՅ expression in mossy fiber terminal regions was not substantially altered following seizure. Taken together, our data suggest that PKC isozymes might be differentially involved in KA-induced neural degeneration and pathological synaptic reorganization.
Keywords: PKCՆ,, PKCՅ,, seizure, excitotoxicity, gene expression