LONG-LASTING INCREASE IN PROTEIN-KINASE-C ACTIVITY IN THE HIPPOCAMPUS OF AMYGDALA-KINDLED RAT

Previous studies have demonstrated that membrane-associated protein kinase C (PKC) activities in the right and left hippocampus of rats kindled from the left hippocampus increased significantly at 4 weeks [9] and 4 months [22] after the last seizure compared with those in matched control rats. In this study, we investigated the effect of kindling from the left amygdala on PKC activities in the amygdala/pyriform cortex and hippocampus at long seizure-free intervals (4 and 16 weeks) from the last amygdala-kindled seizure. Membrane-associated PKC activity of the kindled group increased significantly only in the left hippocampus compared with the left side control (the left hippocampus of rats subjected to a sham operation) at 4 weeks (by 34%, P < 0.03) and 16 weeks (by 24%, P < 0.05) after the last seizure. There was no significant alteration in the membrane-associated PKC activity of the kindled group in the right hippocampus or amygdala/pyriform cortex in any seizure-free interval after the last amygdala seizure. Cytosolic PKC activity did not differ between the kindled and control groups in any brain region examined in any seizure-free interval. At 16 weeks after the last seizure, the PKC activity in the P-1 fraction of the kindled group increased significantly only in the left hippocampus (by 49%, P < 0.005), but not in the right hippocampus. Neither PKC activity in the P-2 fraction nor that in the cytosolic fraction was altered in the kindled group after this seizure-free interval. The prolonged increase in activity of the membrane-associated PKC and that in the P-1 fraction in the hippocampus induced by amygdala-kindling may contribute to long-lasting seizure susceptibility induced by kindling.