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

Citation
K. Akiyama et al., LONG-LASTING INCREASE IN PROTEIN-KINASE-C ACTIVITY IN THE HIPPOCAMPUSOF AMYGDALA-KINDLED RAT, Brain research, 679(2), 1995, pp. 212-220
Citations number
37
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
679
Issue
2
Year of publication
1995
Pages
212 - 220
Database
ISI
SICI code
0006-8993(1995)679:2<212:LIIPAI>2.0.ZU;2-K
Abstract
Previous studies have demonstrated that membrane-associated protein ki nase C (PKC) activities in the right and left hippocampus of rats kind led from the left hippocampus increased significantly at 4 weeks [9] a nd 4 months [22] after the last seizure compared with those in matched control rats. In this study, we investigated the effect of kindling f rom the left amygdala on PKC activities in the amygdala/pyriform corte x and hippocampus at long seizure-free intervals (4 and 16 weeks) from the last amygdala-kindled seizure. Membrane-associated PKC activity o f the kindled group increased significantly only in the left hippocamp us compared with the left side control (the left hippocampus of rats s ubjected to a sham operation) at 4 weeks (by 34%, P < 0.03) and 16 wee ks (by 24%, P < 0.05) after the last seizure. There was no significant alteration in the membrane-associated PKC activity of the kindled gro up 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 re gion 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 in creased significantly only in the left hippocampus (by 49%, P < 0.005) , but not in the right hippocampus. Neither PKC activity in the P-2 fr action nor that in the cytosolic fraction was altered in the kindled g roup after this seizure-free interval. The prolonged increase in activ ity of the membrane-associated PKC and that in the P-1 fraction in the hippocampus induced by amygdala-kindling may contribute to long-lasti ng seizure susceptibility induced by kindling.