Long-lasting increase in protein kinase C activity in the hippocampus of amygdala-kindled rat

• Published in: Brain research Vol. 679; no. 2; pp. 212 - 220
• Main Authors: Akiyama, Kazufumi, Ono, Mitsuhiro, Kohira, Ichiro, Daigen, Akihiro, Ishihara, Takeshi, Kuroda, Shigetoshi
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 15-05-1995; Amsterdam Elsevier; New York, NY
• Subjects: Amygdala; Amygdala - metabolism; Animals; Biological and medical sciences; Cytosol - metabolism; Epilepsy; Epilepsy - metabolism; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Hippocampus; Hippocampus - enzymology; Hippocampus - metabolism; Kindling; Kindling, Neurologic - metabolism; Male; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Neuronal plasticity; Protein kinase C; Protein Kinase C - metabolism; Rats; Rats, Sprague-Dawley; Time Factors; Protein kinase C; Neuronal plasticity; Amygdala; Kindling; Epilepsy; Hippocampus; Nervous system diseases; Rat; Enzyme; Rodentia; Central nervous system; Basal ganglion; Cerebral disorder; Vertebrata; Experimental disease; Mammalia; Enzymatic activity; Animal; Central nervous system disease; Plasticity; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(95)00221-B

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.