Hippocampal kindling enhances excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the hippocampus and amygdala/pyriform cortex

We recently demonstrated that a long-lasting increase in ibotenate-stimulated polyphosphoinositide (PPI) hydrolysis in the amygdala/pyriform cortex (AM/PC) is associated with seizure susceptibility of amygdala (AM)-kindled rats. The present study examined (1) whether ibotenate-stimulated PPI hydrolysis would be lastingly enhanced in the hippocampus (HIPP) and AM/PC of the HIPP-kindled rats and (2) whether similar changes would be found in the early stage of HIPP kindling. Although ibotenate-stimulated accumulation of [³H]inositol 1-phosphate ([³H]IP₁) increased significantly in the HIPP 24 h, 5 days, and 15 days after the last seizure of fully developed HIPP-kindled rats, no statistically significant increase was found in the HIPP 30 days after the last seizure. In the AM/PC, 10^-3 M ibotenate-stimulated [³H]IP₁ accumulation significantly increased by 91%, 91%, 86% and 90%, 24 h, 5 days, 15 days and 30 days after the last seizure, respectively. There was no significant increase in ibotenate-stimulated [³H]IP₁ accumulation 7 days after the last stimulation in the HIPP and AM/PC of rats which had undergone electrical stimulation only 5 times in the HIPP. These results indicate that (1) PPI hydrolysis coupled to excitatory amino acid receptors increases long-lastingly in the AM/PC regardless of the primary kindled site, and (2) these changes do not occur in the early stage of HIPP-kindling.