Increase in ibotenate-stimulated phosphatidylinositol hydrolysis in slices of the amygdala/pyriform cortex and hippocampus of rat by amygdala kindling.

Hydrolysis of membrane phospholipid phosphoinositides following ibotenate stimulation of an excitatory amino acid receptor subtype has recently been demonstrated to be a receptor-mediated biochemical response. The present study examined ibotenate-stimulated phosphoinositides hydrolysis, determined as accumulation of [3H]inositol 1-phosphate, in amygdala/pyriform cortical and hippocampal slices of amygdala-kindled rats which exhibited fully developed kindled seizures on 20 consecutive days. Animals which underwent a sham operation were used as controls. Ibotenate (10(-3) M)-stimulated accumulation of [3H]inositol 1-phosphate increased significantly by 191% in the amygdala/pyriform cortex (P less than 0.01) and by 59% in the hippocampus (P less than 0.05) of the amygdala-kindled rats killed 24 h after the last seizure. One week after the last seizure, a similar magnitude of significant increase (by 171%, P less than 0.05) was maintained in the amygdala/pyriform cortex of the amygdala-kindled rats. In contrast, the increase in the hippocampus had attenuated by this time, although accumulation of [3H]inositol 1-phosphate increased significantly (P less than 0.05) when stimulated by 10(-4) M ibotenate. These results suggest that enhancement of ibotenate-stimulated phosphoinositides hydrolysis in the amygdala/pyriform cortex may be associated with the long-lasting seizure susceptibility of amygdala-kindled rats.