Lasting increase in excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the amygdala/pyriform cortex of amygdala-kindled rats.

We previously demonstrated that ibotenate-stimulated polyphosphoinositide hydrolysis, determined as the accumulation of [3H]inositol 1-phosphate, significantly increased in the amygdala/pyriform cortex (AM/PC) 24 h and 7 days after the last seizure in AM-kindled rats. The present study examined whether the increase in ibotenate-stimulated polyphosphoinositide hydrolysis in the AM/PC is longer lasting. AM-kindled rats with a tripolar electrode implanted into the left AM and sham-operated controls were decapitated either 1, 2 or 4 weeks after the last seizure. Ibotenate (10(-3) M)-stimulated accumulation of [3H]inositol 1-phosphate significantly increased by 90% (P less than 0.01), 110% (P less than 0.001) and 73% (P less than 0.05) in the AM/PC 1, 2 and 4 weeks, respectively, after the last seizure. Four weeks after the last seizure, there were significant increases of a similar magnitude in the contralateral (right) AM/PC (by 83%, P less than 0.001) and the ipsilateral (left) AM/PC (by 63%, P less than 0.01). There was no change in the hippocampus or limbic forebrain at any of these times. Also 4 weeks after the last seizure, accumulation of [3H]inositol 1-phosphate significantly (P less than 0.05) increased at ibotenate concentrations of 2 x 10(-4) M, 5 x 10(-4) M and 10(-3) M in the kindled AM/PC. In light of the view that the AM/PC are the crucial brain structures for sustaining seizure susceptibility, the marked and lasting increase in the ibotenate-stimulated polyphosphoinositide hydrolysis coupled to excitatory amino acid receptors in the kindled AM/PC may be associated with the development of kindling and long-term maintenance of kindled events.