Development of clonic-tonic
flurothyl-induced
seizures was examined in both normal and genetically
epilepsy-prone rats (GEPRs). At each age, from 10 to 30 days, clonus occurred at significantly shorter latencies in GEPRs than in normal rats. The latency to onset of
clonic seizures did not change with age, however, in either GEPRs or normal rats. A different pattern of response was observed in the progression to
tonic seizures. As normal animals matured, the latency to
tonic seizures became longer and, by day 30, the duration of
flurothyl exposure necessary to induce tonus was almost 70% greater in normal rats than in the GEPRs. In contrast, in GEPRs, tonic extension occurred immediately following the onset of clonus throughout development. A subset of GEPRs failed to have audiogenic
seizures in a 40-day posttest. These animals had a
flurothyl response identical to their audiogenic-susceptible litter mates. These data suggest that (a) a protective mechanism which develops against
tonic seizures in normal rats fails to mature in the GEPR, and (b) seizure inducing gene-linked neural abnormalities occur in the GEPR independent of pathologies underlying audiogenic
seizures.