Hippocampal afterdischarges and their post-ictal sequelae in rats: a potential tool for assessment of CNS neurotoxicity.

Two types of AD and post-AD sequences are described. Type 1, which were most common (83%), are followed by a profound post-ictal depression (PID). PIDs can be quantitatively measured by integrating the EEG. The post-ictal EEG power normally returned to 75% of its prestimulation power within 4-5 min. PIDs are usually interrupted by a brief rebound AD, occurring about 1.5 min after the end of the AD. Wet dog shakes (WDSs) often punctuate the end of the AD and the end of the rebound AD. Type II ADs (12% of those recorded) do not have profound PID, but do have irregular post-ictal spikes which may persist for over 30 min. Type IIa ADs do not have the post-ictal spikes or the PID, and represented 5% of the ADs recorded. Females had higher AD thresholds than males, and had more Type IIa ADs than males during threshold testing. AD durations were longest in the subiculum and shortest in the area dentata. Correlations among the different measures of AD activity are discussed. With repeated elicitation, AD and PID durations increased. Stimuli 400% of threshold produced shorter ADs and longer PIDs than stimuli 115% of threshold. High intensity stimuli did not significantly alter frequency of WDSs or rebound AD characteristics. Increasing dosages of sodium pentobarbital decreased AD duration, increased threshold, decreased the probability of a Type I AD and produced depressions which were not accompanied by rebound ADs. At the highest (30 mg/kg) dosage of sodium pentobarbital, the spike frequency within the AD was decreased. When PIDs occurred, they were somewhat longer at higher dosages of sodium pentobarbital. The feasibility of the AD as an index of neurotoxicity is discussed, and it is concluded that it may provide a valuable mirror of dysfunction in the hippocampal formation. Further work must determine its sensitivity to toxicant-induced alterations.