Development of propagated discharge and behavioral arrest in hippocampal and amygdala-kindled animals

Patients with focal temporal lobe seizures often experience transient episodes of impaired awareness with behavioral arrest, but the precise mechanism remains unknown. The Network Inhibition Hypothesis attributes these deficits to a loss of cholinergic input to the cortex. This is presumed to result from increased activation of inhibitory regions that suppress subcortical arousal, giving rise to cortical delta wave activity. Recently, this hypothesis has been tested in animal experiments, where triggering dorsal hippocampal seizures is associated with behavioral arrest. To further test this hypothesis in animals - and, more specifically, to characterize the relationship between propagated discharge, cortical delta waves and behavioral arrest - we performed partial kindling studies in three different limbic sites in rats. We found that seizure discharge took longer to spread from the amygdala than the hippocampus, and took more stimulations to elicit behavioral arrest. In addition, the onset of propagated discharge in subcortical and cortical sites did not always match with the onset of behavioral arrest. Importantly, the activity seen in the cortex did not resemble the slow waves seen in deep sleep. Together, these findings suggest that limbic discharge triggers epileptic discharge in downstream pacemakers, including the cortex, and that these secondarily cause behavioral arrest.