The perirhinal cortex has recently been implicated in the kindling of limbic generalized seizures. The following experiments in rats tested the selectivity of the perirhinal cortex's epileptogenic properties by comparing its kindling profile with those of the adjacent insular cortex, posterior (dorsolateral) claustrum and amygdala. The first experiment examined the kindling and EEG profiles, and found that both the claustrum and insular cortex demonstrated rapid epileptogenic properties similar to the perirhinal cortex, including very rapid kindling rates and short latencies to convulsion. Furthermore, electrical stimulation of all three structures led to a two-phase progression through stage-5 seizures which had characteristics of both neocortical and amygdaloid kindling. In a second experiment rats were suspended in a harness to allow for more detailed documentation of both forelimb and hindlimb convulsions. With this procedure we were able to detect subtle yet unique differences in convulsion characteristics from each of the kindled sites and stage-5 seizure phases. Some of these convulsive parameters were correlated with changes in FosB/DeltaFosB protein and BDNF mRNA expression measured two hours after the last convulsion. Overall, it appears that the perirhinal cortex is not unique in its property of rapid epileptogenesis. Moreover, the posterior claustrum exhibited the fastest kindling and most vigorous patterns of clonus, suggesting that it may be even more intimately associated with the motor substrates responsible for limbic seizure generalization than is the perirhinal cortex.

Summary:Purpose: Lesions of the claustrum in cats and primates have been shown to disrupt the development and expression of amygdaloid-kindled seizures in cats and primates. Because the structure and connectivity of the claustrum can vary between species, we wanted to examine the effects of claustral lesions on kindling in rats.Methods: One group of rats received bilateral radiofrequency lesions of both anterior and posterior regions of the claustrum before amygdaloid kindling. Another group of rats received bilateral anterior and posterior radiofrequency lesions of the claustrum after amygdaloid kindling. Some rats were tested for transfer of kindling to the contralateral amygdala after claustral lesions.Results: Small lesions that destroyed 13% of the claustrum were capable of delaying, but not blocking, amygdaloid kindling. The delay in kindling was due to an increase in the stimulation trials required to kindle to stage 5 seizures. The lesions had no effect on established kindled seizures or on transfer to the contralateral amygdala.Conclusions: As in other species, the claustrum in the rat appears to play a role in kindling from the amygdala. Because of the restricted size of our claustral lesions, however, we were unable to conclusively assess the full extent of the claustrum's participation in limbic kindling.