The Kindling Process and Vulnerability to Status Epilepticus

Abstract

Several years ago, we developed an experimental model of status epilepticus (SE) that exploited the interaction of pilocarpine and seizure discharge upon a background of epileptogenesis resulting from amygdala kindling (1). We were initially interested in using the model to study the mechanisms by which the sustained seizures were initiated and maintained. However, we were struck by the extensive bilateral neuropathology resulting from a relatively short duration of SE in our model compared to other models of SE using pilocarpine (2, 11). We naturally wondered if the kindling process established an increased vulnerability to seizure-induced damage. If so, we reasoned that elucidation of the mechanisms responsible for the enhanced vulnerability might reveal information about the mechanisms underlying the acquisition of kindled seizures. Described here is some of the work that evolved from this idea, the results of which indicate that kindling does indeed alter vulnerability to SE, but also that the picture is more complex than we had originally envisioned.