The Kindling Process and Vulnerability to Status Epilepticus
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.
KeywordsStatus Epilepticus Piriform Cortex Power Spectral Analysis Edge Frequency Seizure Discharge
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- 1.Buterbaugh, G.G., Michelson, H.B. and Keyser, D.O. (1986) Status epilepticus facilitated by pilocarpine in amygdala-kindled rats. Exp. Neurol. 94: 94–102.Google Scholar
- 8.Morimoto, K., M. Dragunow and G.V. Goddard (1986) Deep prepyriform kindling and its relation to amygdala kindling in the rat. Exp. Neurol. 94: 637–648.Google Scholar
- 10.Olney, J.W., Collins, R.C. and Sloviter, R.S. (1986) Excitotoxic mechanisms of epileptic brain damage. In Delgado-Escueta, A.V., Ward, A., Woodbury, D.M. and Porter, R.J. (eds): Advances in Neurology, Volume 44. Raven Press, New York, pp. 857–877.Google Scholar
- 11.Turski, W.A., Cavalheiro, E.A., Schwarz, M., Czuczwar, S.J., Kleinrok, Z. and Turski, L. (1983) Limbic seizures produced by pilocarpine in rats: Behavioral, electroencephalographic and neuropathological study. Behay. Brain Res. 9: 315–335.Google Scholar