Kindling-induced epileptiform potentials in piriform cortex slices originate in the underlying endopiriform nucleus. Hoffman, William H. and Lewis B. Haberly. Neuroscience Training Program and Department of Anatomy, University of Wisconsin, Madison, WI 53706, Department of Anatomy, University of Wisconsin, 1300 University Ave., West Loading Dock, Madison, WI 53706-7306.
APStracts 3:0077N, 1996.
1. Previous studies in vivo and in vitro have shown that kindling from several locations in the limbic system induces the onset of epileptiform activity in the piriform (olfactory) cortex in the rat. The present study tested the hypothesis that kindled epileptiform events in piriform cortex are initiated in the underlying endopiriform nucleus. The experiments were performed in slices taken from rats that were previously kindled by conventional means. 2. Both stimulus-evoked and spontaneous interictal-like epileptiform events were observed in most slices from the anterior piriform cortex, but in few slices from the posterior piriform cortex. These events resembled those described in unanesthetized and urethane-anesthetized rats in previous studies. 3. Findings in support of the hypothesis were as follows: Epileptiform events in the endopiriform nucleus preceded those in the piriform cortex. Epileptiform events could occur in endopiriform nucleus alone, but were only observed in the piriform cortex following occurrence in the endopiriform nucleus. A buildup in population activity preceded the onset of all-or-none epileptiform events in the endopiriform nucleus. Epileptiform events could be triggered by local application of glutamate in the endopiriform nucleus and adjacent claustrum, but not from the piriform cortex. Finally, local application of Co2+ in the endopiriform nucleus, but not in the piriform cortex or elsewhere in the slices, blocked their occurrence. 4. Additional experiments were performed to further characterize the generation process. DNQX blocked epileptiform events and the preceding accelerating buildup in multiunit activity at a concentration below that required to block the monosynaptic EPSP. This suggests that EPSPs mediated by AMPA-type glutamate receptors underlie epileptiform events in slices of piriform cortex, and that multisynaptic interactions within the endopiriform nucleus are required for generation of these epileptiform EPSPs. By contrast, block of NMDA receptors decreased the amplitude of epileptiform EPSPs but did not block their occurrence, indicating that NMDA receptors contribute to generation but are not required. When membrane potential was depolarized to increase driving force, fast IPSPs were found to consistently accompany the buildup process and epileptiform EPSPs. This indicates that if initiation of epileptiform activity in the endopiriform nucleus results from a compromise in feedback inhibition, this compromise is partial rather than complete. 5. Epileptiform EPSPs in slices of piriform cortex from kindled rats displayed similarities in properties, locus of origin, and mechanism of generation to those previously studied in slices from normal rats in which epileptiform activity was induced by a brief period of bursting activity. These similarities suggest that study of bursting-induced epileptiform EPSPs may provide insight into certain aspects of kindling-induced epileptogenesis.

Received 21 July 1995; accepted in final form 27 March 27.
APS Manuscript Number J469-5
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96