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.
SUMMARY AND CONCLUSIONS
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