Journal of Neuroscience, Vol 12, 2211-2224, Copyright © 1992 by Society for Neuroscience
Neuronal processes that underlie expression of kindled epileptiform events in the piriform cortex in vivo
LB Haberly and TP Sutula
Department of Anatomy, University of Wisconsin, Madison 53706.
Recent studies with kindling and convulsant drug models of epilepsy suggest
that the piriform (primary olfactory) cortex may be particularly
susceptible to generation of epileptiform activity. The present study has
examined the generation of interictal epileptiform events in the piriform
cortex of kindled rats in vivo, taking advantage of special features of
this system that facilitate physiological analysis. The investigation
included analysis of extracellular and intracellular potentials, and
membrane currents computed by current source density (CSD) analysis. In
pyramidal cells, epileptiform events consisted of an initial EPSP that
occurred in all-or-none fashion and a long-lasting IPSP with Cl(-)- and
K(+)-mediated components. Onset of the IPSP was sufficiently fast that
firing evoked by the EPSP was consistently limited to single action
potentials. CSD analysis revealed the presence of two distinctly different
excitatory epileptiform currents: an initial inward current of unknown
origin that is widely distributed over depth, and a second much larger
inward current at the depths of proximal apical and basal dendrites of
pyramidal cells. It was concluded that this second component is mediated by
the associational projections of pyramidal cells excited by the first
component. Since these heavy associational projections also extend to
neighboring areas including the amygdala, entorhinal cortex, and insular
and orbitofrontal areas of neocortex, this second component could be widely
propagated within the basal forebrain. An important finding was that the
EPSP generated by this associational pathway was completely blocked in cell
bodies of pyramidal cells in piriform cortex by the IPSP during most
events. This IPSP may therefore play a critical role in limiting seizure
activity by preventing reverberating positive feedback in the pyramidal
cell population. It can be speculated that compromise of this IPSP, as by
repetitive activation by the shock trains used for kindling, leads to
prolonged epileptic activity in the piriform cortex and the many limbic
structures to which it projects.
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