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J Neurophysiol 80: 2727-2742, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 5 November 1998, pp. 2727-2742
Copyright ©1998 The American Physiological Society

Voltage Imaging of Epileptiform Activity in Slices From Rat Piriform Cortex: Onset and Propagation

Rezan Demir1, Lewis B. Haberly1, 2, and Meyer B. Jackson1, 3

3 Department of Physiology and 2 Department of Anatomy, and 1 Center for Neuroscience, University of Wisconsin Medical School, Madison Wisconsin 53706

Demir, Rezan, Lewis B. Haberly, and Meyer B. Jackson. Voltage imaging of epileptiform activity in slices from rat piriform cortex: onset and propagation. J. Neurophysiol. 80: 2727-2742, 1998. The piriform cortex is a temporal lobe structure with a very high seizure susceptibility. To investigate the spatiotemporal characteristics of epileptiform activity, slices of piriform cortex were examined by imaging electrical activity with a voltage-sensitive fluorescent dye. Discharge activity was studied for different sites of stimulation and different planes of slicing along the anterior-posterior axis. Epileptiform behavior was elicited either by disinhibition with a gamma -aminobutyric acid-A receptor antagonist or by induction with a transient period of spontaneous bursting in low-chloride medium. Control activity recorded with fluorescent dye had the same pharmacological and temporal characteristics as control activity reported previously with microelectrodes. Simultaneous optical and extracellular microelectrode recordings of epileptiform discharges showed the same duration, latency, and all-or-none character as described previously with microelectrodes. Under all conditions examined, threshold electrical stimulation applied throughout the piriform cortex evoked all-or-none epileptiform discharges originating in a site that included the endopiriform nucleus, a previously identified site of discharge onset. In induced slices, but not disinhibited slices, the site of onset also included layer VI of the adjoining agranular insular cortex and perirhinal cortex, in slices from anterior and posterior piriform cortex, respectively. These locations had not been identified previously as sites of discharge onset. Thus like the endopiriform nucleus, the deep agranular insular cortex and perirhinal cortex have a very low seizure threshold. Additional subtle differences were noted between the induced and disinhibited models of epileptogenesis. Velocity was determined for discharges after onset, as they propagated outward to the overlying piriform cortex. Propagation in other directions was examined as well. In most cases, velocities were below that for action potential conduction, suggesting that recurrent excitation and/or ephaptic interactions play a role in discharge propagation. Future investigations of the cellular and organizational properties of regions identified in this study should help clarify the neurobiological basis of high seizure susceptibility.




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