Initiation of Electrographic Seizures in the Rat Limbic System [italic]In Vitro[/italic]: Intracellular Characterization of Entorhinal Cortex Neuronal Activity.
Abstract number :
3.032
Submission category :
Year :
2001
Submission ID :
2289
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
M. D[ssquote]Antuono, PhD, Neurology and Neurosurgery, and Physiology, Montreal Neurological Institute, McGill University, Montreal, QC, Canada; V. Tancredi, MD, Neuroscience, University of Rome [dsquote]Tor Vergata[dsquote], Rome, Italy; V. Lopantsev, Ph
RATIONALE: Interictal activity may prevent or facilitate sustained epileptiform discharges, resembling electrographic seizures, in the entorhinal cortex (EC). These opposite actions depend on the interictal discharge frequency and on the associated increases in [K + ] [sub] o [/sub]. Here we used intracellular recordings from EC neurons to characterize the ionic components of these two types of interictal dicharge.
METHODS: Field potential and sharp-electrode intracellular recordings were obtained from combined adult rat slices containing the hippocampus and the EC during bath application of 4-aminopyridine (4AP, 50 [mu]M)
RESULTS: Intracellular recordings with either K-acetate- or K-acetate+QX314-filled electrodes showed that the CA3-driven interictal discharges corresponded in the EC neurons to depolarizations capped by action potential bursts and characterized by reversal potentials of approx. -25mV. A similar reversal potential was found for the intracellular depolarizations generated by EC cells during the slow interictal patterns recorded after cutting the Schaffer collaterals or the hippocampus-EC connections. When recorded with KCl- or KCl+QX314-filled electrodes both types of interictal depolarization had more positive reversal potential values. The interictal-ictal transition in the isolated EC was accompained in cells recorded with K-acetate+QX314-filled electrodes by a progressive shift of the interictal depolarization reversal potential in the depolarizing direction.
CONCLUSIONS: Our data indicate that in the EC both CA3-driven and local interictal discharges are largely contributed by Cl - -mediated conductances presumably caused by the activation of GABA [sub] A [/sub] receptors. However, CA3 outputs entrain EC networks in a fast interictal pattern that prevents electrographic seizures by controlling the expression of Cl - -mediated conductances.
Support: CIHR
Fragile X Research Foundation of Canada
Disclosure: Grant - CHIR
Fragile X Research Foundation of Canada