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Increased Propensity to Seizures After Chronic Cortical Deafferentation In Vivo

Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Québec, Canada

Submitted 14 July 2005; accepted in final form 17 October 2005

Cortical injury may lead to clinical seizures. We investigated the changing patterns of the sleeplike slow oscillation and its tendency to develop into paroxysmal activity consisting of spike-wave (SW) complexes at 2–4 Hz after partial deafferentation of the suprasylvian gyrus. Experiments were carried out in anesthetized cats, at different time intervals (wk 1 to wk 5, W1–W5) after cortical undercut. Multisite field potentials and single or dual intracellular recordings from the whole extent of the deafferented gyrus were used. The field components of the slow oscillation increased in amplitudes and were transformed into paroxysmal patterns, expressed by increased firing rates and tendency to neuronal bursting. The incidence of SW seizures was higher with transition from semiacute (W1) to chronic (W2–W5) stages after cortical undercut. The propagation delay of low-frequency activities decreased from W1 to W5, during both the slow oscillation and seizures. The initiation of seizures took place in territories contiguous to the relatively intact cortex (area 5 in the anterior part of the gyrus), as shown by cross-correlations of field potentials from different sites and simultaneous intracellular recordings from the anterior and posterior parts of the gyrus. The increased amplitudes of both slow oscillation and SW seizures, and their enhanced synchrony expressed by shorter time of propagation, are ascribed to increased neuronal and network excitability after cortical undercut.

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