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J Neurophysiol 82: 3108-3122, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3108-3122
Copyright ©1999 by the American Physiological Society

Intracellular Study of Excitability in the Seizure-Prone Neocortex In Vivo

Mircea Steriade and Florin Amzica

Laboratoire de Neurophysiologie, Faculté de Médicine, Université Laval, Quebec, Canada G1K 7P4

Steriade, Mircea and Florin Amzica. Intracellular Study of Excitability in the Seizure-Prone Neocortex In Vivo. J. Neurophysiol. 82: 3108-3122, 1999. The excitability of neocortical neurons from cat association areas 5-7 was investigated during spontaneously occurring seizures with spike-wave (SW) complexes at 2-3 Hz. We tested the antidromic and orthodromic responsiveness of neocortical neurons during the "spike" and "wave" components of SW complexes, and we placed emphasis on the dynamics of excitability changes from sleeplike patterns to seizures. At the resting membrane potential, an overwhelming majority of neurons displayed seizures over a depolarizing envelope. Cortical as well as thalamic stimuli triggered isolated paroxysmal depolarizing shifts (PDSs) that eventually developed into SW seizures. PDSs could also be elicited by cortical or thalamic volleys during the wave-related hyperpolarization of neurons, but not during the spike-related depolarization. The latencies of evoked excitatory postsynaptic potentials (EPSPs) progressively decreased, and their slope and depolarization surface increased, from the control period preceding the seizure to the climax of paroxysm. Before the occurrence of full-blown seizures, thalamic stimuli evoked PDSs arising from the postinhibitory rebound excitation, whereas cortical stimuli triggered PDSs immediately after the early EPSP. These data shed light on the differential excitability of cortical neurons during the spike and wave components of SW seizures, and on the differential effects of cortical and thalamic volleys leading to such paroxysms. We conclude that the wave-related hyperpolarization does not represent GABA-mediated inhibitory postsynaptic potentials (IPSPs), and we suggest that it is a mixture of disfacilitation and Ca2+-dependent K+ currents, similar to the prolonged hyperpolarization of the slow sleep oscillation.




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