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The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3123-3138
Copyright ©1999 by the American Physiological Society
Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec, Canada G1K 7P4
Amzica, Florin and
Mircea Steriade.
Spontaneous and Artificial Activation of Neocortical Seizures. J. Neurophysiol. 82: 3123-3138, 1999. The aim of this study is to disclose the mechanisms underlying the
recruitment of neocortical networks during slow-wave sleep oscillations
evolving into spike-wave (SW) seizures. 1) We
investigated the activation of SW seizures in a seizure-prone neocortex
by means of electrical stimuli applied within the frequency range of
spontaneous sleep oscillations. Stimuli were grouped in bursts of 10 Hz, similar to sleep spindles, and repeated every 2 s, to reproduce their rhythmic recurrence imposed by the slow (<1 Hz) sleep
oscillation. Either cortical or thalamic stimuli, which were applied
while the cortex displayed sleeplike activity, gradually induced
paroxysmal responses in intracellularly recorded neocortical neurons,
which were virtually identical to those of spontaneous seizures and
consisted of a progressive buildup of paroxysmal depolarizing shifts
(PDSs). 2) The ability of cortical networks to follow
stimuli was tested at various stimulation frequencies (1-3 Hz) and
quantified by calculating the entropy of the ensuing oscillation.
Rhythmic PDSs were optimally induced, and the lowest entropy was
generated, at a stimulation frequency around 1.5 Hz. Fast runs at
10-15 Hz, which often override PDSs, thus contributing to the
polyspike-wave pattern of seizures, were induced by cortical stimuli,
but were disturbed by thalamic stimuli. Spontaneous seizures generally
evolved toward an accelerated discharge of PDSs. It is suggested that
these accelerating trends during SW seizures act as protective
mechanisms by provoking the uncoupling of cortical networks and
eventually arresting the seizure.
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