Changes in neuronal conductance during different components of cortically generated spike-wave seizures.
Neuronal conductance was studied in anesthetized cats during cortically generated spike-wave seizures arising from slow sleep oscillation. Single and dual intracellular recordings from neocortical neurons were used. The changes were similar whether the seizures occurred spontaneously, or were evoked by electrical stimulation or induced by bicuculline. In all seizures, the conductance increased from the very onset of the seizure and returned to control values only at the end of the postictal depression. Simultaneous intracellular recordings from two neurons showed that the neuron leading the other neuron displayed the largest increase in membrane conductance. The changes in neuronal conductance during the two phases of the slow sleep oscillation, i.e. highest during depolarizations and lowest during hyperpolarizations, were similar to those occurring during the "spike" and "wave" components of seizures. (1) Maximal conductance was found during the paroxysmal depolarizing shift corresponding to the electroencephalogram "spike" (median: 252 nS; range: 90 to more than 400 nS). It was highest at the onset of the depolarized plateau and decreased thereafter. (2) During the hyperpolarization corresponding to the electroencephalogram "wave", the conductance was significantly lower (median: 71 nS; range: 41 to 140 nS). (3) The conductance was elevated during the fast runs (median: 230 nS; range: 92 to 350 nS) which occurred in two-thirds of the seizures. (4) The conductance values during postictal depression were situated between those measured during the seizure hyperpolarizations and during sleep hyperpolarizations. The conductance decreased exponentially back to the values of the slow sleep oscillation over the total duration of the postictal depression. The data suggest that the major mechanism underlying the "wave"-related hyperpolarizing component of spike-wave seizures relies mainly not on active inhibition, but on a mixture of disfacilitation and potassium currents.
Neckelmann
D
D
Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Québec, Canada.
Amzica
F
F
Steriade
M
M
D000200:Action Potentials; D000818:Animals; D001640:Bicuculline; D002415:Cats; D002462:Cell Membrane / Q000502:physiology; D003292:Convulsants; D004553:Electric Conductivity; D004558:Electric Stimulation; D004569:Electroencephalography; D004594:Electrophysiology; D019579:Neocortex / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D009991:Oscillometry; D012640:Seizures / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*; D012894:Sleep Stages
D003292:Convulsants; D001640:Bicuculline