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The Journal of Neurophysiology Vol. 82 No. 5 November 1999, pp. 2731-2746
Copyright ©1999 by the American Physiological Society
Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec G1K 7P4, Canada
Amzica, Florin and
Dag Neckelmann.
Membrane Capacitance of Cortical Neurons and Glia During Sleep
Oscillations and Spike-Wave Seizures. J. Neurophysiol. 82: 2731-2746, 1999. Dual intracellular
recordings in vivo were used to disclose relationships between cortical
neurons and glia during spontaneous slow (<1 Hz) sleep oscillations
and spike-wave (SW) seizures in cat. Glial cells displayed a slow
membrane potential oscillation (<1 Hz), in close synchrony with
cortical neurons. In glia, each cycle of this oscillation was made of a
round depolarizing potential of 1.5-3 mV. The depolarizing slope
corresponded to a steady depolarization and sustained synaptic activity
in neurons (duration, 0.5-0.8 s). The repolarization of the glial
membrane (duration, 0.5-0.8 s) coincided with neuronal
hyperpolarization, associated with disfacilitation, and suppressed
synaptic activity in cortical networks. SW seizures in glial cells
displayed phasic events, synchronized with neuronal paroxysmal
potentials, superimposed on a plateau of depolarization, that lasted
for the duration of the seizure. Measurements of the neuronal membrane
capacitance during slow oscillating patterns showed small fluctuations
around the resting values in relation to the phases of the slow
oscillation. In contrast, the glial capacitance displayed a
small-amplitude oscillation of 1-2 Hz, independent of phasic sleep and
seizure activity. Additionally, in both cell types, SW seizures were
associated with a modulatory, slower oscillation (
0.2 Hz) and a
persistent increase of capacitance, developing in parallel with the
progression of the seizure. These capacitance variations were dependent
on the severity of the seizure and the distance between the presumed seizure focus and the recording site. We suggest that the capacitance variations may reflect changes in the membrane surface area (swelling) and/or of the interglial communication via gap junctions, which may
affect the synchronization and propagation of paroxysmal activities.
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