Slow-wave sleep: serotonin, neuronal plasticity, and seizures.

M. Steriade


This article starts by enumerating several data that vindicate Michel Jouvet's hypothesis regarding serotonin as a factor promoting slow-wave sleep. The core of the article is devoted to the description of neuronal bases underlying sleep oscillations, with emphasis on the cortically generated slow oscillation (0.5-1 Hz) that groups both low-frequency (spindles and delta) and high-frequency (beta/gamma) rhythms. The low-frequency rhythms are generated by the synchronous firing of cortical neurons during the depolarizing phase of the slow oscillation, which impacts on the thalamic circuitry to generate spindles and clock-like delta potentials. The fast activity is voltage-dependent and occurs during the depolarization component of the slow cortical oscillation. This coalescence of brain rhythms, discovered in intracellular studies of neocortical and thalamic neurons, is now supported by EEG studies during human sleep. The rich spontaneous activity of neocortical neurons during slow-wave sleep is associated with neuronal plasticity that may play a role in consolidating memory traces acquired during the state of waking. Surprisingly, neuronal plasticity, usually regarded as a beneficial phenomenon implicated in memory and learning, could develop during slow-wave sleep into self-sustained paroxysmal discharges, similar to spike-wave complexes that appear in some epileptic syndromes.

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