Cortical coupling in sleep and paroxysmal oscillations

Abstract

Intracellular and electroencephalographic (EEG) studies in animals and humans show that a major sleep rhythm, the slow oscillation (0.5–1 Hz), is generated and synchronized within intracortical circuits. This cortical oscillation triggers thalamic neurons, and thus, produces complex wave-sequences that include sleep spindles (7–15 Hz). These findings emphasize that the neocortex and thalamus are a unified oscillatory machine. Under special circumstances, such as the reduction in the inhibitory constraint, the slow sleep oscillation may develop into paroxysmal oscillations, consisting of spike-wave (SW) and polyspike-wave (PSW) complexes at 2–3 Hz, which are often associated with fast runs at 10–15 Hz, as in the Lennox–Gastaut syndrome. The SW/PSW seizures are initiated in neocortex and they spread to the thalamus only after a few seconds. During cortical SW seizures, most thalamocortical neurons are hyperpolarized and display phasic inhibitory postsynaptic potentials due to the activity of GABAergic thalamic reticular neurons that faithfully follow the paroxysmal depolarizing shifts arising in cortical neurons.