CELLULAR AND NETWORK MECHANISMS OF SLOW-WAVE SLEEP ELECTRICAL ACTIVITY

Timofeev Igor
Departement d'Anatomie et Physiologie, Universite Laval, Quebec, Canada, G1K 7P4
e-mail: Igor.Timofeev@phs.ulaval.ca

Various forms of oscillatory activity in the thalamocortical network, whose mechanisms and sources of generation are different, characterize the states of vigilance. Slow-wave sleep oscillations are composed of slow rhythm (<1 Hz), which groups delta (1-4 Hz), spindle (7-15 Hz), beta-gamma (20-60 Hz) and epochs of ripples (100-200 Hz). In this presentation I will show that the generation of slow sleep rhythm is an emerging property of cortical network that depends on interaction of spontaneous synaptic events, intrinsic properties of cortical neurons and complexity of neocortical network. This rhythm is composed of active (up) states and of silent (down) states. Silent states are periods of disfacilitation lasting 200-300 ms during which spontaneous synaptic activity is largely reduced. The onset of sleep at cortical level is associated with sudden appearance of periods of disfacilitation. The depolarizing phases of slow-sleep rhythm are accompanied with a high level of synaptic activity leading to neuronal depolarization and firing. The onset of depolarizing phases of slow rhythm induces a strong corticothalamic drive that triggers spindle activities. The spindle activity (7-15 Hz) is generated within intrathalamic networks composed of thalamocortical and reticular thalamic neurons. Burst firing of inhibitory RE neurons induces rhythmic IPSPs in thalamocortical (TC) neurons, which generate rebound spike-bursts and drive cortical networks. Spindles are fully synchronized by RE-TC interconnections and effectively controlled by corticothalamic volleys. Faster cortical rhythms occur when cortical neurons are steadily depolarized. Gamma activities help to transmit synaptic excitation over oligosynaptic chains, while ripples are associated with overexcitation, often leading to the generation of paroxysmal activities.