Chapter 31 - Local and Use-Dependent Aspects of Sleep

Abstract

Ample historical evidence suggests that parts of the brain can be asleep while other parts are awake (e.g., sleepwalking, sleep inertia, dolphin unilateral sleep). The hypothesis that small networks, whether in vivo or in vitro, exhibit sleep-like properties and that sleep within these networks is initiated by local cell activity is elaborated. Many, perhaps all, sleep regulatory molecules are locally synthesized in response to cell activity. Experimentally, local cortical sleep intensity can increase or decrease by prior local activation or inhibition, respectively, whether achieved by enhanced or reduced, localized afferent input, or by treatment with sleep regulatory substances or their inhibitors. Cortical columns oscillate between sleep- and wake-like states; behavior dependent upon a single cortical column is disturbed if the column is in the sleep-like state. Neuronal/glial co-cultures have a default sleep-like state, and their stimulation, electrically or chemically, is followed by enhanced expression of sleep regulatory substances and rebound sleep-like state, indicating sleep homeostasis. The in vitro sleep-like state, like whole animal sleep, is also characterized by neuronal burstiness, synchrony of slow potentials, sleep-associated gene expression, and spontaneous reversibility. We conclude that small neuronal/glial networks constitute a minimal part of the brain capable of sleep states and that sleep-like states are the default state dependent upon prior cell use. This proposition provides greater explanatory parsimony of dissociated brain states, poor behavioral performance, insomnia, sleep inertia, and other sleep anomalies and pathologies.