Abstract

The logic and potential mechanisms for a new paradigm, the local use-dependent view of sleep as a distributed dynamic process in brain, are presented. This new paradigm is needed because the current dominant top-down imposition of sleep on the brain by sleep regulatory centers is either silent or is of inadequate explanatory value for many well-known sleep phenomena, e.g. sleep inertia. Two mechanistic falsifiable hypotheses linking sleep to cell use and the emergence of sleep/wake states are presented. These hypotheses are not mutually exclusive and both firmly link sleep to activitydependent epigenetic brain plasticity and the need to integrate and balance waking activity induced-network connectivity changes. The views presented herein emphasize the inseparability of sleep mechanisms from a connectivity sleep function.

Keywords: Plasticity, local sleep, sleep regulatory substance, ATP, synaptic homeostasis hypothesis, potential mechanisms, inadequate explanatory value, epigenetic brain plasticity, anterior hypothalamus, ATP-cytokine-adenosine, brain's connectivity matrix, synaptic renormalization, emergent phenomenon