The historic sleep regulatory paradigm invokes “top-down” imposition of sleep on the brain by sleep regulatory circuits. While remaining conceptually useful, many sleep phenomena are difficult to explain using that paradigm, including, unilateral sleep, sleep-walking, and poor performance after sleep deprivation. Further, all animals sleep after non-lethal brain lesions, regardless of whether the lesion includes sleep regulatory circuits, suggesting that sleep is a fundamental property of small viable neuronal/glial networks. That small areas of the brain can exhibit non-rapid eye movement sleep-like states is summarized. Further, sleep-like states in neuronal/glial cultures are described. The local sleep states, whether in vivo or in vitro, share electrophysiological properties and molecular regulatory components with whole animal sleep and exhibit sleep homeostasis. The molecular regulatory components of sleep are also involved in plasticity and inflammation. Like sleep, these processes, are initiated by local cell-activity dependent events, yet have at higher levels of tissue organization whole body functions. While there are large literatures dealing with local initiation and regulation of plasticity and inflammation, the literature surrounding local sleep is in its infancy and clinical applications of the local sleep concept are absent. Regardless, the local use-dependent sleep paradigm can advise and advance future research and clinical applications.