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The buildup and resolution of sleep need is correlated with overall cortical, excitatory synaptic strength.

During SWS episodes, the rebound SWS-SWA increase resolves, consistent with resolution of sleep need ( Bjorness et al., 2016). The amplitude of the rebound directly correlates with the previous waking or SD duration ( Borbély, 1982 Franken et al., 2001) implicating rebound SWS, slow wave activity (SWS-SWA) as a biomarker of sleep need. Following an extended period of waking, or sleep deprivation (SD), the mammalian cortex shows an altered pattern of EEG activity characterized by rebound slow wave power (delta power in the frequency range of 0.5–4.5 Hz) during the ensuing slow wave sleep (SWS also referred to as NREM) periods. Sleep abnormalities are commonly observed in numerous neurological disorders, including autism spectrum disorder, major depressive disorder, bipolar disorder, post-traumatic stress disorder, neurodegenerative disorders and many others, but our understanding of sleep need and its regulation and resolution is poorly understood.