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. 2015 Oct 12;2(3):406–417. doi: 10.1080/23328940.2015.1075095

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 2. — Circuit basis of sleep-wake regulation. Model 1 (shown in panel a): Adenosine inhibits the release of acetycholine from basal forebrain (BF) cholinergic neurons to produce slow-wave sleep. Model 2 (shown in panels b-d): a flip–flop switching mechanism involving mutually inhibitory interactions between sleep-promoting neurons in the ventrolateral preoptic area (VLPO) and wake-promoting neurons in the hypothalamus [i.e., histaminergic tuberomammilary nucleus (TMN)], and brainstem [i.e., noradrenergic locus coeruleus (LC), serotonergic dorsal raphe nucleus (DR), and cholinergic laterodorsal tegmental nucleus (LDT)]. The flip-flop switch between the VLPO and hypothalamus and brainstem is stabilized by orexin/hypocretin (OX/Hcrt) inputs. Adenosine is known to act as an endogenous somnogen and promotes sleep via inhibitory A₁ receptors (A₁) in the basal forebrain, VLPO and TMN and excitatory A_2A receptors (A_2A) in the nucleus accumbens (NAc) and VLPO.^98-101 Other Abbreviations: Ach, acetylcholine; 5-HT, serotonin, NE, norepinephrine.