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. 2021 Jun 10;44(11):zsab146. doi: 10.1093/sleep/zsab146

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© The Author(s) 2021. Published by Oxford University Press on behalf of Sleep Research Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 1. — Key components of the model of arousal dynamics. Light activates photoreceptors in the eye, which transmit activation to the central circadian clock in the suprachiasmatic nucleus (SCN). The circadian drive from the SCN suppresses the sleep-active neurons in the ventrolateral preoptic nucleus (VLPO), thereby reducing inhibition of the wake-active monoaminergic neurons in the hypothalamus and brainstem (MA). MA has mutually inhibitory connections with the VLPO, so only one population is active at a time. Activation of the MA leads to increase of the homeostatic sleep drive, which together with the circadian drive from the SCN produce a total sleep drive controlling the switch between sleep and wake. The homeostatic and circadian drives together determine alertness levels. When MA is inactive, sleep state is predicted by the model and the eyelids are closed so the light input is reduced to zero. SCN controls synthesis of melatonin, which is released to blood circulation, diffused to saliva and metabolized into 6-sulphatoxymelatonin (aMT6s) which is excreted in the urine. Circadian phase markers, including aMT6s acrophase and dim light melatonin onset (DLMO) are calculated from the hormone profiles. Shifts and commute are simulated by keeping MA awake.