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Updated: Jan 22, 2026

Optogenetic Manipulation of Neural Circuits During Monitoring Sleep/wakefulness States in Mice
Published on: June 19, 2019
Sleep-wake physiology
Pierre-Hervé Luppi1, Patrice Fort1
1Lyon Neuroscience Research Center, Lyon, France.
Abstract:
This chapter presents hypotheses on the mechanisms responsible for the succession of the three vigilance states, namely waking, nonrapid eye movement (non-REM) (slow-wave sleep-SWS), and REM sleep (paradoxical sleep-PS). It can be proposed that waking is induced by the activity of multiple waking systems, including the serotonergic, noradrenergic, cholinergic, and hypocretin systems. At the onset of sleep, the SWS-active neurons are activated by the circadian clock localized in the suprachiasmatic nucleus and a hypnogenic factor, adenosine, which progressively accumulates in the brain during waking. A number of studies support the hypothesis that SWS results from the activation of GABAergic neurons localized in the ventrolateral preoptic nucleus. However, additional GABAergic systems have been described, localized in the parafacial, accumbens, and reticular thalamic nuclei, and these are also presented. In addition, the chapter discusses the fact that a large body of data strongly suggests that the switch from SWS to PS is due to the interaction of multiple populations of glutamatergic and GABAergic neurons localized in the posterior hypothalamus and the brainstem.
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