Neurocircuitry Mediating Sleep and Waking States

Illness exerts a strong influence on sleep-waking cycles, with the most common result being an increase in non-REM (NREM), particularly slow wave sleep (SWS) (Opp 2005). In order to determine the mechanisms by which illness influences sleep, it is necessary to understand the brain substrates that control transitions between wakefulness and sleep. Recent evidence indicates that sleep wake cycles are controlled by a "switch" mechanism that is exerted by interactions of hypothalamic nuclei (reviewed in Saper, Scammell, and Lu 2005; see Fig. 6.1).

Histaminergic neurons of the tuberomammillary posterior hypothalamus serve an activating role in the brain, becoming functionally quiescent during sleep when behavioral activity is minimal, and are believed to be particularly important in regulating transitions between sleep and arousal (Saper et al. 2005). In contrast, a compact cluster of neurons in the ventrolateral preoptic nucleus (VLPO) promotes sleep, via inhibitory projections to the histaminergic, as well as all other monoaminergic nuclei contributing to arousal, such as the noradrenergic locus coeruleus and the serotonergic raphe nuclei.

The sleep-promoting neurons of the VLPO are under recurrent inhibitory influence by the monoaminergic arousal systems (Chou, Bjorkum, Gaus, Lu, Scammell, and Saper 2002; see Fig. 6.1). The arrangement of this circuitry indicates that any increased drive to sleep due to inflammation or illness would be executed by inhibition of critical monoaminergic arousal systems, including the histaminergic neurons, which as a consequence would release their inhibitory control over the sleep-active neurons within the VLPO.

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