Sleep Switch Hypothalamus

(a) Circadian clock

Brainstem Ascending cortical activation REM/SWS switch

Rem Sws Acetylcholine

Figure 2 Systems regulating sleep-wake biology. Upper panel (a): Sleep-wake states are controlled through a delicate balance of activities between the thalamus (cortical activation and EEG synchronization), the hypothalamus (sleep/wake switch), the superchiasmatic nucleus (SCN or circadian clock) and the brainstem (ascending cortical activation, REM/SWS switch). Lower panel (b): Multiple neurotransmitters are involved in sleep-wake regulation. The ventrolateral preoptic area (VLPO) contains sleep promoting GABA/Galanin (Gal) neurons whereas wake-promoting orexin (hypocretin) neurons reside in the hypothalamus. The VLPO and orexin systems innervate key areas of the ascending arousal system: locus coeruleus (LC; adrenergic), dorsal raphe (DR; serotonergic) and tuberomammillary nucleus (TMN; histaminergic). Other key regions include the dopaminergic ventral tegmental center (VTA or A10 and A11 projections) which plays a role in alertness and may be important in cataplexy and restless leg syndrome. Serotonin plays a role in upper airway resistance control, thus potentially important in obstructive sleep apnea. Histamine is also involved in wakefulness. Other components of the arousal system are: BF (basal forebrain; cholinergic), LDT/PPT (laterodorsal tegmental nuclei/pediculopontine tegmental nuclei), CR (caudal raphe), PRF (pontine reticular formation); NE (norepinephrine); ACh (acetylcholine); GLY (glycine) and GLU (glutamate). (Reprinted with permission from Mignot, E.; Taheri, S.; Nishino, S. Nat. Neurosci. 2002, 5, 1071-1075 © Nature Publishing Group.)

Figure 2 Systems regulating sleep-wake biology. Upper panel (a): Sleep-wake states are controlled through a delicate balance of activities between the thalamus (cortical activation and EEG synchronization), the hypothalamus (sleep/wake switch), the superchiasmatic nucleus (SCN or circadian clock) and the brainstem (ascending cortical activation, REM/SWS switch). Lower panel (b): Multiple neurotransmitters are involved in sleep-wake regulation. The ventrolateral preoptic area (VLPO) contains sleep promoting GABA/Galanin (Gal) neurons whereas wake-promoting orexin (hypocretin) neurons reside in the hypothalamus. The VLPO and orexin systems innervate key areas of the ascending arousal system: locus coeruleus (LC; adrenergic), dorsal raphe (DR; serotonergic) and tuberomammillary nucleus (TMN; histaminergic). Other key regions include the dopaminergic ventral tegmental center (VTA or A10 and A11 projections) which plays a role in alertness and may be important in cataplexy and restless leg syndrome. Serotonin plays a role in upper airway resistance control, thus potentially important in obstructive sleep apnea. Histamine is also involved in wakefulness. Other components of the arousal system are: BF (basal forebrain; cholinergic), LDT/PPT (laterodorsal tegmental nuclei/pediculopontine tegmental nuclei), CR (caudal raphe), PRF (pontine reticular formation); NE (norepinephrine); ACh (acetylcholine); GLY (glycine) and GLU (glutamate). (Reprinted with permission from Mignot, E.; Taheri, S.; Nishino, S. Nat. Neurosci. 2002, 5, 1071-1075 © Nature Publishing Group.)

6.06.1.6.1 Adenosine

Adenosine (Ado), a paracrine neuromodulator produced in response to changes in cellular energy metabolism and tissue trauma, has both direct and indirect effects on neuronal function. Directly, Ado activates four receptors, Ai, A2A, A2B, and A3, which comprise the Pi receptor family. Indirectly, via presynaptic A1 heteroreceptors, Ado inhibits the release of neurotransmitters including ACh, glutamate, and GABA. Ado is released during wake and induces sleep onset, particularly after prolonged wakefulness.17 Adenosine effects on sleep are also thought to involve adenosine A2A receptor activation.98 The alerting effects of caffeine, 1 (see Section 6.06.6), occur via antagonism of Pi receptors. Ado may be the common final pathway for several sleep factors including endogenous somnolytic mediators, e.g., prostaglandin D2 (PGD2), tumor necrosis factor a (TNF-a), and interleukin-1 (IL1).

Natural Prostaglandin Inhibitors
Cl
Sleep Apnea

Sleep Apnea

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