Promotion of sleep mediated by the A2a-adenosine receptor and possible involvement of this receptor in the sleep induced by prostaglandin D2 in rats.

Satoh, Shinsuke; Matsumura, Hitoshi; Suzuki, Fumio; Hayaishi, Osamu

doi:10.1073/pnas.93.12.5980

Cited by 145 publications

(94 citation statements)

References 22 publications

(16 reference statements)

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“…Under pentobarbital anesthesia (50 mg/kg, i.p. ), rats underwent surgery for implantation of electrodes for EEG and EMG recordings and placement of a guide cannula for the microdialysis probe as described (35,36). Brief ly, a guide cannula (outer diameter, 0.6 mm) with an in-dwelling stylet was directed stereotaxically into the TMN.…”

Section: Electroencephalogram (Eeg) and Electromyogram (Emg) Recordingsmentioning

confidence: 99%

Arousal effect of orexin A depends on activation of the histaminergic system

Huang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

503

314

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Orexin neurons are exclusively localized in the lateral hypothalamic area and project their fibers to the entire central nervous system, including the histaminergic tuberomammillary nucleus (TMN). Dysfunction of the orexin system results in the sleep disorder narcolepsy, but the role of orexin in physiological sleep–wake regulation and the mechanisms involved remain to be elucidated. Here we provide several lines of evidence that orexin A induces wakefulness by means of the TMN and histamine H 1 receptor (H1R). Perfusion of orexin A (5 and 25 pmol/min) for 1 hr into the TMN of rats through a microdialysis probe promptly increased wakefulness for 2 hr after starting the perfusion by 2.5- and 4-fold, respectively, concomitant with a reduction in rapid eye movement (REM) and non-REM sleep. Microdialysis studies showed that application of orexin A to the TMN increased histamine release from both the medial preoptic area and the frontal cortex by ≈2-fold over the baseline for 80 to 160 min in a dose-dependent manner. Furthermore, infusion of orexin A (1.5 pmol/min) for 6 hr into the lateral ventricle of mice produced a significant increase in wakefulness during the 8 hr after starting infusion to the same level as the wakefulness observed during the active period in wild-type mice, but not at all in H1R gene knockout mice. These findings strongly indicate that the arousal effect of orexin A depends on the activation of histaminergic neurotransmission mediated by H1R.

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Section: Electroencephalogram (Eeg) and Electromyogram (Emg) Recordingsmentioning

confidence: 99%

Arousal effect of orexin A depends on activation of the histaminergic system

Huang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

503

314

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“…The stimulant effects of caffeine on the central nervous system at doses obtained through normal human consumption are due to caffeine's ability to antagonize adenosine receptors (Fredholm et al, 1999). Numerous reports have corroborated that adenosine is a neuromodulator that is involved in sleep regulation Benington et al, 1995;Porkka-Heiskanen et al, 1997;Radulovacki et al, 1982Radulovacki et al, , 1985Satoh et al, 1996Satoh et al, , 1999Scammell et al, 2001;Schwierin et al, 1996;Strecker et al, 2000;Ticho and Radulovacki, 1991;Urade et al, 2003). It has recently been proposed that in humans, caffeine mimics the effects of a reduction in sleep homeostasis during prolonged wakefulness (Landolt et al, 2004).…”

Section: Discussionmentioning

confidence: 97%

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Carrier

Fernandez‐Bolaños

Robillard

et al. 2006

Neuropsychopharmacol

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Caffeine is often used to counteract sleepiness generated by sleep deprivation, jet lag, and shift-work, and is consumed at different times of day. Caffeine also has effects on sleep. However, little is known about the interaction between sleep deprivation, circadian timing, and caffeine consumption on sleep. In this study, we compared the effects of caffeine on nocturnal sleep initiated at habitual circadian time and on daytime recovery sleep. Thirty-four moderate caffeine consumers participated in both caffeine (200 mg) and placebo (lactose) conditions in a double-blind crossover design. Seventeen subjects followed their habitual sleep-wake cycle and slept in the laboratory during the night (Night), while 17 subjects were sleep deprived for one night and recovery sleep started in the morning (DayRec). All subjects received a capsule of 100 mg of caffeine (or placebo) 3 h before bedtime, and the remaining dose 1 h before bedtime. Compared to placebo, caffeine lengthened sleep latency, increased stage 1, and reduced stage 2 and slow-wave sleep (SWS) in both groups. However, caffeine reduced sleep efficiency more strongly in the DayRec group, and decreased sleep duration and REM sleep only in that group. The stronger effects of caffeine on daytime recovery sleep compared to nocturnal sleep are probably the consequence of the combined influence of increasing circadian wake propensity drive and the dissipation of homeostatic sleep pressure. We propose that the reduction of SWS by caffeine during daytime sleep increases the impact of the circadian wake signal on sleep. These results have implications for individuals using caffeine during night time. Neuropsychopharmacology (2007) 32, 964-972.

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“…Alternatively, we previously showed that a PGD 2 or A 2A R agonist suppresses the histaminergic system (12,13,29) and increases both NREM and REM sleep (4,11). For example, an A 2A R agonist (2 pmol/min) increased slow-wave sleep (NREM sleep) by 71% and paradoxical sleep (REM sleep) by 96% in rats (11), whereas an A 1 R one at 1.5 nmol/side increased NREM sleep by 3.1-fold but did not change the amount of REM sleep at all (Fig. 2C).…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent studies have shown that PGD 2 is involved in both circadian (6,7) and homeostatic regulation of sleep (8). Further studies on the molecular mechanisms of sleep-wake regulation by PGD 2 demonstrated that PGD 2 is produced by the action of lipocalin-type PGD synthase dominantly expressed in the leptomeninges (9), binds with PGD receptors (DPRs) exclusively localized in the arachnoid membrane of the basal forebrain (BF) (10), and promotes sleep through adenosine acting at adenosine A 2A receptors (A 2A R's) (11), followed by activation of sleep-active neurons in the ventrolateral preoptic (VLPO) area (12,13). The somnogenic effect of PGD 2 is mimicked by an A 2A R agonist, but not by an adenosine A 1 receptor (A 1 R) one, and is blocked by an A 2A R antagonist (11).…”

mentioning

confidence: 99%

Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A ₁ receptors and promotes non-rapid eye movement sleep

Oishi

Huang

Fredholm

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

133

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Adenosine has been proposed to promote sleep through A1 receptors (A 1R's) and/or A2A receptors in the brain. We previously reported that A 2A receptors mediate the sleep-promoting effect of prostaglandin D2, an endogenous sleep-inducing substance, and that activation of these receptors induces sleep and blockade of them by caffeine results in wakefulness. On the other hand, A 1R has been suggested to increase sleep by inhibition of the cholinergic region of the basal forebrain. However, the role and target sites of A1R in sleep-wake regulation remained controversial. In this study, immunohistochemistry revealed that A 1R was expressed in histaminergic neurons of the rat tuberomammillary nucleus (TMN). In vivo microdialysis showed that the histamine release in the frontal cortex was decreased by microinjection into the TMN of N 6 -cyclopentyladenosine (CPA), an A1R agonist, adenosine or coformycin, an inhibitor of adenosine deaminase, which catabolizes adenosine to inosine. Bilateral injection of CPA into the rat TMN significantly increased the amount and the delta power density of non-rapid eye movement (non-REM; NREM) sleep but did not affect REM sleep. CPA-promoted sleep was observed in WT mice but not in KO mice for A 1R or histamine H1 receptor, indicating that the NREM sleep promoted by A 1R-specific agonist depended on the histaminergic system. Furthermore, the bilateral injection of adenosine or coformycin into the rat TMN increased NREM sleep, which was completely abolished by coadministration of 1,3-dimethyl-8-cyclopenthylxanthine, a selective A 1R antagonist. These results indicate that endogenous adenosine in the TMN suppresses the histaminergic system via A 1R to promote NREM sleep.Adenosine deaminase ͉ histamine ͉ knockout mouse ͉ rat I n 1954, Feldberg and Sherwood (1) showed that intraventricular injection of micromole quantities of adenosine into cats caused a state resembling natural sleep of 30-min duration. Subsequent pharmacological studies from several laboratories demonstrated that adenosine and its receptor agonists promoted, but antagonists such as caffeine, inhibited both non-rapid eye movement (non-REM; NREM) and REM sleep (for review, see refs. 2, 3). However, the exact molecular mechanisms underlying sleep-wake regulation by adenosine still remained unclear. Since 1983, we have reported that prostaglandin (PG) D 2 is an endogenous sleep-inducing substance in rodents (4) and monkeys (5). PGD 2 -induced sleep was indistinguishable from natural physiological sleep as judged by several electrophysiological and behavioral criteria (5). Subsequent studies have shown that PGD 2 is involved in both circadian (6, 7) and homeostatic regulation of sleep (8). Further studies on the molecular mechanisms of sleep-wake regulation by PGD 2 demonstrated that PGD 2 is produced by the action of lipocalin-type PGD synthase dominantly expressed in the leptomeninges (9), binds with PGD receptors (DPRs) exclusively localized in the arachnoid membrane of the basal forebrain (BF) (10), and promotes sleep thr...

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Promotion of sleep mediated by the A2a-adenosine receptor and possible involvement of this receptor in the sleep induced by prostaglandin D2 in rats.

Cited by 145 publications

References 22 publications

Arousal effect of orexin A depends on activation of the histaminergic system

Arousal effect of orexin A depends on activation of the histaminergic system

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A ₁ receptors and promotes non-rapid eye movement sleep

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Promotion of sleep mediated by the A2a-adenosine receptor and possible involvement of this receptor in the sleep induced by prostaglandin D2 in rats.

Cited by 145 publications

References 22 publications

Arousal effect of orexin A depends on activation of the histaminergic system

Arousal effect of orexin A depends on activation of the histaminergic system

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A 1 receptors and promotes non-rapid eye movement sleep

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Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A ₁ receptors and promotes non-rapid eye movement sleep