An adenosine A2a agonist increases sleep and induces Fos in ventrolateral preoptic neurons

@article{Scammell2001AnAA,
  title={An adenosine A2a agonist increases sleep and induces Fos in ventrolateral preoptic neurons},
  author={Thomas E. Scammell and Dmitry Gerashchenko and Takatoshi Mochizuki and Marie T. McCarthy and Ivy V. Estabrooke and Christina A. Sears and C. B. Saper and Y. Urade and Osamu Hayaishi},
  journal={Neuroscience},
  year={2001},
  volume={107},
  pages={653-663}
}

Adenosine A(2A) receptors regulate the activity of sleep regulatory GABAergic neurons in the preoptic hypothalamus.

Findings support a hypothesis that A2AR-mediated activation of MnPN and VLPO GABAergic neurons contributes to adenosinergic regulation of sleep.

Effects on sleep of microdialysis of adenosine A1 and A2a receptor analogs into the lateral preoptic area of rats.

Observations support a hypothesis that AD mediated effects on sleep-wake cycles are site and receptor dependent, and confirm that NBTI administration in the wake promoting area of the BF increased sleep.

Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A1 receptors and promotes non-rapid eye movement sleep

Ex vivo microdialysis results indicate that endogenous adenosine in the TMN suppresses the histaminergic system via A1R to promote NREM sleep, which was completely abolished by coadministration of 1,3-dimethyl-8-cyclopenthylxanthine, a selective A 1R antagonist.

An adenosine A2A receptor agonist induces sleep by increasing GABA release in the tuberomammillary nucleus to inhibit histaminergic systems in rats

Electroencephalogram and electromyogram recordings coupled with in vivo microdialysis suggest that the A2AR agonist induced sleep by inhibiting the histaminergic system through increasing GABA release in the tuberomammillary nucleus.

Prostaglandins and adenosine in the regulation of sleep and wakefulness.

Minireview: Sleep regulation in adenosine A2A receptor-deficient mice

A2AR is found to be important in sleep regulation by using several A1R and A2AR agonists, including N6-cyclopentyladenosine (CPA) and 2-(4-(2-carboxyethyl)phenylethylamino)- adenosine-5′- N -ethylcarboxamideadenosines (CGS 21680).

Prostaglandin D2 and adenosine as endogenous somnogens

Prostaglandin D2–adenosine system is crucial for the maintenance of physiological sleep, and administration of an inhibitor of lipocalin-type PGD synthase (SeCl4), an antagonist of DP1 receptors (ONO-4127Na) or an antagonists of adenosine A2A receptors (caffeine) results in sleep inhibition in rats and mice.
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PGD2 increased nonrapid eye movement sleep and induced striking expression of Fos in the ventrolateral preoptic area (VLPO), a cluster of neurons that may promote sleep by inhibiting the tuberomammillary nucleus, the source of the ascending histaminergic arousal system.

Afferents to the Ventrolateral Preoptic Nucleus

Robust pathways examined in afferents to the ventrolateral preoptic nucleus (VLPO) suggest candidate mechanisms by which sleep may be influenced by brain systems regulating arousal, autonomic, limbic, and circadian functions.

Adenosinergic modulation of rat basal forebrain neurons during sleep and waking: neuronal recording with microdialysis

It is suggested that in naturally awake and sleeping animals, adenosine exerts tonic inhibitory influences on BF neurons, supporting the hypothesized role ofAdenosine in sleep regulation.

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The data indicate that potent and selective adenosine agonists have little or no effect on sleep states in the rat, while usingAdenosine antagonists it seems that A2A receptors are primarily involved in the modulation of wakefulness.

Hypothalamic Arousal Regions Are Activated during Modafinil-Induced Wakefulness

Modafinil may promote waking via activation of TMN and orexin neurons, two regions implicated in the promotion of normal wakefulness, and Selective pharmacological activation of these hypothalamic regions may represent a novel approach to inducing wakefulness.

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It is proposed that the reciprocal inhibitory interaction of such VLPO neurons with the noradrenergic, serotoninergic and cholinergic waking systems to which they project is a key factor for promoting sleep.