Involvement of adenosine A2A receptor in sleep promotion

Satoh, Shinsuke; Matsumura, Hitoshi; Hayaishi, Osamu

doi:10.1016/s0014-2999(98)00302-1

Cited by 97 publications

(59 citation statements)

References 28 publications

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“…Several studies have reported that sleep can be induced by systemic administration of CGS 21680 or local injections of this drug into the basal forebrain (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Knockout of adenosine A 2A receptors in mice resulted in a loss of sensitivity to the sedative effects of adenosine A 2A agonists, and in these studies, it also was shown that an adenosine A 2A agonist could induce sleep in wild-type mice (Satoh et al 1998). Thus, it is possible that systemic administration of CGS 21680 decreased lever pressing but failed to increase feeding because of a drug-induced sedation effect (i.e., induction of drowsiness, which produced a non-selective suppression of several behaviors), which is consistent with the behavioral observations of rats treated with systemic CGS 21680 (see above).…”

Section: Discussionmentioning

confidence: 94%

“…One of the likely explanations is that systemic administration of an adenosine A 2A agonist such as CGS 21680 produces sedation (i.e., drowsiness). The sedative effects of adenosine have been well characterized (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Systemic or intraventricular injections of adenosine, as well as local infusions into the basal forebrain, have been shown to induce sleep (Stenberg 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Evidence indicates that both adenosine A 1 and A 2A receptors are involved in the regulation of sleep, though probably through different mechanisms and distinct brain areas (Stenberg 2007). Several studies have reported that sleep can be induced by systemic administration of CGS 21680 or local injections of this drug into the basal forebrain (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Knockout of adenosine A 2A receptors in mice resulted in a loss of sensitivity to the sedative effects of adenosine A 2A agonists, and in these studies, it also was shown that an adenosine A 2A agonist could induce sleep in wild-type mice (Satoh et al 1998).…”

Section: Discussionmentioning

confidence: 99%

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Intra-accumbens injections of the adenosine A2A agonist CGS 21680 affect effort-related choice behavior in rats

et al. 2008

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Rationale-Nucleus accumbens dopamine (DA) participates in the modulation of instrumental behavior, including aspects of behavioral activation and effort-related choice behavior. Rats with impaired accumbens DA transmission reallocate their behavior away from food-reinforced activities that have high response requirements and instead select less-effortful types of food-seeking behavior. Although accumbens DA is considered a critical component of the brain circuitry regulating effortrelated processes, emerging evidence also implicates adenosine A 2A receptors.Objective-The present work was undertaken to test the hypothesis that accumbens A 2A receptor stimulation would produce effects similar to those produced by DA depletion or antagonism.Materials and methods-Three experiments assessed the effects of the adenosine A 2A agonist CGS 21680 on performance of a concurrent choice task (lever pressing for preferred food vs. intake of less preferred chow) that is known to be sensitive to DA antagonists and accumbens DA depletions.Results-Systemic injections of CGS 21680 reduced lever pressing but did not increase feeding. In contrast, bilateral infusions of the adenosine A 2A receptor agonist CGS 21680 (6.0-24.0 ng) into the nucleus accumbens decreased lever pressing for the preferred food but substantially increased consumption of the less preferred chow. Injections of CGS 21680 into a control site dorsal to the accumbens were ineffective.Conclusions-Taken together, these results are consistent with the hypothesis that local stimulation of adenosine A 2A receptors in nucleus accumbens produces behavioral effects similar to those induced by accumbens DA depletions. Accumbens adenosine A 2A receptors appear to be a component of the brain circuitry regulating effort-related choice behavior.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Intra-accumbens injections of the adenosine A2A agonist CGS 21680 affect effort-related choice behavior in rats

et al. 2008

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“…PGD 2 -induced sleep is inhibited by pretreatment of rats with the A 2A receptor antagonist, KF17837 (Satoh et al, 1996). A 2A receptor agonists, such as CGS 21680 and APEC, induce non-rapid eye movement (NREM) sleep when infused into the PGD 2 -sensitive zone of the basal forebrain of rats during the night (Satoh et al, 1998). On the other hand, A 1 receptor agonists, such as CPA, are ineffective.…”

Section: Adenosine a 1 And A 2a Receptors In Sleep Regulationmentioning

confidence: 99%

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

Ferré

Diamond

Goldberg

et al. 2007

Progress in Neurobiology

126

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Adenosine A 2A receptors localized in the dorsal striatum are considered as a new target for the development of antiparkinsonian drugs. Co-administration of A 2A receptor antagonists has shown a significant improvement of the effects of L-DOPA. The present review emphasizes the possible application of A 2A receptor antagonists in pathological conditions other than parkinsonism, including drug addiction, sleep disorders and pain. In addition to the dorsal striatum, the ventral striatum (nucleus accumbens) contains a high density of A 2A receptors, which presynaptically and postsynaptically regulate glutamatergic transmission in the cortical glutamatergic projections to the nucleus accumbens. It is currently believed that molecular adaptations of the cortico-accumbens glutamatergic synapses are involved in compulsive drug seeking and relapse. Here we review recent experimental evidence suggesting that A 2A antagonists could become new therapeutic agents for drug addiction. Morphological and functional studies have identified lower levels of A 2A receptors in brain areas other than the striatum, such as the ventrolateral preoptic area of the hypothalamus, where adenosine plays an important role in sleep regulation. Although initially believed to be mostly dependent on A 1 receptors, here we review recent studies that demonstrate that the somnogenic effects of adenosine are largely mediated by hypothalamic A 2A receptors. A 2A receptor antagonists could therefore be considered as a possible treatment for narcolepsy and other sleep-related disorders. Finally, nociception is another adenosine-regulated neural function previously thought to mostly involve A 1 receptors. Although there is some conflicting literature on the effects of agonists and antagonists, which may partly be due to the lack of selectivity of available drugs, the studies in A 2A receptor knockout mice suggest that A 2A receptor antagonists might have some therapeutic potential in pain states, in particular where high intensity stimuli are prevalent.

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“…For example, it was recently demonstrated that the adenosine A 2A antagonist MSX-3 could reverse the effect of haloperidol on a concurrent lever pressing/feeding task that measures aspects of motivation related to response allocation and effort-related choice behavior . Further studies have implicated adenosine A 2A receptors in cognitive function (Takahashi et al, 2008) and sleep (Hong et al, 2005;Porkka-Heiskanen et al, 2000;Satoh et al, 1998;Scammell et al, 2001;Stenberg, 2007).…”

Section: Introductionmentioning

confidence: 99%

Systemic administration of the adenosine A2A agonist CGS 21680 induces sedation at doses that suppress lever pressing and food intake

Mingote

Pereira

Farrar

et al. 2008

Pharmacology Biochemistry and Behavior

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Adenosine A 2A receptors are involved in the regulation of several behavioral functions. Adenosine A 2A antagonists exert antiparkinsonian effects in animal models, and adenosine A 2A agonists suppress locomotion and impair various aspects of motor control. The present experiments were conducted to study the effects of low doses of the adenosine A 2A agonist CGS 21680 on lever pressing, specific parameters of food intake, and sedation. In the first experiment, the effects of CGS 21680 on fixed ratio 5 lever pressing were assessed. In the second experiment, rats were tested in 30 min feeding sessions, and also were observed for drug-induced sedation using a sedation rating scale. CGS 21680 (0.025, 0.05, 0.1 mg/kg IP) produced a dose related suppression of lever pressing, and also reduced the amount of food consumed. The feeding effect was largely dependent upon a slowing of the rate of feeding, and there was only a modest suppression of time spent feeding. Doses of CGS 21680 that suppressed lever pressing and feeding also were associated with sedation/drowsiness. In conjunction with other studies, the present results suggest that sedative effects may play an important role in some of the behavioral effects produced by systemic administration of adenosine A 2A agonists.

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Involvement of adenosine A2A receptor in sleep promotion

Cited by 97 publications

References 28 publications

Intra-accumbens injections of the adenosine A2A agonist CGS 21680 affect effort-related choice behavior in rats

Intra-accumbens injections of the adenosine A2A agonist CGS 21680 affect effort-related choice behavior in rats

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

Systemic administration of the adenosine A2A agonist CGS 21680 induces sedation at doses that suppress lever pressing and food intake

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