Adenosine A1 and A2 receptors modulate extracellular dopamine levels in rat striatum

Okada, Motohiro; Mizuno, Kazuhisa; Kaneko, Sunao

doi:10.1016/0304-3940(96)12780-4

Cited by 137 publications

(133 citation statements)

References 17 publications

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“…In mammals, the antagonistic effect of CAFF on adenosine receptors located on dopaminergic neurons leads to increased release (2,3,19). A similar mechanism might be operating in flies, based on the correlation that we have shown between CAFF responsiveness and functional dDA1 receptors in MBs as well as on the motor-activating effects of dopamine (21).…”

Section: Meth-induced Wakefulness Does Not Involve Modulation Of Dda1mentioning

confidence: 62%

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Drosophila D1 dopamine receptor mediates caffeine-induced arousal

Andretic

Kim

Jones

et al. 2008

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

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The arousing and motor-activating effects of psychostimulants are mediated by multiple systems. In Drosophila, dopaminergic transmission is involved in mediating the arousing effects of methamphetamine, although the neuronal mechanisms of caffeine (CAFF)-induced wakefulness remain unexplored. Here, we show that in Drosophila, as in mammals, the wake-promoting effect of CAFF involves both the adenosinergic and dopaminergic systems. By measuring behavioral responses in mutant and transgenic flies exposed to different drug-feeding regimens, we show that CAFFinduced wakefulness requires the Drosophila D1 dopamine receptor (dDA1) in the mushroom bodies. In WT flies, CAFF exposure leads to downregulation of dDA1 expression, whereas the transgenic overexpression of dDA1 leads to CAFF resistance. The wakepromoting effects of methamphetamine require a functional dopamine transporter as well as the dDA1, and they engage brain areas in addition to the mushroom bodies.ptimal behavioral performance in humans and animals depends on an adequate arousal level, which often involves diffuse afferent inputs from the dopaminergic system. Caffeine (CAFF) displays strong arousing properties and is the most consumed psychoactive drug in the world. CAFF competitively inhibits adenosine A1 and A2 receptors, antagonizing the effects of the sleep-promoting neuromodulator adenosine that accumulates during waking (1). CAFF also leads to increased dopaminergic and glutamatergic transmission in different striatal subcompartments, which has been linked to its activating and reinforcing effects (2-4).Although CAFF-induced wakefulness has been related to modulation of cholinergic and histaminergic arousal systems (5, 6), CAFF's induction of increased dopaminergic transmission and its effect on wakefulness have not been adequately examined. Animals with increased dopaminergic transmission, such as dopamine transporter (DAT) mutant mice, have decreased non-rapid eye movement sleep and increased sensitivity to the wake-promoting action of CAFF (7). Dopaminergic action on both the D1 and D2 receptors contributes to the alert waking state, based on the action of centrally administered D1 and D2 agonists in rodents (8). Molecularly, CAFF modulates D2 transcription in vitro and in vivo (9). Motor-activating effects of CAFF are diminished in D2R mutant mice (10, 11); however, the role of D2R in the arousing effect of CAFF remains unknown, and functional tests of the brain regions mediating these effects are lacking in mammals.We have shown previously that the wake-promoting effects of methamphetamine (METH) in Drosophila are mediated through dopaminergic transmission, indicating some evolutionary conservation in the behavioral and neurochemical effects of psychostimulants (12).Treatment of flies with CAFF induces wakefulness; however, the mechanism underlying this activity is currently unknown (13,14). In the present study, we investigate the role of dopamine signaling in the wake-inducing properties of CAFF and METH, with emphasis on the role of the Dr...

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Section: Meth-induced Wakefulness Does Not Involve Modulation Of Dda1mentioning

confidence: 62%

“…CAFF leads to increased dopaminergic transmission by antagonizing A1 receptors on presynaptic dopaminergic neurons (19). To determine if dDA1 mediates the arousing effects of CAFF, we measured sleep in the CAFF-exposed dDA1 mutant dumb 1 (20).…”

Section: Adenosinergic and Dopaminergic Systems Mediate Wake-promotingmentioning

confidence: 99%

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

Andretic

Kim

Jones

et al. 2008

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

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“…In the striatum, adenosine plays an important role as a modulator of both dopamine and glutamate neurotransmission. At a presynaptic level, adenosine, mostly by acting on adenosine A 1 receptors localized in nerve terminals, inhibits dopamine and glutamate release (Wood et al, 1989;Okada et al, 1996;Golembiowska and Zylewska, 1997;Flagmeyer et al, 1997). At a postsynaptic level, adenosine decreases dopaminergic neurotransmission by means of specific antagonistic interactions between adenosine and dopamine receptors, which modulate the function of the two types of striatal Figure 8 Effect of chronic treatment with caffeine on the motor activation induced by the acute administration of different doses of caffeine and the A 1 and A 2A receptor antagonists CPT and MSX-3 in habituated rats.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Adenosine A1 and A2A Receptors in the Motor Effects of Caffeine after its Acute and Chronic Administration

Karcz-Kubicha¹,

Αντωνίου²,

Terasmaa

et al. 2003

Neuropsychopharmacol

177

189

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The involvement of adenosine A 1 and A 2A receptors in the motor effects of caffeine is still a matter of debate. In the present study, counteraction of the motor-depressant effects of the selective A 1 receptor agonist CPA and the A 2A receptor agonist CGS 21680 by caffeine, the selective A 1 receptor antagonist CPT, and the A 2A receptor antagonist MSX-3 was compared. CPT and MSX-3 produced motor activation at the same doses that selectively counteracted motor depression induced by CPA and CGS 21680, respectively. Caffeine also counteracted motor depression induced by CPA and CGS 21680 at doses that produced motor activation. However, caffeine was less effective than CPT at counteracting CPA and even less effective than MSX-3 at counteracting CGS 21680. On the other hand, when administered alone in habituated animals, caffeine produced stronger motor activation than CPT or MSX-3. An additive effect on motor activation was obtained when CPT and MSX-3 were coadministered. Altogether, these results suggest that the motoractivating effects of acutely administered caffeine in rats involve the central blockade of both A 1 and A 2A receptors. Chronic exposure to caffeine in the drinking water (1.0 mg/ml) resulted in tolerance to the motor effects of an acute administration of caffeine, lack of tolerance to amphetamine, apparent tolerance to MSX-3 (shift to the left of its 'bell-shaped' dose-response curve), and true crosstolerance to CPT. The present results suggest that development of tolerance to the effects of A 1 receptor blockade might be mostly responsible for the tolerance to the motor-activating effects of caffeine and that the residual motor-activating effects of caffeine in tolerant individuals might be mostly because of A 2A receptor blockade.

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“…A 2A R inactivation may prevent behavioral sensitization by modulating presynaptic dopamine release (Zetterstrom and Fillenz 1990;Okada et al, 1996;Dassesse et al, 2001). Since there is no evidence of A 2A Rs expression on nigrostriatal neurons (Rosin et al, 2003), it has been suggested that A 2A R-mediated facilitation of dopamine release may arise indirectly, that is, through regulation of glutamate and GABA release (Sebastiao and Ribeiro, 1996;Wolf, 1998;Corsi et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

A Crucial Role for Forebrain Adenosine A2A Receptors in Amphetamine Sensitization

Bastia

Scibelli

et al. 2004

Neuropsychopharmacol

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Adenosine A 2A receptors (A 2A Rs) are well positioned to influence the maladaptive CNS responses to repeated dopaminergic stimulation in psychostimulant addiction. Expression of A 2A Rs in brain is largely restricted to the nucleus accumbens and striatum, where molecular adaptations mediate chronic effects of psychostimulants such as behavioral sensitization. Using a novel forebrain-specific conditional (Cre/loxP system) knockout of the A 2A R in coordination with classical pharmacological approaches, we investigated the involvement of brain A 2A Rs in amphetamine-induced behavioral sensitization. Tissue-specific, functional disruption of the receptor was confirmed by autoradiography, PCR, and the loss of A 2A antagonist-induced motor stimulation. Daily treatment with amphetamine for 1 week markedly enhanced locomotor responses on day 8 in control mice and the sensitization remained robust after a week of washout. Their conditional knockout littermates however showed no sensitization to amphetamine on day 8 and only a modest sensitization following the washout. Pharmacological blockade of adenosine A 2A Rs also was able to block the development (but not the expression) of sensitization in multiple mouse strains. Thus activation of brain A 2A Rs plays a critical role in developing augmented psychomotor responses to repeated psychostimulant exposure.

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Adenosine A1 and A2 receptors modulate extracellular dopamine levels in rat striatum

Cited by 137 publications

References 17 publications

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

Involvement of Adenosine A1 and A2A Receptors in the Motor Effects of Caffeine after its Acute and Chronic Administration

A Crucial Role for Forebrain Adenosine A2A Receptors in Amphetamine Sensitization

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