Both A<sub>1</sub> and A<sub>2a</sub> Purine Receptors Regulate Striatal Acetylcholine Release

Brown, Susan J.; James, Stephen P.; Reddington, Martin; Richardson, Peter J.

doi:10.1111/j.1471-4159.1990.tb08817.x

Cited by 136 publications

(92 citation statements)

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“…13 -32 These observations have suggested that adenosine has a "universal" depressor effect in the CNS. However, our present results in the NTS (which are the first to demonstrate an increase in glutamate release by adenosine) and studies by others documenting an increase of dopamine 49 and acetylcholine 50 by purines, seriously challenge this concept and indicate that regional brain differences are present. In these last two reports, it was shown that activation of the adenosine receptor subtype A^ increases the release of striatal dopamine 49 or acetylcholine.…”

Section: -45contrasting

confidence: 47%

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

et al. 1991

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Adenosine is an inhibitory neuromodulator in several brain regions. In the nucleus tractus soUtarius (NTS), however, adenosine exerts excitatory cardiovascular effects. The purpose of the present study was to elucidate the involvement of other endogenous mechanisms that could contribute to the final hemodynamic response to adenosine in this nucleus. In normotensive Sprague-Dawley rats, intra-NTS microinjection of adenosine (23 nmol/60 nl) decreased blood pressure and heart rate. These effects were blocked by prior administration of the specific adenosine receptor antagonist l,3-dipropyl-8-p-sulfophenylxanthine (0.92 nmol) and by the two glutamate receptor antagonists kynurenic acid and glutamic diethylester. The specificity of the adenosine-glutamate interaction in the NTS was demonstrated with adrenergic and angiotensin receptor antagonists that did not affect the adenosine response and by experiments with glutamate receptor antagonists that did not affect nicotine actions in the NTS. Furthermore, an increase in glutamate levels was demonstrated during perfusion of adenosine through a microdiatysis probe in the NTS of anesthetized rabbits. These findings indicate that adenosine increases the release of glutamate in the NTS and, thus, are at variance with the concept of a "universal" inhibitory effect of adenosine in the central nervous system. (Hypertension 1991;18:494-502)

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Section: -45contrasting

confidence: 47%

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

et al. 1991

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“…Nonetheless, adenosine anaiogs inhibit central release of acetylcholine (8,17,36) and cholinergic agonists and antagonists have effects on locomotor activity (3,18,30,33). Therefore, both nicotinic and muscarinic agents were investigated in control and caffeinetreated mice.…”

Section: Discussionmentioning

confidence: 99%

Locomotor activity in mice during chronic treatment with caffeine and withdrawal

Nikodijevic

Jacobson

Daly

1993

Pharmacology Biochemistry and Behavior

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Chronic ingestion of caffeine by mice caused a marked reduction in locomotor exploratory activity. At least 4 days of withdrawal were required to restore activity to normal levels. Stimulatory effects of injected caffeine were lower in chronically treated mice and the biphasic dose-response (stimulatory followed by depressant) curve for injected caffeine was left shifted. Seven days of withdrawal were required before the dose-response curve to caffeine was identical to that of control mice. The depressant effects of a potent xanthine phosphodiesterase inhibitor, 1,3-dipropyl-7-methylxanthine, were blunted in caffeine-treated mice. The depressant effects of A 1 -and A 2 -selective adenosine analogs were enhanced after chronic caffeine. There was little or no effect of chronic caffeine on the stimulatory effects of dopaminergic agents (amphetamine, caffeine), while both depressant and stimulatory effects of chollnergic agents (nicotine, oxotremorine, scopolamine) were reduced. The results indicate that chronic caffeine affects functions of adenosine and chollnergic receptors related to regulation of locomotor exploratory activity. KeywordsCaffeine; Adenosine receptors; Cocaine; Amphetamine; Chollnergic receptors; Nicotine; Locomotor activity THE behavioral stimulant activity of caffeine is widely recognized, but the underlying mechanism of action remains poorly defined. At present, it is in general accepted that caffeine, at least in part, owes its behavioral stimulant activity to blockade of adenosine receptors (2). Caffeine and other stimulant xanthines block adenosine receptors and reverse the depressant effects of adenosine analogs (4,19,27,29,39,42). Adenosine analogs appear capable of eliciting behavioral depression through activation of either A 1 or A 2 adenosine receptors (37,38). Indeed, chronic ingestion of caffeine results in an upregulation in levels of adenosine receptors (7,16,20,21,35). Remarkably, caffeine and other xanthines are more potent in reversing the depressant effects of adenosine analogs in vivo than in causing behavioral stimulation of locomotor exploratory activity when administered alone (27). Further, caffeine can become a behavioral depressant at higher doses. It has been suggested that the behavioral depressant effects of caffeine and other xanthines are due to inhibition of a cyclic adenosine monophosphate (cAMP) phosphodiesterase (9). Finally, the well-known ability of caffeine to mobilize intracellular calcium [cf. (5,44) Chronic effects of caffeine, leading to tolerance, are well known in man and rodents (1,10,(22)(23)(24)32). The mechanism(s) underlying such tolerance, as well as the withdrawal syndrome, are not well understood. The increase of levels of adenosine receptors after chronic caffeine (7,16,20,21,35) suggests upregulation of adenosine receptor-mediated functions as a basis for caffeine tolerance. A number of points argue against such a simple explanation: First, in rats the tolerance to caffeine can appear insurmountable (16); second, there are no clear p...

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Section: Influence Of Sch 58261 On D 1 -And D 2 -Dependent Turning Bementioning

confidence: 99%

“…Moreover, the "synergistic" hypothesis can not explain the inhibitory effects exerted by certain doses of an A 2A receptor agonist on both D 1 -and D 2 -induced turning (Morelli et al 1994). Since adenosine A 2A receptors modulate acetylcholine (Brown et al 1990), GABA (Ferré et al 1993) and glutamate release (Popoli et al 1995), other indirect mechanisms may also account for the A 2A /D 1 interaction.As for the ability of SCH58261 to selectively potentiate D 2 -dependent rotations, this finding is in line with a previous study showing that CGS 21680, an adenosine A 2A receptor agonist, antagonized quinpirole-but not SKF 38393-induced turning in 6-OHDA-lesioned rats (Ferré et al 1999). Taken together, these results provide a behavioral support for the view that a specific antagonistic interaction exists between adenosine A 2 and dopamine D 2 receptors in the neostriatum (Ferré et al 1991b), an interaction which was found to be even increased in 6-OHDA-lesioned rats .…”

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Effects of SCH 58261, an Adenosine A2A Receptor Antagonist, on Quinpirole-Induced Turning in 6-Hydroxydopamine-Lesioned Rats Lack of Tolerance after Chronic Caffeine Intake

Popoli

Reggio

Pézzola

2000

Neuropsychopharmacology

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In unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rats, a rodent model of Parkinson's disease (PD), the adenosine A 2A receptor antagonist SCH 58261 significantly increased ( ϩ 180%, p Ͻ .01) the number of rotations induced by a low dose of quinpirole (a dopamine D 2 receptor agonist), while it did not significantly modify the effects of a comparably low dose of SKF 38393 (a dopamine D 1 receptor agonist). The dose-dependent potentiating effects of SCH 58261 on quinpirole-induced turning were similar in caffeine-treated rats (1 g/l in drinking water over 14 days) and control animals (tap water). The selective potentiating effects of SCH 58261 on D 2 -dependent turning confirm the existence of a potent and specific A 2A /D 2 receptor-receptor interaction. The persistence of the potentiating effects of SCH 58261 after chronic caffeine intake suggests that no tolerance should develop towards the antiparkinsonian effects of adenosineThe two major output pathways from the basal ganglia, the direct (striato-nigral) and the indirect (striato-pallidal) pathways, have opposing effects on thalamocortical neurones and subsequently on motor activity (Alexander and Crutcher 1990). A co-ordinated balance of the pathway functions results in normal movements, while predominance of the indirect or the direct pathways is thought to underlie hypo-and hyper-kinetic disorders, respectively (Albin et al. 1989). For instance, over-activity of the indirect pathway (due to the reduction of dopamine D 2 receptor-mediated inhibition of striato-pallidal neurones) is thought to determine the motor deficits of Parkinson's disease (PD) (Alexander and Crutcher 1990;Gerfen et al. 1990).In the striato-pallidal neurones, dopamine D 2 receptors are co-localized with adenosine A 2A receptors (Fink et al. 1992;Schiffmann et al. 1991;Svenningsson et al. 1997a), and a tonic, antagonistic A 2A ր D 2 interaction has been reported. The stimulation of A 2A receptors decreases the affinity of D 2 receptors for the agonist in rat striatal membranes (Ferré et al. 1991b) and in a mouse fibroblast cell line stably cotransfected with A 2A and D 2 receptors (Dasgupta et al. 1996) 29, 1999; revised October 11, 1999; accepted November 11, 1999. N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 22 , NO . 5 SCH 58261 Potentiates Quinpirole-Induced Turning in PD Rat Model 523 tentiate, the effects of D 2 receptor agonists on motor activity, neurotransmitter release and striatal c-Fos expression (Ferré et al. 1991a(Ferré et al. , 1993(Ferré et al. , 1999Jin et al. 1993;Morelli et al. 1995;Pollack and Fink 1995). While much data indicates that A 2A receptors selectively interact with dopamine D 2 receptors (reviewed in Ferré et al. 1997), adenosine A 2A receptor blockade has been reported to potentiate both D 1 -and D 2 -dependent contralateral rotations in 6-hydroxydopamine (6-OHDA)-lesioned rats (Fenu et al. 1997;Pinna et al. 1996) Due to the key role played by adenosine A 2A receptors in the regulation of striatal dopaminergic neurotransmission, drugs acting on these re...

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Both A₁ and A_2a Purine Receptors Regulate Striatal Acetylcholine Release

Cited by 136 publications

References 46 publications

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Locomotor activity in mice during chronic treatment with caffeine and withdrawal

Effects of SCH 58261, an Adenosine A2A Receptor Antagonist, on Quinpirole-Induced Turning in 6-Hydroxydopamine-Lesioned Rats Lack of Tolerance after Chronic Caffeine Intake

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Both A1 and A2a Purine Receptors Regulate Striatal Acetylcholine Release

Cited by 136 publications

References 46 publications

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Locomotor activity in mice during chronic treatment with caffeine and withdrawal

Effects of SCH 58261, an Adenosine A2A Receptor Antagonist, on Quinpirole-Induced Turning in 6-Hydroxydopamine-Lesioned Rats Lack of Tolerance after Chronic Caffeine Intake

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Both A₁ and A_2a Purine Receptors Regulate Striatal Acetylcholine Release