Inhibition of nigrostriatal release of dopamine in the rat by adenosine receptor agonists: A1 receptor mediation

Wood, Paul L.; Kim, Helen S.; Boyar, William C.; Hutchison, Alan J.

doi:10.1016/0028-3908(89)90062-2

Cited by 58 publications

(35 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Wood et al 1989;DawidMilner et al 1994). In a behavioural study by Griebel et al (1991), only slightly decreased locomotion and rearing responses, ataxia and lack of co-ordination were noted after high doses of DPCPX (6 mg/kg) in mice, and no electroencephalographic (EEG) or sleep pattern modulation was noted after the i.p.…”

Section: Discussionmentioning

confidence: 93%

Alkylxanthine adenosine antagonists and epileptiform activity in rat hippocampal slices in vitro

Chesi

Stone

1997

Exp Brain Res

View full text Add to dashboard Cite

Despite its potent proconvulsant effects in vitro, the adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) does not induce seizures when administered in vivo. This contrasts with the effects of less selective adenosine antagonists such as theophylline or cyclopentlytheophylline, and led us to reexamine the nature of DPCPX-induced epileptiform activity. In the present study, we report that proconvulsant effects of bath-applied DPCPX in rat hippocampal slices are only observed after a preceding stimulus such as NMDA receptor activation or brief tetanic stimulation. While this may be due to the absence of a basal "purinergic tone", the relatively high interstitial concentrations of adenosine present in the slice suggest that access of the drug to A1 receptors may instead be prevented by tightly coupled endogenous adenosine, with the ternary adenosine-A1 receptor-G protein complex stabilised in the high-affinity conformation by a coupling cofactor. This implies that a substantial percentage of adenosine A1 receptors are inactive under physiological conditions, but that access of adenosine A1 receptor antagonists may be facilitated under pathological conditions. Once induced, DPCPX-evoked spiking persists for long periods of time. A "kindling" effect of A1 receptor blockade is unlikely, since persistent spiking is not usually observed with less selective A1 antagonists even after prolonged application. Alternatively, endogenous adenosine released during increased neuronal activity may activate A2 receptors during selective A1 blockade. The most important factor determining the duration of DPCPX-induced spiking, however, may be a persistence of the drug in the tissue and subsequent access to the A1 receptor via a membrane-delineated pathway, since DPCPX-induced spiking could be shown to decrease markedly after a transient superfusion of theophylline. This hypothesis, which implies that the apparent affinity of adenosine antagonists for the A1 receptor is in part a function of their membrane partitioning coefficient, is supported by a close correlation between alkylxanthine logP values obtained from the literature and their Ki value at A1 receptors, but not at the enzyme phosphodiesterase, whose xanthine binding site is presented to the cytosol. The implications for the therapeutic value of purinergic drugs are discussed.

show abstract

Section: Discussionmentioning

confidence: 93%

Alkylxanthine adenosine antagonists and epileptiform activity in rat hippocampal slices in vitro

Chesi

Stone

1997

Exp Brain Res

View full text Add to dashboard Cite

show abstract

“…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

179

189

View full text Add to dashboard Cite

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.

show abstract

“…Higher doses of caffeine inhibit phosphodiesterase, block the receptors for γ-aminobutyric acid type A (GABA A ), and cause the release of intracellular Ca 2+ [40]. Caffeine is characterized by a stimulating influence on the cerebral cortex which is related to the release of various neurotransmitters in central nervous system [14,22,26,29,45,59,69]. Effects of caffeine activity are a common issue to investigate in the scientific world.…”

Section: Introductionmentioning

confidence: 99%

The influence of caffeine on the activity of moclobemide, venlafaxine, bupropion and milnacipran in the forced swim test in mice

et al. 2015

View full text Add to dashboard Cite

Inhibition of nigrostriatal release of dopamine in the rat by adenosine receptor agonists: A1 receptor mediation

Cited by 58 publications

References 26 publications

Alkylxanthine adenosine antagonists and epileptiform activity in rat hippocampal slices in vitro

Alkylxanthine adenosine antagonists and epileptiform activity in rat hippocampal slices in vitro

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

The influence of caffeine on the activity of moclobemide, venlafaxine, bupropion and milnacipran in the forced swim test in mice

Contact Info

Product

Resources

About