Effect of Adenosine Receptor Agonists and Antagonists on the Expression of Opiate Withdrawal in Rats

Salem, Abdallah; Hope, Wendy

doi:10.1016/s0091-3057(96)00393-0

Cited by 52 publications

(33 citation statements)

References 46 publications

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“…Thus, adenosine agonists inhibit the expression of morphine withdrawal, while adenosine antagonists increase the incidence of withdrawal signs (Kaplan and Sears, 1996;Salem and Hope, 1997). In agreement, mice lacking A 2A adenosine receptors showed an increased morphine withdrawal in comparison with wild-type mice (Berrendero et al, 2003).…”

Section: Introductionmentioning

confidence: 57%

The Lack of A2A Adenosine Receptors Diminishes the Reinforcing Efficacy of Cocaine

Sòria

Castañé

Ledent

et al. 2005

Neuropsychopharmacol

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Adenosine is an endogenous purine nucleoside, which acts as a neuromodulator in the central nervous system. A 2A adenosine and D 2 dopamine receptors are colocalized in the same neurons in discrete brain areas, and the dopaminergic transmission plays a crucial role in the addictive properties of drugs of abuse, such as cocaine. In the present study, we have investigated the specific role of A 2A adenosine receptors in cocaine-induced behavioral responses related to its addictive properties. For this purpose, we have evaluated the acute locomotor effects produced by cocaine and the development of locomotor sensitization by repeated cocaine administration. In addition, we have also examined cocaine acute rewarding properties using the conditioned place preference. Finally, we used the intravenous drug self-administration paradigm to investigate the acquisition of an operant response maintained by cocaine self-administration and the reinforcing efficacy of the drug in these knockout animals. Acute cocaine induced a similar increase of locomotor activity in mice lacking A 2A adenosine receptors and wild-type littermates. Cocaine-induced locomotor sensitization and conditioned place preference were also maintained in A 2A knockout mice. Nevertheless, these knockout mice showed a lower rate of cocaine self-administration than wildtype mice in both fixed ratio 1 and 3 schedules of reinforcement. Moreover, a reduction in the maximal effort to obtain a cocaine infusion was found in A 2A knockout mice under a progressive ratio schedule. In addition, a vertical shift of the cocaine dose-response curve was observed in mice lacking A 2A adenosine receptors in comparison with wild-type littermates. Our study demonstrates that A 2A adenosine receptors play an important role in cocaine addictive properties, and these receptors seem to be required to develop the addictive effects of this drug. Neuropsychopharmacology (2006) 31, 978-987.

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Section: Introductionmentioning

confidence: 57%

The Lack of A2A Adenosine Receptors Diminishes the Reinforcing Efficacy of Cocaine

Sòria

Castañé

Ledent

et al. 2005

Neuropsychopharmacol

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“…In support of this notion, substantial evidence shows that NMDA receptor antagonists and GABA B receptor agonists prevent the development of opioid dependence and suppress opioid withdrawal signs [49,50]. Meanwhile, accumulating evidence demonstrates that increase of extracellular adenosine levels by adenosine kinase inhibitor and activation of both A 1 and A 2A receptors by their selective agonists attenuate the incidence of some of the morphine withdrawal signs, such as jumping, wetdog shakes and diarrhoea, whereas antagonists exacerbate the symptoms [40,54].…”

Section: Discussionmentioning

confidence: 98%

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

Chen

Lü

Gong³

et al. 2007

Cell Res

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Cell Research (2007) 17:689-700. © 2007 IBCB, SIBS, CAS All rights reserved 1001-0602/07 $ 30.00 www.nature.com/cr npg Dependence and impairment of learning and memory are two well-established features caused by abused drugs such as opioids. The hippocampus is an important region associated with both drug dependence and learning and memory. However, the molecular events in hippocampus following exposure to abused drugs such as opioids are not well understood. Here we examined the effect of chronic morphine treatment on hippocampal protein expression by proteomic analyses. We found that chronic exposure of mice to morphine for 10 days produced robust morphine withdrawal jumping and memory impairment, and also resulted in a significant downregulation of hippocampal protein levels of three metabolic enzymes, including Fe-S protein 1 of NADH dehydrogenase, dihydrolipoamide acetyltransferase or E2 component of the pyruvate dehydrogenase complex and lactate dehydrogenase 2. Further real-time quantitative PCR analyses confirmed that the levels of the corresponding mRNAs were also remarkably reduced. Consistent with these findings, lower ATP levels and an impaired ability to convert glucose into ATP were also observed in the hippocampus of chronically treated mice. Opioid antagonist naltrexone administrated concomitantly with morphine significantly suppressed morphine withdrawal jumping and reversed the downregulation of these proteins. Acute exposure to morphine also produced robust morphine withdrawal jumping and significant memory impairment, but failed to decrease the expression of these three proteins. Intrahippocampal injection of d-glucose before morphine administration significantly enhanced ATP levels and suppressed morphine withdrawal jumping and memory impairment in acute morphine-treated but not in chronic morphine-treated mice. Intraperitoneal injection of high dose of d-glucose shows a similar effect on morphine-induced withdrawal jumping as the central treatment. Taken together, our results suggest that reduced expression of the three metabolic enzymes in the hippocampus as a result of chronic morphine treatment contributes to the development of drug-induced symptoms such as morphine withdrawal jumping and memory impairment.

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“…For example, most studies agree that adenosine A 1 and A 2A receptor agonists attenuate while adenosine receptor antagonists exacerbate morphine-induced withdrawal signs (such as 'wet-dog' shakes, diarrhoea, teeth chattering, jumping, and writhing) of mice (Kaplan and Sears, 1996;Zarrindast et al, 1999) and rats (Salem and Hope, 1997). In view of these considerations, it seems clear that the endogenous adenosine is released during withdrawal from different drugs and acts at its receptors to produce an ongoing inhibitory 'tone' (reducing the specific withdrawal signs associated with each drug) which, when blocked, results in the enhancement of withdrawal behavior.…”

Section: Discussionmentioning

confidence: 99%

Activation of Adenosine A1 Receptors Reduces Anxiety-Like Behavior During Acute Ethanol Withdrawal (Hangover) in Mice

Prediger

Silva

Batista

et al. 2006

Neuropsychopharmacol

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Elevated signs of anxiety are observed in both humans and rodents during withdrawal from chronic as well as acute ethanol exposure, and it represents an important motivational factor for ethanol relapse. Several reports have suggested the involvement of brain adenosine receptors in different actions produced by ethanol such as motor incoordination and hypnotic effects. In addition, we have recently demonstrated that adenosine A 1 receptors modulate the anxiolytic-like effect induced by ethanol in mice. In the present study, we evaluated the potential of adenosine A 1 and A 2A receptor agonists in reducing the anxiety-like behavior during acute ethanol withdrawal (hangover) in mice. Animals received a single intraperitoneal administration of saline or ethanol (4 g/kg) and were tested in the elevated plus maze after an interval of 0.5-24 h. The results indicated that hangover-induced anxiety was most pronounced between 12 and 18 h after ethanol administration, as indicated by a significant reduction in the exploration of the open arms of the maze. At this time interval, ethanol was completely cleared. The acute administration of 'nonanxiolytic' doses of adenosine and the selective adenosine A 1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA), but not the adenosine A 2A receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)ethyl]adenosine (DPMA), at the onset of peak withdrawal (18 h), reduced this anxiogenic-like response. In addition, the effect of CCPA on the anxiety-like behavior of ethanol hangover was reversed by pretreatment with the selective adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). These results reinforce the notion of the involvement of adenosine receptors in the anxiety-like responses and indicate the potential of adenosine A 1 receptor agonists to reduce the anxiogenic effects during ethanol withdrawal.

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Effect of Adenosine Receptor Agonists and Antagonists on the Expression of Opiate Withdrawal in Rats

Cited by 52 publications

References 46 publications

The Lack of A2A Adenosine Receptors Diminishes the Reinforcing Efficacy of Cocaine

The Lack of A2A Adenosine Receptors Diminishes the Reinforcing Efficacy of Cocaine

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

Activation of Adenosine A1 Receptors Reduces Anxiety-Like Behavior During Acute Ethanol Withdrawal (Hangover) in Mice

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