Postsynaptic dopamine/adenosine interaction: II. Postsynaptic dopamine agonism and adenosine antagonism of methylxanthines in short-term reserpinized mice

Ferré, Sergi; Herrera‐Marschitz, Mario; Grabowska-Andén, Maria; Casas, Miquel; Ungerstedt, Urban; Andén, Nils‐Erik

doi:10.1016/0014-2999(91)90065-x

Cited by 98 publications

(39 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These down-to upstate transitions require channels that can be regulated by striatal transmitters acting through GPCRs, such as the interacting A 2A and D 2 receptors in the GABAergic enkephalinergic neurons. In a re- These effects on neurotransmitter release and neuronal excitability are paralleled by effects on motor activity and other behavioral responses, where selective A 2A receptor agonists or antagonists respectively counteract or potentiate the motor activation induced by dopamine D 2 receptor agonists [38][39][40][41][42]. Consequently, we predicted 15 years ago that A 2A receptor antagonists could be useful in Parkinson's disease, especially potentiating the effects of L-dopa or D 2 receptor agonists [43].…”

Section: The Antagonistic a 2a -D 2 Intramembrane Recep-tor Interactionmentioning

confidence: 99%

An Update on Adenosine A2A-Dopamine D2 Receptor Interactions: Implications for the Function of G Protein-Coupled Receptors

Ferré¹,

Quiroz²,

Woods³

et al. 2008

CPD

227

185

View full text Add to dashboard Cite

Adenosine A2A-dopamine D2 receptor interactions play a very important role in striatal function. A2A-D2 receptor interactions provide an example of the capabilities of information processing by just two different G protein-coupled receptors. Thus, there is evidence for the coexistence of two reciprocal antagonistic interactions between A2A and D2 receptors in the same neurons, the GABAergic enkephalinergic neurons. An antagonistic A2A-D2 intramembrane receptor interaction, which depends on A2A-D2 receptor heteromerization and Gq/11-PLC signaling, modulates neuronal excitability and neurotransmitter release. On the other hand, an antagonistic A2A-D2 receptor interaction at the adenylyl-cyclase level, which depends on Gs/olf-and Gi/o-type V adenylyl-cyclase signaling, modulates protein phosphorylation and gene expression. Finally, under conditions of upregulation of an activator of G protein signaling (AGS3), such as during chronic treatment with addictive drugs, a synergistic A2A-D2 receptor interaction can also be demonstrated. AGS3 facilitates a synergistic interaction between Gs/olf -and Gi/o-coupled receptors on the activation of types II/IV adenylyl cyclase, leading to a paradoxical increase in protein phosphorylation and gene expression upon co-activation of A2A and D2 receptors. The analysis of A2-D2 receptor interactions will have implications for the pathophysiology and treatment of basal ganglia disorders and drug addiction.Key Words: Adenosine A 2A Receptor, Dopamine D 2 Receptor, G Protein-Coupled Receptors, Receptor Heteromers, Striatum, Basal Ganglia Disorders, Drug Addiction. LOCALIZATION OF THE A 2A -D 2 RECEPTOR HETERO-MERApplying a broad definition of "neurotransmitter" [1], adenosine can be considered as an important neurotransmitter in the CNS, which acts through different subtypes of G protein-coupled receptors (GPCRs). From the four cloned adenosine receptors (adenosine A 1 , A 2A , A 2B and A 3 receptors ) , A 1 and A 2A receptors are the main targets for the physiological effects of adenosine in the brain [2]. A 1 receptor is widely distributed in the brain, including the striatum, while A 2A receptor is mostly concentrated in the striatum [2,3]. It is becoming increasingly obvious that the modulatory role of adenosine in the striatum is related to the ability of A 1 and A 2A receptors to heteromerize with themselves and with other GPCRs, such as dopamine, glutamate, cannabinoid and ATP receptors [4][5][6][7][8][9][10][11][12][13][14]. The present review focuses on the role of one particular adenosine receptor heteromer, the one constituted by the A 2A and the dopamine D 2 receptor, which is already having important implications for the treatment of neuropathologies involving the striatum (see below).Striatal medium spiny neurons are GABAergic efferent neurons which constitute more that 95% of the striatal neuronal population. They receive two main afferents, cortical-limbic-thalamic glutamatergic inputs and dopaminergic mesencephalic inputs, from the substantia nigra pars compac...

show abstract

Section: The Antagonistic a 2a -D 2 Intramembrane Recep-tor Interactionmentioning

confidence: 99%

An Update on Adenosine A2A-Dopamine D2 Receptor Interactions: Implications for the Function of G Protein-Coupled Receptors

Ferré¹,

Quiroz²,

Woods³

et al. 2008

CPD

227

185

View full text Add to dashboard Cite

show abstract

“…Indeed, the formation of heterodimers between these two receptors has been demonstrated (Canals et al, 2003). Adenosine A 2A receptor activation has been shown to modulate negatively the postsynaptic effects of dopamine at the biochemical, cellular, functional, and behavioral levels (Ferre et al, 1993(Ferre et al, , 1991a. Behaviorally, adenosine A 2A agonists produce dopamine D 2 -like antagonist effects and vice versa (Ferre et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

A Differential Role for the Adenosine A2A Receptor in Opiate Reinforcement vs Opiate-Seeking Behavior

Brown

Short²,

Cowen

et al. 2008

Neuropsychopharmacol

View full text Add to dashboard Cite

The adenosine A 2A receptor is specifically enriched in the medium spiny neurons that make up the 'indirect' output pathway from the ventral striatum, a structure known to have a crucial, integrative role in processes such as reward, motivation, and drug-seeking behavior. In the present study we investigated the impact of adenosine A 2A receptor deletion on behavioral responses to morphine in a number of reward-related paradigms. The acute, rewarding effects of morphine were evaluated using the conditioned place preference paradigm. Operant self-administration of morphine on both fixed and progressive ratio schedules as well as cue-induced drug-seeking was assessed. In addition, the acute locomotor response to morphine as well as sensitization to morphine was evaluated. Decreased morphine selfadministration and breakpoint in A 2A knockout mice was observed. These data support a decrease in motivation to consume the drug, perhaps reflecting diminished rewarding effects of morphine in A 2A knockout mice. In support of this finding, a place preference to morphine was not observed in A 2A knockout mice but was present in wild-type mice. In contrast, robust cue-induced morphine-seeking behavior was exhibited by both A 2A knockout and wild-type mice after a period of withdrawal. The acute locomotor response to morphine in the A 2A knockout was similar to wild-type mice, yet A 2A knockout mice did not display tolerance to chronic morphine under the present paradigm. Both genotypes display locomotor sensitization to morphine, implying a lack of a role for the A 2A receptor in the drug-induced plasticity necessary for the development or expression of sensitization. Collectively, these data suggest a differential role for adenosine A 2A receptors in opiate reinforcement compared to opiate-seeking.

show abstract

“…The basis for this reciprocal influence are attributed to the negative interaction between dopamine D 1 and D 2 receptors and adenosine A 1 and A 2A receptors that are blocked by caffeine (Ferré et al, 1997;Fredholm et al, 1999). Caffeine and theophylline acutely potentiate the motor-activating effects induced by dopamine receptor agonists (Ferré et al, 1991;Fredholm et al, 1983;Garrett and Griffiths, 1997;Kuribara, 1994;Misra et al, 1986) and reverse catalepsy induced by dopamine receptor antagonists (Hauber et al, 2001;Malec, 1997;Mandhane et al, 1997), whereas sensitization or upregulation of dopamine receptors sensitize rats to the motor-activating effect induced by caffeine or theophylline (Fenu et al, 2000;Fenu and Morelli, 1998;Ferré et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Subchronic Caffeine Exposure Induces Sensitization to Caffeine and Cross-Sensitization to Amphetamine Ipsilateral Turning Behavior Independent from Dopamine Release

Cauli

Pinna

Valentini

et al. 2003

Neuropsychopharmacol

View full text Add to dashboard Cite

We have recently shown that repeated exposure to caffeine sensitizes rats to the motor activating effects of dopamine D 1 and D 2 receptor agonists. In order to study the role of dopamine in this effect, sensitization to caffeine and cross-sensitization between caffeine and amphetamine was evaluated by studying turning behavior and in vivo striatal dopamine release in unilaterally 6-hydroxydopaminelesioned rats. Administration of caffeine (15 mg/kg) for 2 weeks, on alternate days, induced a significant increase in ipsilateral turning behavior during the course of treatment, indicating that sensitization to caffeine took place in the intact striatum. Caffeine modestly increased dopamine release in the intact dorsa-lateral striatum and no significant difference between the first (+38%) and the last (+51%) injection was observed. Amphetamine (2 mg/kg) induced a significantly higher ipsilateral turning behavior in caffeine-sensitized rats than in vehicle-pretreated rats, however, a similar increase in dopamine release (+900 and +800%) was observed in the two groups. The results are the first demonstration that caffeine pre-exposure sensitizes the motor-stimulant effects of caffeine itself and of amphetamine. Sensitized ipsilateral turning after caffeine and amphetamine are not correlated to modification in striatal dopamine release, rather, postsynaptic modifications in dopamine and adenosine receptor interaction might be involved in the sensitization phenomena observed.

show abstract

Postsynaptic dopamine/adenosine interaction: II. Postsynaptic dopamine agonism and adenosine antagonism of methylxanthines in short-term reserpinized mice

Cited by 98 publications

References 24 publications

An Update on Adenosine A2A-Dopamine D2 Receptor Interactions: Implications for the Function of G Protein-Coupled Receptors

An Update on Adenosine A2A-Dopamine D2 Receptor Interactions: Implications for the Function of G Protein-Coupled Receptors

A Differential Role for the Adenosine A2A Receptor in Opiate Reinforcement vs Opiate-Seeking Behavior

Subchronic Caffeine Exposure Induces Sensitization to Caffeine and Cross-Sensitization to Amphetamine Ipsilateral Turning Behavior Independent from Dopamine Release

Contact Info

Product

Resources

About