Dopamine D<sub>1</sub> Receptor‐mediated Facilitation of GABAergic Neurotransmission in the Rat Strioentopeduncular Pathway and its Modulation by Adenosine A<sub>1</sub> Receptor‐mediated Mechanisms

Ferré, Sergi; O’Connor, W.T.; Svenningsson, Per; Björklund, Lars; Lindberg, Jakob; Tinner, B.; Strömberg, Ingrid; Goldstein, Menek; Ögren, Sven Ove; Ungerstedt, Urban; Fredholm, Bertil B.; Fuxé, Kjell

doi:10.1111/j.1460-9568.1996.tb01617.x

Cited by 136 publications

(74 citation statements)

References 40 publications

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“…These changes in paired-pulse ratio indicate a presynaptic locus for the A 1 receptors regulating glutamatergic synaptic transmission in the NAcc. Although A 1 receptor mRNA has been located in a minority of striatal neurons (Ferré et al, 1996), postsynaptic A 1 receptors play no obvious role in the effects of adenosine, NMDA, and dopamine described here. Thus glutamate release is likely to be inhibited presynaptically not by D 1 receptors, but by A 1 receptors, which are activated indirectly by dopamine.…”

Section: Discussionmentioning

confidence: 57%

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

1997

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The mechanism underlying dopamine D 1 receptor-mediated attenuation of glutamatergic synaptic input to nucleus accumbens (NAcc) neurons was investigated in slices of rat forebrain, using whole-cell patch-clamp recording. The depression by dopamine of EPSCs evoked by single-shock cortical stimulation was stimulus-dependent. Synaptic activation of NMDA-type glutamate receptors was critical for this effect, because dopamine-induced EPSC depressions were blocked by the competitive NMDA receptor antagonist D/L-2-amino-5-phosphonopentanoate (AP5). Application of NMDA also depressed the EPSC, and both this effect and the dopamine depressions were blocked by the A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), implicating adenosine release in the EPSC depression. A 1 receptor agonists also depressed EPSCs by a presynaptic action, causing increased paired-pulse facilitation, but this was insensitive to AP5. Activation of D 1 receptors enhanced both postsynaptic inward currents evoked by NMDA application and the isolated NMDA receptor-mediated component of synaptic transmission.The biochemical processes underlying the dopamine-induced EPSC depression did not involve either protein kinase A or the production of cAMP and its metabolites, because this effect was resistant to the protein kinase inhibitors H89 and H7 and the cAMP-specific phosphodiesterase inhibitor rolipram. We conclude that activation of postsynaptic D 1 receptors enhances the synaptic activation of NMDA receptors in nucleus accumbens neurons, thereby promoting a transsynaptic feedback inhibition of glutamatergic synaptic transmission via release of adenosine. Unusually for D 1 receptors, this phenomenon occurs independently of adenylyl cyclase stimulation. This process may contribute to the locomotor stimulant action of dopaminergic agents in the NAcc.

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Section: Discussionmentioning

confidence: 57%

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

1997

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“…Previous studies showed evidence for an opposite modulatory role of adenosine in the other major striatal neuronal element, the GABAergic dynorphinergic neuron, where activation of A 1 receptors attenuates dopamine D 1 receptor-mediated release of GABA and increase in the striatal expression of the immediate-early genes NGFI-A, c-fos and jun-B (Ferré et al, 1996. Therefore, under physiological conditions of increased adenosine release, a preferential activation of GABAergic enkephalinergic vs GABAergic dynorphinergic neurons must take place.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Adenosine Receptors Selectively Activates Gene Expression in Striatal Enkephalinergic Neurons

Karcz-Kubicha

Ferré

Diaz-Ruiz

et al. 2006

Neuropsychopharmacol

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In the striatum, adenosine A 2A and dopamine D 2 receptors exert reciprocal antagonistic interactions that modulate the function of GABAergic enkephalinergic neurons. We have previously shown that stimulation of adenosine A 1 receptors allows the stimulation of A 2A receptors to overcome a tonic inhibitory effect of D 2 receptors and induce striatal expression of c-fos. In the present work, by studying co-localization of c-Fos immunoreactivity and preproenkephalin and preprodynorphin transcripts, we show that co-administration of the A 1 receptor agonist CPA and the A 2A receptor agonist CGS 21680 increases the striatal expression of c-fos in GABAergic enkephalinergic but not in GABAergic dynorphinergic neurons. Co-administration of CPA and CGS 21680 also induced a significant increase in the striatal expression of preproenkephalin. The results underscore the role of adenosine in the activation of gene expression in the GABAergic enkephalinergic neuron.

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“…Thus, stimulation of A 1 receptors, but not A 2A receptors (Sebastiao and Ribeiro 1996), inhibits the release of glutamate (Fredholm 1995) and decreases the extracellular levels of dopamine (Zetterström and Fillenz 1990;Ballarin et al 1995;Okada et al 1996), acetylcholine (Bueters et al 2003), and GABA (Ferré et al 1996). Adenosine-induced reductions in these or other intercellular messenger substances could in turn affect glial KYNA synthesis by impairing the signaling of distinct astrocytic membrane receptors (Steinhäuser et al 1994;Zanassi et al 1999;Khan et al 2001;Sharma and Vijayaraghavan 2001;Zhou and Kimelberg 2001;Araque et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Neuronal A₁ receptors mediate increase in extracellular kynurenic acid after local intrastriatal adenosine infusion

Fuxé

Schwarcz

2004

Journal of Neurochemistry

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The naturally occurring purine nucleoside adenosine has pronounced anticonvulsant and neuroprotective properties and plays a neuromodulatory role in the CNS. Kynurenic acid (KYNA) is an astrocyte-derived, endogenous neuroinhibitory compound, which shares several of adenosine's properties. In a first attempt to examine possible interactions between these two biologically active molecules, adenosine was focally applied into the striatum of freely moving rats by reverse microdialysis, and changes in extracellular KYNA were monitored over time. A 2-h infusion of adenosine increased KYNA levels in a dose-dependent manner, with 10 mM of adenosine causing a twofold elevation within 1 h. This effect was reversible and was effectively blocked by coinfusion of the specific A 1 adenosine receptor antagonist 8-cyclopentyltheophylline (100 lM). In contrast, coinfusion of adenosine with MSX-3 (100 lM), an A 2A receptor antagonist, did not affect the adenosine-induced increase in KYNA levels. Local striatal perfusion with the A 1 receptor agonist N 6 -cyclopentyladenosine (100 lM) mimicked the effect of adenosine, whereas perfusion with the A 2A receptor agonist CGS-21680 (100 lM) was ineffective. Finally, we tested the effect of adenosine (10 mM) on extracellular KYNA in striata that had been injected with quinolinate (60 nmol/1 lL) 7 days earlier. In this neuron-depleted tissue, perfusion with adenosine failed to affect extracellular KYNA levels. These data demonstrate that adenosine is capable of raising extracellular KYNA in the rat striatum by interacting with postsynaptic neuronal A 1 receptors. This mechanism may result in a synergism between the neurobiological effects of adenosine and KYNA.

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Dopamine D₁ Receptor‐mediated Facilitation of GABAergic Neurotransmission in the Rat Strioentopeduncular Pathway and its Modulation by Adenosine A₁ Receptor‐mediated Mechanisms

Cited by 136 publications

References 40 publications

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

Stimulation of Adenosine Receptors Selectively Activates Gene Expression in Striatal Enkephalinergic Neurons

Neuronal A₁ receptors mediate increase in extracellular kynurenic acid after local intrastriatal adenosine infusion

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Dopamine D1 Receptor‐mediated Facilitation of GABAergic Neurotransmission in the Rat Strioentopeduncular Pathway and its Modulation by Adenosine A1 Receptor‐mediated Mechanisms

Cited by 136 publications

References 40 publications

A Postsynaptic Interaction between Dopamine D1and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

A Postsynaptic Interaction between Dopamine D1and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

Stimulation of Adenosine Receptors Selectively Activates Gene Expression in Striatal Enkephalinergic Neurons

Neuronal A1 receptors mediate increase in extracellular kynurenic acid after local intrastriatal adenosine infusion

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Dopamine D₁ Receptor‐mediated Facilitation of GABAergic Neurotransmission in the Rat Strioentopeduncular Pathway and its Modulation by Adenosine A₁ Receptor‐mediated Mechanisms

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

A Postsynaptic Interaction between Dopamine D₁and NMDA Receptors Promotes Presynaptic Inhibition in the Rat Nucleus Accumbens via Adenosine Release

Neuronal A₁ receptors mediate increase in extracellular kynurenic acid after local intrastriatal adenosine infusion