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Adenosine receptor-mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N-methyl-D-aspartate receptor stimulation.

Abstract

Adenosine, by acting on adenosine A(1) and A(2A) receptors, exerts opposite modulatory roles on striatal extracellular levels of glutamate and dopamine, with activation of A(1) inhibiting and activation of A(2A) receptors stimulating glutamate and dopamine release. Adenosine-mediated modulation of striatal dopaminergic neurotransmission could be secondary to changes in glutamate neurotransmission, in view of evidence for a preferential colocalization of A(1) and A(2A) receptors in glutamatergic nerve terminals. By using in vivo microdialysis techniques, local perfusion of NMDA (3, 10 microm), the selective A(2A) receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680; 3, 10 microm), the selective A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 300, 1000 microm), or the non-selective A(1)-A(2A) receptor antagonist in vitro caffeine (300, 1000 microm) elicited significant increases in extracellular levels of dopamine in the shell of the nucleus accumbens (NAc). Significant glutamate release was also observed with local perfusion of CGS 21680, CPT and caffeine, but not NMDA. Co-perfusion with the competitive NMDA receptor antagonist dl-2-amino-5-phosphonovaleric acid (APV; 100 microm) counteracted dopamine release induced by NMDA, CGS 21680, CPT and caffeine. Co-perfusion with the selective A(2A) receptor antagonist MSX-3 (1 microm) counteracted dopamine and glutamate release induced by CGS 21680, CPT and caffeine and did not modify dopamine release induced by NMDA. These results indicate that modulation of dopamine release in the shell of the NAc by A(1) and A(2A) receptors is mostly secondary to their opposite modulatory role on glutamatergic neurotransmission and depends on stimulation of NMDA receptors. Furthermore, these results underscore the role of A(1) vs. A(2A) receptor antagonism in the central effects of caffeine.

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  • Authors+Show Affiliations

    ,

    Preclinical Pharmacology Section, Behavioral Neuroscience Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland 21224, USA.

    , , , , , , , , ,

    Source

    Journal of neurochemistry 91:4 2004 Nov pg 873-80

    MeSH

    Adenosine
    Adenosine A1 Receptor Antagonists
    Adenosine A2 Receptor Agonists
    Adenosine A2 Receptor Antagonists
    Animals
    Caffeine
    Dopamine
    Excitatory Amino Acid Agonists
    Excitatory Amino Acid Antagonists
    Glutamic Acid
    Male
    Microdialysis
    N-Methylaspartate
    Nucleus Accumbens
    Phenethylamines
    Purinergic P1 Receptor Agonists
    Purinergic P1 Receptor Antagonists
    Rats
    Rats, Sprague-Dawley
    Receptors, N-Methyl-D-Aspartate
    Receptors, Purinergic P1
    Synaptic Transmission
    Theophylline

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    15525341

    Citation

    Quarta, Davide, et al. "Adenosine Receptor-mediated Modulation of Dopamine Release in the Nucleus Accumbens Depends On Glutamate Neurotransmission and N-methyl-D-aspartate Receptor Stimulation." Journal of Neurochemistry, vol. 91, no. 4, 2004, pp. 873-80.
    Quarta D, Borycz J, Solinas M, et al. Adenosine receptor-mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N-methyl-D-aspartate receptor stimulation. J Neurochem. 2004;91(4):873-80.
    Quarta, D., Borycz, J., Solinas, M., Patkar, K., Hockemeyer, J., Ciruela, F., ... Ferré, S. (2004). Adenosine receptor-mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N-methyl-D-aspartate receptor stimulation. Journal of Neurochemistry, 91(4), pp. 873-80.
    Quarta D, et al. Adenosine Receptor-mediated Modulation of Dopamine Release in the Nucleus Accumbens Depends On Glutamate Neurotransmission and N-methyl-D-aspartate Receptor Stimulation. J Neurochem. 2004;91(4):873-80. PubMed PMID: 15525341.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Adenosine receptor-mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N-methyl-D-aspartate receptor stimulation. AU - Quarta,Davide, AU - Borycz,Janusz, AU - Solinas,Marcello, AU - Patkar,Kshitij, AU - Hockemeyer,Jörg, AU - Ciruela,Francisco, AU - Lluis,Carme, AU - Franco,Rafael, AU - Woods,Amina S, AU - Goldberg,Steven R, AU - Ferré,Sergi, PY - 2004/11/5/pubmed PY - 2005/5/26/medline PY - 2004/11/5/entrez SP - 873 EP - 80 JF - Journal of neurochemistry JO - J. Neurochem. VL - 91 IS - 4 N2 - Adenosine, by acting on adenosine A(1) and A(2A) receptors, exerts opposite modulatory roles on striatal extracellular levels of glutamate and dopamine, with activation of A(1) inhibiting and activation of A(2A) receptors stimulating glutamate and dopamine release. Adenosine-mediated modulation of striatal dopaminergic neurotransmission could be secondary to changes in glutamate neurotransmission, in view of evidence for a preferential colocalization of A(1) and A(2A) receptors in glutamatergic nerve terminals. By using in vivo microdialysis techniques, local perfusion of NMDA (3, 10 microm), the selective A(2A) receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680; 3, 10 microm), the selective A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 300, 1000 microm), or the non-selective A(1)-A(2A) receptor antagonist in vitro caffeine (300, 1000 microm) elicited significant increases in extracellular levels of dopamine in the shell of the nucleus accumbens (NAc). Significant glutamate release was also observed with local perfusion of CGS 21680, CPT and caffeine, but not NMDA. Co-perfusion with the competitive NMDA receptor antagonist dl-2-amino-5-phosphonovaleric acid (APV; 100 microm) counteracted dopamine release induced by NMDA, CGS 21680, CPT and caffeine. Co-perfusion with the selective A(2A) receptor antagonist MSX-3 (1 microm) counteracted dopamine and glutamate release induced by CGS 21680, CPT and caffeine and did not modify dopamine release induced by NMDA. These results indicate that modulation of dopamine release in the shell of the NAc by A(1) and A(2A) receptors is mostly secondary to their opposite modulatory role on glutamatergic neurotransmission and depends on stimulation of NMDA receptors. Furthermore, these results underscore the role of A(1) vs. A(2A) receptor antagonism in the central effects of caffeine. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/15525341/Adenosine_receptor_mediated_modulation_of_dopamine_release_in_the_nucleus_accumbens_depends_on_glutamate_neurotransmission_and_N_methyl_D_aspartate_receptor_stimulation_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0022-3042&date=2004&volume=91&issue=4&spage=873 DB - PRIME DP - Unbound Medicine ER -