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Research ArticleArticle

Chronic Morphine Treatment Selectively Augments Metabotropic Glutamate Receptor-Induced Inhibition of N-Methyl-d-Aspartate Receptor-Mediated Neurotransmission in Nucleus Accumbens

Gilles Martin, Riszard Przewlocki and George R. Siggins
Journal of Pharmacology and Experimental Therapeutics January 1999, 288 (1) 30-35;
Gilles Martin
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Riszard Przewlocki
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George R. Siggins
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Abstract

We compared the effects of different metabotropic glutamate receptor (mGluR) agonists on pharmacologically isolatedN-methyl-d-aspartate-excitatory postsynaptic currents (NMDA-EPSCs) in core nucleus accumbens neurons using conventional intracellular recording in untreated and morphine-treated rats. The rats were treated by s.c. implantation of two morphine pellets and studied over a 3- to 6-day period. This model is known to exhibit opiate tolerance and dependence. We elicited NMDA-EPSCs by stimulating locally in the presence of the α-amino-3-hydroxy-5-methly-4-isoxazolepropionic acid/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM) and the γ-aminobutyric acid receptor antagonist bicuculline (15 μM). We found thattrans-1-aminocyclopentane-1,3-decarboxylic acid, an agonist of group 1 and 2 mGluRs, decreased NMDA-EPSC areas (time-integrals) in a dose-dependent manner (1–10 μM) in slices taken from untreated rats. This inhibitory effect was significantly enhanced after chronic morphine treatment. In contrast, although the group 3 mGluR agonist l(+)-2-amino-4-phosphonobutyric acid also markedly reduced NMDA-EPSC areas, there was no apparent change in this effect after chronic morphine. We found that quisqualate, the group 1 mGluR agonist, failed to elicit any effect on NMDA-EPSCs in either untreated or chronically treated rats. Paired-pulse stimulation of core nucleus accumbens NMDA-EPSCs in slices from these groups showed that chronic morphine enhanced paired-pulse facilitation, consistent with a presynaptic reduction in glutamate release. Because of the relevance to opiate tolerance and dependence of the chronic model used, the brain region (accumbens), and the receptors studied, our data provide a cellular substrate that could account for some aspects of these phenomena.

Footnotes

  • Send reprint requests to: Dr. G.R. Siggins, CVN-12, Department of Neuropharmacology, The Scripps Research Institute, 10550 N. Torrey Pines Road., La Jolla, CA 92037.

  • ↵1 This work was supported by National Institutes of Health/National Institute on Drug Abuse Grant DA03665

  • Abbreviations:
    PKC
    protein kinase C
    CNQX
    6-cyano-7-nitroquinoxaline-2,3-dione
    NAcc
    nucleus accumbens
    mGluRs
    metabotropic glutamate receptors
    NMDA
    N-methyl-d-aspartate
    trans-ACPD
    trans-1-aminocyclopentane-1,3-decarboxylic acid
    EPSC
    excitatory postsynaptic currents
    l-AP4
    l(+)-2-amino-4-phosphonobutyric acid
    ACSF
    artificial cerebrospinal fluid
    • Received April 3, 1998.
    • Accepted July 20, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 1
1 Jan 1999
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Research ArticleArticle

Chronic Morphine Treatment Selectively Augments Metabotropic Glutamate Receptor-Induced Inhibition of N-Methyl-d-Aspartate Receptor-Mediated Neurotransmission in Nucleus Accumbens

Gilles Martin, Riszard Przewlocki and George R. Siggins
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 30-35;

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Research ArticleArticle

Chronic Morphine Treatment Selectively Augments Metabotropic Glutamate Receptor-Induced Inhibition of N-Methyl-d-Aspartate Receptor-Mediated Neurotransmission in Nucleus Accumbens

Gilles Martin, Riszard Przewlocki and George R. Siggins
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 30-35;
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