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OtherANALGESIA AND DRUGS OF ABUSE

Antisense Mapping of the MOR-1 Opioid Receptor Clone: Modulation of Hyperphagia Induced by DAMGO

Liza Leventhal, Lesley B. Stevens, Grace C. Rossi, Gavril W. Pasternak and Richard J. Bodnar
Journal of Pharmacology and Experimental Therapeutics September 1997, 282 (3) 1402-1407;
Liza Leventhal
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Lesley B. Stevens
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Grace C. Rossi
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Gavril W. Pasternak
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Richard J. Bodnar
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Abstract

The mu opioid receptor mediates ingestive behavior:mu-selective agonists stimulate food intake and antagonists reduce intake in many ingestive situations. Antisense oligodeoxynucleotides directed against each of the four exons of the MOR-1 clone were equally effective in reducing spontaneous food intake and body weight in rats. However, antisense probes directed against only exon 1 or 4 of the MOR-1 clone reduced mu-mediated analgesia. The present study examined whether central administration of antisense probes directed against each of the four exons of the MOR-1 clone or a missense control altered hyperphagia elicited by themu agonist DAMGO across a range of doses. Antisense probes directed against only exon 1 or 4 blocked hyperphagia at agonist doses of 0.5 and 1.0 μg; this pattern was identical to that observed formu-mediated analgesia. A missense control failed to exert significant effects, which suggests specificity of antisense actions. The effective antisense probes failed to reduce hyperphagia at a higher (5 μg) agonist dose, a result consistent with limitations in down-regulation of receptor proteins by antisense. The muantagonist β-funaltrexamine produced a similar pattern of effects onmu-mediated hyperphagia. The selective actions of antisense probes directed against different exons of the MOR-1 clone in reducing hyperphagia induced by DAMGO suggest that multiple splice variants of the MOR-1 clone exist and raise the possibility of further opioid receptor subclassifications.

Footnotes

  • Send reprint requests to: Dr. R. J. Bodnar, Department of Psychology, Queens College, CUNY, 65–30 Kissena Blvd., Flushing, NY 11367.

  • ↵1 This research was supported in part by NIDA grants DA05746 (L.L.), DA04194 (R.J.B.), DA07274 (G.W.P.), DA00220 (G.W.P.) and DA00310 (G.C.R.) and by a CUNY Project Ascend undergraduate grant (L.B.S.).

  • Abbreviations:
    AS ODN
    antisense oligodeoxynucleotide
    βFNA
    β-funaltrexamine
    KOR-1
    kappa opioid receptor clone
    KOR-3
    kappa 3 opioid receptor clone
    MS ODN
    mismatch oligodeoxynucleotide
    M6G
    morphine-6β-glucuronide
    MOR-1
    mu opioid receptor clone
    ORL-1
    orphanin opioid-like receptor clone
    VEH
    vehicle
    DOR-1 = delta opioid receptor clone.
    • Received March 11, 1997.
    • Accepted May 29, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 282, Issue 3
1 Sep 1997
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OtherANALGESIA AND DRUGS OF ABUSE

Antisense Mapping of the MOR-1 Opioid Receptor Clone: Modulation of Hyperphagia Induced by DAMGO

Liza Leventhal, Lesley B. Stevens, Grace C. Rossi, Gavril W. Pasternak and Richard J. Bodnar
Journal of Pharmacology and Experimental Therapeutics September 1, 1997, 282 (3) 1402-1407;

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OtherANALGESIA AND DRUGS OF ABUSE

Antisense Mapping of the MOR-1 Opioid Receptor Clone: Modulation of Hyperphagia Induced by DAMGO

Liza Leventhal, Lesley B. Stevens, Grace C. Rossi, Gavril W. Pasternak and Richard J. Bodnar
Journal of Pharmacology and Experimental Therapeutics September 1, 1997, 282 (3) 1402-1407;
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