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OtherANALGESIA AND DRUGS OF ABUSE

Acute Tolerance To Spinally Administered Morphine Compares Mechanistically with Chronically Induced Morphine Tolerance

Carolyn A. Fairbanks and George L. Wilcox
Journal of Pharmacology and Experimental Therapeutics September 1997, 282 (3) 1408-1417;
Carolyn A. Fairbanks
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George L. Wilcox
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Abstract

The mechanistic similarity between acutely and chronically induced morphine tolerance has been previously proposed but remains largely unexplored. Our experiments examined the modulation of acutely induced tolerance to spinally administered morphine by agonists that affect the N-methyl-d-aspartate receptor and nitric oxide synthase systems. Antinociception was detected via the hot water (52.5°C) tail flick test in mice. Intrathecal pretreatment with morphine (40 nmol) produced a 9.6-fold rightward shift in the morphine dose-response curve. This shift confirmed the induction of acute spinal morphine tolerance. Intrathecal copretreatment with the receptor antagonists (competitive and noncompetitive, respectively) dizolcipine (MK801, 3 nmol) or LY235959 (4 pmol) and morphine [40 nmol, intrathecally (i.t.)] attenuated acute tolerance to morphine measured 8 hr later. A 60-min pretreatment of 7-nitroindazole (6 nmol, i.t.), a selective neuronal NOS inhibitor, followed by administration of morphine (40 nmol, i.t.) blocked the induction of morphine tolerance. Intrathecal copretreatment with morphine (40 nmol, i.t.) and agmatine (4 nmol, i.t.), an imidazoline1 receptor agonist and putative nitric oxide synthase inhibitor, almost completely abolished acute spinal morphine tolerance. The results of these experiments agree with previous reports using models of chronically induced morphine tolerance. This evidence supports the proposal that the mechanisms responsible for acute morphine tolerance parallel those underlying chronic morphine tolerance. This study attests to the powerful predictive value of acute induction as a model for morphine tolerance.

Footnotes

  • Send reprint requests to: Dr. George L. Wilcox, Department of Pharmacology, 3-249 Millard Hall, 435 Delaware St. SE, Minneapolis, MN 55455.

  • ↵1 This work was supported by NIH/K02-DA-00145 and NIH/R01-DA-04274 and ADAMHA training Grant T32A07234 awarded by NIDA.

  • Abbreviations:
    ANOVA
    analysis of variance
    CREB
    cAMP-responsive element-binding protein
    I1
    imidazoline1
    i.t.
    intrathecal(ly)
    l-NNA
    l-NG-nitro-l-arginine
    l-NAME
    l-NG-nitro-l-arginine methyl ester
    LY
    LY235959
    MK801
    dizolcipine
    % MPE
    percent maximum possible effect
    NMMA
    NG-monomethyl-l-arginine
    NO2Arg
    NG-nitro-l-arginine
    NO
    nitric oxide
    NOS
    nitric oxide synthase
    7-NI
    7-nitroindazole
    NMDA
    N-methyl-d-aspartate
    pmol
    picomoles
    PKC
    protein kinase C
    • Received October 7, 1996.
    • Accepted May 2, 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

Acute Tolerance To Spinally Administered Morphine Compares Mechanistically with Chronically Induced Morphine Tolerance

Carolyn A. Fairbanks and George L. Wilcox
Journal of Pharmacology and Experimental Therapeutics September 1, 1997, 282 (3) 1408-1417;

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OtherANALGESIA AND DRUGS OF ABUSE

Acute Tolerance To Spinally Administered Morphine Compares Mechanistically with Chronically Induced Morphine Tolerance

Carolyn A. Fairbanks and George L. Wilcox
Journal of Pharmacology and Experimental Therapeutics September 1, 1997, 282 (3) 1408-1417;
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