, Volume 44, Issue 6, pp 460–463 | Cite as

Ethanol-Induced Antinociception in Rodents: Role of the Cholinergic and Opioidergic Systems

  • G. F. Ibironke
  • O. A. Oyekunle

We examined antinociceptive properties of ethanol and the mechanism of its action using two thermal (hot-plate and tail-flick) and two chemical (acetic acid-induced writhing and formalin) nociception tests. The mechanism of antinociception was analyzed using naloxone (an opioid antagonist) and atropine (a cholinergic blocker). It was found that ethanol in a dose-dependent manner produced significant (P < < 0.05) prolongations of both the hot-plate and tail-flick latencies. In the chemical tests, ethanol caused a significant (P < 0.05) reduction in the number of writhings produced by acetic acid and also a significant decrease (P < 0.01) in the licking time produced by formalin within both phases of the respective test. It was also observed that both atropine and naloxone significantly (P < 0.05) suppressed ethanolinduced antinociception effects. We conclude that the antinociceptive action of ethanol may in part be opiodergic- and cholinergic-dependent.


ethanol pain tests antinociception naloxone atropine 


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  1. 1.
    M. B. Gatch, “Effects of ethanol administration and withdrawal on thermal nociception in rats,” Alchohol Clin. Exp. Res., 23, 328–333 (1999).CrossRefGoogle Scholar
  2. 2.
    V. C. Campbell, R. E. Taylor, and Y. Tizabi, “Antinociceptive effects of alcohol and nicotine: involvement of the opioid system,” Brain Res., 1096, 71–77 (2006).CrossRefGoogle Scholar
  3. 3.
    H. J. Franclin and V. Abott, “Pentobarbital, diazepam and ethanol abolish the interphase dimunition of pain in the formalin test: Evidence for pain modulation by GABAA receptors,” Pharmacol. Biochem. Behav., 46, 661–666 (1993).CrossRefGoogle Scholar
  4. 4.
    M. B. Gatch, “Effects of benzodiazipines on acute and chronic ethanol-induced antinociception in rats,” Alcohol Clin. Exp. Res., 23, 1736–1743 (1999).PubMedCrossRefGoogle Scholar
  5. 5.
    L. Pohorecky and P. Shah, “Ethanol-induced analgesia,” Life Sci., 41, 1289–1295 (1987).PubMedCrossRefGoogle Scholar
  6. 6.
    J. S. Mogil, P. Marek, R. Yirmiya, et al., “Antagonism of the nonopioid component of ethanol-induced analgesia by the NMDA receptor antagonist MK-801,” Brain Res., 602, 126–130 (1993).PubMedCrossRefGoogle Scholar
  7. 7.
    H. Jorgensen and K. Hole, “Does ethanol stimulate brain opiate receptors? Studies on receptor binding and naloxone inhibition of ethanol-induced effects,” Eur. J. Pharmacol., 75, 223–229 (1981).PubMedCrossRefGoogle Scholar
  8. 8.
    N. B. Eddy and B. Leimbach, “Synthetic analgesics: II Dithienyl butenyl and Dithienyl butylamines,” J. Pharmacol. Exp. Ther., 107, 385–393 (1953).PubMedGoogle Scholar
  9. 9.
    G. F. Ibironke, O. J. Saba, and F. O. Olopade, “Glycemic control and pain threshold in alloxan diabetic rats,” Afr. J. Biomed. Res., 7, 149–151 (2004).Google Scholar
  10. 10.
    F. E. D’Amour and D. A. Smith, “A method for determining the loss of pain sensation,” J. Pharmacol. Exp. Ther., 72, 74–79 (1941).Google Scholar
  11. 11.
    E. Siegmund, R. Caolmus, and G. Lu, “A method for evaluating both narcotic and non-narcotic analgesics,” Proc. Soc. Exp. Biol. Med., 95, 729–731 (1957).PubMedGoogle Scholar
  12. 12.
    R. Konster, M. Anderson, E. De Beer, “Acetic acid for analgesic screening,” Fed. Proc., 18, 412 (1959).Google Scholar
  13. 13.
    S. Hunskar and K. Hole, “The formalin test in mice: Dissociation between inflammatory and noninflammatory pain,” Pain, 30, 103–114 (1997).CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2012

Authors and Affiliations

  1. 1.University of IbadanIbadanNigeria
  2. 2.Ladoke Akintola University of TechnologyOgbomosoNigeria

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