| RESEARCH ARTICLE
|Year : 2013 | Volume
| Issue : 6 | Page : 593-596
Sucrose-induced analgesia in mice: Role of nitric oxide and opioid receptor-mediated system
Abtin Shahlaee1, Ali Farahanchi2, Shiva Javadi2, Bahram Delfan3, Ahmad Reza Dehpour2
1 Department of Pharmacology, School of Medicine; Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran
2 Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
3 Department of Pharmacology, Lorestan University of Medical Sciences, Faculty of Medicine, Khoram Abad, Iran
Background: The mechanism of action of sweet substance-induced analgesia is thought to involve activation of the endogenous opioid system. The nitric oxide (NO) pathway has a pivotal role in pain modulation of analgesic compounds such as opioids.
Objectives: We investigated the role of NO and the opioid receptor-mediated system in the analgesic effect of sucrose ingestion in mice.
Materials and Methods: We evaluated the effect of intraperitoneal administration of 10 mg/kg of NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME) and 20 mg/kg of opioid receptor antagonist, naltrexone on the tail flick response in sucrose ingesting mice.
Results: Sucrose ingestion for 12 days induced a statistically significant increase in the latency of tail flick response which was unmodified by L-NAME, but partially inhibited by naltrexone administration.
Conclusions: Sucrose-induced nociception may be explained by facilitating the release of endogenous opioid peptides. Contrary to some previously studied pain models, the NO/cyclic guanosine monophosphate (cGMP) pathway had no role in thermal hyperalgesia in our study. We recommend further studies on the involvement of NO in other animals and pain models.
Ahmad Reza Dehpour
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran
Source of Support: None, Conflict of Interest: None
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