| RESEARCH ARTICLE |
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| Year : 2013 | Volume
: 45
| 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
Correspondence Address:
Ahmad Reza Dehpour
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.121370
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.
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