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Indian J Pharmacol. 2013 Nov-Dec;45(6):593-6. doi: 10.4103/0253-7613.121370.

Sucrose-induced analgesia in mice: role of nitric oxide and opioid receptor-mediated system.

Author information

1
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran ; 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.

Abstract

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.

KEYWORDS:

N-nitro-L-arginine methyl ester; Naltrexone; opioid; tail flick test

PMID:
24347767
PMCID:
PMC3847249
DOI:
10.4103/0253-7613.121370
[Indexed for MEDLINE]
Free PMC Article

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