Endocannabinoid mechanism for orofacial antinociception induced by electroacupuncture in acupoint St36 in rats.

Autor: Almeida RT; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Romero TR; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Romero MG; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., de Souza GG; Department of Physiotherapy, Federal University of Alfenas, Alfenas, Minas Gerais, Brazil., Perez AC; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Duarte ID; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address: dimitri@icb.ufmg.br.
Jazyk: angličtina
Zdroj: Pharmacological reports : PR [Pharmacol Rep] 2016 Dec; Vol. 68 (6), pp. 1095-1101. Date of Electronic Publication: 2016 Jul 21.
DOI: 10.1016/j.pharep.2016.07.004
Abstrakt: Introduction: This study was conducted with the aim of evaluating whether electroacupuncture (EA) at acupoint St36 could produce antinociception through the activation of an endocannabinoid mechanism.
Methods: Male Wistar rats were divided into experimental groups. Heat was applied to the faces of rats, and the latency to withdraw the face was measured. Furthermore, the influence of electrical stimulation (100HzP) of acupoint St36, at a 0.5mA intensity, was investigated in the facial withdrawal threshold.
Results: The EA produced antinociception, which lasted for 180min. This effect was antagonized by the pre-injection of AM 251, a CB 1 cannabinoid receptor antagonist, but not by AM 630, a CB 2 cannabinoid receptor antagonist. Additionally, pretreatment with an endocannabinoid metabolizing enzyme inhibitor (MAFP) and an anandamide reuptake inhibitor (VDM11) prolonged and intensified the antinociceptive effect produced by EA.
Conclusion: This study demonstrated for the first time that the CB1 cannabinoid receptor participates in the antinociceptive effect induced by EA.
(Copyright © 2016 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: