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

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 CB1 cannabinoid receptor antagonist, but not by AM 630, a CB2 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.

Nitric oxide/cGMP pathway mediates orofacial antinociception induced by electroacupuncture at the St36 acupoint.

The aim of the present study was to test the hypothesis that electroacupuncture (EA) at acupoint St36 induces antinociception by activation of the L-arg/NO/cGMP pathway. Nociception was produced by thermal stimuli applied to the face of Wistar rats and latency was measured by face withdrawal. Electric stimulation of acupoint St36 for 20 min induced antinociception in this model, which was maintained for 150 min. For comparison, a so-called dry needle group (DN) was used, which received needling at the same point without stimulation. The antinociception obtained by stimulation of acupoint St36 was only achieved when high frequency (100 Hz) was used, whereas low frequencies (5 and 30 Hz) were not capable of achieving this effect. Subcutaneous administration of both inhibitors of NO synthase (N-nitro-L-arginine) and guanylyl cyclase (ODQ) and intraperitoneal administration of specific antagonists of neuronal NO synthase (L-NNA) and inductible NO synthase (aminoguanidine) antagonized the antinociception induced by St36 stimulation. The results of this paper suggest that stimulation of acupoint St36 at high frequency induces antinociception, which seems to be related to L-arg/NO/cGMP pathway activation.