Alpha 2 adrenoceptors but not GABA participate in electroacupuncture-induced orofacial antinociception at ST36 point in rats

Orofacial pain represents a significant portion of the complaints from patients seeking treatment at pain management centers worldwide. Although the treatment for orofacial pain is primarily pharmacological, there has been an increase in reports showing significant clinical results from non-pharmacological therapies, including electroacupuncture (EA). Recently, EA has been recognized as an effective and affordable non-pharmacological strategy with minimal side effects. However, the mechanisms underlying its pain-relieving (antinociceptive) effects remain poorly understood. The present study aimed to evaluate the roles of α2 adrenoreceptors and GABA in the antinociception induced by electroacupuncture. Male Wistar rats underwent EA stimulation at the acupoint St36 for 20 minutes at a frequency of 100 Hz and an intensity of 0.5 mA. To assess the thermal nociceptive response, a stimulus was applied to the vibrissae (whiskers) of the rats, and the time taken for facial withdrawal was measured before the EA stimulation and at 15-minute intervals afterward until the effects diminished. EA at acupoint St36 for 20 minutes effectively reversed thermal nociception, with this effect lasting for 150 minutes. The antinociceptive effects of EA were blocked by the pre-injection of yohimbine, an antagonist of α2 adrenoreceptors, at doses of 2 and 4 mg/kg. However, it was primarily observed at the onset, indicating that α2 adrenoreceptors play a role in the initial antinociceptive effect of EA. To investigate the involvement of GABA in this effect, intraperitoneal injections of a GABAB antagonist (sacoflen) and a GABA reuptake inhibitor (guvacine) were administered 10 minutes before EA. Neither of these drugs affected the antinociceptive effect produced by EA. Thus, this study suggests that GABA does not participate in the antinociception induced by electroacupuncture.