Electroacupuncture (EA) possesses various therapeutic effects, including alleviation of pain, reduction of inflammation and improvement of sleep disturbance. The mechanisms of EA on sleep improvement, however, remain to be determined. It has been stated in ancient Chinese literature that the Anmian (EX17) acupoint is one of the trigger points that alleviates insomnia. We previously demonstrated that EA stimulation of Anmian acupoints in rats during the dark period enhances non-rapid eye movement (NREM) sleep, which involves the induction of cholinergic activity in the nucleus tractus solitarius (NTS). In addition to cholinergic activation of the NTS, activation of the endogenous opioidergic system may also be a mechanism by which acupuncture affects sleep. Therefore, this study was designed to investigate the involvement of the NTS opioidergic system in EA-induced alterations in sleep. Our present results indicate that EA of Anmian acupoints increased NREM sleep, but not rapid eye movement sleep, during the dark period in rats. This enhancement in NREM sleep was dose-dependently blocked by microinjection of opioid receptor antagonist, naloxone, and the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-receptor antagonist, nor-binaltrophimine, however, did not affect EA-induced alterations in sleep. Furthermore, β-endorphin was significantly increased in both the brainstem and hippocampus after the EA stimuli, an effect blocked by administration of the muscarinic antagonist scopolamine into the NTS. Our findings suggest that mechanisms of EA-induced NREM sleep enhancement may be mediated, in part, by cholinergic activation, stimulation of the opiodergic neurons to increase the concentrations of β-endorphin and the involvement of the μ-opioid receptors.

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These observations argue that amygdala-kindling-induced sleep-wake alterations are modulated by central increases in CRH or IL-1.

Evidence in the past decade indicates that the mechanisms of anti-nociception of electroacupuncture (EAc) involve actions of neuropeptides (i.e., enkephalin and endorphin) and monoamines (i.e., serotonin and norepinephrine) in the central nervous system. Our present results using a subcutaneous injection of formalin to test pain sensation in mice provide further understanding of the involvement of serotonin in the actions of EAc-induced analgesia. Our observations show that (1) EAc at three different frequencies (2, 10 and 100 Hz) elicited an anti-nociceptive effect as determined by behavioral observations of reduced hindpaw licking; (2) exogenously intracerebroventricular administration of 5-hydroxytryptamine (5-HT) exhibited an analgesic effect, which partially mimicked the analgesic actions of EAc; (3) the anti-nociception of EAc at different frequencies was attenuated after reduced biosynthesis of serotonin by the administration of the tryptophan hydroxylase inhibitor, p-chlorophenylalanine, and (4) the 5-HT_1A and 5-HT₃ receptor antagonists, pindobind-5-HT_1A and LY-278584, respectively, blocked three different frequencies of EAc-induced analgesic effects, but the anti-nociceptive effect of 100 Hz EAc was potentiated by the 5-HT₂ receptor antagonist, ketanserin. These observations suggest that 5-HT_1A and 5-HT₃ receptors partially mediate the analgesic effects of EAc, but that the 5-HT₂ receptor is conversely involved in the nociceptive response.