Yi P.-L.Lu C.-Y.Cheng C.-H.Tsai Y.-F.Lin C.-T.FANG-CHIA CHANGCHUNG-TIEN LIN2020-01-072020-01-0720131472-6882https://scholars.lib.ntu.edu.tw/handle/123456789/446393Background: The effect of seizure suppression by acupuncture of Feng-Chi (GB20) acupoints has been documented in the ancient Chinese literature, Lingshu Jing (Classic of the Miraculous Pivot), however, there is a lack of scientific evidence to prove it. This current study was designed to elucidate the effect of electroacupuncture (EA) stimulation of bilateral Feng-Chi (GB20) acupoints on the epileptic activity by employing an animal model of focal epilepsy.Methods: Administration of pilocarpine into the left central nucleus of amygdala (CeA) induced the focal epilepsy in rats. Rats received a 30-min 100?Hz EA stimulation of bilateral Feng-Chi acupoints per day, beginning at 30?minutes before the dark period and performing in three consecutive days. The broad-spectrum opioid receptor antagonist (naloxone), μ-receptor antagonist (naloxonazine), δ-receptor antagonist (naltrindole) and κ-receptor antagonist (nor-binaltorphimine) were administered directly into the CeA to elucidate the involvement of CeA opioid receptors in the EA effect.Results: High-frequency (100?Hz) EA stimulation of bilateral Feng-Chi acupoints did not suppress the pilocarpine-induced epileptiform electroencephalograms (EEGs), whereas it further increased the duration of epileptiform EEGs. We also observed that epilepsy occurred while 100?Hz EA stimulation of Feng-Chi acupoints was delivered into na?ve rats. EA-induced augmentation of epileptic activity was blocked by microinjection of naloxone, μ- (naloxonazine), κ- (nor-binaltorphimine) or δ-receptor antagonists (natrindole) into the CeA, suggesting that activation of opioid receptors in the CeA mediates EA-exacerbated epilepsy.Conclusions: The present study suggests that high-frequency (100?Hz) EA stimulation of bilateral Feng-Chi acupoints has no effect to protect against pilocarpine-induced focal epilepsy; in contrast, EA further exacerbated focal epilepsy induced by pilocarpine. Opioid receptors in the CeA mediated EA-induced exacerbation of focal epilepsy. ? 2013 Yi et al.; licensee BioMed Central Ltd.[SDGs]SDG3naloxonazine; naloxone; naltrindole; norbinaltorphimine; opiate receptor; pilocarpine; amygdaloid nucleus; animal experiment; animal model; article; cerebellum; controlled study; disease exacerbation; drug response; electroacupuncture; electrode; electroencephalography; epileptic discharge; focal epilepsy; frontal lobe; male; nonhuman; occipital lobe; parietal lobe; rat; right hemisphere; Acupuncture Points; Amygdala; Animals; Electroacupuncture; Epilepsies, Partial; Humans; Male; Narcotic Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Opioidjournal article10.1186/1472-6882-13-2902-s2.0-84886391030https://www2.scopus.com/inward/record.uri?eid=2-s2.0-84886391030&doi=10.1186%2f1472-6882-13-290&partnerID=40&md5=fd7e6b9cabc48fabcbee2c7bc11026ae