title: Activation of amygdala opioid receptors by electroacupuncture of Feng-Chi (GB20) acupoints exacerbates focal epilepsy.
abstract: BACKGROUND
  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 naïve 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.
authors.forename: Pei-Lu
authors.initials: PL
authors.lastname: Yi
authors.forename: Chin-Yu
authors.initials: CY
authors.lastname: Lu
authors.forename: Chiung-Hsiang
authors.initials: CH
authors.lastname: Cheng
authors.forename: Yi-Fong
authors.initials: YF
authors.lastname: Tsai
authors.affiliation: Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, No, 1, Sec, 4,, Roosevelt Road, Taipei 106, Taiwan. ctlin@ntu.edu.tw.
authors.forename: Chung-Tien
authors.initials: CT
authors.lastname: Lin
authors.forename: Fang-Chia
authors.initials: FC
authors.lastname: Chang
mesh_terms: D015669:Acupuncture Points; D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D015671:Electroacupuncture; D004828:Epilepsies, Partial / Q000378:metabolism / Q000628:therapy*; D006801:Humans; D008297:Male; D009292:Narcotic Antagonists / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011957:Receptors, Opioid / Q000235:genetics / Q000378:metabolism*
chemical_list: D009292:Narcotic Antagonists; D011957:Receptors, Opioid