title: Electroacupuncture induces Fos expression in the nucleus tractus solitarius via cholecystokinin A receptor signaling in rats.
abstract: OBJECTIVE
  Cholecystokinin, a satiety hormone, acts on cholecystokinin A receptor on vagal afferent neurons that project to the nucleus tractus solitarius, resulting in inhibition of feeding. Cholecystokinin is known to be released by electroacupuncture stimulation at certain body sites which elicits profound psychophysiological responses. Our previous study has revealed the involvement of cholecystokinin and cholecystokinin A receptor in the electroacupuncture stimulation-induced modulation of feeding. The aim of the present study was to examine whether electroacupuncture stimulation at the acupuncture point ST36 (Joksamni) activates the nucleus tractus solitarius neurons and whether such effect is mediated by cholecystokinin A receptor.
  
  
  METHODS
  Using an immunofluorescent analysis of Fos, a neuronal activation marker, we compared the Fos immunoreactivity of the nucleus tractus solitarius among three groups of Sprague-Dawley rats: (1) control (48 hour fasting + saline pre-treatment + no electroacupuncture stimulation); (2) SalEA (48 hour fasting + saline pre-treatment + ST36 electroacupuncture stimulation); (3) LorEA (48 hour fasting + pre-treatment of cholecystokinin A receptor antagonist, lorglumide + ST36 electroacupuncture stimulation).
  
  
  RESULTS
  ST36 electroacupuncture stimulation significantly reduced 30 minute food intake (p<0.05, SalEA versus control) and increased Fos expression in the nucleus tractus solitarius (p<0.01, SalEA versus control). The effects of electroacupuncture on food intake and Fos were blocked by a lorglumide pre-treatment (p>0.05, LorEA versus control).
  
  
  CONCLUSIONS
  Our finding suggests that ST36 electroacupuncture stimulation activates the nucleus tractus solitarius neurons via cholecystokinin A receptor signaling pathway, which may be the underlying central mechanism of electroacupuncture-induced satiety effect.
authors.affiliation: Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Korea; Acupuncture and Meridian Science Research Center, Kyung Hee University, Seoul 130-701, Korea.
authors.forename: Sun Kwang
authors.initials: SK
authors.lastname: Kim
authors.forename: Jongyoon
authors.initials: J
authors.lastname: Kim
authors.forename: Hyun Su
authors.initials: HS
authors.lastname: Woo
authors.forename: Hyunjeong
authors.initials: H
authors.lastname: Jeong
authors.forename: Hyejung
authors.initials: H
authors.lastname: Lee
authors.forename: Byung-Il
authors.initials: BI
authors.lastname: Min
authors.forename: Sangsoo
authors.initials: S
authors.lastname: Nam
authors.forename: Hyunsu
authors.initials: H
authors.lastname: Bae
mesh_terms: D000818:Animals; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D015671:Electroacupuncture / Q000379:methods*; D005215:Fasting / Q000502:physiology*; D005455:Fluorescent Antibody Technique; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043886:Receptor, Cholecystokinin A / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*
chemical_list: D006727:Hormone Antagonists; D016760:Proto-Oncogene Proteins c-fos; D043886:Receptor, Cholecystokinin A; D011377:Proglumide; C048181:lorglumide