title: NK-1 receptor is involved in the decreased movement in a rat chronic acid reflux oesophagitis model.
abstract: BACKGROUND
  We previously reported that rats with reflux oesophagitis (RE) show a decrease in voluntary movement, which could be used as a measure of chronic visceral symptoms. However, what mediates these symptoms is still unknown, and pain-related neuropeptides or their receptors in oesophageal mucosa are possibly related to the symptom generation of oesophagitis. In the present study, we investigated the role of NK-1 receptor (NK-1R) as a mediator of oesophagitis symptoms.
  
  
  METHODS
  Chronic RE was surgically induced using rats. The degree or severity of oesophageal symptoms was evaluated by assessing voluntary movement, which was monitored using an infrared sensor system. The NK-1R antagonist, L-732,138, was administered and changes in voluntary movement were assessed. Ten days after surgery, the rats were killed to examine the oesophagus. NK-1R and tachykinin-1 mRNA were detected by real-time RT-PCR. NK-1R protein expression was examined by Western blotting.
  
  
  RESULTS
  Voluntary movement of the oesophagitis model rats was significantly lower than that of the sham-operated rats on day 10. The size of oesophageal mucosal erosion did not correlate with the amount of voluntary movement. The amount of NK-1R protein and mRNA in the oesophageal tissue was significantly higher at both the erosion and non-erosion sites. The amount of tachykinin-1 mRNA in oesophageal tissue at the non-erosion sites was significantly higher in oesophagitis rats. The voluntary movement of oesophagitis rats was significantly increased by the administration of L-732,138.
  
  
  CONCLUSIONS
  The NK-1R and related neuropeptides are possibly involved in the decrease in voluntary movement of RE.
authors.affiliation: Division of Upper Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Oshima
authors.forename: J
authors.initials: J
authors.lastname: Koseki
authors.forename: J
authors.initials: J
authors.lastname: Sakurai
authors.forename: J
authors.initials: J
authors.lastname: Watari
authors.forename: T
authors.initials: T
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Miwa
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D004942:Esophagitis, Peptic / Q000378:metabolism*; D004947:Esophagus / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D009068:Movement / Q000187:drug effects / Q000502:physiology*; D064729:Neurokinin-1 Receptor Antagonists; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018040:Receptors, Neurokinin-1 / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015320:Tachykinins / Q000378:metabolism; D014364:Tryptophan / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D064729:Neurokinin-1 Receptor Antagonists; D012333:RNA, Messenger; D018040:Receptors, Neurokinin-1; D015320:Tachykinins; C086089:3,5-bis(trifluoromethyl)benzyl N-acetyltryptophan; D014364:Tryptophan