title: Characterization of ghrelin-sensitive neurons in the lumbosacral defecation center in rats.
abstract: BACKGROUND
  Ghrelin is involved in the regulation of somatic growth, feeding behavior and energy homeostasis. Ghrelin stimulates neuropeptide Y (NPY) neurons and activates intracellular AMP-activated protein kinase (AMPK) in the hypothalamus. These NPY neurons also express the leptin receptor and leptin inhibits ghrelin-induced activation of NPY neurons. In the spinal cord, we have demonstrated colokinetic action of ghrelin. However, the precise characteristics of the ghrelin-sensitive neurons remain to be clarified. The aim of this study was firstly to confirm that the action of ghrelin is mediated via a neurogenic pathway in the spinal cord, and secondly to characterize the ghrelin-sensitive neurons by comparing with hypothalamic ghrelin-sensitive neurons.
  
  
  METHODS
  Rats were anesthetised with alpha-chloralose and ketamine, and colorectal intraluminal pressure and expelled volume were recorded in vivo. Drugs were applied intrathecally.
  
  
  RESULTS
  Ghrelin caused enhancement of propulsive contractions. Tetrodotoxin completely blocked the colokinetic effect of ghrelin. An AMPK activator, aminoimidazole carboxamide ribonucleotide, failed to mimic the ghrelin effect. Leptin had no effect on the spontaneous contractions and did not exert a suppressive effect on the ghrelin-enhanced colorectal motility. An NPY Y1 receptor antagonist did not affect the action of ghrelin. NPY had no effect on the colorectal motility.
  
  
  CONCLUSIONS
  This study showed that intrathecal injection of ghrelin stimulates colorectal motility by acting on ghrelin-sensitive neurons in the lumbosacral defecation center. The characteristics of ghrelin-sensitive neurons in the spinal cord are quite different from those of ghrelin-sensitive neurons in the hypothalamus.
authors.affiliation: Department of Basic Veterinary Science, Laboratory of Physiology, The United Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Naitou
authors.forename: T
authors.initials: T
authors.lastname: Shiina
authors.forename: R
authors.initials: R
authors.lastname: Sugita
authors.forename: H
authors.initials: H
authors.lastname: Nakamori
authors.forename: Y
authors.initials: Y
authors.lastname: Shimizu
mesh_terms: D000818:Animals; D003672:Defecation / Q000187:drug effects / Q000502:physiology; D005769:Gastrointestinal Motility / Q000187:drug effects; D054439:Ghrelin / Q000494:pharmacology / Q000502:physiology*; D007278:Injections, Spinal; D007420:Intestine, Large / Q000187:drug effects / Q000294:innervation* / Q000502:physiology*; D020738:Leptin / Q000494:pharmacology / Q000502:physiology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009478:Neuropeptide Y / Q000494:pharmacology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000502:physiology; D018013:Receptors, Neuropeptide / Q000037:antagonists & inhibitors / Q000502:physiology
chemical_list: D054439:Ghrelin; D020738:Leptin; D009478:Neuropeptide Y; C066211:Npy1r protein, rat; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide
keywords: AMPK; NPY; TTX; colorectal motility; in vivo; leptin