title: Spinal cord FAAH in normal micturition control and bladder overactivity in awake rats.
abstract: OBJECTIVE
  We assessed whether spinal inhibition of the cannabinoid degrading enzyme FAAH would have urodynamic effects in normal rats and rats with bladder overactivity induced by partial urethral obstruction or prostaglandin E2. We also determined the expression of FAAH, and the cannabinoid receptors CB1 and CB2 in the sacral spinal cord.
  
  
  METHODS
  We used 44 rats for functional (cystometry) and Western blot experiments. The FAAH inhibitor oleoyl ethyl amide (3 to 300 nmol) was administered intrathecally (subarachnoidally) or intravenously. The expression of FAAH and CB1/CB2 receptors was determined by Western blot.
  
  
  RESULTS
  Oleoyl ethyl amide given intrathecally affected micturition in normal rats and rats with bladder overactivity but effects were more pronounced in the latter. In normal rats oleoyl ethyl amide only decreased micturition frequency, while it decreased frequency and bladder pressures in rats with bladder overactivity. Intravenous oleoyl ethyl amide (3 to 300 nmol) had no urodynamic effect. FAAH and CB1/CB2 receptors were expressed in the rat sacral spinal cord. The expression of CB1/CB2 receptors but not FAAH was higher in obstructed than in normal rats.
  
  
  CONCLUSIONS
  FAAH inhibition in the sacral spinal cord by oleoyl ethyl amide resulted in urodynamic effects in normal rats and rats with bladder overactivity. The spinal endocannabinoid system may be involved in normal micturition control and it appears altered when there is bladder overactivity.
authors.affiliation: Department of Urology, Ludwig-Maximilians-Universitat, Munich, Germany. claudius.fuellhase@med.uni-muenchen.de
authors.forename: Claudius
authors.initials: C
authors.lastname: Füllhase
authors.forename: Andrea
authors.initials: A
authors.lastname: Russo
authors.forename: Fabio
authors.initials: F
authors.lastname: Castiglione
authors.forename: Fabio
authors.initials: F
authors.lastname: Benigni
authors.forename: Lysanne
authors.initials: L
authors.lastname: Campeau
authors.forename: Francesco
authors.initials: F
authors.lastname: Montorsi
authors.forename: Christian
authors.initials: C
authors.lastname: Gratzke
authors.forename: Arianna
authors.initials: A
authors.lastname: Bettiga
authors.forename: Christian
authors.initials: C
authors.lastname: Stief
authors.forename: Karl-Erik
authors.initials: KE
authors.lastname: Andersson
authors.forename: Petter
authors.initials: P
authors.lastname: Hedlund
mesh_terms: D000581:Amidohydrolases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D015232:Dinoprostone / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D007275:Injections, Intravenous; D007278:Injections, Spinal; D009829:Oleic Acids / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D043885:Receptor, Cannabinoid, CB2 / Q000378:metabolism; D012016:Reference Values; D013116:Spinal Cord / Q000187:drug effects* / Q000378:metabolism; D014524:Urethral Obstruction / Q000188:drug therapy; D053201:Urinary Bladder, Overactive / Q000188:drug therapy*; D014554:Urination / Q000187:drug effects; D014563:Urodynamics / Q000187:drug effects; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000581:Amidohydrolases; D015232:Dinoprostone; D009829:Oleic Acids; D043885:Receptor, Cannabinoid, CB2; D000099252:Fatty Acid Amide Hydrolases; C571010:oleoyl ethyl amide