title: Fluoxetine differentially suppresses sucrose solution consumption in free-fed and food-deprived rats--reversal by amantadine.
abstract: BACKGROUND
  Clinical use of fluoxetine and similar medications is often associated with appetite suppression and weight loss that may warrant drug discontinuation. It is unclear, however, if fluoxetine-induced consummatory suppression may be influenced by factors such as dietary status and if appetite suppressant effects of fluoxetine may be pharmacologically attenuated.
  
  
  METHODS
  Fluoxetine (0.5-10 mg/kg, i.p.) was administered to free-fed and 24 hr food-deprived adult male rats either 30 min or 4 hr prior to presentation of a sucrose solution (10% v/v). Further, amantadine (5-10 mg/kg, i.p.) and fluoxetine (5 mg/kg) were both administered either 30 min or 4 hr prior to sucrose solution presentation and intake of the solution was assessed after 2 hours of exposure.
  
  
  RESULTS
  Fluoxetine (2-10 mg/kg) administration significantly reduced sucrose solution intake in both free-fed and food-deprived rats. However, a brief treatment-test interval (30 min) resulted in a greater suppression of intake and food-deprived rats were more resistant to the suppressant effects of fluoxetine than were sated rats. Finally, the suppressant effect of fluoxetine were reversed by acute administration of amantadine (8 mg/kg) prior to sucrose solution presentation, a dose producing no inherent stimulation of consumption.
  
  
  CONCLUSIONS
  Acute fluoxetine administration produces a reduction in palatable substance intake that is decreased in potency with a longer treatment-test interval, an effect likely not related to pharmacokinetic considerations. Further, fluoxetine-induced consummatory suppression is reduced by prior food-deprivation. Evidence that the dopamine agonist amantadine reversed fluoxetine-induced consummatory suppression suggests a role for dopaminergic antagonism in the appetite suppressant effects of fluoxetine.
authors.affiliation: Department of Psychology, University of Nebraska at Omaha, NE 68182, USA.
authors.forename: Mark A
authors.initials: MA
authors.lastname: Prendergast
authors.forename: David P
authors.initials: DP
authors.lastname: Yells
authors.forename: Scott E
authors.initials: SE
authors.lastname: Balogh
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Paige
authors.forename: Shelton E
authors.initials: SE
authors.lastname: Hendricks
mesh_terms: D000547:Amantadine / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D015259:Dopamine Agents / Q000378:metabolism / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004327:Drinking Behavior / Q000187:drug effects*; D005473:Fluoxetine / Q000378:metabolism / Q000494:pharmacology*; D005508:Food Deprivation; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D017367:Selective Serotonin Reuptake Inhibitors / Q000378:metabolism / Q000494:pharmacology*; D013395:Sucrose / Q000008:administration & dosage*
chemical_list: D000547:Amantadine; D015259:Dopamine Agents; D005473:Fluoxetine; D017367:Selective Serotonin Reuptake Inhibitors; D013395:Sucrose