title: Decreased consumption of sweet fluids in μ opioid receptor knockout mice: a microstructural analysis of licking behavior.
abstract: BACKGROUND
  Evidence suggests that the palatability of food (i.e., the hedonic impact produced by its sensory features) can promote feeding and may underlie compulsive eating, leading to obesity. Pharmacological studies implicate opioid transmission in the hedonic control of feeding, though these studies often rely on agents lacking specificity for particular opioid receptors.
  
  
  OBJECTIVE
  Here, we investigated the role of mu opioid receptors (MORs) specifically in determining hedonic responses to palatable sweet stimuli.
  
  
  METHODS
  In Experiment 1, licking microstructure when consuming sucrose solution (2 to 20 %) was compared in MOR knockout and wildtype mice as a function of sucrose concentration and level of food deprivation. In Experiment 2, a similar examination was conducted using the palatable but calorie-free stimulus sucralose (0.001 to 1 %), allowing study of licking behavior independent of homeostatic variables.
  
  
  RESULTS
  In Experiment 1, MOR knockout mice exhibited several alterations in sucrose licking. Although wildtype mice exhibited a twofold increase in the burst length when food deprived, relative to the nondeprived test, this aspect of sucrose licking was generally insensitive to manipulations of food deprivation for MOR knockout mice. Furthermore, during concentration testing, their rate of sucrose licking was less than half that of wildtype mice. During sucralose testing (Experiment 2), MOR knockout mice licked at approximately half the wildtype rate, providing more direct evidence that MOR knockout mice were impaired in processing stimulus palatability.
  
  
  CONCLUSIONS
  These results suggest that transmission through MORs mediates hedonic responses to palatable stimuli, and therefore likely contributes to normal and pathological eating.
authors.affiliation: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, 760 Westwood Plaza, Los Angeles, CA 90024-1759, USA. sostlund@ucla.edu
authors.forename: Sean B
authors.initials: SB
authors.lastname: Ostlund
authors.forename: Alisa
authors.initials: A
authors.lastname: Kosheleff
authors.forename: Nigel T
authors.initials: NT
authors.lastname: Maidment
authors.forename: Niall P
authors.initials: NP
authors.lastname: Murphy
mesh_terms: D000818:Animals; D004435:Eating / Q000502:physiology*; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D005508:Food Deprivation / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017450:Receptors, Opioid, mu / Q000172:deficiency* / Q000235:genetics; D012201:Reward; D013395:Sucrose / Q000008:administration & dosage* / Q000031:analogs & derivatives*
chemical_list: D017450:Receptors, Opioid, mu; D013395:Sucrose; C026285:trichlorosucrose