title: Sweetened-fat intake sensitizes gamma-aminobutyric acid-mediated feeding responses elicited from the nucleus accumbens shell.
abstract: BACKGROUND
  There is much interest in exploring whether reward-driven feeding can produce druglike plasticity in the brain. The gamma-aminobutyric acid (GABA) system in the nucleus accumbens (Acb) shell, which modulates hypothalamic feeding systems, is well placed to "usurp" homeostatic control of feeding. Nevertheless, it is unknown whether feeding-induced neuroadaptations occur in this system.
  
  
  METHODS
  Separate groups of ad libitum-maintained rats were exposed to daily bouts of sweetened-fat intake, predator stress, or intra-Acb shell infusions of either d-amphetamine (2 or 10 μg) or the μ-opioid agonist D-[Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO, 2.5 μg), then challenged with intra-Acb shell infusion of the GABAA agonist, muscimol (10 ng).
  
  
  RESULTS
  Exposure to sweetened fat robustly sensitized muscimol-induced feeding. Sensitization was present 1 week after cessation of the palatable feeding regimen but had abated by 2 weeks. Rats exposed to sweetened fat did not show an altered feeding response to food deprivation. Repeated intra-Acb shell infusions of DAMGO (2.5 μg) also sensitized intra-Acb shell muscimol-driven feeding. However, neither repeated intra-Acb shell d-amphetamine infusions (2 or 10 μg) nor intermittent exposure to an aversive stimulus (predator stress) altered sensitivity to muscimol.
  
  
  CONCLUSIONS
  Palatable feeding engenders hypersensitivity of Acb shell GABA responses; this effect may involve feeding-induced release of opioid peptides. Heightened arousal, aversive experiences, or increased catecholamine transmission alone are insufficient to produce the effect, and a hunger-induced feeding drive is insufficient to reveal the effect. These findings reveal a novel type of food-induced neuroadaptation within the Acb; possible implications for understanding crossover effects between food reward and drug reward are discussed.
authors: Department of Psychiatry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
authors: Sarah
authors: S
authors: Newman
authors: Lindsay
authors: L
authors: Pascal
authors: Ken
authors: K
authors: Sadeghian
authors: Brian A
authors: BA
authors: Baldo
mesh_terms: D000818:Animals; D003913:Dextroamphetamine / Q000494:pharmacology; D004041:Dietary Fats / Q000494:pharmacology*; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology; D005247:Feeding Behavior / Q000187:drug effects*; D058785:GABA-A Receptor Agonists / Q000494:pharmacology; D008297:Male; D009118:Muscimol / Q000494:pharmacology; D009714:Nucleus Accumbens / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013315:Stress, Psychological / Q000503:physiopathology*; D013395:Sucrose / Q000494:pharmacology*; D013549:Sweetening Agents / Q000494:pharmacology
chemical_list: D004041:Dietary Fats; D018765:Dopamine Uptake Inhibitors; D058785:GABA-A Receptor Agonists; D013549:Sweetening Agents; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D009118:Muscimol; D013395:Sucrose; D003913:Dextroamphetamine