title: Contributions of the orbitofrontal cortex to impulsive choice: interactions with basal levels of impulsivity, dopamine signalling, and reward-related cues.
abstract: BACKGROUND
  Individual differences in impulsive decision-making may be critical determinants of vulnerability to impulse control disorders and substance abuse, yet little is known of their biological or behavioural basis. The orbitofrontal cortex (OFC) has been heavily implicated in the regulation of impulsive decision-making. However, lesions of the OFC in rats have both increased and decreased impulsivity in delay-discounting paradigms, where impulsive choice is defined as the selection of small immediate over larger delayed rewards.
  
  
  OBJECTIVE
  Reviewing the different methods used, we hypothesized that the effects of OFC inactivation on delay discounting may be critically affected by both subjects' baseline level of impulsive choice and the presence or absence of a cue to bridge the delay between selection and delivery of the large reward.
  
  
  RESULTS
  Here, we show that OFC inactivation increased impulsive choice in less impulsive rats when the delay was cued, but decreased impulsive choice in highly impulsive rats in an uncued condition.
  
  
  CONCLUSIONS
  Providing explicit environmental cues to signal the delay-to-reinforcement appears to change the way in which the OFC is recruited in the decision-making process in a baseline-dependent fashion. This change may reflect activation of the dopamine system, as intra-OFC infusions of dopamine receptor antagonists increased impulsive choice but only when the delay was cued.
authors.affiliation: Department of Psychology, University of British Columbia, 2136 West Mall, Vancouver, BC, V6T 1Z4, Canada. fzeeb@psych.ubc.ca
authors.forename: Fiona D
authors.initials: FD
authors.lastname: Zeeb
authors.forename: Stan B
authors.initials: SB
authors.lastname: Floresco
authors.forename: Catharine A
authors.initials: CA
authors.lastname: Winstanley
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D002755:Choice Behavior / Q000502:physiology*; D003216:Conditioning, Operant / Q000187:drug effects; D003463:Cues; D004298:Dopamine / Q000378:metabolism*; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D018755:GABA Agonists / Q000494:pharmacology; D007175:Impulsive Behavior / Q000503:physiopathology*; D008297:Male; D009118:Muscimol / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D020318:Rats, Long-Evans; D012055:Reinforcement Schedule; D012201:Reward; D012457:Salicylamides / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
chemical_list: D001552:Benzazepines; D018492:Dopamine Antagonists; D018755:GABA Agonists; C534628:SCH 23390; D012457:Salicylamides; D009118:Muscimol; D001418:Baclofen; C045989:eticlopride; D004298:Dopamine