title: Impaired flexibility in decision making in rats after administration of the pharmacological stressor yohimbine.
abstract: BACKGROUND
  Stress-induced disruption of decision making has been hypothesized to contribute to drug-seeking behaviors and addiction. Noradrenergic signaling plays a central role in mediating stress responses. However, the effects of acute stress on decision making, and the role of noradrenergic signaling in regulating these effects, have not been well characterized.
  
  
  OBJECTIVE
  To characterize changes in decision making caused by acute pharmacological stress, the effects of yohimbine (an α2-adrenergic antagonist) were examined in a delay discounting task. Noradrenergic contributions to decision making were further characterized by examining the effects of propranolol (a β antagonist), prazosin (an α1 antagonist), and guanfacine (an α2 agonist).
  
  
  METHODS
  Sprague-Dawley rats were administered drugs prior to performance on a delay discounting task, in which the delay preceding the large reward increased within each session (ascending delays). To dissociate drug-induced changes in delay sensitivity from behavioral inflexibility, drug effects were subsequently tested in a modified version of the discounting task, in which the delay preceding the large reward decreased within each session (descending delays).
  
  
  RESULTS
  Yohimbine increased choice of the large reward when tested with ascending delays but decreased choice of the same large reward when tested with descending delays, suggesting that drug effects could be attributed to perseverative choice of the lever preferred at the beginning of the session. Propranolol increased choice of the large reward when tested with ascending delays. Prazosin and guanfacine had no effect on reward choice.
  
  
  CONCLUSIONS
  The stress-like effects of yohimbine administration may impair decision making by causing inflexible, perseverative behavior.
authors.affiliation: Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT, USA.
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Schwager
authors.forename: Andrew K
authors.initials: AK
authors.lastname: Haack
authors.forename: Sharif A
authors.initials: SA
authors.lastname: Taha
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D058647:Adrenergic alpha-2 Receptor Agonists / Q000494:pharmacology; D058669:Adrenergic alpha-2 Receptor Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D002755:Choice Behavior / Q000187:drug effects; D003216:Conditioning, Operant / Q000187:drug effects; D003657:Decision Making / Q000187:drug effects*; D065786:Delay Discounting / Q000187:drug effects*; D016316:Guanfacine / Q000494:pharmacology; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012201:Reward; D015016:Yohimbine / Q000494:pharmacology*
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D015016:Yohimbine; D016316:Guanfacine; D011433:Propranolol; D011224:Prazosin