title: Natural reward-related learning in rats with neonatal ventral hippocampal lesions and prior cocaine exposure.
abstract: BACKGROUND
  Psychostimulant injections in rats have been shown to alter future performance in natural reward conditioning. These effects may represent a persistent impact of drugs on neurocircuits that interface cognitive and motivational processes, which may be further altered in neuropsychiatric conditions that entail increased addiction vulnerability.
  
  
  OBJECTIVE
  This study investigated whether a rat model of schizophrenia with cocaine addiction vulnerability shows altered natural reward conditioning with or without prior cocaine exposure.
  
  
  METHODS
  Adult rats with SHAM or neonatal ventral hippocampal lesions were given cocaine (15 mg/kg per day for 5 days) or saline injections, followed 7 days later by natural reward-conditioned learning. Over ten daily sessions, water-restricted rats were assessed for durations of head entries into a magazine during random water presentations, a conditioning stimulus phase predictive of the water reward, and an "inappropriate" phase when conditioning stimuli were absent and reward presentation would be delayed.
  
  
  RESULTS
  Over repeated sessions, lesioned and SHAM rats showed similar reductions in total magazine entry durations, with similar increases in the allocations of entry times during the water presentation. However, lesioned rats, especially those exposed to cocaine, demonstrated reduced allocations of magazine entry times during the conditioning stimulus phase, and increased allocations during the inappropriate phase.
  
  
  CONCLUSIONS
  Intact natural reward motivation accompanied by deficient learning of complex contingencies to guide efficient reward approach may represent a form of impulsivity as an addiction vulnerability trait marker in an animal model of schizophrenia.
authors.affiliation: Laboratory for Translational Neuroscience of Dual Diagnosis Disorders, Institute of Psychiatric Research, Indiana University School of Medicine, 791 Union Drive, Indianapolis, IN 46202, USA. robchamb@iupui.edu
authors.forename: R Andrew
authors.initials: RA
authors.lastname: Chambers
authors.forename: Rachel M
authors.initials: RM
authors.lastname: Jones
authors.forename: Scott
authors.initials: S
authors.lastname: Brown
authors.forename: Jane R
authors.initials: JR
authors.lastname: Taylor
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D003042:Cocaine / Q000494:pharmacology*; D003216:Conditioning, Operant / Q000187:drug effects / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005260:Female; D006624:Hippocampus / Q000293:injuries / Q000502:physiology*; D007051:Ibotenic Acid / Q000633:toxicity; D007858:Learning / Q000187:drug effects* / Q000502:physiology*; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012055:Reinforcement Schedule; D012201:Reward
chemical_list: D018690:Excitatory Amino Acid Agonists; D007051:Ibotenic Acid; D003042:Cocaine