title: Nucleus accumbens lesions decrease sensitivity to rapid changes in the delay to reinforcement.
abstract: Both humans and non-humans discount the value of rewards that are delayed or uncertain, and individuals that discount delayed rewards at a relatively high rate are considered impulsive. To investigate the neural mechanisms that mediate delay discounting, the present study examined the effects of excitotoxic lesions of the nucleus accumbens (NAC) on discounting of reward value by delay and probability. Rats were trained on delay (n=24) or probability discounting (n=24) tasks. Following training, excitotoxic lesions of the NAC were made by intracranial injections of 0.5 microl 0.15 M quinolinic acid (n=12) or vehicle (n=12) aimed at the NAC (AP +1.6, ML +/-1.5, DV -7.1). NAC lesions did not alter performance in animals tested with a constant delay (4s) or probability (0.4) of reinforcement. However, when tested with between session changes in the delay (0, 1, 2, 4, and 8s) of reinforcement, the lesioned rats had flatter discount curves than the sham group, indicating that they were less sensitive to frequent changes in the delay to reward. In contrast, the NAC lesions did not affect discounting of probabilistic rewards. NAC lesions impaired the ability to adapt to frequent between session changes in the delay to reward but did not increase or decrease discounting when the delay was held constant across sessions. NAC lesions may disrupt the ability of the animals to predict the timing of delayed rewards when the delay to reward is changed frequently.
authors.affiliation: University of Chicago, Department of Psychiatry, Chicago, IL 60637, United States.
authors.forename: Ashley
authors.initials: A
authors.lastname: Acheson
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Farrar
authors.forename: Michele
authors.initials: M
authors.lastname: Patak
authors.forename: Kathryn A
authors.initials: KA
authors.lastname: Hausknecht
authors.forename: Artur K
authors.initials: AK
authors.lastname: Kieres
authors.forename: Seulgi
authors.initials: S
authors.lastname: Choi
authors.forename: Harriet
authors.initials: H
authors.lastname: de Wit
authors.forename: Jerry B
authors.initials: JB
authors.lastname: Richards
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D001930:Brain Injuries / Q000139:chemically induced / Q000473:pathology*; D003216:Conditioning, Operant / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009714:Nucleus Accumbens / Q000293:injuries / Q000503:physiopathology*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D011336:Probability; D017378:Quinolinic Acid / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000502:physiology*; D012055:Reinforcement Schedule; D012054:Reinforcement, Psychology; D013997:Time Factors
chemical_list: D010751:Phosphopyruvate Hydratase; D017378:Quinolinic Acid