The role of prelimbic cortex in instrumental conditioning.
Numerous studies have implicated human and primate prefrontal cortex in the ability to hold and manipulate goal or outcome-related information in working memory to guide the performance of forthcoming actions. Here we report that cell-body lesions of prelimbic cortex impair the ability of rats to select an action based on previously encoded action-outcome associations. Rats were food deprived and trained to press two levers, one delivering food pellets and the other a sucrose solution. All rats acquired the lever-press response although the initial acquisition in the prelimbic rats was significantly slower than in sham controls. Furthermore, whereas in sham-lesioned rats, post-training devaluation of one of the two outcomes using a specific satiety procedure produced a selective reduction in performance on the lever that in training delivered the prefed outcome, prelimbic rats failed to show a selective devaluation effect and appeared to reduce performance on both levers non-selectively. Importantly, this impairment only emerged in extinction; in subsequent experiments it was found that, when a specific action-outcome association was cued either by presentation of the outcome itself or by presenting a stimulus previously paired with the outcome, rats demonstrated an ability to select the associated action. These results suggest that action-outcome encoding may be intact in prelimbic rats and that the lesion impaired their ability to retain this learning in working memory in order to establish a course of action. Alternatively, the lesion may have altered the relative contribution of action-outcome and outcome-action associations to instrumental performance. On this account, prelimbic lesions affect action-outcome encoding but leave outcome-action associations intact providing the basis for outcome-mediated initiation of an action sufficient, perhaps, to support acquisition and performance in the lesioned rats.
Corbit
Laura H
LH
Department of Psychology and the Brain Research Institute, University of California, Box 951563, Los Angeles, CA 90095, USA.
Balleine
Bernard W
BW
D000818:Animals; D001245:Association Learning / Q000187:drug effects / Q000502:physiology*; D001522:Behavior, Animal; D003214:Conditioning, Classical; D003216:Conditioning, Operant / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005108:Extinction, Psychological / Q000502:physiology*; D005508:Food Deprivation; D008032:Limbic System / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008568:Memory / Q000502:physiology; D016202:N-Methylaspartate / Q000633:toxicity; D017397:Prefrontal Cortex / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D020318:Rats, Long-Evans; D012055:Reinforcement Schedule; D012054:Reinforcement, Psychology; D014163:Transfer, Psychology / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D016202:N-Methylaspartate