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      Appetitive overshadowing is disrupted by systemic amphetamine but not by electrolytic lesions to the nucleus accumbens shell.

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          Abstract

          There is evidence that the indirect dopamine (DA) agonist amphetamine (AMP) can disrupt selective learning in an aversive overshadowing task, consistent with a role for the DA system in this form of salience manipulation. In the following experiments we assessed in the male Wistar rat: (1) whether amphetamine disruption of overshadowing extends to an appetitively motivated overshadowing task; and (2) whether selective electrolytic lesions to the n.acc (shell versus core subfields) disrupt appetitively motivated overshadowing. The experiments used sucrose reward pellets as the unconditioned stimulus (UCS). In each case, a conditioned stimulus (CS, light) was either conditioned alone or in compound together with a more intense CS (noise or tone). The presence of overshadowing was demonstrated as reduced conditioning to the light when it had been previously conditioned in compound compared to when it had been conditioned alone. It was predicted that AMP and lesions to the n.acc shell would disrupt overshadowing. AMP was found to abolish overshadowing at 0.5 mg/kg, but not at 1 mg/kg. Contrary to prediction, the shell lesioned animals did not differ from shams. The results of Experiment 1 add to the evidence that the DA system can moderate salience processing of weaker predictors, also in cases where CS salience is manipulated directly via the physical intensities of the stimuli, as here. However, in terms of the brain structures involved, Experiment 2 suggests that, overshadowing is moderated by projections of the DA system without n.acc.

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          Author and article information

          Journal
          J. Psychopharmacol. (Oxford)
          Journal of psychopharmacology (Oxford, England)
          SAGE Publications
          0269-8811
          0269-8811
          Mar 2008
          : 22
          : 2
          Affiliations
          [1 ] School of Psychology, Institute of Neuroscience, University of Nottingham, Nottingham, UK.
          Article
          0269881107079062
          10.1177/0269881107079062
          18208926
          dfca540e-e341-483b-924a-186eb10eb437
          History

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