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Cerebral Cortex Advance Access published online on December 19, 2007
Cerebral Cortex, doi:10.1093/cercor/bhm236
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© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Evidence of Temporal Cortical Dysfunction in Rhesus Monkeys following Chronic Cocaine Self-Administration

S. Liu1, R. P. Heitz2, A. R. Sampson3, W. Zhang3 and C. W. Bradberry1,4,5

1 Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15261, USA, 2 Center for Integrative and Cognitive Neuroscience, Vanderbilt University, Nashville, TN 37203, USA, 3 Department of Statistics, 4 Department of Neuroscience, 5 VA Pittsburgh Healthcare System, University of Pittsburgh, Pittsburgh, PA 15261, USA

Address correspondence to C. W. Bradberry, Department of Psychiatry, Rm. 4078, 3501 Fifth Ave., Pittsburgh, PA 15261, USA. Email: bradberrycw{at}upmc.edu.

Cocaine abusers show impaired performance on cognitive tasks that engage prefrontal cortex. These deficits may contribute to impaired control and relapse in abusers. Understanding the neuronal substrates that lead to these deficits requires animal models that are relevant to the human condition. However, to date, models have mostly focused on behaviors mediated by subcortical systems. Here we evaluated the impact of long-term self-administration of cocaine in the rhesus monkey on cognitive performance. Tests included stimulus discrimination (SD)/reversal and delayed alternation tasks. The chronic cocaine animals showed marked deficits in ability to organize their behavior for maximal reward. This was demonstrated by an increased time needed to acquire SDs. Deficits were also indicated by an increased time to initially learn the delayed alternation task, and to adapt strategies for bypassing a reliance on working memory to respond accurately. Working memory per se (delay dependent performance) was not affected by chronic self-administration. This pattern of cognitive deficits suggests dysfunction that extends beyond localized prefrontal cortical areas. In particular, it appears that temporal cortical function is also compromised. This agrees with other recent clinical and preclinical findings, and suggests further study into addiction related dysfunction across more widespread cortical networks is warranted.

Key Words: addiction • cognition • prefrontal • primate • psychostimulant


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