Impaired object recognition following prolonged withdrawal from extended-access cocaine self-administration

Abstract

Cocaine addicts have a number of cognitive deficits that persist following prolonged abstinence. These include impairments in executive functions dependent on the prefrontal cortex, as well as deficits on learning and memory tasks sensitive to hippocampal function. Recent preclinical studies using non-human animals have demonstrated that cocaine treatment can produce persistent deficits in executive functions, but there is relatively little evidence that treatment with cocaine produces persistent deficits in performance on hippocampal-dependent tasks. We recently demonstrated that extended (but not limited) access to self-administered cocaine is especially effective in producing persistent deficits on a test of cognitive vigilance, and therefore, we used this procedure to examine the effects of limited or extended access to cocaine self-administration on recognition memory performance, which is sensitive to hippocampal function. We found that extended access to cocaine produced deficits in recognition memory that persisted for at least 2 weeks after the cessation of drug use. We conclude that the deficits in learning and memory observed in cocaine addicts may be at least in part due to repeated drug use, rather than just due to a pre-existing condition, and that in studying the neural basis of such deficits procedures involving extended access to self-administered cocaine may be especially useful. Keywordsself-administration; memory; cocaine; object recognition Cocaine addicts present with a number of cognitive deficits even following prolonged abstinence. These include impaired performance on tasks involving attention and cognitive flexibility that are thought to be mediated by the medial and orbital prefrontal cortex, as well as spatial, verbal, and recognition memory impairments on tasks thought to be mediated by the hippocampus (Manschreck et al. 1990;Ardila et al. 1991;Berry et al. 1993;Beatty et al. 1995;Hoff et al. 1996;Bolla et al. 2003). Given that cognitive deficits are known to negatively impact treatment outcomes (Aharonovich et al. 2003;Aharonovich et al. 2006), the development of an animal model of persistent cocaine-induced cognitive deficits would be useful in exploring the nature of the deficit. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2009 July 31. Published in final edited form as:Neuroscience. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptA number of preclinical studies have reported that treatment with cocaine produces cognit...

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