| Reduction in phencyclidine induced sensorimotor gating deficits in the rat following increased system x(c) (-) activity in the medial prefrontal cortex. | |
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MedLine Citation:
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PMID: 23192314 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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RATIONALE: Aspects of schizophrenia, including deficits in sensorimotor gating, have been linked to glutamate dysfunction and/or oxidative stress in the prefrontal cortex. System x(c) (-), a cystine-glutamate antiporter, is a poorly understood mechanism that contributes to both cellular antioxidant capacity and glutamate homeostasis. OBJECTIVES: Our goal was to determine whether increased system x(c) (-) activity within the prefrontal cortex would normalize a rodent measure of sensorimotor gating. METHODS: In situ hybridization was used to map messenger RNA (mRNA) expression of xCT, the active subunit of system x(c) (-), in the prefrontal cortex. Prepulse inhibition was used to measure sensorimotor gating; deficits in prepulse inhibition were produced using phencyclidine (0.3-3 mg/kg, sc). N-Acetylcysteine (10-100 μM) and the system x(c) (-) inhibitor (S)-4-carboxyphenylglycine (CPG, 0.5 μM) were used to increase and decrease system x(c) (-) activity, respectively. The uptake of (14)C-cystine into tissue punches obtained from the prefrontal cortex was used to assay system x(c) (-) activity. RESULTS: The expression of xCT mRNA in the prefrontal cortex was most prominent in a lateral band spanning primarily the prelimbic cortex. Although phencyclidine did not alter the uptake of (14)C-cystine in prefrontal cortical tissue punches, intraprefrontal cortical infusion of N-acetylcysteine (10-100 μM) significantly reduced phencyclidine- (1.5 mg/kg, sc) induced deficits in prepulse inhibition. N-Acetylcysteine was without effect when coinfused with CPG (0.5 μM), indicating an involvement of system x(c) (-). CONCLUSIONS: These results indicate that phencyclidine disrupts sensorimotor gating through system x(c) (-) independent mechanisms, but that increasing cystine-glutamate exchange in the prefrontal cortex is sufficient to reduce behavioral deficits produced by phencyclidine. |
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Authors:
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Victoria Lutgen; Krista Qualmann; Jon Resch; Linghai Kong; Sujean Choi; David A Baker |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-11-29 |
Journal Detail:
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Title: Psychopharmacology Volume: - ISSN: 1432-2072 ISO Abbreviation: Psychopharmacology (Berl.) Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-11-29 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7608025 Medline TA: Psychopharmacology (Berl) Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Biomedical Sciences, Marquette University, Suite 446, 561 N. 15th St, Milwaukee, WI, 53233, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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