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    Methamphetamine-Induced Short-Term Increase and Long-Term Decrease in Spatial Working Memory Affects Protein Kinase M Zeta (PKMζ), Dopamine, and Glutamate Receptors

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    https://ezproxy.stevenson.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=psyh&AN=2015-05445-001&site=eds-live&scope=site
    Permanent Link
    10.3389/fnbeh.2014.00438
    http://hdl.handle.net/11603/7459
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    • Stevenson University Faculty and Staff Works
    • Stevenson University School of Humanities and Social Sciences Faculty and Staff Works
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    Author/Creator
    Braren, Stephen H.
    Drapala, Damian
    Tulloch, Ingrid K.
    Serrano, Peter A.
    Date
    2014-12-18
    Type of Work
    Text
    Subjects
    methamphetamine
    Short Term Memory
    Spatial Memory
    Animal Learning
    Dopamine; Kinases
    Mice
    Visuospatial Memory
    Abstract
    Methamphetamine (MA) is a toxic, addictive drug shown to modulate learning and memory, yet the neural mechanisms are not fully understood. We investigated the effects of 2 weekly injections of MA (30 mg/kg) on working memory using the radial 8-arm maze (RAM) across 5 weeks in adolescent-age mice. MA-treated mice show a significant improvement in working memory performance 1 week following the first MA injection compared to saline-injected controls. Following 5 weeks of MA abstinence mice were re-trained on a reference and working memory version of the RAM to assess cognitive flexibility. MA-treated mice show significantly more working memory errors without effects on reference memory performance. The hippocampus and dorsal striatum were assessed for expression of glutamate receptors subunits, GluA2 and GluN2B; dopamine markers, dopamine 1 receptor (D1), dopamine transporter (DAT) and tyrosine hydroxylase (TH); and memory markers, protein kinase M zeta (PKMζ) and protein kinase C zeta (PKCζ). Within the hippocampus, PKMζ and GluA2 are both significantly reduced after MA supporting the poor memory performance. Additionally, a significant increase in GluN2B and decrease in D1 identifies dysregulated synaptic function. In the striatum, MA treatment increased cytosolic DAT and TH levels associated with dopamine hyperfunction. MA treatment significantly reduced GluN2B while increasing both PKMζ and PKCζ within the striatum. We discuss the potential role of PKMζ/PKCζ in modulating dopamine and glutamate receptors after MA treatment. These results identify potential underlying mechanisms for working memory deficits induced by MA. (PsycINFO Database Record (c) 2016 APA, all rights reserved)


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    Stevenson University Library
    1525 Greenspring Valley Road
    Stevenson, MD 21153

    Website: http://stevensonlibrary.org

    Contact information:
    Elizabeth Fields
    efields2@stevenson.edu
    http://stevenson.libguides.com/sse


    If you wish to submit a copyright complaint or withdrawal request, please email mdsoar-help@umd.edu.