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    Interplay of chemical neurotransmitters regulates developmental increase in electrical synapses

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    Park_ku_0099D_11625_DATA_1.pdf (2.108Mb)
    Issue Date
    2011-08-31
    Author
    Park, Won-Mee
    Publisher
    University of Kansas
    Format
    113 pages
    Type
    Dissertation
    Degree Level
    Ph.D.
    Discipline
    Molecular & Integrative Physiology
    Rights
    This item is protected by copyright and unless otherwise specified the copyright of this thesis/dissertation is held by the author.
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    Abstract
    Coupling of neurons by electrical synapses (gap junctions) transiently increases during embryonic and/or early postnatal development of the mammalian central nervous system and plays an important role in a number of developmental events. A previous study revealed the mechanisms that control the developmental uncoupling of neuronal gap junctions, however, developmental regulation of neuronal gap junction coupling is largely unknown and is addressed in this dissertation. The current study revealed that the developmental increase in neuronal gap junction coupling is regulated by the interplay between the activity of group II metabotropic glutamate receptors (mGluR) and GABAA receptors (GABAAR). Specifically, the experiments including dye coupling, electrotonic coupling, western blots and siRNA technology in the rat and mouse hypothalamus and cortex in vivo and in vitro demonstrated that activation of group II mGluRs augments, and inactivation prevents, the developmental increase in neuronal gap junction coupling and connexin36 (Cx36, neuronal gap junction protein) expression. In contrast, changes in GABAA receptor activity have the opposite effects. The regulation by group II mGluRs is through cyclic AMP/protein kinase A-dependent signaling, while the GABAAR-dependent regulation is via influx of Ca2+ through L-type voltage-gated Ca2+ channels and activation of protein kinase C-dependent signaling. Further, the receptor mediated up-regulation of Cx36 requires a neuron-restrictive silencer element in the Cx36 gene promoter and the down-regulation involves the 3' untranslated region of the Cx36 mRNA, as shown using real-time quantitative polymerase chain reaction and luciferase reporter activity analysis. In addition, the methyl thiazolyl tetrazolium analysis indicates that mechanism for the developmental increase in neuronal gap junction coupling directly control the death/survival mechanisms in developing neurons. Altogether, the results suggest a multi-tiered strategy for chemical synapses in developmental regulation of electrical synapses.
    URI
    http://hdl.handle.net/1808/8175
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    • Dissertations [4475]
    • Molecular Biosciences Dissertations and Theses [270]

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    785-864-8983
    KU Libraries
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    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
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    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

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