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    Increased expression of the nicotinic acetylcholine receptor in stimulated muscle


    O'Reilly, Clare and Pette, Dirk and Ohlendieck, Kay (2003) Increased expression of the nicotinic acetylcholine receptor in stimulated muscle. Biochemical and Biophysical Research Communications, 300 (2). pp. 585-591. ISSN 0006-291X

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    Abstract

    Chronic low-frequency stimulation has been used as a model for investigating responses of skeletal muscle fibres to enhanced neuromuscular activity under conditions of maximum activation. Fast-to-slow isoform shifting of markers of the sarcoplasmic reticulum and the contractile apparatus demonstrated successful fibre transitions prior to studying the effect of chronic electro-stimulation on the expression of the nicotinic acetylcholine receptor. Comparative immunoblotting revealed that the alpha- and delta-subunits of the receptor were increased in 10-78 day stimulated specimens, while an associated component of the surface utrophin-glycoprotein complex, beta-dystroglycan, was not drastically changed in stimulated fast skeletal muscle. Previous studies have shown that electro-stimulation induces degeneration of fast glycolytic fibres, trans-differentiation leading to fast-to-slow fibre transitions and activation of muscle precursor cells. In analogy, our results indicate a molecular modification of the central functional unit of the post-synaptic muscle surface within existing neuromuscular junctions and/or during remodelling of nerve-muscle contacts.

    Item Type: Article
    Keywords: Low-frequency stimulation; Skeletal muscle; Fast-to-slow transition; Nicotinic acetylcholine receptor; Neuromuscular junction; Calcium-ATPase; Calsequestrin; Agrin; Dystroglycan; Dystrophin;
    Academic Unit: Faculty of Science and Engineering > Biology
    Item ID: 7513
    Identification Number: https://doi.org/10.1016/S0006-291X(02)02898-X
    Depositing User: Prof. Kay Ohlendieck
    Date Deposited: 14 Oct 2016 14:51
    Journal or Publication Title: Biochemical and Biophysical Research Communications
    Publisher: Elsevier
    Refereed: Yes
    Funders: Health Research Board (HRB), European Commission, Deutsche Forschungsgemeinschaft
    URI:

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