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Abstract Neurotrophin-dependent activation of the tyrosine kinase receptor trkB.FL modulates neuromuscular synapse maintenance and function; however, it is unclear what role the alternative splice variant, truncated trkB ( trkB.T1 ), may have in the peripheral neuromuscular axis. We examined this question in trkB.T1 null mice and demonstrate that in vivo neuromuscular performance and nerve-evoked muscle tension are significantly increased. In vitro assays indicated that the gain-in-function in trkB.T1 −/− animals resulted specifically from an increased muscle contractility, and increased electrically evoked calcium release. In the trkB.T1 null muscle, we identified an increase in Akt activation in resting muscle as well as a significant increase in trkB.FL and Akt activation in response to contractile activity. On the basis of these findings, we conclude that the trkB signaling pathway might represent a novel target for intervention across diseases characterized by deficits in neuromuscular function. neurotrophin neuromuscular junction calcium knockout mouse Copyright © 2012 the American Physiological Society « Previous | Next Article » Table of Contents This Article Published online before print August 2011 , doi: 10.​1152/​ajpcell.​00469.​2010 Am J Physiol Cell Physiol January 2012 vol. 302 no. 1 C141-C153 » Abstract Free Full Text Full Text (PDF) Supplemental Figures and Tables All Versions of this Article: ajpcell.00469.2010v3 302/1/C141 most recent Classifications Muscle Cell Biology and Cell Motility Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Dorsey, S. G. Articles by Ward, C. W. PubMed PubMed citation Articles by Dorsey, S. G. Articles by Ward, C. W. Related Content Load related web page information Current Issue January 2012, 302 (1) Alert me to new issues of Am J Physiol Cell Physiol About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2011 the American Physiological Society Print ISSN: 0363-6143 Online ISSN: 1522-1563 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview();

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Genetic deletion of trkB.T1 increases neuromuscular function

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  • Publisher American Physiological Society
  • Copyright Copyright © 2011 the American Physiological Society
  • ISSN 0363-6143
  • eISSN 1522-1563
  • D.O.I. 10.1152/ajpcell.00469.2010
  • Publisher site Get PDF  

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