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Am J Physiol Cell Physiol. 2012 Jan 1;302(1):C141-53. doi: 10.1152/ajpcell.00469.2010. Epub 2011 Oct 5.

Genetic deletion of trkB.T1 increases neuromuscular function.

Author information

1
University of Maryland Baltimore School of Nursing, Baltimore, Maryland 21201, USA. sdorsey@son.umaryland.edu

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.

PMID:
21865582
PMCID:
PMC3328911
DOI:
10.1152/ajpcell.00469.2010
[Indexed for MEDLINE]
Free PMC Article

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