American journal of physiology. Cell physiology · 2011
Genetic deletion of trkB.T1 increases neuromuscular function.
Сравнительное исследованиеСтатьяПоддержка NIH: внешняя программаResearch Support, N.I.H., IntramuralНазвание и аннотация: Перевод пока не подготовлен
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Dorsey Susan G, Lovering Richard M, Renn Cynthia L, Leitch Carmen C, Liu Xinyue, Tallon Luke J, Sadzewicz Lisa DeShong, Pratap Abhishek, Ott Sandra, Sengamalay Naomi, Jones Kristie M, Barrick Colleen, Fulgenzi Gianluca, Becker Jodi, Voelker Kevin, Talmadge Robert, Harvey Brandon K, Wyatt Ryan M, Vernon-Pitts Elizabeth, Zhang Chao, Shokat Kevan, Fraser-Liggett Claire, Balice-Gordon Rita J, Tessarollo Lino, Ward Christopher W
Аннотация
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.