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Open Access Publications from the University of California

Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation.

  • Author(s): Feng, Ning
  • Huke, Sabine
  • Zhu, Guangshuo
  • Tocchetti, Carlo G
  • Shi, Sa
  • Aiba, Takeshi
  • Kaludercic, Nina
  • Hoover, Donald B
  • Beck, Sarah E
  • Mankowski, Joseph L
  • Tomaselli, Gordon F
  • Bers, Donald M
  • Kass, David A
  • Paolocci, Nazareno
  • et al.

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BDNF and its associated tropomyosin-related kinase receptor B (TrkB) nurture vessels and nerves serving the heart. However, the direct effect of BDNF/TrkB signaling on the myocardium is poorly understood. Here we report that cardiac-specific TrkB knockout mice (TrkB(-/-)) display impaired cardiac contraction and relaxation, showing that BDNF/TrkB signaling acts constitutively to sustain in vivo myocardial performance. BDNF enhances normal cardiomyocyte Ca(2+) cycling, contractility, and relaxation via Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Conversely, failing myocytes, which have increased truncated TrkB lacking tyrosine kinase activity and chronically activated CaMKII, are insensitive to BDNF. Thus, BDNF/TrkB signaling represents a previously unidentified pathway by which the peripheral nervous system directly and tonically influences myocardial function in parallel with β-adrenergic control. Deficits in this system are likely additional contributors to acute and chronic cardiac dysfunction.

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