Neuronal involvement in muscular atrophy

Bruno A. Cisterna, Christopher Cardozo, Juan C. Sáez

Research output: Contribution to journalReview articlepeer-review

36 Citations (Scopus)


The innervation of skeletal myofibers exerts a crucial influence on the maintenance of muscle tone and normal operation. Consequently, denervated myofibers manifest atrophy, which is preceded by an increase in sarcolemma permeability. Recently, de novo expression of hemichannels (HCs) formed by connexins (Cxs) and other none selective channels, including P2X7 receptors (P2X7Rs), and transient receptor potential, sub-family V, member 2 (TRPV2) channels was demonstrated in denervated fast skeletal muscles. The denervation-induced atrophy was drastically reduced in denervated muscles deficient in Cxs 43 and 45. Nonetheless, the transduction mechanism by which the nerve represses the expression of the above mentioned non-selective channels remains unknown. The paracrine action of extracellular signaling molecules including ATP, neurotrophic factors (i.e., brain-derived neurotrophic factor (BDNF)), agrin/LDL receptor-related protein 4 (Lrp4)/muscle-specific receptor kinase (MuSK) and acetylcholine (Ach) are among the possible signals for repression for connexin expression. This review discusses the possible role of relevant factors in maintaining the normal functioning of fast skeletal muscles and suppression of connexin hemichannel expression.

Original languageEnglish
Article number405
JournalFrontiers in Cellular Neuroscience
Issue numberDEC
Publication statusPublished - 10 Dec 2014


  • Acetylcholine
  • Connexins
  • Electrical activity
  • Hemichannels
  • Trophic factors

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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