PMID- 25540609
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20141225
LR  - 20200929
IS  - 1662-5102 (Print)
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 8
DP  - 2014
TI  - Neuronal involvement in muscular atrophy.
PG  - 405
LID - 10.3389/fncel.2014.00405 [doi]
LID - 405
AB  - 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.
FAU - Cisterna, Bruno A
AU  - Cisterna BA
AD  - Departamento de Fisiologia, Pontificia Universidad Catolica de Chile Santiago, 
      Chile.
FAU - Cardozo, Christopher
AU  - Cardozo C
AD  - Center of Excellence for the Medical Consequences of Spinal Cord Injury, James J. 
      Peters Veterans Affairs Medical Center Bronx, NY, USA ; Departments of Medicine 
      and Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai New York, 
      NY, USA.
FAU - Saez, Juan C
AU  - Saez JC
AD  - Departamento de Fisiologia, Pontificia Universidad Catolica de Chile Santiago, 
      Chile ; Instituto Milenio, Centro Interdisciplinario de Neurociencias de 
      Valparaiso, Universidad de Valparaiso Valparaiso, Chile.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20141210
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC4261799
OTO - NOTNLM
OT  - acetylcholine
OT  - connexins
OT  - electrical activity
OT  - hemichannels
OT  - trophic factors
EDAT- 2014/12/30 06:00
MHDA- 2014/12/30 06:01
PMCR- 2014/01/01
CRDT- 2014/12/26 06:00
PHST- 2014/05/07 00:00 [received]
PHST- 2014/11/10 00:00 [accepted]
PHST- 2014/12/26 06:00 [entrez]
PHST- 2014/12/30 06:00 [pubmed]
PHST- 2014/12/30 06:01 [medline]
PHST- 2014/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2014.00405 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2014 Dec 10;8:405. doi: 10.3389/fncel.2014.00405. 
      eCollection 2014.