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Related Experiment Video

Updated: Apr 19, 2026

Dissection of Single Skeletal Muscle Fibers for Immunofluorescent and Morphometric Analyses of Whole-Mount Neuromuscular Junctions

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Published on: August 14, 2021

Neuronal involvement in muscular atrophy.

Bruno A Cisterna¹, Christopher Cardozo², Juan C Sáez³

¹Departamento de Fisiología, Pontificia Universidad Católica de Chile Santiago, Chile.

Frontiers in Cellular Neuroscience

|December 26, 2014

Summary

Nerve signals normally suppress muscle cell channels like connexins (Cxs). Denervation increases these channels, causing muscle atrophy, but this is reduced when Cxs are absent, suggesting Cxs contribute to muscle wasting.

Keywords:

acetylcholine connexins electrical activity hemichannels trophic factors

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Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice

Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice

Published on: November 3, 2013

Area of Science:

Muscle physiology
Cellular biology
Neuroscience

Background:

Skeletal muscle innervation is vital for tone and function.
Denervation leads to myofiber atrophy and increased sarcolemma permeability.
De novo expression of hemichannels (HCs) and non-selective channels (P2X7Rs, TRPV2) occurs in denervated fast skeletal muscles.

Purpose of the Study:

To explore the mechanism by which nerve signals repress non-selective channel expression in skeletal muscle.
To review factors involved in maintaining fast skeletal muscle function and suppressing connexin hemichannel expression.

Main Methods:

This review discusses potential signaling pathways and molecules involved in regulating channel expression.
Focuses on the role of connexins (Cxs) and other channels in denervated muscle.

Main Results:

Denervation-induced muscle atrophy is significantly reduced in muscles lacking connexins 43 and 45.
The precise nerve-mediated repression mechanism for these channels remains unclear.

Conclusions:

Connexin hemichannels and other non-selective channels likely play a role in denervation-induced muscle atrophy.
Extracellular signaling molecules (ATP, BDNF, agrin/Lrp4/MuSK, Ach) are potential repressors of connexin expression.