by J. Glen House, MD

It is common medical knowledge that nerves are able to talk to each other and relay information to muscles that control movement.   However, recently it has been discovered that muscles are also able to talk back to nerves, and play an important role in nerve development and survival.

At the Medical College of Georgia, Dr. Lin Mei recently performed animal studies in which he triggered a deletion of the muscle cell protein beta-catenin.  The results showed that the protein beta-catenin was responsible for communicating back to the nerve and aiding its development and function.  The normal nerve sends out sprouts to the muscle tissue and releases chemicals called neurotransmitters.  When beta-catenin was missing from the muscle tissue, the nerve terminals were unable to align properly and the release of neurotransmitters was impaired.  As a result, the nerve fibers were unable to survive.  In contrast, when beta-catenin was deleted from the nerve tissue the neurons were able to develop normally and survive.

This information is potentially very useful in conditions such as muscular dystrophy and ALS (Amyotrophic Lateral Sclerosis, Lou Gehrig's disease), where it is unknown why some neurons do not survive.  The presence of beta-catenin in the muscle tissue supports the "retrograde hypothesis", in which the downstream signal in the muscle controls the nerve. 

The researchers are now comparing the genetic code between the muscles with the beta-catenin deletion to that of normal muscle.  Identifying this genetic code could be significant in further research and treatment in individuals with neuromuscular diseases.

Source: 2-way cell talk provides clues about neuromuscular disease, Medical College of Georgia, February 17, 2008, http://www.eurekalert.org/pub_releases/2008-02/mcog-tct021408.php