Response of Neuromuscular Junctions to BaCl2 and Capacity of Mitochondrial Transfer Therapy to Mitigate the Negative Effects of that Insult

Neuromuscular diseases and damage affect many people of all ages and are responsible for an exorbitant medical cost, more than $200 million annually. Finding an appropriate model to investigate potential curative interventions is necessary. One currently used involves the application of toxic agents on skeletal muscle followed by treatment interventions. A question regarding this model is whether such toxins impact not only muscle tissue, but also the neuromuscular junctions (NMJs) responsible for exciting the muscle tissue. This question was addressed here by forming 4 experimental groups: 1) Controls whose muscles had not been injured or treated, 2) muscles taken from mice that were injured and then treated with mitochondrial supplement, 3) muscles that had not been injured but still treated with mitochondria, and 4) muscles that were injured and received no mitochondrial treatment. Several pre- and post-synaptic features of NMJs received immunofluorescent staining before having morphological features assessed with confocal microscopy. Results revealed that only pre-synaptic acetylcholine (ACh) receptors showed any significant (p0.05) among treatment groups and structural features were not different between groups with the exception of dispersion of post-synaptic receptors. Overall, these results suggest that skeletal muscles damaged with toxin accurately mimic what occurs during toxin-induced damage and post-injury recovery.