FIG. 3.

Physiological Ca²⁺ transients induced by motor neuron impulses help prevent mitochondrial Ca²⁺ overload and ROS overproduction. After denervation, elevated nAChR expression likely contributed to the increase of cytosolic Ca²⁺ in the skeletal muscle, which overloads mitochondrial matrix Ca²⁺ content. This promotes the production of ROS, increases structural damage to the mitochondria, and facilitates mPTP opening. However, the elevated ROS production could be reversed by the application of electric field stimulation that simulates physiological Ca²⁺ transients induced by neuronal impulses. nAChR, nicotinic acetylcholine receptor; ROS, reactive oxygen species.