Autoimmune disorders of the muscle

In normal neuromuscular function, an impulse that is carried down an axon ends at the neuromuscular junction. Here, the impulse triggers the release of calcium in the presynaptic nerve terminal by opening voltage-gated calcium channels. The influx of calcium results in synaptic vesicle fusion with the plasma membrane and release of acetylcholine into the synaptic cleft. This acetylcholine activates acetylcholine receptors on the muscle causing the muscle to contract.

Myasthenia gravis is a chronic autoimmune neuromuscular disease that results in weakness of the skeletal muscles especially during periods of activity. In myasthenia gravis, the body produces antibodies against the acetylcholine receptor hampering the effects of acetylcholine on muscle contraction. A related autoimmune disorder called Lambert-Eaton myasthenic syndrome also causes muscle weakness. In this syndrome the body makes antibodies against presynaptic voltage-gated calcium channels. This causes a reduction in the amount of calcium that can enter the nerve ending and therefore less acetylcholine is released into the neuromuscular junction.