In skeletal muscles, acetylcholine is released by nerve terminals at the motor end plate—the point of synaptic communication between motor neurons and muscle fibers. Binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle stimulation.
Individuals with the disorder myasthenia gravis, develop antibodies against the acetylcholine receptor. This prevents transmission of electrical signals between the motor neuron and muscle fiber and impairs skeletal muscle contraction. Myasthenia gravis is treated using drugs that inhibit acetylcholinesterase (allowing more opportunities for the neurotransmitter to stimulate the remaining receptors) or suppress the immune system (preventing the formation of antibodies).
Unlike skeletal muscles, smooth muscles present in the walls of internal organs are innervated by the autonomic nervous system and undergo involuntary contractions. Contraction is mediated by the interaction between two filament proteins—actin and myosin. The interaction of actin and myosin is closely linked to intracellular calcium concentration. In response to neurotransmitter or hormone signals or stretching of the muscle, extracellular calcium enters the cell through calcium channels on the sarcolemma or is released intracellularly from the sarcoplasmic reticulum. Inside the cell, calcium binds to the regulatory protein calmodulin. The calcium-calmodulin complex then activates the enzyme myosin light chain kinase, which phosphorylates myosin and allows it to interact with actin, causing the muscle to contract.
