Summary
Highlights
Skeletal muscles contract only when stimulated by nerve impulses from a motor neuron. A motor unit consists of a motor neuron and the muscle fibers it innervates, which contract in unison. The size of motor units varies, with small units for fine control (e.g., eye muscles) and large units for strength (e.g., limb muscles). Muscle fibers of a motor unit are scattered to ensure a uniform effect on the whole muscle. Muscle contraction strength depends on the number of activated motor units, and even at rest, muscle tonus is maintained by alternating activation of a few units.
The connection between a motor neuron and a muscle fiber is the neuromuscular junction, a chemical synapse. An action potential reaching the nerve terminal releases acetylcholine, which binds to nicotinic receptors on the motor end-plate. These ligand-gated ion channels open, allowing sodium influx and depolarizing the membrane, creating an end-plate potential. If this potential reaches a threshold, voltage-gated sodium channels open, generating an action potential in the muscle cell.
Once generated, the action potential spreads throughout the muscle fiber and deep into T-tubules to reach the sarcoplasmic reticulum. This activates voltage-gated calcium channels, releasing calcium into the muscle cell's cytosol. This calcium then initiates muscle contraction through the 'sliding filament mechanism'.
Acetylcholinesterase, an enzyme at the neuromuscular junction, removes acetylcholine to terminate synaptic activation, allowing muscles to relax and preventing continuous contraction. Substances can interfere with the neuromuscular junction: Botulinum toxin prevents acetylcholine release, some toxins block nicotinic receptors, and certain drugs block sodium channels, all leading to flaccid paralysis. Conversely, pesticides can inhibit acetylcholinesterase, causing continuous muscle activation, spasms, and spastic paralysis.