Muscle Contraction Overview
Muscle fibers are excitable, meaning they respond to chemical signals.
The site of muscle fiber stimulation is the neuromuscular junction (NMJ), where the motor neuron connects with the muscle fiber.
Components of the Neuromuscular Junction
Motor end plate: This is a specialized area of the muscle cell's membrane that interacts with the motor neuron.
Axon terminal: The end of a motor neuron where neurotransmitters are stored.
Synaptic cleft: The narrow space that separates the axon terminal from the muscle fiber.
Neurotransmitter: Acetylcholine is the chemical responsible for transmitting the signal from the neuron to the muscle fiber.
Process of Muscle Contraction
Excitation Phase
An action potential from the brain travels down the motor nerve to the axon terminal.
This action potential opens calcium channels at the terminal, allowing calcium to enter.
Calcium triggers exocytosis of synaptic vesicles, releasing acetylcholine into the synaptic cleft.
Acetylcholine binds to receptors on the motor end plate, specifically ligand-gated sodium channels.
Binding opens these channels, allowing sodium ions to flow into the muscle fiber and causing depolarization (localized depolarization is called end plate potential).
Multiple end plate potentials are required to generate a full muscle contraction.
Action of Acetylcholine
Acetylcholine must be cleared from the synaptic cleft to stop its effects.
Acetylcholine esterase is the enzyme that breaks down acetylcholine, ending the stimulation of the muscle.
Excitation-Contraction Coupling Phase
The depolarization of the motor end plate spreads along the sarcolemma (muscle membrane) and down the T-tubules, leading to the opening of voltage-gated sodium channels.
This results in a larger action potential propagation in the muscle fiber.
Depolarization activates calcium channels in the sarcoplasmic reticulum, releasing stored calcium into the cytoplasm.
Contraction Phase
Calcium binds to troponin, leading to a change in the conformation of tropomyosin.
The move of tropomyosin exposes the binding sites on actin molecules.
Myosin heads bind to the exposed active sites on actin, initiating the crossbridge cycle and leading to muscle contraction.
The contraction mechanism continues as long as calcium remains present in the cytoplasm and the ATP is available.