Acetylcholine initiates skeletal muscle contraction by transmitting a motor neuron's signal across the neuromuscular junction to the muscle fibre. It causes depolarization of the muscle membrane, leading to calcium release and the start of cross-bridge cycling.
The Mechanism
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An action potential reaches the axon terminal of a motor neuron, opening voltage-gated calcium ion channels. Calcium ions enter the terminal and cause vesicles containing acetylcholine to fuse with the presynaptic membrane.
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Acetylcholine is released by exocytosis into the synaptic cleft. It diffuses across the cleft and binds to nicotinic acetylcholine receptors on the motor end plate of the muscle fibre.
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These receptors are ligand-gated ion channels. Their opening produces a net influx of sodium ions, depolarizing the sarcolemma. If the threshold is reached, a muscle action potential is generated.
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The action potential travels along the sarcolemma and down the transverse tubules. This stimulates the sarcoplasmic reticulum to release calcium ions into the sarcoplasm.
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Calcium ions bind to troponin, changing its shape and moving tropomyosin away from the myosin-binding sites on actin. Myosin heads can then form cross-bridges with actin, allowing the sliding filament mechanism to produce contraction.
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Acetylcholinesterase rapidly breaks down acetylcholine in the synaptic cleft. This prevents continuous stimulation and allows the muscle fibre to relax when motor neuron activity stops and calcium is pumped back into the sarcoplasmic reticulum.
A common misconception is that acetylcholine directly makes actin and myosin slide. It does not: acetylcholine initiates the electrical signal that causes calcium release, while calcium permits cross-bridge formation.
Exam Technique
For IB SEHS subtopic B.1.3, explain the sequence in causal order: acetylcholine release, receptor binding, sarcolemma depolarization, calcium release, troponin binding, exposure of actin sites, and cross-bridge cycling. Distinguish clearly between events at the neuromuscular junction and events inside the muscle fibre.
