An action potential reaches the neuromuscular junction simultaneously causing the calcium ion channels to open and calcuim ions to move into the synapticknob.
The calcuim ions cause the synaptic vesicles to fuse with the presynaptic membrane and release acetylcholine into the synaptic cleft.
Acetylcholine diffuses across th synaptic cleft and binds with receptors on the postsynaptic membrane causing it to depolarise.
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Muscle contraction 1
The action potential travels deep into the fibre through a system of T tubules that branch throughout the sarcoplasm.
The tubules are in contact with the Sarcoplasmic reticulum which has actively absorbed calcuim ions from the sarcoplasm.
The action potential opens the calcuim ion channels on the endoplasmic reticulum and calcuim ions flood into the muscle cytoplasm down a diffusion gradient.
The calcium ions cause the troposmyosin molecules that were blocking the binding sites on the action to pull away.
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Muscle contraction 2
The ADP molecule attached to the myosin heads means they are now in a state to bind to the actin filament and form a cross bridge.
Once attached to the actin filament the myosin heads change their angle pulling the actin filament along as they do releasing a molecule of ADP.
An ATP molecule attaches to the myosin head causing it to become detached from the actin filament.
The calcium ions then activate the enzyme ATPase which hydrolyses ATP to ADP providing the energy for the myosin head to return to its normal position.
The myosin head binds to the actin filament as long as the muscle stimulation continues.
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Muscle relaxation
When the nervous stimulation ceases calcuim ions are actively transported back into the endoplasmic reticulum using energy from the hydrolysis of ATP.
The reabsoption of calcium ions causes the tropomyosin to block the actin filament again.
Myosin heads are now unable to bind to actin filamentd and contraction stops so muscle relaxes.
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