- 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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- 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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