Lecture 7 : The Neuromuscular Junction

Question 1

What is a neuromuscular junction

Answer 1

Between a motor neuron and a muscle cell, rapid neurotransmission

Question 2

End plate potential

Answer 2

• -20mV is threshold, +40mV is end of action potential
• Generated by ligand-gated channels
• Threshold easily passed because there is a high density of voltage-gated Na+ channels at end plate

Question 3

How does an action potential get converted to a muscular contraction?

Answer 3

1. Action potential reaches axon terminal, depolarisation causes voltage-gated calcium channels in axon terminal to open, influx of Ca2+ occurs
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2. Influx of Ca2+ triggers synaptic vesicles containing ACh to fuse with presynaptic membrane releasing ACh into synaptic cleft by exocytosis
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3. ACh binds to post synaptic receptors, (nicotinic acetylcholine receptors) on the muscle fibre’s sarcolemma. This binding causes ligand-gated ion channels to open, allowing Na+ ions to flow into muscle cell, and K+ to flow out, generating depolarisation which is called the END PLATE POTENTIAL (-20mV is threshold, +40mV is end of action potential)
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4. If end plate potential is strong enough to reach the threshold, an action potential in the muscle fiber’s sarcolemma occurs, which travels along sarcolemma and into the muscle fibre’s T-Tubules.
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5. T-Tubules are depolarised and dihydropyridine receptors (DHPRs), which are voltage-sensitive proteins, undergo conformational change which activates ryanodine receptors on sarcoplasmic reticulum that causes Ca2+ to release from sarcoplasmic reticulum.
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6. Ca2+ released into cytoplasm of muscle fibre.
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7. Ca2+ in cytoplasm binds to troponin which is a regulatory protein attached to actin filaments. Conformational change occurs in troponin-tropomyosin complex, and the myosin-binding site on the actin filaments are exposed
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8. Myosin heads bind to the exposed binding sites on actin, forming a CROSS BRIDGE. The myosin heads undergo a power-stroke, actin filament is pulled closer to the sarcomere, muscle fibre is shortened and tension is generated which leads to muscle contraction.
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9. After power-stroke, myosin head binds to new ATP molecule causing it to detach from actin and regain its original conformation, and the process repeats in this cycle, further pulling the actin filament closer to the sarcomere until the muscle is fully contracted and all the Ca2+ is removed
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10. After action potential ceases, Ca2+ is actively pumped back into sarcoplasmic reticulum by Ca2+ ATPase pumps. As Ca2+ concentration in cytoplasm decreases troponin returns to its original shape and tropomyosin blocks actin-myosin binding sites. The cross-bridge cycle has stopped and the muscle fibre relaxes.
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    Simpler sumary
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11. Action potential in the motor neuron causes ACh release.
12. ACh binds to receptors on the sarcolemma, generating an end plate potential (EPP).
13. The muscle action potential travels along the sarcolemma and T-tubules.
14. Action potential activates the sarcoplasmic reticulum, releasing Ca²⁺.
15. Ca²⁺ binds to troponin, exposing myosin-binding sites on actin.
16. Cross-bridge formation and the power stroke lead to muscle contraction.
17. Ca²⁺ reuptake leads to muscle relaxation.