muscle contraction

what is a motor unit

• one motor neuron and all the nerves it innervates

• ratio of nerves to muscle fibres varies depending on muscle function

• strength- many fibres by one nerve

• control- few

• can control muscle force by recruiting more/ fewer motor units or by controlling force within a motor unit

key events at the NMJ including what is end plate potential

1. action potential propagates down the axon.

2. depolarised pre synaptic membrane causes opening of voltage gates calcium channels.

3. calcium ions diffuse into presynaptic nerve cytoplasm.

4. Presence of Ca2+ ions causes synaptic vesicles to move and fuse to presynaptic membrane. Acetylcholine is released into synaptic cleft.

5. Acetylcholine diffuses across cleft and binds with receptors on postsynaptic membrane.

6. Binding of Acetylcholine causes ligand-gated ion channels to open. Na+ ions move into the muscle cell causing depolarisation of the motor end plate (END PLATE POTENTIAL).

7. End Plate Potential causes opening of further voltage-gated ion channels along the muscle fibre – an action potential is propagated.

8. Acetylcholinesterase breaks down Acetylcholine to acetyl and choline molecules.

excitation contraction coupling

1. muscle action potential propagated

2. depolarisation of t-tubules causes opening of calcium channel between the myoplasm and SR

3. calcium released from sarcoplasmic reticulum- calcium transient

4. calcium binds to troponin c

dihydropyridine receptor and ryanodine receptor

• DHPR is voltage gated, when a muscle cell membrane depolarises it undergoes a conformational change triggering RyR to open

• RyR released stored calcium ions from SR or ER

After contraction

• calcium ions in myoplasm are pumped back into the sarcoplasmic reticulum

• pump is Ca2+ ATPase

• required ATP

• absence of calcium ions in the sarcoplasm means the muscle no longer contract

classes of neurotoxin

• presynaptic/ transmitter release inhibitor

• receptor inhibitor

• acetylcholinesterase inhibitor