Skeletal muscle

[Ref: WG21:Chp3]

RMP: -90mV
Duration: 2-4ms
Absolute refractory period: 1-3 ms
Conduction velocity: 5 m/s
Ionic changes are similar to nerve
* Depolarisation: Na+ influx
* Repolarisation: K+ efflux
Depolarisation starts at neuromuscular end-plate

Starts 2ms after start of depolarisation, before repolarisation is complete

Troponin I is tightly bound to actin
Tropomyosin covers the sites where myosin heads bind to actin (thus inhibiting preventing interaction between myosin and actin)

AP travels down nerve

--> Acetylcholine at neuromuscular junction (NMJ)

--> Acetylcholine binds to nicotinic acetylcholine receptors on muscle end-plate

--> Depolarisation of the end-plate

--> AP propagated over muscle membrane

--> AP travels along T-tubules

--> Triggers release of Ca2+ from terminal cisterns
* via dihydropyridine receptors

--> Ca2+ binds to troponin C

--> Weakens binding of troponin I to actin

--> Tropomyosin moves laterally

--> Binding site on actin (for myosin) exposed

When binding site on actin is exposed

--> Myosin head binds to actin

--> Myosin head bends and utilises one ATP

--> Sarcomere shortens by about 10nm

--> Myosin head detaches

Channel protein for voltage-dependent L-type Ca2+ channel
High affinity to dihydropyridine (antagonist)
In cardiac muscles, AP triggers Ca2+ influx via these channels which in turn triggers release of more Ca2+ from SR (via a non-voltage-gated Ca2+ channel on SR (ryanodine receptor))
In skeletal muscles, it senses voltage changes and directly opens ryanodine receptor channel, causing Ca2+ release from SR
In skeletal muscles, influx of Ca2+ from ECF via dihydropyridine is not necessary to trigger Ca2+ release from SR

--> Sarcoplasmic reticulum actively transport Ca2+ back into its longitudinal portion
* by Ca-Mg ATPase pump

--> Ca2+ diffuse back into terminal cisterns

--> Ready for release when AP arrives

--> Once Ca2+ outside the reticulum dropped enough, contraction ceases

NB: