Action potential of a skeletal muscle fibre,where is calcium?

[sameeralord]

Now I follow this pic, there is no mention of opening of calcium channels anywhere. So how do skeletal muscles contract, without calcium. Incontrast action potential of a cardiac muscle has plateu phase and calcium channel involvement. Thanks

 

[mtc1973]

Much of the following refers to skeletal muscle only - At the end plate - the conneection between the motor nerve and the muscle - ACh is released by the neuron and the nictotinic receptors (Nm) on the muscle membrane open in response. This non selective cation channel allows the influx of sodium predominantly (although it is quite permeable to K too) which results in depolarization of the muscle membrane under the end plate. The action potential propogates throughout the muscle membrane, including the t tubules (invaginations of the plasma membrane than run deep into the cell interior) by opening of voltage sensitive Na channels (that can be blocked by tetrodotoxin).
There is very close association between the sarcoplasmic reticular membrane and the t tubule (which is an extension of the plasma membrane). The SR basically acts as a calcium resevoir, so a large store of calcium. The t tubule membrane has a voltage sensor, the dihydropyridine receptor - which is basically a calcium channel. But - they are not the source of calcium for contraction. So they are voltage sensors but it is not a calcium influc through this channel that stimulates contraction. Instead, the dihydroporidine sensitive Ca channel senses the depolarization of the t tubule - because of the opening of the voltage gates Na channels - and communicates this depolarization to the SR membrane. On the SR membrane there are ryanodine receptors (which are also calcium channels). Basically, the dihydropiridine receptor on the t tubule is in very close apposition to the ryanodine receptor on the SR membrane. So the depolarization of the t tubule (by the Na channels) is sensed by the dihydropiridine calcium channel and it then passes that information directly to the ryandoine receptor on the SR - which causes the ryanodien receptor to open and calcium to spill out of the SR into the myoplasm. There seems to be direct protein to protein interaction between the dihydropiridine receptor/channel and the ryanodine receptor/channel complex.

It is interesting that the dihydropiridine receptor/channel can conduct calcium - but it is not here as a calcium channel - it is here as a voltage sensor and to pass that info to the ryanodine receptor - which releases stored calcium. Hence skeletal muscle can contract in the absence of external calcium, i.e. has all the calcium it requires to contract stored within the cell.

So the short answer to your question - calcium channels do not confer excitability (i.e. do not contribute to the propogation of the depolarization) in skeletal muscle cells. This is different in cardiac muscle where the sustained depolarization is due to calcium entry - not Na entry as you see in your figure here.

 

[sameeralord]

Much of the following refers to skeletal muscle only - At the end plate - the conneection between the motor nerve and the muscle - ACh is released by the neuron and the nictotinic receptors (Nm) on the muscle membrane open in response. This non selective cation channel allows the influx of sodium predominantly (although it is quite permeable to K too) which results in depolarization of the muscle membrane under the end plate. The action potential propogates throughout the muscle membrane, including the t tubules (invaginations of the plasma membrane than run deep into the cell interior) by opening of voltage sensitive Na channels (that can be blocked by tetrodotoxin).
There is very close association between the sarcoplasmic reticular membrane and the t tubule (which is an extension of the plasma membrane). The SR basically acts as a calcium resevoir, so a large store of calcium. The t tubule membrane has a voltage sensor, the dihydropyridine receptor - which is basically a calcium channel. But - they are not the source of calcium for contraction. So they are voltage sensors but it is not a calcium influc through this channel that stimulates contraction. Instead, the dihydroporidine sensitive Ca channel senses the depolarization of the t tubule - because of the opening of the voltage gates Na channels - and communicates this depolarization to the SR membrane. On the SR membrane there are ryanodine receptors (which are also calcium channels). Basically, the dihydropiridine receptor on the t tubule is in very close apposition to the ryanodine receptor on the SR membrane. So the depolarization of the t tubule (by the Na channels) is sensed by the dihydropiridine calcium channel and it then passes that information directly to the ryandoine receptor on the SR - which causes the ryanodien receptor to open and calcium to spill out of the SR into the myoplasm. There seems to be direct protein to protein interaction between the dihydropiridine receptor/channel and the ryanodine receptor/channel complex.

It is interesting that the dihydropiridine receptor/channel can conduct calcium - but it is not here as a calcium channel - it is here as a voltage sensor and to pass that info to the ryanodine receptor - which releases stored calcium. Hence skeletal muscle can contract in the absence of external calcium, i.e. has all the calcium it requires to contract stored within the cell.

So the short answer to your question - calcium channels do not confer excitability (i.e. do not contribute to the propogation of the depolarization) in skeletal muscle cells. This is different in cardiac muscle where the sustained depolarization is due to calcium entry - not Na entry as you see in your figure here.

Thanks. You always pass on great information