Question about action potentials

[591489]

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Hello,

I am studying the nervous system and I had two questions I was hoping you could help me with.

1) I have read that the refractory period in action potentials sets a limit on the frequency with which an actions potentials can occur. If that is so, then how come tetanus can provide a seemingly constant supply of action potentials?

2) Action potentials are all or nothing. So, I am assuming this means that the voltage gated Na channels only open with a certain voltage. But, we can also get depolarization at values less than the threshold voltage. What channels are causing this depolarization? I assume the are Na channels but arent those voltage gated? Are there some Na channels that are not voltage gated but are gradient gated?

Thanks!

 

[ChEMD]

1) Tetany is reffering to the constant contraction of a muscle, a slightly different concept than just supply of action potentials. Basically, in order for a muscle to contract, calcium must be released from the sarcoplasmic reticulum (SR) within the muscle cells into the cell cytoplasm, which is a voltage-gated process. When an action potential depolarizes the cell, the calcium channels on the SR open and release Ca into the cytoplasm, which leads to contraction via the actin/myosin system. Tetany basically means that the calcium concentration in the cytoplasm remains high, and thus, the muscle keeps contracting. It requires a certain rate of depolarization by the action potentials. If the cell is allowed to re-polarize, the calcium will be taken back up into the SR and the contraction will stop. That's why you get tetany when you have a constant supply of action potentials. It's not that the action potential is always there, but they are being fired at a rate that keeps the cell depolarized and the calcium concentration within the cell high.

2) Depolarization of cells without action potentials can occur via non-specific cation channels. Some of these channels are always open, which is why the resting potential of normal cells is higher than the nernst potential for potassium. These channels can also be triggered to open in different ways, such as voltage-gated or ligand-gated. For instance, the channels that actually cause the initial depolarization of muscle cells on the post-synaptic membrane are triggered to open when they bind to acetylcholine. These channels are non-specific cation channels and lead to depolarization of the muscle cell to the threshold potential, which then triggers the opening of the sodium channels.

Sorry if these answers were in more depth than you've studied, but once you get to the material it'll all make sense! Hope this helped.

 

[591489]

1) Tetany is reffering to the constant contraction of a muscle, a slightly different concept than just supply of action potentials. Basically, in order for a muscle to contract, calcium must be released from the sarcoplasmic reticulum (SR) within the muscle cells into the cell cytoplasm, which is a voltage-gated process. When an action potential depolarizes the cell, the calcium channels on the SR open and release Ca into the cytoplasm, which leads to contraction via the actin/myosin system. Tetany basically means that the calcium concentration in the cytoplasm remains high, and thus, the muscle keeps contracting. It requires a certain rate of depolarization by the action potentials. If the cell is allowed to re-polarize, the calcium will be taken back up into the SR and the contraction will stop. That's why you get tetany when you have a constant supply of action potentials. It's not that the action potential is always there, but they are being fired at a rate that keeps the cell depolarized and the calcium concentration within the cell high.

2) Depolarization of cells without action potentials can occur via non-specific cation channels. Some of these channels are always open, which is why the resting potential of normal cells is higher than the nernst potential for potassium. These channels can also be triggered to open in different ways, such as voltage-gated or ligand-gated. For instance, the channels that actually cause the initial depolarization of muscle cells on the post-synaptic membrane are triggered to open when they bind to acetylcholine. These channels are non-specific cation channels and lead to depolarization of the muscle cell to the threshold potential, which then triggers the opening of the sodium channels.

Sorry if these answers were in more depth than you've studied, but once you get to the material it'll all make sense! Hope this helped.

Oh I see now. Thanks!

As for your response to 1), you mentioned that "If the cell is allowed to re-polarize, the calcium will be taken back up into the SR and the contraction will stop." But doesn't repolarization happen during the second half of every action potential? If it does, then wouldn't calcium be taken back up into the SR with every action potential?

 

[ChEMD]

I think you may be confusing nerve axons with muscle cells. Like I mentioned before, as long as acetylcholine is in the synaptic cleft, the muscle cell will remain stimulated and depolarized. As long as the frequency of the action potentials is high enough, aceytlcholine will continue to be released into the synaptic cleft faster than it is gotten rid of, leading to the constant muscle stimulation.

 

[SN2ed]

Thread closed. These types of questions belong in the MCAT Study Q&A only.