Active Transport?

[DeathandTaxes]

In passage 45 of TPRHL science workbook, there's a question that states:

The movement of sodium during an action potential is an example of
1. Facilitated Diffusion
2. Simple Diffusion
3. Active Transport

A. I only
B. II only.
C. I and III only
D. I, II, and III

I thought that since the Na+/K+ ATPase requires ATP to maintain the gradient, that this would be considered an example of active transport. However, the answer is that it is A.

Can someone explain why this reasoning is wrong?

On a side note: can anyone explain why the opening of K+ channels toward the end of the action potential makes it difficult to elicit another action potential immediately after first one?

 

[gettheleadout]

In passage 45 of TPRHL science workbook, there's a question that states:

The movement of sodium during an action potential is an example of
1. Facilitated Diffusion
2. Simple Diffusion
3. Active Transport

A. I only
B. II only.
C. I and III only
D. I, II, and III

I thought that since the Na+/K+ ATPase requires ATP to maintain the gradient, that this would be considered an example of active transport. However, the answer is that it is A.

Can someone explain why this reasoning is wrong?

On a side note: can anyone explain why the opening of K+ channels toward the end of the action potential makes it difficult to elicit another action potential immediately after first one?

Given the wording of the question, you are correct.

As you know, the sodium-potassium pump is continually running, so during the conduction of an action potential, there is transmembrane flow of sodium in two manners: 1) sodium influx through the voltage-gated Na+ channels and 2) sodium efflux via the sodium-potassium pump. The mechanism of (1) is facilitated diffusion and that of (2) is active transport.

The mindset of the question writer was presumably to refer only to the portion of sodium movement that is unique to the state of conducting an action potential, the (1) above. However, the question is not sufficiently specific to justify the answer given in the key. The correct answer is in fact (C), as you said.

The contribution of the voltage-gated potassium channels in resisting immediate initiation of a consequent action potential is to the relative refractory period. The relative refractory period encompasses the hyperpolarization phase of the action potential, wherein the voltage-gated potassium channels (largely responsible for the repolarization phase) lag in closing and thus the repolarization overshoots the resting potential. The sodium-potassium pump slowly restores the transmembrane potential to the resting potential, but during this period of time, a larger-than-normal excitatory post-synaptic potential (EPSP) would be necessary to initiate a new action potential.

 

[Vybe]

Basically, during an action potential, membrane pores that are specific for Na+ open up, which ALLOW Na+ to move into the cell, requiring no ATP for the time being; thus issuing the action potential. The negative charge of the membrane becomes exceedingly negative, and this is the time when it is called depolarization. So DURING the actual action potential, Na+ does not need ATP, since it has already been primed (I'll explain this in a second).

After depolarization, the Na+ pores close. The next step is, bringing the potential back down. How do we do this? We efflux (bring out) Na+ and potassium ions.

1. Na+ is brought back out with the help of Na+/K+ ATPase and ATP, (the priming of the Na+ concentration outside the membrane).
-- You can look at this as one of the main reasons why we need ATP to live. Think of a wind-up toy car. You have to rotate the little crank on the back of a toy a bunch of times before it can start driving. Once you let go, the little rotating metal piece is rotating OPPOSITE the direction you primed it to... It keeps going until it is done with its priming. It can only go again if you prime the cranker. Just like that, a cell needs to be primed by Na+ being pushed outside the cell. (Pushing 3Na+ out, 2K+ in), eventually reaching a small negative, resting potential.

2. K+ comes out through the pores that automatically open after depolarization.

So eventually, there is a point where too much of those ions goes out of the cell, which causes the introduction of the term, hyperpolarization (too positive)...
The cell works to close the K+ pores, and bring the potential back to its initial position --> The resting potential!

During the time of hyperpolarization and reaching resting potential... it is called the refractory period. (No action potential can occur because the the K+ needs to be closed. If they are open, there will be continuous outward flow of K+, which decreases the negative potential of the cell. The goal of action potentials is to have a huge influx of Na+ which makes the cell extremely negatively charged)

I hope this helps you out.

 

[gettheleadout]

Basically, during an action potential, membrane pores that are specific for Na+ open up, which ALLOW Na+ to move into the cell, requiring no ATP for the time being; thus issuing the action potential.

But the Na+/K+ ATPase is still running elsewhere in the membrane, so active transport of sodium is still occurring.

The negative charge of the membrane becomes exceedingly negative, and this is the time when it is called depolarization. So DURING the actual action potential, Na+ does not need ATP, since it has already been primed (I'll explain this in a second).

You mean positive.

1. Na+ is brought back out with the help of Na+/K+ ATPase and ATP, (the priming of the Na+ concentration outside the membrane).

-- You can look at this as one of the main reasons why we need ATP to live. Think of a wind-up toy car. You have to rotate the little crank on the back of a toy a bunch of times before it can start driving. Once you let go, the little rotating metal piece is rotating OPPOSITE the direction you primed it to... It keeps going until it is done with its priming. It can only go again if you prime the cranker. Just like that, a cell needs to be primed by Na+ being pushed outside the cell. (Pushing 3Na+ out, 2K+ in), eventually reaching a small negative, resting potential.

This paragraph is misleading because 1) the Na+/K+ ATPase is constantly running in cells, as I've stated already, and 2) the charge imbalance of ion transport by the Na+/K+ ATPase is not responsible for the resting potential being negative (you don't explicitly state that it does but it seems implied to me).

2. K+ comes out through the pores that automatically open after depolarization.

So eventually, there is a point where too much of those ions goes out of the cell, which causes the introduction of the term, hyperpolarization (too positive)...

You mean too negative.

The cell works to close the K+ pores, and bring the potential back to its initial position --> The resting potential!

During the time of hyperpolarization and reaching resting potential... it is called the refractory period. (No action potential can occur because the the K+ needs to be closed.

This is incorrect. During the absolute refractory period no new action potential can be generated, but this has nothing to do with the voltage-gated K+ channels. During the relative refractory period new action potentials can in fact be generated.

If they are open, there will be continuous outward flow of K+, which decreases the negative potential of the cell. The goal of action potentials is to have a huge influx of Na+ which makes the cell extremely negatively charged)

I hope this helps you out.

The influx of Na+ during depolarization in an action potential actually makes the cell's transmembrane potential more positive.

 

[Vybe]

Ah yes. you are right. I apologize!! Need to check with my resources better

 

[gettheleadout]

Ah yes. you are right. I apologize!! Need to check with my resources better

No worries! I'm just here to help.

 

[sillyjoe]

But the Na+/K+ ATPase is still running elsewhere in the membrane, so active transport of sodium is still occurring.


You mean positive.


This paragraph is misleading because 1) the Na+/K+ ATPase is constantly running in cells, as I've stated already, and 2) the charge imbalance of ion transport by the Na+/K+ ATPase is not responsible for the resting potential being negative (you don't explicitly state that it does but it seems implied to me).


You mean too negative.


This is incorrect. During the absolute refractory period no new action potential can be generated, but this has nothing to do with the voltage-gated K+ channels. During the relative refractory period new action potentials can in fact be generated.

The influx of Na+ during depolarization in an action potential actually makes the cell's transmembrane potential more positive.

What is responsible for the resting potential being negative?

 

[gettheleadout]

What is responsible for the resting potential being negative?

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[sillyjoe]

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You pointed out earlier that this question would be incorrect due to the fact that the Na/K ATPase is still running during an action potential. Is there a membrane potential at which the Na/K ATPase either reverses direction? If so, would there be a brief period where it stops working?

 

[Vybe]

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Ok let me get this straight..

The REASON for the negative resting potential of the cell membrane is due to the highly permeable K+ pores on the cell membrane, which allows K+ to move out of the cell.. causing the more negative charge inside the cell. The action potential allows for Na+ permeability INTO the cell and shuts off K+ permeability, to exponentially increase the positive charge of the cell, thus leading to the depolarization.

Refractory period --> Still a bit confused on this... Aren't there 2 refractory periods? One absolute (during the action potential) and one relative (between hyperpolarization and resting potential) Need better understanding of this

The take away..
What I concluded from the video is that the reason for the negative resting potential is not majorly depenent ON the Na+/K+ ATPase pump.

The pump is responsible for maintenance of the negative potential.

Correct?

 

[sillyjoe]

Ok let me get this straight..

The REASON for the negative resting potential of the cell membrane is due to the highly permeable K+ pores on the cell membrane, which allows K+ to move out of the cell.. causing the more negative charge inside the cell. The action potential allows for Na+ permeability INTO the cell and shuts off K+ permeability, to exponentially increase the positive charge of the cell, thus leading to the depolarization.

Refractory period --> Still a bit confused on this... Aren't there 2 refractory periods? One absolute (during the action potential) and one relative (between hyperpolarization and resting potential) Need better understanding of this

The take away..
What I concluded from the video is that the reason for the negative resting potential is not majorly depenent ON the Na+/K+ ATPase pump.

The pump is responsible for maintenance of the negative potential.

Correct?

You are correct about the reasoning for the membrane potential being negative. The pump sets up the concentration gradient and the leakage of K+ relative to Na+ sets up the negative membrane potential.

Once the action potential starts there is a short period called the absolute refractory period where NO stimulus will create an action potential. This lasts from depolarization to repolarization.

The relative refractory period occurs during the hyperpolarization phase of the action potential (following repolarization). During the relative refractory period you need a big stimulus to reach threshold and get an action potential.

Two important notes:

1. Do not mistake needing a big stimulus to creating a smaller action potential.

2. When I say big stimulus I mean a stimulus that is relatively larger than the stimulus needed when the cell is not in any refractory period.

 

[Vybe]

You are correct about the reasoning for the membrane potential being negative. The pump sets up the concentration gradient and the leakage of K+ relative to Na+ sets up the negative membrane potential.

Once the action potential starts there is a short period called the absolute refractory period where NO stimulus will create an action potential. This lasts from depolarization to repolarization.

The relative refractory period occurs during the hyperpolarization phase of the action potential (following repolarization). During the relative refractory period you need a big stimulus to reach threshold and get an action potential.

Two important notes:

1. Do not mistake needing a big stimulus to creating a smaller action potential.

2. When I say big stimulus I mean a stimulus that is relatively larger than the stimulus needed when the cell is not in any refractory period.

Ok. So what is the science behind why there cannot be another action potential during the absolute refractory period?

Is it due to the state of the membrane pores? Or is it more dependent on the current charge of the cell? Or both?

 

[sillyjoe]

Ok. So what is the science behind why there cannot be another action potential during the absolute refractory period?

Is it due to the state of the membrane pores? Or is it more dependent on the current charge of the cell? Or both?

It is mainly due to the inactivation of Na+ channels.

 

[Vybe]

Aren't Na+ channels active because they are open during the action potentials though? How do you distinguish if the channels are active or inactive then?

 

[sillyjoe]

Aren't Na+ channels active because they are open during the action potentials though? How do you distinguish if the channels are active or inactive then?

The absolute refractory period coincides with nearly all of the action potential. In the very beginning of an action potential the membrane becomes permeable to Na+ because the voltage gated sodium channels open. However, they inactivate shortly after the depolarization and remain inactive until the cell HYPERpolarizes. The Na+ channels have to inactivate following depolarization or the cell cannot repolarize.

Now conceptually, I don't think you need to really distinguish the short amount of time between the onset of the action potential and the start of the absolute refractory period. Just know that after the quick depolarization the Na+ channels deactivate allowing for repolarization of the cell and the subsequent inability to stimulate the Na+ channels until the cell hyperpolarizes.

For a deeper understand you should know there is a gate that opens the Na+ channel and a different gate that closes the Na+ channel. Because of this there are really 3 states a Na+ channel can be in. Open, inactivated, and closed. When it is closed you can stimulate it and it will open. When it is inactivated it CANNOT be opened no matter how much you stimulate it. This leads to a period called the absolute refractory period where no stimulus can activate the channel.

Think of it like this: I'm sure you have seen movies where banks have vaults and during the day you can open and close it. However, at night, the entry code inactivates and even if you have the correct code you cannot get in. Vault = Na+ channel

 

[Vybe]

Ok I get it now, thanks!

 

[WierdScience]

I think of it like this. During the absolute refractory phase, there are points when the cell is in depolarization and repolarization which is the difference of when the sodium channels are open, closing, or closed. But the reason another stimulus cannot create an action potential is because the membrane potential is too positive, meaning that there is too much sodium inside the cell, which means that opening the sodium channels, if you could, would not have a great effect because there's already a large amount of sodium in the cell. The reason that you can have an action potential during hyperpolarization which is the relative refractory period is because sodium and potassium are in the right place; they have just been over corrected but a large enough stimulus can overcome that.

 

[sillyjoe]

I think of it like this. During the absolute refractory phase, there are points when the cell is in depolarization and repolarization which is the difference of when the sodium channels are open, closing, or closed. But the reason another stimulus cannot create an action potential is because the membrane potential is too positive, meaning that there is too much sodium inside the cell, which means that opening the sodium channels, if you could, would not have a great effect because there's already a large amount of sodium in the cell. The reason that you can have an action potential during hyperpolarization which is the relative refractory period is because sodium and potassium are in the right place; they have just been over corrected but a large enough stimulus can overcome that.

While this is a contributing factor, the major reason why the cell cannot have a second action potential occur during the absolute refractory period is due to the inactivation of the Na+ channels.

What you are talking about is actually more of a determinant for the relative refractory period which is due to the hyperpolarized membrane.

 

[WierdScience]

I found a geat link that explains this in detail and well.

https://www.inkling.com/read/medica...es-david-bell-4th/chapter-3/action-potentials

 

[gettheleadout]

You pointed out earlier that this question would be incorrect due to the fact that the Na/K ATPase is still running during an action potential. Is there a membrane potential at which the Na/K ATPase either reverses direction? If so, would there be a brief period where it stops working?

My first thought when I read this was "I don't know," but let's consider the implications of a reversal. The Na+/K+ ATPase catalyzes the hydrolysis of ATP to ADP and inorganic phosphate. The exergonic nature of the hydrolysis reaction is coupled to the transport of the Na+ and K+ ions against both of their concentration gradients. Because there is a slight charge imbalance in the ion antiport (even though it doesn't "account" for the resting potential being negative), the transport also effectively works against the electric potential gradient as well. So, the normal function of the pump requires energy from ATP to act against the electrochemical gradient that exists across the cell membrane as a whole.

If the pump reversed, we would observe transport of the Na+ and K+ ions in the opposite directions, but we would also see synthesis of ATP on the intracellular side of the membrane. Consider just how favorable the reversed antiport of the ions would have to be in order to drive ATP synthesis via the pump. This would require an enormous electrochemical gradient (and if we want to only consider the transmembrane potential, as you specified in your question, we would need to determine how the membrane potential might become this great without changing the concentration gradients for the Na+ and K+ ions.) Further, reaching the point where the gradient exists with this magnitude would require passing through a time where, as the gradient increased in strength, the hydrolysis of ATP became insufficiently energetic to drive the pump's normal function.

I would speculate that if you could artificially establish such a gradient across the cell membrane, via increase in the strength of the existing gradient, you would pass through a point where the thermodynamic favorabilities of the two directions of pump function were equivalent, and the pump could stop (and technically, all this would necessarily mean is that the net work by the set of pumps in the membrane is 0; you might have individual pumps going in different directions.) However, I wouldn't be surprised if establishing such a strong gradient caused the cell membrane to rupture altogether or something like that.

While yours is definitely a question for a molecular biologist and not something I'm qualified to answer outright, I would be surprised if the pump ever stops or reverses for the reasons you've suggested.