So lets start by summarizing what I told you in the last lecture. There's an electrical gradient across the membranes of all livingcells. What's that electrical gradient called? The membrane potential.How big is it?
It's tiny, but significant. 70 millivolts.
And we need to know about 4 facts in order to begin to explainthe cause of the membrane. What is the first of those facts thatI gave you? Concentration of potassium inside is very different.It's like a 140 versus 4 millimolar.
Big difference in concentration.
Second fact?
STUDENT: It's permeable.
INSTRUCTOR: The membrane is permeable to potassium. Is thatthe same thing as saying that potassium is permeable to the membrane?
STUDENT: No.
INSTRUCTOR: No. So don't say it that way. The membrane is permeable.Saying it the other way is, like, saying the membrane can getthrough potassium. That's not true. The membrane is permeableto potassium.
Third fact.
Majority of the anions are proteins.
So there is almost a perfect balance of negative and positivecharge inside the cell; there has to be. And the majority of thenegatively charged ions inside the cell are parts of humongousmolecules --
Fact number 4.
Membrane is not permeable to protein. Now, there is a verb thatallows you to say that the other way, but it's so similar to thefirst one, how many of you want to hear it? You could say it theother way. You could say protein is not permeant to the membrane.But that's too confusing. So the net effect of all of that is,if this is a diagramatic reputation of the cell --
This is our membrane, our cell. Potassium can escape from thiscell moving down its concentration gradient by diffusion, physiologistsuse a dashed line for diffusion, can escape from the cell throughthe potassium channels that are responsible for Fact Number 2.The permeability of the membrane.
And there are these negatively charged proteins inside the cellthat cannot get out. So there is a very slight separation of charge.The potassium ions, and you can imagine the potassium ions sittinghere in the channel. And there is a force tending to push it outof the cell, which is the difference in concentration. And thereis a force which is tending to hold it inside of the cell.
And that is the attraction of the positively charged potassiumfor the negative charge that has accumulated inside the cell.And that's the membrane potential, and it's 70 millivolts.
All cells have that. Liver cells have it. All the differentkinds of living cells that you have read about or seen in thelab. All of them have it to some extent because they all havethese same basic 4 facts.
Now, the thing that really distinguishes nerve and muscle tissuesis that they are excitable tissues.
All the other kinds of tissues that you are learning about inlab and histology are not excitable, that is they can't be stimulatedand respond in some measurable way.
Now, the measurable way is a change in the membrane potential.That's what distinguishes never and muscle from other tissues.The biggest difference is that nerve and muscle tissues' membranepotential can change when they are stimulated. Now, that mightbe mechanically stimulated. It might be electrically stimulated,or chemically stimulated. There are different ways that that stimulationcan occur.
But the bottom line is that they do not have a stable membranepotential. After they are stimulated, their membrane potentialundergoes a change, which is called and "action" potential.
And so one of the things that I'm going to talk about in thelecture today is an action potential. That is the change in amembrane potential that occurs in a nerve cell.
A synonym -- not quite as good from a scientific point view,but a synonym for an action potential is a nerve impulse. Thisis an electrical signal that travels along a nerve cell, goesfrom one place in the body to another place in the body, representsa piece of information going from one place in the body to anotherplace in the body.
And that information might be going from the brain to a muscleand telling the muscle to contract. In other words, in you raiseyour hand, you have activated a bunch of muscles in order to applysome forces and elevate the mass of your arm against gravity.
And so that piece of information went from your brain and, says,"Okay, muscles get in action, I want to raise my hand."And so the muscle is contracted.
One of the things that nerves do frequently is they cause musclesto become active. And that's what we're going to be talking aboutin here today and on Wednesday is that process that starts with-- in the brain, with a piece of information that says, "Okay, muscle become active."
And what happens? The nerve impulse or active potential travelsalong a real long segment of a nerve cell and it finally getsout there in the body someplace to the muscle cell. And then someinformation is transferred from the nerve cell to the muscle cell.And there is a special kind of connection between the two, calledthe neuromuscular junction.
And then that causes the muscle cell to go through a bunch ofactivity that results in it contracting, generating force andgetting shorter.
Now, before I go on to that, we need to talk a little bit moreabout these, about this typical cell, because some of the samekinds of things that are going on in this typical cell are alsogoing to be happening in the muscle cell.
A long time ago both chemists who were studying cells, biochemists,and physiologists discovered that there is located in the membraneof all of these cells there is another membrane-bound protein.What is the first membrane-bound protein that I have mentionedso far? There is a membrane-bound protein on the board there.
What is this right here?
STUDENT: Potassium channel.
INSTRUCTOR: What kind of membrane protein is that? What functionis it performing?
Carrier-Mediated Transport.
There are 2 kinds of functions involved in Carrier-MediatedTransport. This one is not active transport, it is the secondone. Facilitated diffusion. So the channel is the main, the functionis facilitated diffusion.
Now, there is another membrane-bound protein in all of thesecells as well, which is called a "sodium channel." Actually,what it should be called is the "sodium potassium exchangepump."
And that's the more correct and complete name of this membrane-boundprotein, which is sometimes just called a "sodium pump."Sodium potassium exchange pump.
Now, given that name, what function is this performing?
STUDENT: Exchange of sodium and potassium.
INSTRUCTOR: But remember, a membrane-bound proteins performCarrier-Mediated Transport. There is two classes; Active transport,because this is called a pump, this is called active transport.And what this thing is doing is it is taking potassium from outsidethe cell and moving it in and in exchange for kicking sodium out.
Sodium and potassium are both univalent, positively charged,single to positive charge and they are fairly similar in size.But the interesting thing that is while there is high concentrationof potassium on the inside of the cell there is very, very lowconcentration of sodium on the inside of the cell.
And we know that there is a low concentration of potassium onthe outside, but there is a big concentration of sodium. So these2 ions, that are very similar to one another and similar in size,they appear one right below the other on the chemical chart, theyeach have a positive charge, but they have very different placesinside of a living system.
Okay. This is inside the cell. Now, there is lots of fluidssurrounding the cells in your body. There is body fluid. Thereis other -- there is blood, all kinds of parts of your body thatare outside the cells as well, but inside of cells we find highpotassium, and outside of cells we find high sodium.
And this exchange pump is the cause for that differential concentration.Any -- this potassium tends to leak out. But the cell can't allowthat to go on indefinitely, because if it did, then the concentrationof potassium in here would drop down, and the first of our 4 factswould disappear. And, in fact, the cell would be dead.
So the cell has to do something continually to replace any potassiumthat's leaking out. And there is also going to be a slow leakof sodium in.
Think about it. If you were one of these sodium ions out hereon the outside of the cell, remember the 2 forces acting on potassium?What are the 2 forces acting on potassium? Concentration and electriccharge.
Now, think about it from the standpoint of a sodium ion. Same2 forces, but are they operating in opposition to one another?Are the 2 forces that cause this potassium to be kind of -- thesetwo forces are sort of balancing one another. Ionic force, concentrationforce, operating in that direction, attraction of positive fornegative operating in that direction.
So that potassium ion sits there in a dynamic equilibrium; ithas 2 forces operating in opposite directions.
Now, think about a sodium ion, are the 2 forces operating inopposition to one another?
STUDENT: No.
INSTRUCTOR: What direction is the concentration force operating?
STUDENT: Inside.
INSTRUCTOR: In, sure. Huge concentration gradient in. Do youthink that sodium is attracted to the negative charge? Okay. Sothe 2 forces that are operating and balancing one another forpotassium are operating in the same direction for sodium. So thereare 2 forces favoring the leakage of sodium into this cell.
And so there is, in fact, a slow leak of sodium into the cell.It burrows its way past the phospholipid bilayer. So the sodiumpotassium exchange point must operate continually in order tomaintain the concentrations inside the cell at the right level.In order to keep the sodium concentration low and the potassiumconcentration high, the pump does that.
So in the first of these facts, the high potassium concentrationor potassium gradient is in fact produced by the sodium potassiumexchange pump. It is kind of indirectly involved. The sodium potassiumexchange pump is indirectly involved in the production of themembrane potential.
And there was a time when physiologists were curious as to knowjust how directly involved is that pump. How important is thatpump, because it's moving ions. Maybe, it's, in fact, the wholeexplanation for the membrane potential. That was before they figuredout -- they had to eliminate that hypothesis before they couldcome up this hypothesis.
And so they discovered that there is chemical that kills thesodium potassium exchange pump called "wouabain." Thebiochemist discovered that this chemical, which can be extractedfrom some plants, it's a plant alkaloid, would inactivate thesodium potassium exchange pump.
So they said, "Great, let's take a cell and we'll stickwouabain into the solution surrounding the cell and see if thatdestroys the membrane potential.
So they had a hypothesis that they were testing. What was thehypothesis? If you were going to do an experiment where you weremeasuring the membrane potential and you wanted to know how importantis the sodium potassium exchange pump in producing that potentialand you had this chemical wouabain that you could kill the pumpwith. What would be a hypothesis that you could test?
STUDENT: That wouabain would -- if used wouabain, that wouldstop -- the cell wouldn't have a membrane potential.
INSTRUCTOR: Right. The idea would be, you're measuring the membranepotential. You stick in wouabain, if the pump the critical, thenthe membrane potential goes away. And that's what they did. Andthe membrane potential didn't go away. You can kill this pump chemically with wouabain, and you still have a membrane potential.It sort of gradually goes away over the course of hours. But it'sa much longer time course than the time course for wouabain inactivating the pump.
So the wouabain kills the pump virtually immediately. The membranepotential goes away over the course of 6 or 8 hours. So clearlythe pump is not part of the explanation. That's why it's not listedhere as one of the 4 causes of the membrane potential.
Let's talk about the action potential then. And then we'll talkabout the neuromuscular junction now that we understand what ishappening for the basis of the membrane potential itself.
A nerve cell, they come in billions and billions of differentshapes and sizes, but basically a very simplified diagram of anerve cell might be something like this.
It has a cell body. And you are going to see this in lab. Ithas a cell body which is this part here called the soma, Latinfor body. It has a nucleous. It has these little pointy extensions,which are called "dendrites." The root there of dendritehas to do with tree.
So it looks kind of like branches of a tree extending away.And then it has this long fairly large extension called an "axon."
Now that axon can really be long. I mean, it could be a millimeteror a 10th of a millimeter in diameter, but it can be 3 meterslong. There are nerve cells that originate in the spinal cordof an animal and go all the way out to the foot, a single cell.Maybe a giraffe. Think about that.
A single cell, a 10th of a millimeter in diameter and a coupleof meters long. And that would be the axon part of the cell thatwas traveling all of that distance. Then it branches at the end,and it has this expanded area at the end which is called a synapticknob.
And a physiologists can study the function of this nerve cellby making a microscopic electrode, take a piece of very fine glasstubing, you heat it up and pull it and it ends up with a hollowmicroscopic tip that you can then mount on a thing called a "micro-manipulator."
It's like, you know, the microscope stage that you have, ithas the little knobs and the gears on it, and you can move thingsin 2 directions. Well, it's possible to construct those so theyoperate things in 3 directions as well.
And a micro manipulator can have this hollow-glass electrode,which me might fill with a salt solution so that it can conductelectricity. And we can stick a an electrode into this axon,and we can hook it up to an oscilloscope, which is a device thatmeasures voltages and can measure things that happen very, veryquickly, displays it on a screen. It's like the most primitivepossible sort of TV picture.
And you need to complete the circuit so have another electrodethat is sitting in the solution surrounding the axon. And youcan measure the membrane potential across this membrane and thatparticular area of the axon.
And what you'll see is this changing membrane potential. Whenthis cell is stimulated, there will be a changing membrane potentialcalled an "action potential."
So I'm going to make a graph.
And anytime that I make a graph and you copy it down so thatyou are prepared to reproduce it on an exam, you should be surethat you know what is on the 2 axes of the graph.
You should be sure you label your graph and know what the unitsare. I was having a conversation with my son last night who isa freshman in college, and he was trying to tell me somethingabout economics. And he drew this graph, and he had all theselines all over it. And I said, "What's on the axis?"And he said, "Well, you don't need to know that in orderto understand this graph." Then he tried to explain thegraph, and he couldn't because he didn't remember what was onthe axis.
You have to know what is on the axis.
On these axes we are going to put "time." And we aregoing to measure time in milliseconds.
MSEC; not M/SES. What would M/SEC be?
STUDENT: Speed.
INSTRUCTOR: That would be speed. We're not graphing speed onthis axis, we're graphing time, milliseconds.
and then on the "Y" axis, we're going to plot themembrane potential. And the symbol for membrane potential E subM. "E" because it's the electro motive force. That'ssymbol that chemists use for voltage. And "M" for membrane.And the units are going to be what? Millivolts.
And we're going to put zero, it's going to be near the middleof this graph so that we can get our minus 70 down here somewhere.Not all the way at the bottom, because part of our graph is goingto go below minus 70.
All right. So that is the graph. You have to remember -- I willabsolutely guarantee you that every time, absolutely every singlesolitaire time in any class you have ever taken from me now orcomparative physiology, if I ask you to graph something, willbe points allocated in the answer key for labelling the axes.
Now, we're going to see what happens in this membrane. It'sstable at minus 70 until the cell gets stimulated. All of suddenit goes up to plus 35 or so. And then it comes back down again,and it overshoots, and then it goes back to minus 70.
So this over here is back up at the same value.
Now, what is the time scale? We'll start our time when the cellis stimulated, when it first starts to change from minus 70. Sothat's time zero. When it gets back down here, having gone throughthis first little part of it, time is going to be one millisecond,one one thousandths of a second required for that little part,which, by the way, is called the "spike phase" of theaction potential.
The next part ends at time ten.
How long does that mean it lasts?
This phase from here to here is called "hyperpolarization."How long does it last? 9 milliseconds.
One millisecond for the spike phase. 9 milliseconds for hyperpolarization.
Now, can anybody tell me why that phase is called hyperpolarizationand not hypo polarization? I mean, it's kind of lower down onthe graph. We know "hypo" means low and "hyper"means extra. Since it's lower on the graph during this phase,why isn't that hypo polarization? Why do we call it hyperpolarization?Does anybody have a clue.
STUDENT: There is a higher electric charge.
INSTRUCTOR: Actually, polarized refers to the separation ofcharge. We even use that word "polarized" when we talkabout politics. The opinion is polarized on abortion, for example.It means there is separation of differences. Polarization meansa difference.
Depolarized would be right here at zero. But it's polarizedin the resting state. And it's even more polarized than normal.And that's why it's called hyperpolarization, more polarized thannormal. Minus 70 is the normal resting state. This thing getsdown to about minus 90, at the bottom of that little U-shapedtrough. So it's more polarized than normal. And it's called "hyperpolarization."
Remember this is a time course of what happened in this littletiny segment of membrane that are we are studying right here.
This is what happened in ten milliseconds in the life of thisaxon, in this particular piece of the axon, because we stuck ourmicro-electrode in right there. So we're measuring what is happeningthere. This is the time course of a membrane potential followingthe stimulation of this cell.
If we were to stick another micro-electrode in over here, orif this was giraffe nerve cell, you know, 2 meters further downthe axon over here, we would find exactly the same thing. Exactly,but it would happen a little bit later in time.
This action potential which we would measure right here is goingto spread along the axon at an incredibly fast speed, 50 metersper second. At 50 meters per second, think what a good -- howwell you could do in the Olympics if you could cover 50 metersa second.
At 50 meters a second this thing is going to spread down theaxon. And when it gets down here a couple of meters down, we'regoing to see exactly the same time course. Each of the littlesegments of membrane, it's going to go through the exactly thesame time course of change as its membrane potential.
Okay.
And that's how information gets transferred from one place inthe body to another place in the body at very high speed by nerveimpulses going from the brain out to muscles, for example.
That process is called "propagation."
Propagation is the spread of an action potential along theaxon from one part of the nerve cell to another part of the nervecell. Notice, this is just one nerve cell we're talking about.One continuous membrane surrounding a single cell.
And it's spreading very, very rapidly.
Now, what is it that's happening at the cellular molecular levelto produce this action potential? That's what I want to tell youabout next, is what is it that makes this cell an excitable cell.Remember the difference between nerve and muscle is that nerveand muscle cells are excitable. They can make action potentials.
They must have something more in their membrane that distinguishesthem and gives them that ability that the other cells, that arenot excitable, don't have.
And the only thing they have is they have another channel. Theyhave a sodium channel. So here we have -- remember this cell haspotassium channels and all that, but now it has a whole bunchof sodium channels as well.
Now, you'll notice that when I drew that potassium channel --I'll put a potassium channel in this cell as well. The potassiumchannel is a channel that is open all the time. So the way I drawthat is kind of like a cross section of a little donut with awhole in the middle of it.
Well, so that's a potassium channel. I drew that sodium channel-- it doesn't have an open hole all the time. In fact, it onlyopens during the spike phase. That's what causes the spike phaseis the sodium channel opens up and closes down in a millisecond.In one one thousandths of a second, all the sodium channels, hundredsof sodium channels in this one segment of membrane that we'restudying, all of the sodium channels open up and close back downagain in a millisecond, and that produces the spike.
STUDENT: Your sodium channel, is that the same thing as thesodium potassium pump?
INSTRUCTOR: No. If it was the same thing; it would have thesame name. It's a channel. So what does it do? What is its function?
STUDENT: To let the sodium out?
INSTRUCTOR: No. Give me the generic name for the function ofa channel.
STUDENT: Facilitated diffusion.
INSTRUCTOR: So what direction is sodium moving, then, in ourout?
STUDENT: Out.
STUDENT: In.
INSTRUCTOR: You had a 50/50 chance. Remember high sodium onthe outside; low sodium on the inside. This is a channel. Itis allowing sodium to move in the direction in which it wouldnormally defuse anyway. So when this sodium channel opens up,then some sodium can diffuse in.
It doesn't take any energy. The sodium potassium exchange pumprequires ATP in order to move sodium in the opposite direction.This sodium channel just says, "Open up. Okay. You guys gotin," and it closes in a thousandth of a second.
Now, that causes the inside of the cell to become positive.Remember, I said the top of this spike is up here, plus 35.
STUDENT: So the sodium channel opens up and let's the sodiumin, that's what causes the spike?
INSTRUCTOR: Right. It makes it go up to a positive value. Itchanges the membrane potential from negative, when there was separationof charge and there was some of that positive potassium left alittle lonely negative proteins behind, and the inside was negative,then as soon as the sodium channels open up, both of those forces,that are headed in the same direction, are both headed in thesame direction, drives extra sodium into the cell.
And for a short period of time there are, maybe, 500 more sodiumchannels open than there are potassium channels. Potassium channelsare sitting there open all the time, but they get totally swampedout. And so what happens is for a millisecond or half a millisecondthe inside of this cell is positive rather than negative.
And that's why the spike is up here at plus 35.
STUDENT: When causes the channel to open?
INSTRUCTOR: The stimulation, whether it a was chemical stimulationor an electrical stimulation or mechanical stimulation. Any oneof those things, that because this is an excitable tissue, itcan respond to those things.
And when we get through talking about the neuromuscular junction,you will have a better idea of what kind it normally causes thisnormally to start.
What normal starts is a nerve cell sends some information tothis cell. And this cell then sends the information out to themuscle. So we can do it electrically. We can have another pairof electrodes here and electrically stimulate this thing and causeit to do this.
In a living cell, it's information coming in from in from someother nerve cell and the mechanism of that is complicated. We'llunderstand that better in a minute. The same thing is going tohappen down here, because down here is a muscle cell. And we haveto get information across from this nerve cell to this musclecell and that will cause the muscle cell -- the first thing themuscle cell will do is it will generate an action potential, ithas a different time course.
So if you can wait just a second to understand how and whatcaused that stimulation in this living system, I think you willhave a better understanding by the time we get through with theperiod.
So these sodium channels are what are normal closed. So youcan use the little "n.c." as an abbreviation to remindyourself that in the resting state, when this cell has not beenstimulated, these sodium channels are closed. And you might wantto remind yourself that these potassium channels, that I talkedabout so far, are normally open. Okay? So you can use the abbreviation"n.o." for normally open.
In the resting state these potassium channels are open all thetime, normally open. And these sodium channels are called -- forthose of you that have a little more physiology, these are voltage-gatedsodium channels, it's when a membrane potential changes, thesethings open up.
If that's a not a familiar term, don't worry about it. I wantto talk about the cellular molecular basis for the period or thephase of hyperpolarization. In other words, if we can explainthis thing in terms of membrane-bound proteins, then we can alsoexplain this thing in terms of membrane-bound proteins.
And it turns out that in addition to the normally open potassiumchannels that are found in this cell, there are also normallyclosed potassium channels.
So a cross section of donut with a bar in the middle of it.Okay? These are potassium channels normally closed. And they'realso voltage-gated, so that as soon as the sodium channels startto open up and cause the spike phase, and they open and closevery rapidly by themselves, these normally closed potassium channels,they also start to open up. But they are much slower to open andmuch slower to close.
And so if you were to make a graph of the opening and closingof those channels, what you would find is that it would go somethinglike this --
In other words, they start to open as soon as the spike phasestarts, but they are very slow. And then they close -- start toclose by themselves. And when they are done, when these normallyclosed potassium channels, when they close that's the end of theaction potential. That's the end of hyperpolarization. It takesten milliseconds for that whole entire opening and closing tooccur.
STUDENT: Under the spike phase, though?
INSTRUCTOR: No, it's not the spike phase. The spike phase isthe sodium channels. They open up and close in a millisecond.The hyperpolarization are the normally closed potassium channels.And they open up, and then they slow back down in ten milliseconds.
STUDENT: Why wouldn't it be hypo?
INSTRUCTOR: I'm saying that they are opening. That's sodiumpermeability, if you will. Increased in -- I mean, potassium.It's an increase in potassium permeability due to the presenceof more potassium channels that are open than there is addressed.
So in a sense, this increase in potassium permeability, is whatcauses the membrane to be even more negative than it is at rest.So you can think of it as allowing extra potassiums to leak out.
Any questions?
All right.
So now we have 4 different membrane-bound proteins, all involveda Carrier-Mediated Transport, because a little tiny bit of sodiumcame into the cell to make the spike phase. And a little extrapotassium left the cell in order to produce this hyperpolarizationphase.
Notice that we haven't said anything about sodium leaving thecell. What left through these normally closed potassium channels,was not the sodium that came in and made the spike phase; itwas the little extra potassium.
So now the cell has moved a tiny, almost unmeasurable, distanceaway from its normal concentration of sodium and potassium. It'slost a little extra potassium; it's gained a little extra sodium.And so our other friend, the sodium potassium exchange pump hasto sit here and restore conditions.
So it pulls potassium in and kicks the sodium out.
So we have 4 membrane-bound proteins that are involved in thiswhole explanation of a cellular molecular basis for the functionof a nerve cell we. We have the potassium channels that explainthat, those are the ones that normally open. Then we have thesodium channels right here that are responsible for the spikephase.
And then we have the normally closed potassium channels thatare responsible for hyperpolarization. And then we have the sodiumpotassium exchange pump that puts the whole thing back to whereit used to be, back to rest.
One pump, 3 channels.
We can now understand that some channels are open all the time,and other channels can be closed and caused to open and closethemselves back down again.
STUDENT: So sodium does not cause hyperpolarization?
INSTRUCTOR: No.
STUDENT: Even though it's on the graph that you drew the firsttime where the concentration of sodium is lower than negative-- or the electro --
INSTRUCTOR: The hyperpolarization, where the membrane is morenegative than normal, is going to be caused by the same basicthing that causes it to be negative to begin with, and that ispositive charge leaving the cell. And potassium is a positivecharge that leaves the cell by diffusion.
STUDENT: But you have sodium coming in, which is positive.
INSTRUCTOR: Positive charge coming in makes the inside positive.This is more negative.
STUDENT: You are talking about potassium making it more negative,because there is less concentration of potassium inside at themoment of sodium coming in. But doesn't the sodium make a lesselectro-negative because it it has a positive charge as well?
INSTRUCTOR: The sodium coming in makes it positive.
STUDENT: Okay.
INSTRUCTOR: So at rest, the inside is negative and that's becauseof the positive charge leaving the cell. That would be what'shappening over here.
Up here at the peak, what's happened is a whole bunch of positionactive charge has come in, moving down the diffusion gradientfor sodium, making the inside of the cell positive. That's positiveup there, plus 35.
Now, down here where the membrane is more negative, what's happenedis that we had extra potassium channels open up, and so therehas been even more potassium leaving the cell and the cell ismore negative than it is in the resting state.
STUDENT: Even with the presence of sodium.
INSTRUCTOR: Right. Again, the amount of sodium that is movingin is very, very tiny in comparison with the total volume of thisinterior of just this part of the cell. It only takes, you know,a dozen or a couple dozen sodium ions to produce this very, verylittle ion actually moving in any of this stuff.
And so the little tiny bit of sodium that comes in, immediatelygets swamped out by the extra potassium that's leaked -- the sodiumdoes eventually need to be removed, but the charge effect of itis swamped out by potassiums that leak.
STUDENT: When does the sodium potassium pump kick in?
INSTRUCTOR: It kind of sits there and cranks away all thetime. And, in fact, the same experiment that we did with wouabainbefore can be done here. You can administer wouabain and cause-- and if you are electrically this axon, it will generate a thousandaction potentials with its sodium exchange pump killed. Then theconcentration of sodium in here finally rises to the level thatthe thing doesn't work anymore.
So the sodium exchange pump is necessary to the long-term survivalof the cell. It sets up the conditions that allow all this stuffto happen, but it doesn't actually have to functioning duringan action potential for an action potential to be produced. It'sjust the opening of 2 sets of channels.
Any other questions about this material?
We'll talk about the neuromuscular junction and muscle functionon Wednesday.