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  • Now that we know how a signal can spread through a neuron,

  • through an electrotonic potential and action

  • potential and combinations of the two, let's

  • put it all together by looking again

  • at the structure of a neuron, the anatomy of a neuron,

  • and thinking about why it has that anatomy

  • and how it all can work.

  • So we've already talked about the dendrites

  • as being where the neuron can be stimulated

  • from multiple inputs.

  • If we're in the brain, these dendrites

  • might be near the terminal ends of axons of other neurons.

  • If we're some type of sensory cell,

  • these dendrites could be stimulated

  • by some type of sensory input.

  • But let's just say, for the sake of argument,

  • they are stimulated in some way.

  • And because they're stimulated in some way,

  • it allows positive ions to flood into the neuron

  • from the outside.

  • As we know, there's a potential difference.

  • It's more negative inside of the neuron

  • than outside of the neuron.

  • And so if a channel gets opened up

  • because of some stimulus, that would

  • allow positive ions to flow in.

  • And the primary positive ions we've been talking about

  • are the sodium ions.

  • Maybe this is some type of sodium gate

  • that gets opened up because of this stimulus.

  • So when that happens, you will have electrotonic spread.

  • You will have an electrotonic potential being spread.

  • So let's say that we had a voltmeter

  • right here on the axon hillock.

  • It's kind of the hill that leads to the axon right over here.

  • So what you might see happening after some amount of time--

  • so let me draw.

  • So let's say this is our voltage in millivolts

  • across the membrane-- our voltage difference,

  • I should say.

  • This is the passage of time.

  • Let's say the stimulus happens at time 0.

  • But right at time 0, we haven't really

  • noticed it with our voltmeter.

  • Our voltage right across the membrane right over there

  • is at that equilibrium, negative 70 millivolts.

  • But after some small amount of time,

  • this electrotonic potential has gotten to this point,

  • because all of these positive charges

  • are trying to get away from each other.

  • It's gotten to that point.

  • And you might see a bump in the voltage--

  • in the voltage difference, I guess I should say.

  • This thing might go up.

  • So it might look something like that.

  • Now, that by itself might not be--

  • we might have gotten the voltage difference low enough,

  • I guess we could say.

  • Or we might not have gotten the voltage inside of the cell

  • positive enough in order to trigger the voltage-gated ion

  • channels.

  • And so maybe nothing happens.

  • Maybe this right over here, this is negative 55 millivolts.

  • And so that's what you have to get the voltage up to,

  • the voltage difference up to, in order

  • to trigger the ion channels right over there.

  • So those are the sodium channels to get positive charge in.

  • Here's the potassium channels to get the positive charge out.

  • The axon hillock has a ton of these,

  • because these are really there.

  • Once they get triggered, they can trigger an impulse

  • that can then go down the entire axon,

  • and maybe stimulate other things, maybe in the brain

  • or whatever else this neuron might be connected to.

  • So maybe that stimulus by itself didn't trigger it.

  • But let's say that there's another stimulus that

  • happens right at the same time, or around the same time.

  • And that happens.

  • And on its own, that might have caused

  • a similar type of bump right over here.

  • But when you add the two together

  • and they're happening at the same time,

  • their combined bumps are enough to trigger

  • an action potential in the hillock,

  • or a series of action potentials in the hillock.

  • And so then, you really have, essentially, fired the neuron.

  • So now all sorts of positive charge

  • gets flushed into the neuron.

  • And then purely through electrotonic spread,

  • you will have this electrotonic potential spread down the axon.

  • Now, this is the interesting part,

  • because we can think a little bit about,

  • what is the best way for an axon to be designed?

  • In general, if you're trying to transfer a current,

  • the ideal thing to do is, the thing that you're transferring

  • the current down should conduct really well.

  • Or you could say it has low resistance.

  • But you want it to be surrounded by an insulator.

  • You want it to be surrounded.

  • So if this was a cross section, you

  • want it to be surrounded by an insulator that

  • has high resistance.

  • And the reason is because you don't want the potential

  • to leak across your membrane-- high resistance

  • right over here.

  • If you didn't have something high resistance around it,

  • your current would actually go slower.

  • This is true if you're just dealing with electronics.

  • If you just had a bunch of copper wires on one side,

  • and you had some copper wires that

  • were surrounded by a really good insulator,

  • a really good resistor-- for example, plastic or rubber

  • of some kind.

  • The current is actually going to have less energy loss.

  • It's going to travel faster when it's

  • surrounded by an insulator.

  • So you might say, OK, well gee.

  • The best thing to do would be to surround this entire axon

  • with a good insulator.

  • And for the most part, that is true.

  • It is surrounded by a good insulator.

  • That is what the myelin sheath is.

  • So let's say we want to surround this whole thing with just one

  • big grouping of Schwann's cells, so one big myelin

  • sheath-- which is a good insulator.

  • It does not conduct current well.

  • So this right over here is just one big myelin sheath right

  • over here.

  • Now, what's the problem with this?

  • Well, if this axon is really long-- and let's say,

  • you know, you're a dinosaur or something.

  • And you're trying to go up your neck,

  • and your neck is 20 feet long.

  • Or even a human being, we're a reasonable size.

  • And you're going several feet, or even whatever,

  • you want to go a reasonable distance

  • purely with electrotonic spread, your signal, remember,

  • it dissipates.

  • Your signal is going to be really weak right over here.

  • You're going to have a weak signal on the other end.

  • It might not be even strong enough

  • to make anything interesting happen

  • at these terminals, which wouldn't be strong enough

  • to trigger, maybe, other neurons,

  • or whatever else might need to happen at this other end.

  • So then you say, OK, well then why

  • don't we try to boost the signal?

  • Well, how would you boost the signal?

  • You say, OK.

  • I like having this myelin sheath.

  • But why don't we put gaps in the myelin sheath every so often?

  • And then those gaps would allow the membrane

  • to interface with the outside.

  • And in those areas, we could put some voltage-gated channels

  • that can release action potentials,

  • in order to essentially boost the signal.

  • And that's is exactly what the anatomy of a typical neuron

  • is like.

  • So instead of just one big insulating sheath like this,

  • it would-- let me make some gaps here.

  • Whoops, I'm going to do that in black.

  • So actually, let me just draw it like this.

  • Let me just erase this.

  • So clear, and let me clear this.

  • That's good enough.

  • And so what we could do is we could put gaps in it

  • right over here where the axon, the axonal

  • membrane itself can interface with its surroundings.

  • And of course, we know we call those

  • gaps the nodes of Ranvier, or Ran-Veer.

  • I'm not really sure how to pronounce it.

  • So let me put those gaps in here.

  • So you put those gaps in here, so these are the myelin sheath.

  • And this right over here is a node of Ranvier.

  • These are nodes of Ran-Veer, or Ranvier.

  • And right in those little nodes, right in those nodes, right

  • where the myelin sheath isn't, we

  • can put these voltage-gated channels to essentially boost

  • the signal.

  • If the signal had to go electrotonically

  • all the way over here, it'd be very weak.

  • It's going to dissipate as it goes down,

  • but it could be just strong enough right at this point

  • in order to trigger these voltage-gated channels,

  • in order to essentially boost the signal again, in order

  • to trigger an action potential, boost the signal.

  • And now the signal is boosted, it'll

  • dissipate, dissipate, dissipate, boost.

  • And it'll boost right over here again.

  • And then it'll dissipate, dissipate, dissipate,

  • and boost.

  • Dissipate, dissipate, boost.

  • And so by having this combination,

  • you want the myelin sheath.

  • You want the insulator in order to keep the transmission

  • of the current to fast, in order to have minimal energy loss.

  • But you do need these areas where the myelin sheath isn't

  • in order to boost the signal, in order for the action potentials

  • to get triggered, and so your signal can keep being-- well,

  • I guess keep being amplified, if we

  • wanted to talk in kind of electrical engineering speak.

  • And this type of conduction, where the signal just

  • keeps boosting, and if you were just to superficially observe

  • it, it looks like the signal is almost jumping.

  • It gets triggered here, then it gets triggered,

  • here then it gets triggered here,

  • then it gets triggered here, then it gets triggered here.

  • This is called saltatory conduction.

  • It comes from the Latin word saltare-- once again,

  • I don't know how to pronounce.

  • My Latin isn't too good.

  • But it comes from the Latin word saltare,

  • which means to jump around or to hop around.

  • And that's because it looks like the signal is hopping around.

  • But that's not exactly what's happening.

  • The signal is traveling passively through.

  • It gets triggered here in the axon hillock.

  • Then it travels passively through electrotonic spread.

  • And then it gets boosted.

  • And you have the myelin sheath around it

  • to make sure it goes as fast as possible,

  • and you get very little loss of signal.

  • And then it gets boosted at the nodes of Ranvier,

  • because it triggers these voltage-gated channels again.

  • That triggers an action potential.

  • And then your signal gets boosted,

  • and then it dissipates-- boosted, dissipates, boosted,

  • dissipates, boosted, dissipates.

  • Maybe it could even get boosted again.

  • And then it can trigger whatever else it has to trigger.

Now that we know how a signal can spread through a neuron,

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B2 UK signal sheath voltage axon myelin neuron

Saltatory conduction in neurons

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    fung posted on 2016/12/01
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