- Anatomy of a neuron
- Overview of neuron structure and function
- The membrane potential
- Electrotonic and action potentials
- Saltatory conduction in neurons
- Neuronal synapses (chemical)
- The synapse
- Neurotransmitters and receptors
- Q & A: Neuron depolarization, hyperpolarization, and action potentials
- Overview of the functions of the cerebral cortex
Myelin sheaths, nodes of Ranvier, and saltatory conduction in neurons. Created by Sal Khan.
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- how the nodes can boast the signal of ions??(26 votes)
- At the nodes there are huge quantities of voltage gated ion channels, so when the action potential reaches these channels they open and there is a huge influx of ions. This influx creates a high electrochemical gradient near the ion channels and so the ions rapidly diffuse down their electrochemical gradient, along the neuron.(62 votes)
- Is myelin sheath same as Schwann cells?(25 votes)
- In the peripheral nervous system, yes. Each segment of myelin on an axon in the PNS is made by a Schwann cell.
In the central nervous system, myelin is provided by oligodendrocytes. One oligodendrocyte can provide myelin for multiple axons; this also helps the astrocytes to stabilise brain tissue.(27 votes)
- What disease occurs when the myelin sheath is damaged or missing?(15 votes)
- Multiple Sclerosis. It is an auto-immune disease in which your body's own defenses attack the myelin sheath, causing symptoms ranging from fatigue and tingling to depression, seizures, and massive amounts of pain.(31 votes)
- When the action potential is initiated at the Axon Hillock, what prevents the inflow of ions from migrating (diffusing) back towards the cell body/dendrites? If this does occur, is there any consiquence of this happening?(13 votes)
- Ions are not supposed to migrate back towards the soma (neuron cell body). This is mainly due to the refractory period. It is period of time after an action potential occurs at one point of the axon when it is impossible to produce another action potential at this point. So, ions cannot go backward because they would diffuse passively and ion channels that maintain the resting potential would get the ions back in proper place (K+ inside, Na+ outside, etc.).:17.207Z/v/neuron-action-potential-mechanism" rel="nofollow">https://en.khanacademy.org/science/health-and-medicine/nervous-system-and-sensory-infor/neuron-membrane-potentials-2014-03-27T
Mechanisms of the neuron action potential are well explained there: 17:5817:58:17.207Z/v/neuron-action-potential-mechanism
At7:38, he explains what is the refractory period.(9 votes)
why are there only sodium and potassium as positive and negative ions in a neuron. why not any other positive or negative ions ?
- There are are other positive and negative ions, but first I want to point out that both sodium and potassium are both positively charged ions, Potassium is just less positive in comparison to Sodium.
Though there are ions such as sodium, magnesium, chlorine,bicarbonate, polyatomic ions, and negatively charged protein side chains inside the cell, potassium is the most abundant. The same is true for the extracellular side to but at different concentrations, but this time there is more sodium, making the outside more positive at resting state.
The reason that there is more sodium and potassium cations than the other stuff is probably because of dietary intake.(7 votes)
Is myelin sheath same as schwann cells ??
- The Schwann cells pretty much wrap themselves and the axon with myelin. It produces the myelin and surrounds the surrounding area. Each myelin sheath contains a Schwann cell, so you have to be careful if you doing a matching or fill in the blank question while looking at a diagram. The myelin sheath is the product of the Schwann cells which are trapped inside, it's very easy for people to get confused between the two.
An analogy would be a very hairy dog. The hair itself is not the dog, it's the product of the dog and not the dog itself. The dog is underneath all of those layers of fur. They are not the same. I can't think of a great analogy, that's the best I could think of.
Hope this solves any confusion.(11 votes)
This question might be weird but, if the Na+ Atoms repel each other then cant they repel to go in the opposite direction of the axon and not necessarily go through it?
- I was just asking the same question. I guess, it is because the other side is more negative than where they are flowing from and thats why they flow along the axon not the other side. Just a thought...(5 votes)
I am confused as to how the myelin sheath speeds up signal propagation. I find the copper wire analogy not very satisfying because it has a potential difference axially whereas the axon membrane has a radial potential difference. (also does copper really work that way? Would the speed of a signal be affected if say the wire was in a salt bath instead of simply in the air?)
One last question, are there any ion channels and Na/K pumps under the Schwann cells? Are they attached to the axon (can they rotate)?
One last question, are there any ion channels and Na/K pumps under the Schwann cells? Are they attached to the axon (can they rotate)?
- Myelin can greatly increase the speed of electrical impulses in neurons because it insulates the axon and assembles voltage-gated sodium channel clusters at discrete nodes along its length.
The energy loss is still the same since it has an insulator. Regardless of the environment (you mentioned salt bath or air).(2 votes)
How do positively charged ions carry a signal? At
9:22wouldn't the signal be diluted at the nodes of Ranvier when it just gets flooded with more ions? Is the signal shared?
- The signal isn't a horizontal transmission of ions at all, but a "wave." There is a very slight time lag (on the order of milliseconds) between the ion channels opening at one node versus the next, and these are all dependent on the membrane potential upstream. If the signal were left to diffusion alone, the ions wouldn't travel more than 1/100th down the length of an axon. But because the ion channels open/close in response to local voltages, the signal propagates very quickly.(3 votes)
Does a signal always travel from Dendrite to axon to terminal or can it traveled from terminal to dendrite
- Yes. Millions of axons are communicating with each other in our nervous system. That communication happens when one neuron (the presynaptic cell) sends it's signal down its axons where the terminals are sending a signal to other neurons (postsynaptic cell).(4 votes)
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.