This was a great explanation. I was a neuroscience major (way back in the day) and no professor explained WHY the AP was faster under the myelin sheaths, they always just said THAT it was faster and you just had to take that at face value.
By watching your video, I could remember this process for over a year, when I was the only one in a class of 38 to answer why action potential is faster in myelinated axon and how. Studying the book helped but is dry as hell. Thank you so much
Really appreciate you guys. Such a great explanation. I was so confused about how myelination increases the velocity . Now I got it. Thanx . Keep up the good work 💪
In the myelinated portion, what happened to the "obstacles" such as the vesicles/large proteins/filaments (basically organelles)? Is it still there leading to the degrading conduction along the myelinated portion? Also, the decreased capacitance is because the charges are pushing away from each other onto the axon hillock or onto the nodes right?
I think I'm pretty close to understanding this but I still have a few issues that I need to clear up: 1) Does the surface of the myelin also contain voltage gated Na+ channels? The speaker seems to insinuate this around the 8:50 mark. I want to say that, no, it doesn't. But how then exactly is the positive charge traveling through the insulated portion of the axon to the next node? Is it via electrotonic conduction? 2) Why, after the opening of voltage gated Na+ channels are the + and - charges "leaving"? For example, wouldn't an influx of positive charge into the cell cause a local attraction of negative charges in the region (as opposed to the negative charges moving away)? What am I missing here?
I just want to note something that I did not like about the explanation - the action potential does NOT propagate faster because the membrane potential (voltage across the membrane) changes faster in the myelinated segments of the axon, the action potential is simply conducted faster because the membrane resistance of the axon (i.e. how permeable it is to ions) is GREATER in the myelinated segments - therefore less ions are able to flow out of the membrane at the myelinated segments (Because there are practically no leak channels at the myelinated segments), as opposed to the unmyelinated segments, which DO have leak channels in them - therefore, the action potential, which is made up ions, will decrease in magnitude faster in the unmyelinated segments simply because ions are going to leave the axon at these segments at a much greater rate as opposed to the myelinated segments. It is true that the myelinated segments have a smaller capacitance than the unmyelinated segments, but I do not think it plays any role with the speed at which the action potential is being propagated - this is due, again, to the increased membrane resistance that the myelin sheath confers to the membrane.
I think he's saying the low capacitance means less time is needed to charge the capacitor (myelin), which means speed increases. Towards the end at 9:36 he then talks about the leakage I think you're referring to, where he says myelin sheath is more resistant to leakage, therefore action potential depolarization is maintained for longer.
I have a related question: How can sensory nerves transmit fast enough without myelin? Many sensory nerves (i.e., pseudounipolar) consist of a long dendritic nerve fibre that may travel (say) from the far periphery of a limb, all the way to the DRG of the spinal chord. Since only axons are myelinated (or so I have always been taught) how can the conduction speed be adequate for a useful response time to any stimuli?
Wouldn't a larger diameter axon have more surface area to accommodate more voltage-gated channels, thereby also contributing to the increased action potential speed?
what? why do we care about whats going on on the membrane? we want a positive charge to travel toward the axon terminal... what does that have to do with negative charges coming in (I understand they do cause they are attracted to the na+ but why do we care about it?) If you would have said it slows down the current because the Na is connected to the Cl and is no longer serving as a positive charge flow I wouldve understand. can someome help me with this?
I think you're thinking that the Na+ only travel down the axon, but it seems the Na+ goes in and out of the membrane every step of the way. It's called signal propagation. This means its travel across the membrane also matters (i.e capacitance of the membrane).
you are only considering the resistance of the citoplasm, you are not considering that with a bigger diameter there's a bigger surface and a lower membrane resistance. I was hoping for a more complete explanation, i think this is overly simplified, though i liked the way you explain how the citoplasm resistance lowers with a bigger diameter. (sorry if you said it later, i stopped the video when you started talking about myelin).
This isn't really a suitable explanation for how the signal propagates down the axon faster due to myelination. The ions leaving the areas of high capacitance is not the signal, but rather the result of the signal, which is essentially the influx of positive sodium ions. If you think about it, myelin sheaths should actually interfere with the positive signal activating the next voltage gated ion channels on the other side of the sheath. There is probably another mechanism at work here.
Current flow is due to electrons ... if you don't understand basics of the subject you comment on, why do you make authoritative claims? Current flow, generally, is due to flow of electrical charge. Remember that complacent ignorants injure this world.
+Marwellus and as far as current flow is due to electrons statement is concerned, I meant that without a negative charge movement, simple movement of sodium ions in one direction does not constitute current. I would be really happy to learn more but with my limited knowledge I know that action potential propagation can not be explained by flow of only one type of charge down the axon. Sodium ions with their positive charge represent loss of negative charge and not its gain. besides, the idea of using electrons (should have been cautious, it was not appropriate) was to highlight that size of charge carriers is way below the obstacles being talked about. I would welcome any healthy discussion.
This is THE BEST explanation I found!
This was a great explanation. I was a neuroscience major (way back in the day) and no professor explained WHY the AP was faster under the myelin sheaths, they always just said THAT it was faster and you just had to take that at face value.
Without a doubt, The BEST explanation I've found on the subject. WOW WOW WOW. Thank you very much
dude your pronunciation of node of ranvier is pefect!
By watching your video, I could remember this process for over a year, when I was the only one in a class of 38 to answer why action potential is faster in myelinated axon and how. Studying the book helped but is dry as hell. Thank you so much
Props for the in depth explanation. None of my courses or any other sources explain the underlying cause of saltatory conduction this well.
the way you explained the lack of resistance is nothing less than artistic
This explanation is beautifully comprehensive.
Really appreciate you guys. Such a great explanation. I was so confused about how myelination increases the velocity . Now I got it. Thanx . Keep up the good work 💪
thank you for the explanation, it makes much more sense because I was super confused by the description of jumping
i discharged @ 9:00. great explanation
I think it can't be explained better than this!
Explanation is plain awesome😮!
6 years later and still the best explanation video I've found. Thank you!!!!
6 years passed and u still couldn't learn the topic properly 🤣😂🤣😂😂🤣😂🤣😂🤣😂🤣
Really best explanation 🥰🤩🤩
THE BEST EXPLANATION! THANK YOU SO MUCH!!!!!
Quite mechanistic explanation for saltatory conduction
In the myelinated portion, what happened to the "obstacles" such as the vesicles/large proteins/filaments (basically organelles)? Is it still there leading to the degrading conduction along the myelinated portion? Also, the decreased capacitance is because the charges are pushing away from each other onto the axon hillock or onto the nodes right?
So easy to follow and understand. Thank you
I think I'm pretty close to understanding this but I still have a few issues that I need to clear up:
1) Does the surface of the myelin also contain voltage gated Na+ channels? The speaker seems to insinuate this around the 8:50 mark. I want to say that, no, it doesn't. But how then exactly is the positive charge traveling through the insulated portion of the axon to the next node? Is it via electrotonic conduction?
2) Why, after the opening of voltage gated Na+ channels are the + and - charges "leaving"? For example, wouldn't an influx of positive charge into the cell cause a local attraction of negative charges in the region (as opposed to the negative charges moving away)?
What am I missing here?
I just want to note something that I did not like about the explanation - the action potential does NOT propagate faster because the membrane potential (voltage across the membrane) changes faster in the myelinated segments of the axon, the action potential is simply conducted faster because the membrane resistance of the axon (i.e. how permeable it is to ions) is GREATER in the myelinated segments - therefore less ions are able to flow out of the membrane at the myelinated segments (Because there are practically no leak channels at the myelinated segments), as opposed to the unmyelinated segments, which DO have leak channels in them - therefore, the action potential, which is made up ions, will decrease in magnitude faster in the unmyelinated segments simply because ions are going to leave the axon at these segments at a much greater rate as opposed to the myelinated segments.
It is true that the myelinated segments have a smaller capacitance than the unmyelinated segments, but I do not think it plays any role with the speed at which the action potential is being propagated - this is due, again, to the increased membrane resistance that the myelin sheath confers to the membrane.
I think he's saying the low capacitance means less time is needed to charge the capacitor (myelin), which means speed increases.
Towards the end at 9:36 he then talks about the leakage I think you're referring to, where he says myelin sheath is more resistant to leakage, therefore action potential depolarization is maintained for longer.
excellent video. thank you.
Best Explanation 👌
Thanks! Awesome explanation.
Thank you!
great video
this helped me so much thank you.
Good work. Thank you.
I have a related question: How can sensory nerves transmit fast enough without myelin?
Many sensory nerves (i.e., pseudounipolar) consist of a long dendritic nerve fibre that may travel (say) from the far periphery of a limb, all the way to the DRG of the spinal chord. Since only axons are myelinated (or so I have always been taught) how can the conduction speed be adequate for a useful response time to any stimuli?
Ah thanks!!
Super helpful thank you :)
Wouldn't a larger diameter axon have more surface area to accommodate more voltage-gated channels, thereby also contributing to the increased action potential speed?
yes increased diameter leads to greater conduction veloccity
save my life now
Fewer charges*
LOL, I was looking for this comment
Increible
My book says that myelination prevents leakage of ions. What is that supposed to mean
Leakage of the potassium ions results in hyperpolarization , the myelin serves as a protective envelope which would prevent the leakage!
what? why do we care about whats going on on the membrane? we want a positive charge to travel toward the axon terminal... what does that have to do with negative charges coming in (I understand they do cause they are attracted to the na+ but why do we care about it?) If you would have said it slows down the current because the Na is connected to the Cl and is no longer serving as a positive charge flow I wouldve understand. can someome help me with this?
I think you're thinking that the Na+ only travel down the axon, but it seems the Na+ goes in and out of the membrane every step of the way. It's called signal propagation. This means its travel across the membrane also matters (i.e capacitance of the membrane).
you are only considering the resistance of the citoplasm, you are not considering that with a bigger diameter there's a bigger surface and a lower membrane resistance. I was hoping for a more complete explanation, i think this is overly simplified, though i liked the way you explain how the citoplasm resistance lowers with a bigger diameter. (sorry if you said it later, i stopped the video when you started talking about myelin).
This isn't really a suitable explanation for how the signal propagates down the axon faster due to myelination. The ions leaving the areas of high capacitance is not the signal, but rather the result of the signal, which is essentially the influx of positive sodium ions. If you think about it, myelin sheaths should actually interfere with the positive signal activating the next voltage gated ion channels on the other side of the sheath. There is probably another mechanism at work here.
Sos un crack
1000!
the explanations about diameter effects here are wrong
Can you elaborate? I don’t want to learn incorrect information, thank you
❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤❤
the magnitude of obstacles that are being described here and sodium ions are totally different. The first part is totally misleading concept.
Current flow is due to electrons ... if you don't understand basics of the subject you comment on, why do you make authoritative claims? Current flow, generally, is due to flow of electrical charge. Remember that complacent ignorants injure this world.
+Marwellus hey, thanks for correcting. I have edited my response.
+Marwellus and as far as current flow is due to electrons statement is concerned, I meant that without a negative charge movement, simple movement of sodium ions in one direction does not constitute current. I would be really happy to learn more but with my limited knowledge I know that action potential propagation can not be explained by flow of only one type of charge down the axon. Sodium ions with their positive charge represent loss of negative charge and not its gain. besides, the idea of using electrons (should have been cautious, it was not appropriate) was to highlight that size of charge carriers is way below the obstacles being talked about. I would welcome any healthy discussion.
Also I would be glad to go through any link which shows the physical
movement of sodium ions during action potential propagation.
Sudheendra Rao did you ever figure this part out? I'm stuck at the same understanding point as you
on a myelinated fiber, where is the site of the fastest conduction velocity? Why?
Love khan academy's videos, but i find this chaps accent so annoying I cant concentrate, so sorry mate, I know it probably shouldn't affect me ....
Bless you for this