THE ACTION POTENTIAL
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- Опубліковано 8 сер 2018
- Neurons have 3 different kinds of potentials - resting, graded, and the action potential. The neuron maintains a resting potential of -70 mV due to differences in permeability of ions on either side of its cell membrane, as well as the sodium potassium pump. The ions contributing to the charges on either side of the membrane are proteins, chloride, sodium, and potassium.
Several kinds of channels found in cell membranes, allowing for the transport of substances from one side to the other. Two kinds are important for action potentials - leaky channels and voltage-gated channels. Leaky channels allow the free flow of substances through them. Voltage-gated channels only open at certain voltages.
Back to the ions - chloride and the proteins stay put. However, the neuron has leaky sodium and potassium channels. These are always open and allow flux of these ions.
There’s a lot more potassium in the cell than outside the cell. The potassium wants to rush out because of the chemical gradient but wants to stay in the cell because of the electrical gradient. Similarly, there is a lot more sodium outside the cell than in it, and it has its own electrochemical gradient.
A graded potential is a change in potential that can vary in size, with magnitude depending on the intensity of the stimulus, and occurs when the neurons get excitatory post-synaptic potentials or inhibitory post-synaptic potentials.
Dendrites are a neuron’s input zone. The neuron cell body is like a calculator, integrating these signals. When the summation of graded potentials results in a potential of -55 mV at the axon hillock, an action potential occurs. Hence, EPSPs make it more likely that an action potential will occur, while IPSPs make it less likely. Unlike graded potentials, which are changes in potential varying in size, action potentials are all or nothing. More intense stimuli simply mean a higher frequency of firing.
At resting potential, voltage-gated sodium and potassium channels are closed. A stimulus causes some voltage-gated sodium channels to open. Once we get to the threshold of -55 mV, the action potential begins, with lots of other voltage-gated sodium channels opening. With sodium channels open, depolarization occurs - sodium rapidly rushes into the cell, and the voltage soars up to +30 mV, at which point the voltage-gated sodium channels close. Potassium channels now open, as repolarization occurs as potassium rapidly rushes out of the cell. The voltage zooms down and overshoots the -70 mV before the potassium channels can close. Finally, the sodium potassium pump restores the resting membrane potential. It does a conformational change thanks to an ATP molecule being hydrolysed. Again, this conformational change results in 3 sodium atoms being shuttled out of the cell, and two potassium atoms being shuttled in.
We’ve now seen what happens locally at one segment of the axon, but how does the action potential propagate? Well, when the sodium ions are rushing in during depolarization, they repel each other and so they spread out. This makes the next section of the axon reach threshold and also have an action potential. Why doesn’t the action potential travel backwards though? At the same time as the first section is depolarizing, the section of axon behind it is experiencing repolarization, and the potassium rushing out results in a refractory period. There is an absolute and relative refractory period. During the absolute refractory period, which coincides with most of the action potential’s duration, you can’t trigger another action potential, because the sodium channels are briefly inactivated - the membrane needs to be hyperpolarized before that can happen. During the relative refractory period, only a very strong stimulus can cause an action potential, since the membrane is below the resting potential and you need a stronger EPSP to get to threshold.
Another important point - action potential propagation is slow. That’s why most of your neurons have myelin sheaths, with are rich in lipids. Myelin sheaths are made by oligodendrocytes in the central nervous system and schwann cells in the peripheral nervous system. They insulate the axon and prevent leakage of charged ions. Instead, you get what’s called “saltatory conduction”, in which action potentials only occur in the spaces between the myelin, called “nodes of Ranvier”. In addition to myelin sheaths, neurons with larger diameters also have faster transmission speeds.
Once the action potential reaches the end of the axon, there are terminal buttons there. The depolarization triggers the opening of voltage-gated calcium channels on the presynaptic membrane, and calcium rushes into the terminal button. This causes exocytosis of vesicles full of neurotransmitter molecules, and neurotransmitter is released into the synaptic cleft, where the neurotransmitters attach to the receptors.
You are teaching me more than all 4 of my Anatomy professors combined
Of course he is teaching more than the anatomy professors, this is physiology
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@Wanderlust my first year, first semester, Anat and physio 😂
Edit for context: it was all online because of 2020s chaos so all of the professors combined to teach the sections like one class online. So I had 3 lecture instructors and 1 lab and it was an absolute nightmare smh. Good news, I made it 😂
From now..when ever I 'll get bored of book-reading I will come to this channel. We medical students need more videos like this and the songs.. whenever you end with human physiology I would like you to go towards plant physiology which is also imp. for many pre -medical students...❤😍thanks alot
Super helpful! I have a rare genetic mutation that causes a malformation of sodium and potassium voltage gated ion channels and it is very helpful for me to learn more about how these systems (are supposed to) work.
I've never understood this since my premed years, never thought I can get it at all. Thanks to you guys I finally get it now. Huge thanks.
I love this channel. You've been helping me a lot making sure I'm writing correct answers for my study guide for school.
Thank you so much. Going to watch this on repeat probably until I get it all.
By far the best explained video about action potential!
Animation have always helped me understand the material better. Thank you!
Hope you guys will become popular soon, the videos are such high quality!
Aww, thank you so so much! :-D We're excited because the channel is growing so quickly! Comments and likes and subscribes and shares really help!
this was amazing. makes everything very understandable. 100% recommended the video to anybody.
the best video out there on the action potential....thank you so much for helping me learn this.
you answered the 2 questions that none of my teachers from highschool AP to university was never able to teach me. and you did it in 5 minutes.
1. how do action potentials cause depolarization to move down the axon..what it actually looks like...na spreading out
2. what it actually means when they say "resting potential is maintained by na/k pump"
I really understood the concept. Thank you. It was done very well. I hope you complete other videos.
Loved it ..brief and to the point
Excellent , one of the best explanations I’ve seen
Your teaching way is amazing! Thank you buddy!
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Excellent video and explanation! I understood everything very easily, thank you.
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Lovely animation ♥️♥️♥️ thanks
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Oh god thank you. Understood this very easily!
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Perfect explanation!
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After 3 videos, 5 chapters, 2 books and 1 hour crying FINALLY I understand
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Super helpful
Thank you
hi this was so useful to watch thank u!! i just have a q abt the relative proportions of charges in the short bit after hyperpolarisation? u said the Na/K pump will bring it back to resting mem potential. if the Na/K pump is transporting net 1 positive ion out, so the inside goes from negative to even more negative, why isnt it hyperpolarising further away from resting mem potential?
Understood very easily thanks
Hello...how does hypocalcemia lead to muscle spasms? How does calcium in hypocalcemia cause increased depolarization? Thank you for this video.
Thank you so much
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You deserve many likes
Wonderful
So helpful!!!!!
nicely explained
How Could Na and K Pump maintain back hyperpolarization from -90 to -70 ???
just wondering- you said na channels close at +30, but don't they first inactivate... and don't actually close until we reach hyperpolarization.. which gives the absolute and relative refractory periods?
Thank you
Awsome video!!!! Im stunned im studying medicine and not even my orofessor could explain like that perfect speed
we all understand now thanks to you
Loved it
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Hermoso todo.
Perfect
Interessante! Il passaggio di elettricità dei neuroni, sembra simile ad una corrente alternata
great
Is there anything that has to do with blockades on the voltage-gated sodium channels and inactivation?
Also, are the sodium channels closed at rest?
Hi Jakari, Not sure I understand your first question, but there are definitely sodium channel blocking drugs - e.g. lidocaine - the local anesthetic. Voltage-gated sodium channels are closed at rest, but there are leaky sodium and potassium channels that are open at rest. Hope that helps!
@@NeuralAcademy Sorry for the misunderstanding. I believed that there was a structure connected to the membrane that hangs down and begins to block the voltage-gated sodium channels as the action potential begins to repolarize.
No problem! The voltage gated sodium channels close quickly at the peak of the action potential.
@@jakarigainer91 You're probably referring to the *inactivation* gate, which this video has ignored, and called just a 'second gate'. It's sometimes referred to as a 'ball and chain' gate. And you're right as to when it operates. And when the voltage gate is closed, that inactivation gate is *not* also closed, as shown in the video, it's *open* . It only begins to close sometime after the voltage gate has opened, with the time delay determined mostly by the *length* of the tether that attaches to the blocking inactivating 'ball'.
I’m a grad student and this is saving my ass rn
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this video and so many others disregard the fact of sodium inactivation that begins and the peak of the action potential and ends after hyperpolarization
If you'd like, I can help with the voice narration free of charge!
4:44
60th n
all of these happen when i flex my arm
all of these happen when you blink
way better than john green. takes him way too long to get to the point and goes off track a lot