I have sat through so many neuroscience lectures the past few weeks, watched more youtube videos than I can remember and read that many books trying to understand this stuff and FINALLY you have made it make sense. THANK YOU!
Correct, in fact the contribution of the NaK ATPase Pump is calculated to account for merely -4mV, whereas the diffusion alone accounts for nearly -86mV.
Yes that's true... Not because of atp channel... Atp channel is used for attaining the state from hyperpolarization to resting ... Once the action potential is generated... To reversal to resting membrane potebtial
Na+/K+ ATPase absolutely does play a role resting membrane potential. Let's take a step back: Recall that the *equilibrium potentials* of K+ and Na+ are -90 mV and 60 mV, respectively. (That is, if you had a membrane in a lab with just K+ around, the resting potential of that membrane would be -90 mV, at which point *no net ion flow would occur, meaning no leaking.* Similarly, the RP with just Na+ present would be 60 mV.) But RP in real life involves both K+ and Na+, and results in an RP of about -70 mV. Since -70 mV =/= -90 mV or 60 mV, _neither ion ever reaches its equilibrium potential,_ so we *must have net ion flow.* Thus, we have constant leaking. With ions constantly leaking, in their attempt to reach their own equilibrium potentials, if we wish to maintain a nice -70 mV environment for the neuron to function properly, at some point we'll need to move these ions back across the membrane, *against their concentration gradients.* (Recall that there is more K+ inside the cell and more Na+ outside the cell). This will not happen spontaneously. We need energy to do this (ATP), and a structure to use this energy to move these ions (Na+/K+ ATPase). Interestingly, our bodies use more ATP for this activity than for any other singular purpose. By this alone we might conclude that the role of this ATPase in maintaining the resting potential is actually quite significant. NOTE: This is 4 years late, I just discovered this channel. But I hope this helps someone out there. Like my great great grandfather used to say, "Always believe strangers on the Internet."
This does not answer _why_ the channels open or close. And I'd want to mention that once a depolarization happened the cell is hyperpolarized and active transport of both sodium and potassium ions is required to restore the resting membrane potential.
K+ and Na+ leak channels are less relevant to this video about the action potential specifically. Leak channels are more relevant to resting potential, along with the Na+/K+ATPase (Sodium/Potassium pump), which work together to establish and maintain the _resting_ potential. So leak channels are a slightly different section, but you're in the right ballpark. For a test, know this: Resting potential (RP) = - 70 mV 1. *voltage-gated* Na+ channels open @ ~ -50 mV. Na+ influx [DEpolarization] 2. AP occurs at 35 mV and voltage-gated Na+ channels close 3. *voltage-gated* K+ channels open (after delay). K+ efflux [REploarization] 4. "Overshoot" [HYPERpolarization] 5. Na+/K+ATPase moves ions *against* concentration gradients. Reestablish RP. Note: In step 5, yes, there will be some activity through the leak channels (they always leak), even during steps 1-4. This activity is negligible though, even during the return to normal in step 5 because the pumping of ions back across the membrane, *against their concentration gradients,* has a far greater effect on the membrane potential. Thus, the pump is the only relevant structure for _re_ -establishing the membrane's RP.
Can you explain how the new drug pregablin works that is prescribed to people with epilepsy and who may suffer from anxiety. Those who supply this drug cannot explain the mechanism of this drug - but they suspect that it binds calcium to the alpha 1 gated receptor. Pregabalin is an anticonvulsant drug used for neuropathic pain, epilepsy and generalized anxiety disorder.[4] It presents antihyperalgesic actions by binding to the α2δ subunit of the voltage-dependent calcium channels without presenting antinociceptive actions.[5] Pregabalin is marketed by Pfizer under the trade name Lyrica and Lyrica Cr (extended release).[13] It is considered to have a dependence liability if misused, and is classified as a Schedule V drug in the U.S.[4]
Optimum for what? Do you mean we must maintain the concentrations in order to maintain the resting potential? If so, then yes. Something must maintain the concentrations such that the resting potential is stable at around -70 mV. The Na+/K+ pump does this along with Na+ leak channels and K+ leak channels.
ungated ion channels cause maintenance of the resting membrane potential while voltage-gated ion channels cause deviation from the resting membrane potential.
I have sat through so many neuroscience lectures the past few weeks, watched more youtube videos than I can remember and read that many books trying to understand this stuff and FINALLY you have made it make sense. THANK YOU!
You are a terrific illustrator!!!
thank you guys soooo much! i have a midterm tomorrow, and you are life savers!
shoutout to all my boys and girls in cell bio ry------ iz lit if u here
this really help me a lot , thank u so much ;)
Resting membrane potential is not caused by na+/k+ atpase. It is cause by passive diffusion. Only membrane potential is caused by the atpase.
Correct, in fact the contribution of the NaK ATPase Pump is calculated to account for merely -4mV, whereas the diffusion alone accounts for nearly -86mV.
Yes that's true...
Not because of atp channel...
Atp channel is used for attaining the state from hyperpolarization to resting ...
Once the action potential is generated...
To reversal to resting membrane potebtial
Na+/K+ ATPase absolutely does play a role resting membrane potential. Let's take a step back:
Recall that the *equilibrium potentials* of K+ and Na+ are -90 mV and 60 mV, respectively. (That is, if you had a membrane in a lab with just K+ around, the resting potential of that membrane would be -90 mV, at which point *no net ion flow would occur, meaning no leaking.* Similarly, the RP with just Na+ present would be 60 mV.) But RP in real life involves both K+ and Na+, and results in an RP of about -70 mV. Since -70 mV =/= -90 mV or 60 mV, _neither ion ever reaches its equilibrium potential,_ so we *must have net ion flow.* Thus, we have constant leaking.
With ions constantly leaking, in their attempt to reach their own equilibrium potentials, if we wish to maintain a nice -70 mV environment for the neuron to function properly, at some point we'll need to move these ions back across the membrane, *against their concentration gradients.* (Recall that there is more K+ inside the cell and more Na+ outside the cell). This will not happen spontaneously. We need energy to do this (ATP), and a structure to use this energy to move these ions (Na+/K+ ATPase).
Interestingly, our bodies use more ATP for this activity than for any other singular purpose. By this alone we might conclude that the role of this ATPase in maintaining the resting potential is actually quite significant.
NOTE: This is 4 years late, I just discovered this channel. But I hope this helps someone out there. Like my great great grandfather used to say, "Always believe strangers on the Internet."
RMP is maintained by :
1.Unequal distribution of ions b/w ecf and icf
2.Potassium leak channels
3.Na-K ATPase (minor contribution)
Love the diagrams but more information on the specific voltages for example how resting potential is -60mV
This does not answer _why_ the channels open or close. And I'd want to mention that once a depolarization happened the cell is hyperpolarized and active transport of both sodium and potassium ions is required to restore the resting membrane potential.
This channel would be so much better with color coding
but what about leak channels?
Go to the website and watch all his videos. He may get into the k+ leak channels.
K+ and Na+ leak channels are less relevant to this video about the action potential specifically. Leak channels are more relevant to resting potential, along with the Na+/K+ATPase (Sodium/Potassium pump), which work together to establish and maintain the _resting_ potential. So leak channels are a slightly different section, but you're in the right ballpark.
For a test, know this:
Resting potential (RP) = - 70 mV
1. *voltage-gated* Na+ channels open @ ~ -50 mV. Na+ influx [DEpolarization]
2. AP occurs at 35 mV and voltage-gated Na+ channels close
3. *voltage-gated* K+ channels open (after delay). K+ efflux [REploarization]
4. "Overshoot" [HYPERpolarization]
5. Na+/K+ATPase moves ions *against* concentration gradients. Reestablish RP.
Note: In step 5, yes, there will be some activity through the leak channels (they always leak), even during steps 1-4. This activity is negligible though, even during the return to normal in step 5 because the pumping of ions back across the membrane, *against their concentration gradients,* has a far greater effect on the membrane potential. Thus, the pump is the only relevant structure for _re_ -establishing the membrane's RP.
Great video!!!! Thank you so much!
hand writing is so pretty :)
Kya baat !!!! Maza aa gya❤️
This is awesome !
this was soo helpful! Thanks!
Can you explain how the new drug pregablin works that is prescribed to people with epilepsy and who may suffer from anxiety. Those who supply this drug cannot explain the mechanism of this drug - but they suspect that it binds calcium to the alpha 1 gated receptor.
Pregabalin is an anticonvulsant drug used for neuropathic pain, epilepsy and generalized anxiety disorder.[4] It presents antihyperalgesic actions by binding to the α2δ subunit of the voltage-dependent calcium channels without presenting antinociceptive actions.[5] Pregabalin is marketed by Pfizer under the trade name Lyrica and Lyrica Cr (extended release).[13] It is considered to have a dependence liability if misused, and is classified as a Schedule V drug in the U.S.[4]
easy and simple! Thanks buddy and God bless........................
this help me a lot ..Thanks
He drew the potassium channel as a ball and chain inactivation method which is considered an n-type, but isn’t it actually a c-type channel?
Good job mate!
What about the concentration of na+ and k+??? They should also maintain an optimum level ,right?
Optimum for what? Do you mean we must maintain the concentrations in order to maintain the resting potential?
If so, then yes. Something must maintain the concentrations such that the resting potential is stable at around -70 mV. The Na+/K+ pump does this along with Na+ leak channels and K+ leak channels.
ungated ion channels cause maintenance of the resting membrane potential while voltage-gated ion channels cause deviation from the resting membrane potential.
Also the Na+/K+ pump helps maintain resting potential along with the leak (ungated) channels.
good stuff for high schooler's and maybe even for biology 101 students.. def not enf info for advanced human physiology courses..
At what transmembrane potential does the voltage gated potassium channel open? 10mV 35mV? or something else?
OyreGot. what is voltage gated calcium channel. my Dr said this what wrong with me what this mean
It's open at 35 mV, but it begins around 10 mV. Remember, the voltage-gated K+ channel is slow to open.
Helps a lot...
Thanks...!!
Brilliant tutorial, thank you!
you are the best
Thank you
thanks martin
what about excess amount of Na inside the celll Please answer and thanks
arohe that's controlled by the action of the sodium-potassium pump, pulling K+ in the cell and releasing Na+ out of the cell
TakeYourPills! A
Thanku so much !
Why black and white color is good for the brain 🧠 memories
its awesome
nice tq
He keeps saying ITPIse.......I thought it was ATPase.
Nice but imperfect, missing Na+/K+ pumps to restore
hey dude u fall in dinamo
its awesome