Health and medicine
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- Neuron resting potential mechanism
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- Neuron graded potential mechanism
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- Neuron action potential mechanism
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- Action potential patterns
- Electrotonic and action potentials
- Saltatory conduction in neurons
Neuron action potential mechanism
Created by Matthew Barry Jensen.
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- Do the voltage-gated channels detect voltage by a protein or a enzyme?(13 votes)
- Voltage-gated channels are proteins embedded in the membrane. Proteins are made up of different combinations of amino acids.
This is how my professor explained how voltage-gated channels worked to me: There are positively charged amino acids that make up this channel in a coil, so it's shaped like a screw. At resting potential, those amino acids would be attracted to the inside of the cell, as it is negatively charged.
But when depolarization occurs, the positively charged amino acids making up a voltage gated ion channel are repelled and move upwards, unscrewing and opening the channel. Hope this helps!(50 votes)
- How is the initial concentration of sodium and potassium ions restored?(6 votes)
- Apparently the initial concentrations are restored mostly through the potassium ion leak channels (which do not require energy,) but also through the active work of sodium-potassium-pumps in the cell membrane. The pumps require ATP and pushes 3 x Na+ ions out of the cell, at the same time allowing 2 x K+ ions to move into the cell.
More on this subject is found in these videos "neuron resting potential mechanism" and "sodium potassium pump" in addition to the very important "correction to the sodium potassium pump video".(8 votes)
- How do channels selectively leak certain ions?(3 votes)
- Most membrane leak channels are highly conserved in their primary structure (the amino acid sequence). Slight differences in only one or a few amino acids can cause selectivity for one ion over another (for example, selectivity to leak sodium over potassium). Ions usually have a sphere of hydration around them, consisting of a few water molecules. Each channel protein has slightly different size channels as a result of the slightly different amino acid compositions. The size of the channel correlates to the sphere of hydration of the ion (potassium has a different size sphere of hydration than sodium, for example).
In summary: the amino acid sequence determines the size of the channel, which determines the ions that can flow in or out.(5 votes)
- In my biology book, there is one sentence that says: "positive charge travels between two nodes, through the axon, and when it arrives in the node, positive charge leave through the membrane, thus making the action potential."
I'm sorry if I didn't translate it very good, I hope you get what they meant.
So, the problem is this: I understood that action potential is caused by Na+ getting into the axon, and it disappears when K+ leaves the axon. How can 'leaving of the positive charge' cause the making of action potential? Which ions leave the cell? I would be very thankful if someone could explain.
And, I'm not sure if there could be a mistake in the book, since it's an official school book for quite some years. :/
- at a resting state the neuron has a charge of about -60mV, so allowing positive ions such as Na+ into the cell the overall charge will get closer to 0mV. Once the inside of the cell reaches a threshold it begins its action potential. the potential makes the inside of the cell reach about a +40mV charge, the decrease is caused by the leaving of a positive ion such as K+. so with positive ions leaving this +40mV cell it will continue towards 0, then into a negative charge closely resembling its resting state. so in short the action potential is started by positive ions bringing the inner voltage closer to 0 from a negative number and is reset to a resting state by positive ions leaving the cell causing the inner charge to shift from positive(+40mV) back to negative(-60mV)
i hope this gives you a better way of looking at how the flow of ions cause neural mechanism to work. if you have any other question or are looking for clarity about anything i wrote please ask.
- At the end of this video Matt mentions that the action potential cant be triggered by itself to travel back the axon. What did he mean by that?(3 votes)
- The action potential is unidirectional. It will go from the hillock (area where the axon starts) to the terminus (end of the axon near the synapse) in a wave like manner. He was saying that the reason for this is because the membrane is hyper polarized for a while after the action potential has past (more negative then the resting potential).(3 votes)
- These Voltage - Gated Channels, do they embed in the membrane only along the axon?
Or the soma's membrane has these channels too?
(sorry for my english)(1 vote)
- First, let me tell you how wonderful you are to work so hard in English, which is not your language. Second let me apologize for the fact that English is so hard and neurology is hard so together, the work is very difficult . Channels on the axon are voltage-gated, they open when the voltage on the axon hillock reaches threshold ( around -55volts). They open up letting Na ions in, that changes the inside of the axon there, so the next channel opens, and so on all the way down to the end or the axon terminal. The dendrites and cell body or soma have chemically-gated channels. This means that when their receptors bind to the neurotransmitter (the chemical) those channels open letting Na ions in, changing the inside environment to be closer to threshold or depolarizing the soma. If enough gates on the soma open up, and cause the axon hillock to reach threshold, then the voltage gates on the axon will open, moving the action potential down the axon. When it reaches the axon terminal, then the neuron releases a neurotransmitter on another neuron so the process can continue and we can have thoughts. When we say voltage-gated, we mean the key to opening the channels is the change in voltage. When we say the channels are chemically-gated, we mean the key to opening the channels is the chemical. I hope this helps.(4 votes)
- Our professor explained to us that the absolute refractory period occurs during the time span of the rising period and falling period(when sodium floods in and potassium flows out) until hyperpolarization. Then he had explained that the relative refractory period was the point from hyperpolarization back to the resting potential? Could someone please clarify on this?(2 votes)
- It sounds like you have the general idea. Here's why it happens:
The absolute refractory period is when the voltage-gated sodium channels are inactivated. There is absolutely no way for sodium to flow back into the cell during this time, hence the name. Once the cell is hyper polarized (below -65 mV, which is resting membrane potential), the voltage-gated sodium channels start to regain their ability to open (in other words, they are de-inactivated). So from hyper polarization to returning to the resting membrane potential, the voltage-gated sodium channels are starting to open up. If there is a very strong depolarization of the nerve, another action potential can be triggered. This is why it is called the relative refractory period (it is relative to the strength of the next depolarization event).(2 votes)
- I believe there is something wrong when he explained the absolute refractory period. After watching this video, I read many sources--most of them state that the absolute refractory period occurs when voltage-gated Na+ channel are either open or inactive, which occurs during the positive slope until the peak is reached on the action potential graph. Once the voltage-gated Na+ channels begin to close (during the downward region after the peak), K+ channels open, and this is when the relative refractory period begins. At this point, another action potential can be generated, but the stimuli will have to have a greater intensity. I could be wrong, but the region of the graph to which he pointed to indicated the absolute refractory period was not accurate. Can someone clear up this conundrum? Please.(1 vote)
- Hmmm if K+ ions leaves neuron via voltage gated potassium channels and leaks out via leak channels and are transported into neuron with ratio 2 K+ ions in and 3 Na + out I wonder how neuron doesn't run out of K+ ions? Because it losses much more potassium than transports in to or leak channels works both ways in and out?(1 vote)
- Astrocytes that insulate the synapses with their end-foot processes uptake and recycle glutamate and GABA as well as sequester K+.(1 vote)
- As far as I have read the action potential is not uni-directional. It travels both sides from where it is triggered in a neuron. Is that right?(1 vote)
- Generally an action potential should only go in one direction. It can go in both directions, but that's usually only done in experiments.(1 vote)
In this video, I want to talk about how action potentials are generated the trigger zone and how they're conducted down the axon. So I've drawn a soma here in red and one axon in green. And I've blown up the axon to a very large size just so I had some room to draw. Here's our graph of the membrane potential on the y-axis and time on the x-axis. And now I've put a couple of different kinds of ion channels in the membrane of the axon. The first in this lighter grey are the leak channels that we talked about when we talked about the neuron resting potential. These channels are open all the time. They're not gated. And I have not drawn any ligand gated ion channels like the neurotransmitter receptors that occur on the soma and the dendrites. But to talk about the action potential, I need to introduce an entirely new type of channel that I've drawn in dark grey with this little v. And these are voltage gated ion channels. The membrane of an axon as many voltage gated ion channels, most of which open when the membrane potential crosses a threshold value. So we've talked about the threshold potential before. And all of these numbers may vary between different types of neurons, but these would be fairly common values. So many neurons would have a resting membrane potential of around negative 60 millivolts and a threshold potential of around negative 50 millivolts or so that I've drawn with a dashed line. And the importance of this threshold potential is that it determines if these voltage gated ion channels will open. So when there is enough temporal and spatial summation of excitatory grad potentials to get us toward the threshold, here at the trigger zone, at the initial segment of the axon, so let me just draw that, that we have temporal and spatial summation of excitatory potentials spreading across the membrane of the soma into the initial segment of the axon, the trigger zone. This voltage gated ion channel has a mechanism to sense this voltage change. And when the threshold potential is crossed, it's going to open. And these are going to be sodium channels. Recall that the electrical and diffusion forces acting on sodium ions are strongly trying to drive them into the neuron. So when this voltage gated sodium channel opens, sodium is going to flow into the neuron through the open channel causing that part of the membrane to depolarize from all these positive charges now on the inside. This is going to cause an explosive chain reaction by triggering the voltage gated sodium channels in the next piece of the membrane so that more sodium is going to flow in further depolarizing the membrane and opening the next voltage gated sodium channel. These voltage gated sodium channels open very quickly triggering each other in a wave that rapidly spreads down the axon. The trigger zone has the greatest density of these voltage gated sodium channels which is why action potentials usually starts at the trigger zone. So many of these voltage gated sodium channels will open that the membrane permeability to sodium is dramatically increased. This is going to cause the membrane potential, which has already gone from the resting potential to the threshold potential from the grated potentials, but now that all this sodium is flowing in through these open channels, the membrane potential is going to dramatically rise trying to head toward the equilibrium potential of sodium, which is usually somewhere around positive 50 millivolts. This rapid increase in the membrane potential values is due to these voltage gated sodium channels. And this is called the rising phase of the action potential. And in fact, it becomes more positive inside the neuron membrane during this period that it's the reverse of the resting potential because normally it's more negative inside than outside the neuron membrane. But now so much sodium has entered, that it's more positive inside the membrane than outside. The action potential usually peaks though some where around positive 40 millivolts. So it doesn't make it up to the sodium equilibrium potential that's often around positive 50 millivolts. And the reason for that is that these voltage gated sodium channels automatically start to close at the higher potential values so that sodium stops flowing into the neuron. And after they close, they're in a special state called the inactivated state and they're unable to open at any membrane potential for a brief time. The next thing we see happen to the action potential, basically just as fast as the membrane potential went from the resting potential to the peak of the action potential, it then rapidly descends back toward the resting potential and then actually goes farther. It goes more negative than the resting potential and then it levels off. The reason for this part of the action potential, which is called the falling phase, is because potassium starts to exit the neuron and it does so through a couple of types of channels. The first are the leak channels that we talked about when we talked about the resting membrane potential. Now a little potassium as exiting through the leak channels at the resting potential, but even more potassium than normal starts to exit. Because during these parts of the action potential, the membrane potential is positive so that during this part of the action potential, both the diffusion force and the electrical force are strongly trying to drive potassium out of the neuron so that more leaves through the leak channels that normally does during the resting potential. The second type of channel that allows potassium to exit are voltage gated potassium channels. These also open when the membrane potential crosses the threshold, but they're a little slower to open than the voltage gated sodium channels. So that at first, all the voltage gated sodium channels snap open, allowing sodium to rush in causing the rising phase of the action potential. And then a little slower the voltage gated potassium channels open, allowing potassium to flow out of the neuron contributing to the falling phase of the action potential. And then the action potential stops falling because now it's more negative inside the neuron again so there's less driving force pushing potassium out through the leak channels. And also the voltage gated potassium channels automatically close at the lower potential values just like the voltage gated sodium channels automatically closed. But just like the voltage gated potassium channels were a little slower to open than the voltage gated sodium channels, the voltage gated potassium channels are also a little slower to close so that it takes a little longer for this exit of potassium to stop. And that's why there's this little bit of a longer period at the end of the action potential until we kind of slowly settle back into the resting membrane potential. Because as these voltage gated potassium channels are slowly closing, the membrane permeability to potassium is returning to the normal amount you get during the resting potential through the leak channels. And as that permeability to potassium returns back to the normal resting potential level, the membrane potential returns to the resting potential. This movement of sodium ions and potassium ions across the membrane causing the wave form of the action potential starts here at the trigger zone at the axon initial segment, but then rapidly spreads in waves down the axon. First, there's the wave of depolarization from opening up the voltage gated sodium channels. So a wave of depolarization rapidly spreads down the axon, but following right behind it, right on its heels, is this wave of hyper-polarization caused by potassium exciting through the voltage gated potassium channels and the leak channels. So we have the rising phase of the action potential, the peak of the action potential, the falling phase of the action potential, and then this period of hyper-polarization at the end of the action potential has a couple of names. It can be called the after hyper-polarization because it's the hyper-polarization that happens after this part of the action potential. But it's also called the refractory period. Let me just write that down. Refractory period right there. And it's called the refractory period because during this time, it's difficult or impossible to trigger another action potential in that part of the membrane. The refractory period is divided into two parts. The first part is called the absolute refractory period. And it's absolute because the voltage gated sodium channels when they first close they're in a special state called the inactivated state. And they are unable to open at any membrane potential for a brief time so that no matter how much excitatory input comes into the neuron, you can't trigger another action potential during the absolute refractory period. The second part is called the relative refractory period. And during this time, the voltage gated sodium channels have become functional again. They can respond to depolarization, however, the membrane potential is hyper-polarized. It's not yet back to the resting potential. Therefore, it would take more excitatory input than normal to trigger an action potential during the relative refractory period. One important effect of the refractory period is that action potentials travel from the trigger zone to the axon terminals. And they don't turn around and head right back the other direction because the membrane right behind the action potential is refractory. It can't be triggered by itself to send the action potential back the other way.