Human biology
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The Lungs and Pulmonary System
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Red blood cells
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Circulatory System and the Heart
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Hemoglobin
-
Anatomy of a Neuron
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Sodium Potassium Pump
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Correction to Sodium and Potassium Pump Video
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Electrotonic and Action Potentials
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Saltatory Conduction in Neurons
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Neuronal Synapses (Chemical)
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Myosin and Actin
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Tropomyosin and troponin and their role in regulating muscle contraction
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Role of the Sarcoplasmic Reticulum in Muscle Cells
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Anatomy of a muscle cell
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The Kidney and Nephron
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Secondary Active Transport in the Nephron
Saltatory Conduction in Neurons Saltatory conduction or how neurons use both electrotonic and action potentials to have signals move quickly while not losing strength.
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- In the last video, we got an overview of electrotonic
- potentials and action potentials and how they
- essentially can transmit potential differences through
- a cell or how they can move a potential
- difference through a cell.
- And just as a bit of review, electrotonic is if you have
- some type of charge disruption-- let's say a
- sodium gate opens and a bunch of positive ions flow in, that
- very quickly is going to make things nearby
- more positive, right?
- It's very quickly because the positive charges are going to
- move away from their positive brethren.
- Positives and positives repel each other.
- And so if we go some point further off in the cell--
- let's say we were looking at that point right here-- the
- positive charges-- if there's a positive charge here, it's
- going to want to move in that direction.
- If you have a positive charge here, it's going to move in
- this direction.
- So it's going to become more positive very quickly.
- So that's what we talk about electrotonic potential.
- And the benefit is, it happens very, very quickly.
- If we're looking at this point, as soon as these
- positive charges move in, a positive charge here that's
- right there is going to want to move there and a positive
- charge that's here is going to want to move to the right, but
- not as quickly because the the effect gets diffused, right?
- The impact on this charge is less than this charge because
- it's further away.
- And we could think more, we could run computer simulations
- about it, but I think you get the general idea.
- Positive things flow in.
- Other positive things want to move away.
- That makes any point that's some distance away from that
- disruption a little bit more positive so it'll affect its
- voltage almost immediately.
- So it's very fast, but the problem is it
- dissipates with distance.
- If we go really far from that-- if we went all the way
- down here, this guy would have almost no impact from what's
- happening at this opening of this sodium gate.
- So that's its negative.
- On the other hand, on the other side of the spectrum, we
- looked at action potentials.
- Action potentials are all about--
- you have some stimulus.
- In general, it's getting a little bit of a positive
- charge near a sodium gate.
- So normally, we're resting at minus 70 millvolts.
- Maybe you have a little bit of a positive charge come, maybe
- through some type of electrotonic interaction, but
- that's not enough.
- But maybe another one comes by and it gets you to minus 55
- millvolts and then the gate opens, sodium floods in, we
- become much more positive.
- Then the sodium gates close.
- Potassium gates open.
- The potassium wants to flow out of the cell because we're
- positive in the cell now and there's a lot of potassium on
- the inside because of the sodium potassium pumps.
- So then we go back to negative.
- We actually overshoot.
- And just in case you want to know, at this point, we're
- kind of in this refractory period.
- And the original gate that just opened and closed-- it's
- deactivated for a short period of time.
- So there's some period of time that another stimulus won't be
- able to do it, but then our sodium potassium pumps can get
- us back to normal.
- But the whole time that that was happening, as the gate
- that was to the left got all charged up, as the sodium
- started flowing in, it's obviously going to make it a
- little bit more positive to the gate that's directly to
- the right of it.
- So the gate that's to the right of it, its charge is
- going to go slightly up and then bam, it hits its
- threshold for firing.
- So then that sodium gate opens and the same thing happens a
- little bit further to the right.
- And I could keep doing that, maybe even a little bit
- further to right.
- A gate's potential might look something like that and that's
- how it travels.
- Now the benefit of this is that the signal never loses
- strength, right?
- We can just keep going down the cell like this.
- We could do that for millions of miles if we had to.
- The negative is that it's slower than electrotonic in
- that you have to open and close these gates and it also
- requires energy because you're always having to re-balance
- the charge potential between the inside and the
- outside of the cell.
- So we need to think about, how could a cell use both of these
- things to optimize those tradeoffs between signal
- dissipation and speed?
- And this is exactly what the neuron does do.
- So let's go back.
- Now we're ready to close the loop and actually talk about
- the neuron.
- So when I talked about a neuron getting excited on the
- dendrite-- if I zoom in on a dendrite-- let's say this is a
- dendrite's membrane right here.
- Let me zoom in on a dendrite.
- So that's the dendrite right there.
- Let's say that this is a drawing of
- that point right there.
- When I say stimulated, what's happening is, some channel is
- being triggered, some gate is being opened.
- And so let's say that this is a sodium channel and it
- stimulates-- the stimulus, it could be-- like in our action
- potential-- it could be voltage gated.
- A higher voltage might cause it to happen.
- It might be some chemical stimulus from some other
- terminal end of some other axon.
- It could be pressure.
- It could be, who knows?
- It could be some molecule that stimulates it, but something
- is making a gate open and maybe it's a sodium gate and
- so positive charge is going to flood in here.
- Positive charge is going to flow into the cell.
- We know why it does that.
- There's a lot of sodium on the outside.
- That's what the sodium potassium pump does.
- So positive charge flows into the cell.
- So immediately, it's going to have some impact.
- If we measure the voltage here, immediately the positive
- charge here is going to want to travel away and so this
- point is going to become a little bit more positive.
- If we look at this point, it's going to become a little bit
- more positive, but it's so far away from the original
- reaction that maybe it doesn't become as positive because the
- ions are becoming dissipated as we go through the cell.
- So as we go right here to our axon hillock,
- we have more gates.
- Let's say that that's a sodium gate.
- Let's say that this is a potassium gate.
- Let's say that we have another sodium gate.
- Doesn't have to be configured this way.
- We have another potassium gate right there.
- Now if we just had one event here, we're so far away from
- that event that maybe if we measured the potential at that
- point, at the axon hillock-- remember, that's the little
- bulge that turns into the axon.
- Let's do that same chart that I had before, where we have
- membrane potential.
- So potential across the membrane.
- And then we have time.
- So if we look at this point-- let's say we're looking at
- this point right here, that point and we're comparing it
- to the outside of the membrane.
- So it's starting at minus 70 millivolts.
- That's its resting.
- And let's say that some event happened out here and
- electrotonically it's going to increase the potential a
- little bit because positive charge is going to make its
- way and they're all going to push each other.
- They're all going to get away from each other and this one's
- going to become slightly positive.
- But let's say it only goes to minus 65, nothing happens.
- Then your sodium potassium pumps come into effect so
- nothing really happened.
- It didn't trigger the neuron, but let's say that gets
- stimulated again and let's say there's a couple more that get
- stimulated and their combined effects-- because all of them
- are flooding with positive ions now-- their combined
- effects are enough to get this point to the threshold.
- So they're enough to get this point to minus 55.
- And we know what's going to happen here.
- As soon as this sodium gate gets to minus 55, it's going
- to open up.
- It's going to open up and sodium is going to flood in.
- Sodium is going to flood in until we get to positive 40.
- then it's going to close.
- Then the potassium gate's going to open and get us back
- to where we were before.
- We're going to overshoot a little bit and then our sodium
- potassium pump's going to get back to where we wanted.
- That's going to happen there, but as the sodium is floating
- in into that first gate, this guy's going to become positive
- here and then this gate, this sodium gate, is going to
- become triggered.
- And this is that action potential idea.
- Now, we could just keep going our action potential all the
- way down the axon because we said the benefit of the
- electrotonic is that it goes fast, but doesn't cover a lot
- of distance.
- This is a relatively short distance, while the axon is
- super-long.
- So you might say, OK, I see, electrotonic from the dendrite
- to the axon hillock-- and then we use action potential all
- the way down the axon.
- That would be reasonable because we're not going to
- lose our signal strength.
- We would keep having that domino, that chain reaction
- going all the way until we get to our terminal end, but the
- problem there is, it's slow.
- I mean, if this is a five foot long axon, I don't want to
- have a slow signal.
- If someone just bit me, I want to move my hand.
- If I just touched a stove, I want to move my hand quickly.
- I don't want all that signal to take so much time, all
- these gates to open and close along the whole four or five
- feet-- of if I'm a dinosaur, move my arm.
- It needs to happen quickly.
- So what happens is that there's a combination.
- You get your signal and this amplifies the signal.
- The signal is very weak here, right?
- It only got us to minus 55, but then when that first
- sodium gate opens, it creates a huge positive potential that
- opens the next gate.
- So we have a huge positive potential here.
- Now the axons have these huge spaces where
- they're covered up.
- They're covered up by these Schwann cells or by these
- myelin sheaths.
- So even if there are gates underneath
- them, they're useless.
- They can't interface with the outside sodiums and
- potassiums. So over this distance of the axon, you
- cannot have a straight-up action potential.
- What happened is, your action potential here, it made
- everything a lot more positive than it would have been had
- there not been that opening of the gate and now you can have
- an electrotonic effect again.
- So you kind of boosted your signal.
- So now this might get to plus 40.
- Maybe over here we only get to minus 50, but minus 50, once
- again is enough to trigger a sodium gate, which then makes
- everything really positive again.
- It boosts the signal.
- It makes everything positive again, then your potassium
- gates, everything, comes out of the cell again.
- So everything gets back to normal, but
- it boosted the signal.
- Now electrotonically, this is super positive.
- Now the electrotonic effect, if we go some distance down
- the axon, this'll be less positive, but it'll be just
- enough to trigger another action potential.
- And then that happens again.
- So we have this combination of action potentials with
- electrotonics.
- So electrotonic-- this is very fast. This is a fast
- interaction.
- It happens immediately, but it dissipates
- as it covers distance.
- So we can't have these nodes of Ranvier being super far
- from each other.
- They have to be just far enough so that when one action
- potential happens, that it's still enough to
- trigger the next one.
- It's not going to boost its potential to plus 40, but as
- long as it boosts it to minus 55, we're still going to
- produce a signal to keep moving on.
- So this is a really good tradeoff because we get fast,
- slow, but it boosts the signal.
- Fast signal dies down, but it's enough to essentially
- trigger this guy and then it boosts the signal.
- It's slow, but then we travel fast again.
- Signal dies, boosts the signal slow, and we keep traveling
- that way down the axon.
- And this is actually called a saltatory conduction.
- Let me write this down.
- Saltatory conduction, which I think comes from
- the Latin for hopping.
- I remember when I first learned this in biology class,
- they kind of talked about it.
- Somehow putting the myelin sheath there just magically
- made it happen faster and these things just hop from one
- action potential reaction to another, but
- that's not what's happening.
- You're boosting the signal here with an action potential.
- When these gates open, it becomes super positive.
- When it becomes super positive here-- from a maybe not so
- positive trigger becomes super positive, that allows this
- point to become reasonably positive, enough to trigger
- the next reaction.
- When that triggers, then it becomes super positive, makes
- this reasonably positive or less negative, it
- triggers the next one.
- So it's a combination of action potentials that boosts
- the signal.
- And electrotonic effects that move the signal, that gives us
- this saltatory conduction.
- So that's actually how neurons are able to make that tradeoff
- between traveling huge distances, but not losing
- their signal.
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At 5:31, how is the moon large enough to block the sun? Isn't the sun way larger?
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