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Neuronal Synapses (Chemical)

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Neuronal Synapses (Chemical) : How one neuron can stimulate (or inhibit) another neuron at a chemical synapse

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I think we have a decent idea of how a signal is transmitted
along the neuron.
We saw that a couple of dendrites, maybe that one and
that one and that one, might get excited or triggered.
And when we say it gets triggered, we're saying that
some type of channel gets opened.
That's probably the trigger.
That channel allows ions to be released into the cell-- or
actually, there are situations where ions can be released out
of the cell.
It would be inhibitory, but let's take the case where ions
are released into the cells in an electrotonic fashion.
It changes the charge or the voltage gradient across the
membrane and if the combined effects of the change in the
voltage gradient is just enough at the axon hillock to
meet that threshold, then the sodium channels over here will
open up, sodium floods in, and then we have the situation
where the voltage becomes very positive.
Potassium channels open up to change things again, but by
the time we went very positive, then that
eletrotonically affects the next sodium pump.
But then we have the situation where that will allow sodium
ions to flood in and then the signal keeps getting
transmitted.
Now the next natural question is, what happens at the neuron
to neuron junctions?
We said that this dendrite gets
triggered or gets excited.
In most cases, it's getting triggered or excited by
another neuron.
It could be something else.
And over here, when this axon fires, it should be exciting
either another cell.
It could be a muscle cell or-- in probably most cases of the
human body-- it's exciting another neuron.
And so how does it do that?
So this is the terminal end of the axon.
There could be the dendrite of another neuron right here.
This is another neuron with its own axon, its own cell.
This would trigger the dendrite right there.
So the question is, how does that happen?
How does the signal go from one neuron's axon to the next
neuron's dendrite?
It actually always doesn't have to go from axon to
dendrite, but that's the most typical.
You can actually go from axon to axon, dendrite to dendrite,
axon to soma-- but let's just focus on axon to dendrite
because that's the most traditional way that neurons
transmit information from one to the other.
So let's zoom in.
Let's zoom in right here.
This little box right there, let's zoom at the base, the
terminal end of this axon and let's zoom in
on this whole area.
Then we'll also zoom in-- we're also going to get the
dendrite of this next neuron-- and I'm going to rotate it.
Actually, I don't even have to rotate it.
So to do that, let me draw the terminal end.
So let's say the terminal end looks something like this.
I'm zoomed in big time.
This is the terminal end of the neuron.
This is inside the neuron and then the next dendrite-- let
me draw it right here.
So we've really zoomed in.
So this is the dendrite of the next neuron.
This is inside the first neuron.
So we have this action potential that
keeps traveling along.
Eventually for maybe right over here-- I don't know if
you can zoom in-- which would be over here, the action
potential makes the electrical potential or the voltage
potential across this membrane just positive enough to
trigger this sodium channel.
So actually, maybe I'm really close.
This channel is this one right here.
So then it allows a flood of sodium to enter the cell.
And then the the whole thing happens.
You have potassium that can then take it out, but by the
time this comes in, this positive charge, it can
trigger another channel and it could trigger another sodium
channel if there's other sodium channels further down,
but near the end of the axon there are
actually calcium channels.
I'll do that in pink.
So this is a calcium channel that is traditionally closed.
So this is a calcium ion channel.
Calcium has a plus 2 charge.
It tends to be closed, but it's also voltage gated.
When the voltage gets high enough, it's very similar to a
sodium voltage gated channel is that if it becomes positive
enough near the gate, it will open up and when it opens up,
it allows calcium ions to flood into the cell.
So the calcium ions, their plus 2 charge, to
flood into the cells.
Now you're saying, hey Sal, why are calcium ions flooding
into the cells?
These have positive charge.
I just thought you said that the cell is becoming positive
because of all the sodium flowing in.
Why would this calcium want to flow in?
And the reason why it wants to flow in is because the cell
also-- just like it pumps out sodium and pumps in potassium,
the cell also has calcium ion pumps and the mechanism is
nearly identical to what I showed you on the sodium
potassium pump, but it just deals with calcium.
So you literally have these proteins that are sitting
across the membrane.
This is a phospobilipid layer membrane.
Maybe I'll draw two layers here just so you realize it's
a bi-layer membrane.
Let me draw it like that.
That makes it look a little bit more realistic, although
the whole thing is not very realistic.
And this is also going to be a bilipid membrane.
You get the idea, but let me just do it to
make the point clear.
So there are also these calcium ion pumps that are
also subsets of ATPases, which they're just like the sodium
potassium pumps.
You give them one ATP and a calcium will bond someplace
else and it'll pull apart the phosphate from the ATP and
that'll be enough energy to change the confirmation of
this protein and it'll push the calcium out.
Essentially, what was the calcium will bond and then
it'll open up so the calcium can only exit the cell.
It's just like the sodium potassium pumps, but it's good
to know in the resting state, you have a high concentration
of calcium ions out here and it's all driven by ATP.
A much higher concentration on the outside than you have on
the inside and it's driven by those ion pumps.
So once you have this action potential, instead of
triggering another sodium gate, it starts triggering
calcium gates and these calcium ions flood into the
terminal end of this axon.
Now, these calcium ions, they bond to other proteins.
And before I go to those other proteins, we have to keep in
mind what's going on near this junction right here.
And I've used the word synapse already--
actually, maybe I haven't.
The place where this axon is meeting with this dendrite,
this is the synapse.
Or you can kind of view it as the touching point or the
communication point or the connection point.
And this neuron right here, this is called
the presynaptic neuron.
Let me write that down.
It's good to have a little terminology under our belt.
This is the post-synaptic neuron.
And the space between the two neurons, between this axon and
this dendrite, this is called the synaptic cleft.
It's a really small space in the terms of-- so what we're
going to deal with in this video is a chemical synapse.
In general, when people talk about synapses, they're
talking about chemical synapses.
There also are electrical synapses, but I won't go into
detail on those.
This is kind of the most traditional one that people
talk about.
So your synaptic cleft in chemical synapses is about 20
nanometers, which is really small.
If you think about the average width of a cell as about 10 to
100 microns-- this micron is 10 to the minus 6.
This is 20 times 10 to the minus 9 meters.
So this is a very small distance and it makes sense
because look how big the cells look next
to this small distance.
So it's a very small distance and you have-- on the
presynaptic neuron near the terminal end,
you have these vesicles.
Remember what vesicles were.
These are just membrane bound things inside of the cell.
So you have these vesicles.
They also have their phospobilipid layers, their
little membranes.
So you have these vesicles so these are just-- you can kind
of view them as containers.
I'll just draw one more just like that.
And they can train these molecules called
neurotransmitters and I'll draw the
neurotransmitters in green.
So they have these molecules called
neurotransmitters in them.
You've probably heard the word before.
In fact, a lot of drugs that people use for depression or
other things related to our mental state, they affect
neurotransmitters.
I won't go into detail there, but they contain these
neurotransmitters.
And when the calcium channels-- they're voltage
gated-- when it becomes a little more positive, they
open calcium floods in and what the calcium does is, it
bonds to these proteins that have docked these vesciles.
So these little vesicles, they're docked to the
presynpatic membrane or to this axon terminal membrane
right there.
These proteins are actually called SNARE proteins.
It's an acronym, but it's also a good word because they've
literally snared the vesicles to this membrane.
So that's what these proteins are.
And when these calcium ions flood in, they bond to these
proteins, they attach to these proteins, and they change the
confirmation of the proteins just enough that these
proteins bring these vesicles closer to the membrane and
also kind of pull apart the two membranes so that the
membranes merge.
Let me do a zoom in of that just to make it clear
what's going on.
So after they've bonded-- this is kind of before the calcium
comes in, bonds to those SNARE proteins, then the SNARE
protein will bring the vesicle ultra-close to
the presynaptic membrane.
So that's the vesicle and then the presynaptic membrane will
look like this and then you have your SNARE proteins.
And I'm not obviously drawing it exactly how it looks in the
cell, but it'll give you the idea of what's going on.
Your SNARE proteins have essentially pulled the things
together and have pulled them apart so that these two
membranes merge.
And then the main side effect-- the reason why all
this is happening-- is it allows those neurotransmitters
to be dumped into the synaptic cleft.
So those neurotransmitters that were inside of our
vesicle then get dumped into the synaptic cleft.
This process right here is called exocytosis.
It's exiting the cytoplasm, you could say, of the
presynaptic neuron.
These neurotransmitters-- and you've probably heard the
specific names of many of these-- serotonin, dopamine,
epinephrine-- which is also adrenaline, but that's also a
hormone, but it also acts as a neurotransmitter.
Norepinephrine, also both a hormone and a
neurotransmitter.
So these are words that you've probably heard before.
But anyway, these enter into the synaptic cleft and then
they bond on the surface of the membrane of the
post-synaptic neuron or this dendrite.
Let's say they bond here, they bond here, and they bond here.
So they bond on special proteins on this membrane
surface, but the main effect of that is, that will trigger
ion channels.
So let's say that this neuron is exciting this dendrite.
So when these neurotransmitters bond on this
membrane, maybe sodium channels open up.
So maybe that will cause a sodium channel to open up.
So instead of being voltage gated, it's
neurotransmitter gated.
So this will cause a sodium channel to open up and then
sodium will flow in and then, just like we said before, if
we go to the original one, that's like this getting
excited, it'll become a little bit positive and then if it's
enough positive, it'll electrotonically increase the
potential at this point on the axon hillock and then we'll
have another neuron-- in this case, this neuron being
stimulated.
So that's essentially how it happens.
It actually could be inhibitory.
You could imagine if this, instead of triggering a sodium
ion channel, if it triggered a potassium ion channel.
If it triggered a potassium ion channel, potassium ion's
concentration gradient will make it want to go
outside of the cell.
So positive things are going to leave the
cell if it's potassium.
Remember, I used triangles for potassium.
And so if positive things leave the cell, then if you go
further down the neuron, it'll become less positive and so
it'll be even harder for the action potential to start up
because it'll need even more positive someplace else to
make the threshold gradient.
I hope I'm not confusing you when I say that.
So this connection, the way I first
described it, it's exciting.
When this guy gets excited from an action potential,
calcium floods in.
It makes these vesicles dump their contents in the synaptic
cleft and then that will make other sodium gates open up and
then that will stimulate this neuron, but if it makes
potassium gates open up, then it will inhibit it-- and
that's how, frankly, these synapses work.
I was about to say there's millions of synapses, but
that'd be incorrect.
There's trillions of synapses.
The best estimate of the number of synapses in our
cerebral cortex is 100 to 500 trillion synapses just in the
cerebral cortex.
The reason why we can have so many is that one neuron can
actually form many, many, many, many synapses.
I mean, you can imagine if this original drawing of a
cell, you might have a synapse here, a synapse here, a
synapse there.
You could have hundreds or thousands of synapses even,
into one neuron or going out of one neuron.
This might be a synapse with one neuron, another one,
another one, another one.
So you'd have many, many, many, many, many connections.
And so synapses are really what give us the complexity of
what probably make us tick in terms of our human mind and
all of that.
But anyway, hopefully you found this useful.

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Neuronal Synapses (Chemical)

Neuronal Synapses (Chemical) : How one neuron can stimulate (or inhibit) another neuron at a chemical synapse