Neuronal synapses (chemical) | Human anatomy and physiology | Health & Medicine | Khan Academy

Neuronal synapses (chemical) | Human anatomy and physiology | Health & Medicine | Khan Academy

December 2, 2019 100 By Kody Olson


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.