We know from the last video that if we have a high calcium
ion concentration inside of the muscle cell, those calcium
ions will bond to the troponin proteins which will then
change their shape in such a way that the tropomyosin will
be moved out of the way and so then the myosin heads can
crawl along the actin filaments and them we'll
actually have muscle contractions.
So high calcium concentration, or calcium ion concentration,
we have contraction.
Low calcium ion concentration, these troponin proteins go to
their standard confirmation and they pull-- or you can say
they move the tropomyosin back in the way of the myosin
heads-- and we have no contraction.
So the next obvious question is, how does the muscle
regulate whether we have high calcium concentration and
contraction or low calcium concentration and relaxation?
Or even a better question is, how does the
nervous system do it?
How does the nervous system tell the muscle to contract,
to make its calcium concentration high and
contract or to make it low again and relax?
And to understand that, let's do a little bit a review of
what we learned on the videos on neurons.
Let me draw the terminal junction of
an axon right here.
Instead of having a synapse with a dendrite of another
neuron, it's going to have a synapse with an
actual muscle cell.
So this is its synapse with the actual muscle cell.
This is a synapse with an actual muscle cell.
Let me label everything just so you don't get confused.
This is the axon.
We could call it the terminal end of an axon.
This is the synapse.
Just a little terminology from the neuron videos-- this space
was a synaptic cleft.
This is the presynaptic neuron.
This is-- I guess you could kind of view it-- the
post-synaptic cell.
It's not a neuron in this case.
And then just so we have-- this is our
membrane of muscle cell.
And I'm going to do-- probably the next video or maybe a
video after that, I'll actually show you the anatomy
of a muscle cell.
In this, it'll be a little abstract because we really
want to understand how the calcium ion
concentration is regulated.
This is called a sarcolemma.
So this is the membrane of the muscle cell.
And this right here-- you could imagine it's just a fold
into the membrane of the muscle cell.
If I were to look at the surface of the muscle cell,
then it would look like a little bit of a hole or an
indentation that goes into the cell, but here we did a cross
section so you can imagine it folding in, but if you poked
it in with a needle or something, this is
what you would get.
You would get a fold in the membrane.
And this right here is called a T-tubule.
And the T just stands for transverse.
It's going transverse to the surface of the membrane.
And over here-- and this is the really important thing in
this video, or the really important
organelle in this video.
You have this organelle inside of the muscle cell called the
sarcoplasmic reticulum.
And it actually is very similar to an endoplasmic
reticulum in somewhat of what it is or maybe how it's
related to an endoplasmic reiticulum-- but here its main
function is storage.
While an endoplasmic reticulum, it's involved in
protein development and it has ribosomes attached to it, but
this is purely a storage organelle.
What the sarcoplasmic reticulum does it has calcium
ion pumps on its membrane and what these do is they're ATP
ases, which means that they use ATP to fuel the pump.
So you have ATP come in, ATP attaches to it, and maybe a
calcium ion will attach to it, and when the ATP hydrolyzes
into ADP plus a phosphate group, that changes the
confirmation of this protein and it pumps
the calcium ion in.
So the calcium ions get pumped in.
So the net effect of all of these calcium ion pumps on the
membrane of the sarcoplasmic reticulum is in a resting
muscle, we'll have a very high concentration of calcium ions
on the inside.
Now, I think you could probably guess
where this is going.
When the muscle needs to contract, these calcium ions
get dumped out into the cytoplasm of the cell.
And then they're able to bond to the troponin right here,
and do everything we talked about in the last video.
So what we care about is, just how does it know when to dump
its calcium ions into the rest of the cell?
This is the inside of the cell.
And so this area is what the actin filaments and the myosin
heads and all of the rest, and the troponin, and the
tropomyosin-- they're all exposed to the environment
that is over here.
So you can imagine-- I could just draw it here
just to make it clear.
I'm drawing it very abstract.
We'll see more of the structure in a future video.
This is a very abstract drawing, but I think this'll
give you a sense of what's going on.
So let's say this neuron-- and we'll call this a motor
neuron-- it's signaling for a muscle contraction.
So first of all, we know how signals travel across neurons,
especially across axons with an action potential.
We could have a sodium channel right here.
It's voltage gated so you have a little bit of a positive
voltage there.
That tells this voltage gated sodium channel to open up.
So it opens up and allows even more of the sodium to flow in.
That makes it a little bit more positive here.
So then that triggers the next voltage gated channel to open
up-- and so it keeps traveling down the membrane of the
axon-- and eventually, when you get enough of a positive
threshold, voltage gated calcium channels open up.
This is all a review of what we learned
in the neuron videos.
So eventually, when it gets positive enough close to these
calcium ion channels, they allow the calcium
ions to flow in.
And the calcium ions flow in and they bond to those special
proteins near the synaptic membrane or the presynaptic
membrane right there.
These are calcium ions.
They bond to proteins that were docking vesicles.
Remember, vesicles were just these membranes around
neurotransmitters.
When the calcium binds to those proteins, it allows
exocytosis to occur.
It allows the membrane of the vesicles to merge with the
membrane of the actual neuron and the
contents get dumped out.
This is all review from the neuron videos.
I explained it in much more detail in those videos, but
you have-- all of these
neurotransmitters get dumped out.
And we were talking about the synapse between a neuron and a
muscle cell.
The neurotransmitter here is acetylcholine.
But just like what would happen at a dendrite, the
acetylcholine binds to receptors on the sarcolemma or
the membrane of the muscle cell and that opens sodium
channels on the muscle cell.
So the muscle cell also has a a voltage gradient across its
membrane, just like a neuron does.
So when this guy gets some acetylcholene, it allows
sodium to flow inside the muscle cell.
So you have a plus there and that causes an action
potential in the muscle cell.
So then you have a little bit of a positive charge.
If it gets high enough to a threshold level, it'll trigger
this voltage gated channel right here, which will allow
more sodium to flow in.
So it'll become a little bit positive over here.
Of course, it also has potassium to reverse it.
It's just like what's going on in a neuron.
So eventually this action potential-- you have a sodium
channel over here.
It gets a little bit positive.
When it gets enough positive, then it opens up and allows
even more sodium to flow in.
So you have this action potential.
and then that action potential-- so you have a
sodium channel over here-- it goes down this T-tubule.
So the information from the neuron-- you could imagine the
action potential then turns into kind of a chemical signal
which triggers another action potential that
goes down the T-tubule.
And this is the interesting part-- and actually this is an
area of open research right now and I'll give you some
leads if you want to read more about this research-- is that
you have a protein complex that essentially bridges the
sarcoplasmic reticulum to the T-tubule.
And I'll just draw it as a big box right here.
So you have this protein complex right there.
And I'll actually show it-- people believe-- I'll sort
some words out here.
It involves the proteins triadin, junctin,
calsequestrin, and ryanodine.
But they're somehow involved in a protein complex here that
bridges between the T-tubule the sarcoplasmic reticulum,
but the big picture is what happens when this action
potential travels down here-- so we get positive enough
right around here, this complex of proteins triggers
the release of calcium.
And they think that the ryanodine is actually the part
that actually releases the calcium, but we could just say
that it-- maybe it's triggered right here.
When the action potential travels down-- let me switch
to another color.
I'm using this purple too much.
When the action potential gets far enough-- I'll use red
right here-- when the action potential gets far enough-- so
this environment gets a little positive with all those sodium
ions flowing in, this mystery box-- and you could do web
searches for these proteins.
People are still trying to understand exactly how this
mystery box works-- it triggers an opening for all of
these calcium ions to escape the sarcoplasmic reticulum.
So then all these calcium ions get dumped into the outside of
the sarcoplasmic reticulum into-- just the inside of the
cell, into the cytoplasm of the cell.
Now when that happens, what's doing to happen?
Well, the high calcium concentration, the calcium
ions bond to the troponin, just like what we said at the
beginning of the video.
The calcium ions bond to the troponin, move the tropomyosin
out of the way, and then the myosin using ATP like we
learned two videos ago can start crawling up the actin--
and at the same time, once the signal disappears, this thing
shuts down and then these calcium ion pumps will reduce
the calcium ion concentration again.
And then our contraction will stop and the muscle will get
relaxed again.
So the whole big thing here is that we have this container of
calcium ions that, when the muscles relax, is essentially
taking the calcium ions out of the inside of the cell so the
muscle is relaxed so that you can't have your myosin climb
up the actin.
But then when it gets the signal, it dumps it back in
and then we actually have a muscle contraction because the
tropomyosin gets moved out of the way by the troponin., So I
don't know. That's pretty fascinating.
It's actually even fascinating that this is still not
completely well understood.
This is an active-- if you want to become a biological
researcher, this could be an interesting thing to try to
understand.
One, it's interesting just from a scientific point of
view of how this actually functions, but there's
actually-- there's maybe potential diseases that are
byproducts of malfunctioning proteins right here.
Maybe you can somehow make these things perform better or
worse, or who knows.
So there actually are positive impacts that you could have if
you actually figured out what exactly is going on here when
the action potential shows up to open up
this calcium channel.
So now we have the big picture.
We know how a motor neuron can stimulate a contraction of a
cell by allowing the sarcoplasmic reticulum to
allow calcium ions to travel across this membrane in the
cytoplasm of the cell.
And I was doing a little bit of reading before this video.
These pumps are very efficient.
So once the signal goes away and this door is closed right
here, this this sarcoplasmic reticulum can get back the ion
concentration in about 30 milliseconds.
So that's why we're so good at stopping contractions, why I
can punch and then pull back my arm and then have it relax
all within split-seconds because we can stop the
contraction in 30 milliseconds, which is less
than 1/30 of a second.
So anyway, I'll see in the next video, where we'll study
the actual anatomy of a muscle cell in a
little bit more detail.