Role of the Sarcoplasmic Reticulum in Muscle Cells

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 verticulum,

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.