Muscle Contraction: The Big Picture

Muscle Contraction: The Big Picture


Hi everybody. This is a big picture view
of muscle contraction, because I know it’s hard to keep that big picture in
mind when you’re also thinking about all the different components of it. So when
you move your skeletal muscles, the ones that are attached to your skeleton and
move your body around, including those that control speech, then there’s a
neuron in your spinal cord– the cell body is in your spinal cord– and it is
told by the brain to send an action potential down its axon to the muscle.
And as you can see in this picture, typically these axons– not always but
typically these axons– divide, and have many axon terminals. So even though
there’s only one signal that’s being sent down from the motor neuron in the
spinal cord, it is received by several different muscle cells, muscle fibers.
This is different than the autonomic nervous system in which you would have
*two* neurons between the spinal cord and the target tissue. With skeletal muscle
there’s only one neuron in that chain. Furthermore, the signal, in contrast to
the autonomic nervous system, is always excitatory; that is, it’s impossible for
the nervous system to tell a muscle to STOP contracting; all it can do is stop
telling it *to* contract. which is very effective; that does make it not contract.
So an action potential has “traveled”– as you know, it doesn’t really travel but is
regenerated– down this axon, and then when it gets to the axon terminal, you have
really what happens at *any* axon terminal, right– is, here you have the vesicles full
of neurotransmitter, in this case acetylcholine, and then when you get to
the axon terminal, voltage-gated calcium channels will open, and calcium will
enter the cell and cause exocytosis of the neurotransmitter, as you learned
before. So these little red dots are supposed to
be acetylcholine that’s now been released into the synapse, into the
synaptic cleft; and it binds to its receptors, which on skeletal muscle are
the nicotinic type. And this is a type that’s an ionotropic receptor, which
means that that the receptor itself is also an ion channel. So acetylcholine
binds to its receptor and when two molecules of acetylcholine are bound, the
channel opens, and both sodium and potassium can actually pass through this
channel, but it doesn’t really matter in real life about the potassium, because
sodium has a much greater driving force, and the movement of ions through that
open channel during the brief time that it’s open is dominated by the movement
of sodium. And that’s the only one shown in this picture. So sodium comes into the
muscle cell, and depolarizes it, and *it* has an action potential. That action potential
spreads along the muscle membrane and muscles have these pockets in them,
called T-tubules, to allow the depolarization to spread to the interior
of the muscle. As that depolarization spreads, it activates these voltage-gated
proteins which are very much like voltage-gated ion channels, but here, the
voltage-gated protein is on the T-tubule membrane– so on the muscle cell membrane–
but it’s physically connected to this other molecule, with a very
confusing name, called the ryanodine receptor, but you can just think of it as
a calcium channel. All right, so the ryanodine receptor (RyR), as soon as you get
the voltage activating this dihydropyridine receptor (“DHP” is fine)
then it activates the RyR and calcium flows out into the cell. So all you need
to really think about here is that the depolarization, the spread of the action
potential, has opened calcium channels. Okay?
So the calcium– which is not coming from outside the cell but rather from the
sacks of calcium within the cell called sarcoplasmic reticulum– the calcium comes
out into the cell, and then of course it can bind to troponin, and this is now the
part of the process that you may be more familiar with from Cell Bio, that you get
an increase in calcium in the cytoplasm, that it binds here to troponin, which
they’re abbreviating TN, and when troponin changes shape when bound by calcium, you
then get a change of shape in tropomyosin, and that exposes, as it’s
always stated, a place on actin for myosin to bind. Once myosin is able to
bind there, it will; so it always is sitting there “waiting” to bind, and it
will bind there as soon as that as that site is activated. So once you have
myosin binding to actin, then we’re here at the contraction cycle, which has many
names as well; and the contraction cycle again is something that you I think
were familiar with in Cell Bio, but probably need to refamiliarize with.
But basically it’s a cycle of myosin and actin attaching, and then moving relative
to each other, and then reattaching. So if you imagine that this is the, part of the,
excuse me, part of the myosin that’s attaching to the actin, right, the sort of
“head,” myosin head; so it binds to the actin, and then you have a power stroke,
right? And then it binds to the actin again, power stroke, so you can see that –
myosin and actin are moving relative to each other, right, that we’re moving my hand
relatively across the screen, right? So at the moment of letting go, you would
expect the actin to just snap back to its original position, and actually
that’s exactly what will happen. And the reason that it *doesn’t* happen is
that, even though in textbooks we always see one myosin head moving, actually
there are hundreds or thousands of them, and at any given point, some of them are
attached and some of them are released, so when one of them releases to rebind,
there are others that are attached and holding it in place. So it’s kind of like
if you were doing tug-of-war, and you let go of the rope to get a better grip, your
team wouldn’t immediately lose, unless you were about to do so anyway; so
there’s this asynchronous binding and rebinding of the actin and myosin. And
all this will continue, if we go back to the first slide here, all this will
continue while we’re getting action potentials in these motor neurons. And
when the action potentials stop, then the depolarization, right– there’s
no acetylcholine release, there’s no depolarization, and the calcium is being
constantly pumped into the sarcoplasmic reticulum, so as soon as the action
potentials stop, the calcium will still be being pumped back in, but it’ll be no
longer being released, and so pretty soon there won’t be enough calcium left in
the cytoplasm of the cell to activate that whole cycle, and
contraction stops. Okay if you have any questions, let me know!

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