The phototransduction cascade | Processing the Environment | MCAT | Khan Academy

The phototransduction cascade | Processing the Environment | MCAT | Khan Academy

Last video, we looked at
how light from the sun can enter the eye–
and this is the eye. So it enters the eye,
hits the back of the eye, and somehow through
a set of steps, it gets converted
into neural impulse. And the impulse gets
sent to the brain for you to make sense of
the information. So we looked at something called
the retina in the last video. And we talked about how
the retina is made up of a bunch of different cells. And the two main cells
are rods and cones. So we’re going to look at
just the rods in this video. So the rod, which
is shaped like this. Let’s give him a little smiley
face because he’s happy. And what he does is that as soon
as light is presented to him, he basically takes that
light and then converts it into a neural impulse. So normally, he is turned on. When there’s no light,
the rod is turned on. But when light is present,
it actually turns him off. So with light, he’s turned off. So how does this happen? So this occurs
through this thing called the
phototransduction cascade. So the phototransduction
cascade is the set of steps that occurs at
the molecular level that basically takes this
rod and turns him off. And in turning him
off, he’s actually able to turn on a
bunch of other cells that eventually lets the brain
know, hey, there’s light here. So it allows the brain to
realize that there’s light and allows it to
comprehend what’s going on make
sense of the world. So let’s go ahead and examine
this phototransduction cascade. So let’s give ourselves
a little bit of space here, just look at it in
a little bit more detail. So let’s look at just
a part of the rod. So I’m going to redraw
the rod over here. And let’s just look at
this part of the rod, just this very top
little bit of the rod. And I’m going to
draw it a lot bigger, so that we can really make
sense of what’s going on here. So inside the rod, which
we just made much bigger, there are a bunch of
these little disks. So they are really
thin little disks, and they’re just stacked
on top of one another, and there are hundreds of them. And basically they
are like this. They just go stacked
on top of one another, and they fill up the entire rod. Same thing with cones but we’re
just going to look at the rods here. So inside of these
little disks, there are a whole bunch of different
proteins all interspersed throughout the disks. So this protein that
I’m drawing in red– let me just go ahead and
draw it a lot bigger, so we’re going to go ahead
and blow this protein up. And it’s basically this
multimeric protein, so it consists of a bunch
of different subunits. There are actually
seven subunits, so there are 5, 6, and 7. So there are all
these subunits that make up this little
protein right here. So this protein as a
whole is called rhodopsin. And it’s called rhodopsin
because it’s in a rod. If it were in a cone, it
would be called cone opsin, but it’s basically
the same protein. And sitting inside of this
protein is a small molecule, and it sits just inside. Let’s go ahead and just
zoom in a little bit, so we can make a
little bit more sense of what we’re looking at here. Let’s go ahead and
zoom in over here. So this little molecule is just
sitting inside of rhodopsin, and it’s kind of bent. You can see here how I drew
it just a little bit bent. So this little molecule
is called retinal. And in this bent confirmation,
we call it 11-cis retinal. And so what happens is
light comes in from the sun, goes in through the
pupil, hits the retina, and then hits this little rod. Some of the light will
actually hit this molecule. So it’ll hit rhodopsin,
and it’ll actually hit this molecule. So here’s the light
wave, it comes in, and it just hits the
molecule right there. So an interesting
thing happens when the light hits the molecule
right at this region. And what it actually causes,
is it causes the retinal to actually change confirmation. So the light provides
enough energy that the retinal goes from
this bent confirmation, and it causes it to
look more like this. I’ll draw it over here. I’ll draw a little carbon
ring, so it becomes straight. So it went from being
bent to being straight. So the light does this,
and basically goes from being 11-cis retinal
to all-trans retinal. So when the retinal
changes shape, it actually causes the rhodopsin
molecule to also change shape. So the two are really
closely linked, so when the retinal
changes shape, the rhodopsin changes shape. So let’s go ahead and pretend
that maybe it looks like this. So this region that I’m
shading in right here is what the new rhodopsin looks
like after the retinal has changed shape after
the light hit it. So rhodopsin now changes
shape, and that basically begins this big
cascade of events. So what happens next
is there’s a molecule– and I’m going to draw that
molecule right here in green– and it’s made up of
three different parts. So there’s this alpha subunit,
there’s a beta subunit, and there’s a gamma subunit. And this molecule as a
whole is called transducin. So transducin, basically
as soon as retinal changes shape and causes
rhodopsin to change shape, transducin breaks
away from rhodopsin. And the alpha subunit
actually comes over here to another part of
the disk and binds to a protein called
phosphodiesterase, which I’ll just draw as
this little box over here. So this little protein is called
cyclic GMP phosphodiesterase, or PDE for short. So PDE, basically
what it does– let’s go ahead and zoom
out a little bit. What PDE does when
it’s activated is it takes cyclic GMP,
which is floating all around the cell– it’s a
little molecule, it’s tiny– and it basically
takes the cyclic GMP and converts it into
just regular GMP. So this basically reduces the
concentration of cyclic GMP and increases the
concentration of GMP. And the reason that
this is important is because there’s
another channel over here, so there’s a whole bunch
of these sodium channels and they’re all over the cell. So they’re just a
whole bunch of them, and basically what
they let the cell do is they allow the cell to take
in sodium from the outside. So let’s just say there’s
a little sodium ion, and it allows it to
come inside the cell. So in order for this
sodium channel to be open, it actually needs cyclic
GMP to be bound to it. So as long as cyclic GMP is
bound, the channel is open. But as the concentration of
cyclic GMP decreases because of the phosphodiesterase,
it actually causes sodium channels to close. So now we have a closing
of sodium channels, and now we basically have
less sodium entering the cell. And as less sodium
enters the cell, it actually causes the cell
to hyperpolarize and turn off. So as the sodium channels
close, it actually causes the rods to turn off. So basically, without
light, the rods are on because these
sodium channels are open. Sodium is flowing through,
and the rods are turned on. They can actually produce
an action potential and activate the
next cell and so on. But as soon as
they’re turned off, what happens is very
interesting because– let’s just look at this rod over here. So what happens is
really interesting, because there’s this
other cell over here that is called the bipolar cell. And we’ll just give it a kind
of a neutral base, because it’s bipolar. This cell, there are actually
two different variants, so there are on-center and there
are off-center bipolar cells. So the on-center
bipolar cells normally are being turned off when
this rod cell is turned on. But as we mentioned, due to
the phototransduction cascade, the rods turn off,
which actually turns on the bipolar cell. So basically, on-center bipolar
cells get turned on with light and get turned off
when there’s no light. So that’s how they
get their names. So when the bipolar
cell gets turned on, it activates a
retinal ganglion cell, which then sends an
axon to the optic nerve, and then into the brain. And so that process is known as
the phototransduction cascade, and it basically
allows your brain to recognize that there’s
light entering the eyeball.

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53 thoughts on “The phototransduction cascade | Processing the Environment | MCAT | Khan Academy

  1. And arent the ganglion cells the one that initiate action potentials, not bipolar cells? Im just making sure b/c i have a physio test thursday and im panicing HEEHOOHEEHOO

  2. The 11-cis conformation drawing is a little misleading. The branch should be angled downward  after carbon 11 to indicate it being "bent"

  3. Nice way of telling a boring subject, thank you very much for the explanation :))) Now that I understand the mechanism,  I don't have to memorise it 😉

  4. I dont understand. Wouldnt the rod be releasing inhibitory neurotransmitters in its "on" state since the bipolar cell is off when the rod cell is on??

  5. Really nice explanation, but the rod does not hyperpolarise only due to the Na channels being blocked, but also due to K channels remaining open and pumping K outside the cell. Other than that, great! 😉

  6. maybe someone mentioned this in previous comment (apologies if so): opsins don't have seven subunits, they have seven transmembrane helices

  7. This was such a great help! My physiology lecturer literally had no idea when he was teaching me this… Thank you! 🙂

  8. hey, i'd like to amend what you said about the naming of the bipolar cells, its actually not "bipolar" because it's on or off, its actually referencing the structure of the cell (it has two poles). This differentiates it from a unipolar cell, which is like a rod with only a single pole, transmitting a signal in 1 direction.

  9. THank you so much for the video, it helped me so much! I do belive though that the word "rhodopsine" does not come from "rods" but from the Greek "rhodon" meaning "pink", but I am sure someone mentioned it already.

  10. I think you are wrong when you said that when there is no light the channels are open and they hyperpolarize and produce an action potential. Yes the channels open and hyperpolarize but photoreceptors do not produce action potential

  11. Thank you!!!!! I'm trying to absorb information for my Neuro final, this was super helpful

  12. So does GMP attach to the the GCPR therefore not allowing in any Na+ molecules therefore causing hyperpolarization within the discs of the rod. Therefore this will not produce glutamate?

  13. Good pointless babble.

    Anyone who believes that this process originated by pure chance is ripe for the lunatic asylum!

  14. so the photon moves through 8 layers to interact with the membranes of photoreceptors? The photon does not interact with any of the other nerves, their nuclei and nuclear inclusions until it reaches rods and cones? cause there're no any "photon pathways" for light to travel to the photoreceptors.

  15. I've read that there are 'on-centre bipolar cells' and 'off-centre bipolar cells', correct?

    When light hits rods, the off-centre bipolar cell depolarizes and releases a neurotransmitter.

    when no light= rod on= off-centre bipolar cell depolarizes and releases neurotransmitters.

    My question is which neurotransmitters the bipolar cells release and if we need to know that on the MCAT.

  16. "We'll just give it kind of a neutral face because it's … bipolar." :'D
    I love this, makes me remember things way better!

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