Now, as I said, this is
a complicated process.
So first, I’m going to step
you through a description
of what happens inside
of the eye cell.
And then I’ll show a representation
about what’s actually occurring.
The first step in the process involves
absorption of a photon of light
by the 11-cis retinal that’s
contained in the opsin.
Now, if this is a rod
cell, that’s rhodopsin.
If this is a cone
cell, it’s photopsin.
The retinal isomerizes in
response to this photon of light
to change from the 11-cis
form to the all-trans form.
This physical change in
the structure of retinal
affects the rhodopsin or
photopsin that contains it.
This protein change is
communicated into the cell.
Now, rhodopsin photopsin
is a membrane protein
and it’s found in the
membrane of these cells.
An outside portion and an inside portion.
The change in structure changes
the inside portion of the cell
and on the inside portion of the cell is
located a G protein known as transducin.
In other lectures, I've
described what G proteins do
and I’ll described a little bit here, but
I won’t go into detail at this point.
The transducin that has been activated
ultimately by this photon of light
goes and activates another enzyme
known as cGMP phosphodiesterase
whereas we will probably refer to it
here simply as phosphodiesterase.
The phosphodiesterase cleaves cyclic GMP
or cGMP as you see here to produce GMP.
Now, cGMP is very important in the eye
cell for keeping the unpolarized state.
At the darkness, remember that
the eye cell is unpolarized
and that unpolarization
is happening because
ions can move into and
out of the nerve cell.
The movement of ions into
and out of the nerve cell
channels to be open.
So if we close the channels,
then what happens is the cell
will start to hyperpolarize.
This happens because the ions can’t move.
Nerve cells have an important
protein that pumps sodium ions out,
the potassium ions in.
So if potassium ions are getting pumped in
and the sodium ions are getting pumped out,
but the sodium ions can’t come
back in, what’s going to happen?
Well, the sodium ion concentration
is going to increase
and that’s what hyperpolarization
is actually all about.
The hyperpolarization that results
is the next part of the signal
of telling the brain that
the eye has detected light.
The hyperpolarization causes in the
next step calcium gates to close.
Now, calcium gates
are also important
for the movement of ions, calcium,
into and out of the cell.
Cells are normally pumping
calcium out of the cell.
But when the gates are open, the
calcium can come right back in.
So we imagine a sort of a
cycle of calcium movement.
If we close the calcium gates and the
calcium concentration begins to change
and calcium concentration inside
the cell begins to decrease.
As the calcium concentration
inside the cell decreases,
Calcium is needed for eye cells
to put out neurotransmitters.
Now, neurotransmitters released by eye
cells are there to tell the brain,
“I’m not getting any light.”
That’s kind of unusual.
I’ll repeat that.
Calcium is necessary for the eye cell
to be releasing neurotransmitter,
which tells the brain
"No light detected."
When the calcium ion
concentration begins to fall,
release begins to fall.
And as the neurotransmitter
release begins to fall,
the brain learns light
has been detected.
Now, as I said, eye cells are very
different from other nerve cells.
First of all, they are in the
unstimulated state, they’re unpolarized.
It is the stimulated state that
causes them to be polarized,
that’s different from
a regular nerve cell.
Second regular nerve cells release
neurotransmitters when signals are received.
But eye cells releasing
neurotransmitters all the time
and only when the cease
is a signal received by the brain.
So it’s a very different kind of a
system than a regular nerve cell.
Well, let’s take a look and see what’s
actually happening at the level of the cell.
First is I described
rhodopsin or photopsin,
depending upon whether we’re talking
about a rod cell or a cone cells,
is located in the membrane
of the retina cell.
And we can see here that the 11-cis
form is present on the left.
It has that bent structure that
I described to you earlier.
The detection or the absorption
of a photon of light
by that 11-cis retinal causes it to
flip to the all-trans configuration.
And you can see that it is
moved from being the bent form
to being in the straight chain
form as you can see here.
That causes the rhodopsin or
photopsin to change its structure
and on the inside of the cell, that activates
this G protein known as transducin.
actually grabs a GTP.
The GTP causes it
to become active.
As transducin is activated in this way,
it goes to this
to cause the phosphodiasterase to begin
to break down cyclic GMP and produce GMP.
That causes the cyclic GMP
concentration to fall.
And as the cyclic GMP
the ions channels that I
described to you earlier
where sodium and calcium
begin to close.
and when hyperpolarization occurs,
release of neurotransmitters ceases
and the brain learns therefore a
photon of light has been absorbed.