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PROFESSOR: So today, we are going
to talk about the midget and parasol channels.
I will begin by reminding you of what these two channels are
that I very briefly talked about before.
Namely, if you look at the Golgi stain of cross sections
of the retina, when you look at just the ganglion cells,
it was discovered initially by the inventors,
if you will, of the Golgi stain, namely,
Golgi himself and Cajal.
Cajal did this, initially.
And then, subsequently, a fellow whose name is down here,
Polyak, has used the same technique to study the retina.
And what he discovered was-- not Polyak initially,
but Cajal initially discovered, and then was
verified by Polyak using these anatomical techniques,
namely, the Golgi stain-- that there's
one class of cells that have very small dendritic arbors,
as you can see here, and another set that
has much, much larger arbors.
Now, once this was discovered, subsequently when
it became possible to record from individual cells
and to study their receptive fields
and their basic organization, and also to look
at them from a different point of view,
it was, first of all, shown that these
are two very distinct classes of cells
in terms of the dendritic arbors they create.
And as I mentioned to you before,
these cells are called parasol cells
because the dendritic arbors look like an umbrella.
And at comparable eccentricities,
the midget cells are three times smaller in diameter
than are the so-called parasol cells.
And then I showed you some data the last time
indicating that these two types of cells
conduct at different velocities to the central nervous system,
with these bigger cells having bigger axons conducting
significantly faster than the midget cells,
and that you get a distribution when you record
from all the axons in the retinal geniculate pathway
that they form separate populations because, initially,
the argument was that maybe this is just
a continuous population of cells.
But it turns out these are indeed
two very distinct classes on the anatomical level
as well as the conduction velocity level.
Then when it became possible to record from single neurons
and to study their receptive fields,
it was shown-- I showed you this picture
before as well-- that you have, first
of all, center-surround organization as discovered
by Kuffler; and secondly, that the midget and parasol cells
are very different in size as far as the receptive fields
are concerned as well as the dendritic arbors;
and that the midget cells in central retina
receive an input from just a single cone,
whereas the parasol cells got a multiple input.
And another distinction that was, at that time, made
is that the neuronal responses are
such that midget cells respond in a much more sustained
fashion when you activate the center
mechanism than do the parasol cells.
So these respond much more transiently.
So this, then, were initial cues as to what
might be involved as to why we have these two systems.
And there were all kinds of hypotheses.
And then, eventually, in the '60s and '70s
and especially in the '80s and '90s, all kinds of experiments
were carried out to try to establish just
why these two separate systems have evolved.
So now, when the anatomical work was further progressing,
it was found, as I have mentioned also the last time
to you, that each cone in the retina-- certainly true
for the red and the green cones, which
would be equivalent to the midget system--
gives rise to an ON and an OFF bipolar cell.
Those are the ones we discussed the last time.
What I did not discuss the last time,
and I'm not going to discuss today either
but will the next time we talk about color perception,
is that the blue cones-- how many of you
remember what is the frequency of blue cones in the retina?
AUDIENCE: 1 in 8.
PROFESSOR: 1 in 8.
Very good.
Excellent.
So that being the case, that already makes them different
because the numerosity's so much lower.
And then people have done all kinds of recordings,
and to this day, it's not quite clear
what the connection or pattern is.
But as I said, next time, we will talk about it
in some detail when we talk about color.
But here, don't get frightened, we will discuss this
the next time.
But at any rate, we have the blue cones.
And when we talk about color opponency
that I will explain the next time,
we think of the opponency to blue being yellow,
and the opponency to red being green.
And so the assumption here was made
that the connections in this case,
somehow, must take place to create color opponency.
And since we have only three kinds of cones in the retina,
in the primate-- red, green, and blue--
the opponency here must, somehow,
involve both the red and green cones.
So that's the complication that we will discuss the next time.
And so the assumption was made that we
have some so-called yellow/blue cells and blue/yellow cells.
And so I just want to keep you puzzled
as to what this means, especially
what it means with respect to how we can see colors.
And that's what we will talk about the next time.
So now, here we have, by contrast-- and we
go back here-- here, this is, then, the midget system.
And I showed you the two extremes,
which are very clear, and in between, which
would be somehow creating the blue system.
So that's the midget system with very small receptive fields
and very small cells.
Now, by contrast, when you look at the parasol system, what
you see here is, as indicated by the picture I showed you
just a minute ago, is that the receptive fields are bigger.
The ganglion cell's a lot bigger.
And the dendritic arbors are much more extensive.
Now, that means, by the way-- I shouldn't even say
"by the way"-- that means, very importantly,
that the ON and OFF bipolar cells that connect with the ON
and OFF cells of the parasol system are also much bigger
and have much more extensive arbors, dendritic arbors,
because they sample many cells instead of just one.
But overall, what this means is that when
you look at the bipolar cells in the retina,
there are about three times as many bipolar cells
than there are photoreceptors.
Now, if you think about this-- somebody
remembered the last time-- that in the retina,
we have about 50 million cones, and we
have about 120 to 150 rods.
And so, then, if you think about the fact, at least,
for the cone system, we have three times as many bipolar
cells.
This only applies fully to the cone system.
That still means that we have 150 million bipolar
cells in the retina.
So it's absolutely incredible, then,
this tiny little thing that you have in your head, which
is less than an inch in diameter,
you have these millions and millions and millions of cells.
Amazing.
So this is then the arrangement for the parasol system.
And now, we can progress and make
another point about how clever the wiring became
in the course of evolution.
The cleverness here is that, as you know,
we only have a single layer of photoreceptors, which,
outside the fovea, has a mix of rods and cones.
But then if you look at the receptive fields of ganglion
cells, what you find is that they have overlapping receptive
fields for many of the attributes.
So you have overlapping for ON and OFF, of course.
And that's obvious from the wiring.
But you also have overlap for the midget
and the parasol cells.
And lastly, there's an overlap-- even if you just
look at the rod input-- which results
in realizing that the receptive fields become larger
during dark adaptation by virtue of the connections of the rod
photoreceptors to the rod bipolars than to the A,
to amacrine cells, which then connect with the same ganglion
cells as do the cones.
So this is, then, an incredibly clever arrangement
which enables you to see things extremely well.
And it's an incredible feat of wiring
that accomplish this incredible arrangement.
So now, another important thing to consider, in addition
to what I've said so far about the midget
and the parasol cells, is that they
have distribution over space.
If you look at it from, say, from the center of the eye,
meaning the fovea, going to the periphery,
the ratio of midget and parasol cells changes dramatically.
In the center here, in the fovea,
you have a huge difference in number of cells.
But as you get to the periphery, these two types of cells
eventually become equally numerous.
Now, to show this in relationship
to the lateral geniculate nucleus--
again, to repeat, in the fovea, you have an 8 to 1 ratio;
in the periphery, they have 1 to 1 ratio.
And this is directly reflected in the lateral geniculate
nucleus.
Everything I've shown you so far about the geniculate
was a six-layered structure.
But those six layers exist only to about
an 18-degree eccentricity from the fovea.
And after that, the lateral geniculate nucleus
becomes a four-layered structure.
And as done here in a schematic fashion,
the four layers for the left and right eyes
are pretty much equal in numerosity.
And that creates, then, the 1 to 1 ratio.
So that makes one think, why do we have this shift?
There must be something very important in central vision
for which the midget system is good for.
And in peripheral retina, the parasol system
becomes more important.
So we are going to pay attention to that
as we examine what the functions are of these two systems.
So how do we go about finding out
the functions of these two systems?
Well, there are several methods.
The first one I'm going to tell you about
is to record from individual neurons-- say, in the cortex--
and determine what kinds of inputs
they get from the midget and the parasol cells.
So to do that, you first want to look at the exact projections
of the retinal ganglion cells again.
Just to remind you, here's the lateral geniculate nucleus,
again, in the region where there are six layers.
I already showed you this picture before.
And I told you that the parvocellular layers project
to 4C alpha; the magnocellular layers to 4C beta;
and those other cells, which we'll talk about eventually,
its lateral layers project to the upper parts of the cortex.
So now, we have a good idea that even
if the inputs to the visual cortex-- meaning,
in this case, of course, the V1-- the two systems are
separate in the input layers, in 4C alpha and beta.
And then the question comes up, well,
what happens when you look at cells above and below the input
layers?
Do they converge?
Or what's going on?
So that's the kind of questions we're going to ask.
And we are going to look at this more
carefully here to find out just how do you
do an experiment like that.
Well, one thing you can do here, you can use a reversible agent
that you can inject either in the parvocellular
or magnocellular layers of the geniculate.
And if you do that, if in the parvocellular layers,
this would be a blocking agent.
Xylocaine is something that's used frequently.
There are several other agents.
And so if you inject that substance in here,
you render the cells in the geniculate unresponsive.
It's to serve the same idea as what we talked about
with APB in the last time, except this is not quite as
neat because it's not a pure chemical
treatment like you did with APB.
Secondly, you can do it in the magnocellular layers as well
and block that region.
Now, if you do this kind of experiment,
let's first talk about what happens in area of V1.
Now, this is a very difficult and complicated experiment.
Sometimes, you can spend days recording from a single animal
because, first of all, what you have to do
is you have to put in electrodes into the lateral geniculate
nucleus, which is way down, preferably into both regions,
but there are many experiments just to one or the other.
And then put an electrode into V1.
Now, the next important task, of course,
is that you've got to record from V1 in the region to which
these cells or these cells project.
So to find that overlap in the receptive fields
that you need to do when you record here, here,
and here is that you have to take many, many electrode
penetrations until, finally, you have an overlap.
And once you have that overlap, you
can be sure that when you inactivate this region
by injecting the Xylocaine, you can
assess what the responses are in the V1
before, during, and after the injection.
And most importantly, before and during, naturally.
So let's look at that.
This has been done studying many cells
to get an overview of what's going on.
And I'm going to show you, initially,
just one example of a cell to give you
a feel for what that's like.
So here we have the cell respond.
What you do is you take a bar of light
and move it across the receptive field-- brrp,
brrp-- for each edge.
So those are the two cumulative responses.
[INAUDIBLE]
That's the normal.
Now, you inject into the parvocellular portions
of the geniculate.
And lo and behold, the cell keeps responding.
Then you inject into the magno portions.
And then lo and behold, the cell still keeps responding.
But when you inject into both-- bango!
There's no response.
So that means that this particular cell
gets a convergent input from the midget and the parasol cells
as they pass through the lateral geniculate nucleus.
Now, if one then does a systematic study
and then records from many cells, what has been found here
is that some cells do get an exclusive input
from the midget cells.
Some get an exclusive input from the parasol cells.
And some are just like the one I've shown you here-- namely,
they get a convergent input.
So that tells us, then, what the very, very basic nature is
of the input to the visual cortex, you, to some degree,
keep separate the two systems.
And to some degree, you also have
a condition where they are united.
So that's what happens in area V1.
So now, the next thing you are going to ask
is, well, what happens in other cortical areas?
So here, then, I'm showing you the same method picture.
But now, you have recording in V4 and MT,
doing the similar kinds of injections
that I just described in the lateral geniculate nucleus.
So when one does this, some interesting results
had been obtained.
And as always, before this kind of experiment
that actually tested this question,
there were, of course, hypotheses.
Some people hypothesized that area
of V4, which had at one time been
proclaimed to be a color area-- and we'll
come back to that shortly-- it was claimed, therefore,
that this area gets input only from the midget system.
And this area-- since it has motion-selective cells,
if you remember-- only gets input from the parasol cells.
So, therefore, we can now have the acid test,
thanks to some remarkable work that
had been done, much of it by John Maunsell
over at Harvard, who had actually
worked here at MIT before then.
And he did an experiment like that.
And here's an example of a single cell recording from V4.
This is a magno block, and this is the parvo block.
This is before the block, and this is after the block.
So what you can see here, this cell, again,
response to a bar moving across-- brrp,
brrp-- like that.
Here are the two responses shown here as
to how they come across the receptive field.
And you can see a vigorous response after you do this
and before you inject Xylocaine into the geniculate
to block, in this case, the magno system;
and in this case, the parvo system.
This is backwards from the way I usually presented.
I usually like to put parvo first.
Preference-- it's the bias.
At any rate, you can see what happens
is dramatic for this particular cell after you injected,
you blocked the magno system.
The cell-- we said has spontaneous activity--
but it no longer responds to the edges.
By contrast, when you do a parvo block,
you only get a small effect.
There is a reduction for this particular cell,
but it's still responding.
So that is the example of a recording in area of V4.
Now, let us go and ask the question, what about MT?
Now, here's an example.
Same arrangement-- magno first, parvo second, before the block,
after the block.
In this case, in MT, you get a cell
that totally stopped responding after magno block
to this moving stimulus.
And here, what you see is after parvo block,
the response continues.
So now, this is just two cells.
Now, to be sure that these two cells are generally
representative of these observations, what you need
to do is to collect this kind of information from many cells,
and then come up with a qualitative statement.
So what you can do is you can, for each cell,
when you do this experiment, you can't
determine how much the cell fired here to the stimulus
and how much it fired here.
And then you can get a ratio of that response.
You can turn it into, like, a percentage or maybe just
to score them as 0 to 1 number.
And then if you do that for a whole bunch of cells,
what you find is shown here.
This is a bunch of cells in V4.
This is a bunch of cells in MT.
And what you can see here is that in V4, first of all,
you have a medium degree of blockage, nothing major,
but some blockage.
But most importantly, you get blockage
both for parvocellular and magnocellular inactivation.
By contrast, in MT, what you find
is that when you block magnocellular geniculate,
most of the cells are dramatically affected.
Only a few cells are blocked as a result of a parvocellular
block.
So the outcome of this is that the hypothesis pertaining
to MT, that it gets mostly an input from the parasol system,
is correct.
But the idea that V4 gets an input only
from the midget system is obviously incorrect,
showing that it gets an input from both.
So to then summarize the wiring diagram here,
what you have here is the eye, of course.
And then you have the midget and parasol cells
that project, respectively, to the parvocellular
and magnocellular layers of the lateral geniculate nucleus,
then they go off to the cortex.
And if you remember, in the cortex,
they terminated 4C alpha and beta.
And then, also, as I told you, up here, you already
have many cells above and below the input layers
that get a convergent input from the midget and parasol cells.
So what happens then, in terms of the projections to higher
cortical areas-- to talk about V2, for example--
you get some cells which are purely
driven by the midget system, some cells purely
driven by the parasol, and many cells that are driven by both.
So V2 becomes very complicated because they
have different subdivisions.
Maybe in V2-- we talked about it a little bit--
that may be receiving different input from area of V1
in terms of whether they are driven
by the midget or the parasol cells.
Now, most notably, when from V2 and from V1,
you look at the projections to area MT,
the middle temporal area, what you find
is that this is heavily dominated
by the input from the parasol cells.
Then if you go beyond that, this continues
to the parietal lobe from MT.
But then, when you go from V2 to V4,
then temporal, then the frontal lobe, what you
find that there's a mix of inputs
from both of these systems.
So it highlights the fact that, indeed, these things
are quite complicated.
And so we need to now turn to a different method
to try to ferret out beyond just establishing the connections
as to what on earth these two systems are for.
And needless to say, hypotheses were rampant about this.
And what I'm going to do now, I'm
going to tell you about how one can go about
and how many investigators have gone about trying to determine
what the functions are of these two systems in processing
visual information.
So how do you do that?
Well, the way you do that is you can
use what is called lesion studies.
What you can do is you can selectively
block either the parvocellular or magnocellular
systems at the level of lateral geniculate nucleus
because, by lucky happenstance, the parvocellular layer is
getting input from midget, and the magnocellular layer is
from the from the parasol cells.
So you can make lesions, then.
How do you make lesions?
There are variety of ways of making lesions.
That's a huge field.
It applies not only to vision, to many, many other areas,
to try to make carefully selective lesions
in various parts of the brain.
Now, it's not easy to do that in the geniculate.
So what you have to do is, again, you
go in to the lateral geniculate nucleus with a microelectrode.
Once you do that-- you already know
the layout of the geniculate-- you
can find out where the receptive fields are located,
and you can determine whether you
are recording from the parvocellular or magnocellular
layers.
You're going to adjust the depth of the electrode
to be either in the parvocellular or magnocellular
layers.
And once you have established the receptive field location
and were certain about in what parts of the geniculate
you are recording, you can then proceed to make a lesion.
Now, there are a number of ways of making lesions.
One of them is called heat lesions.
You should take a metal microelectrode.
You take it down there, and then you
pass some current to make the tip of the electrode hot,
you can affect, as you know, maybe a millimeter area
or something like that in the lateral geniculate nucleus.
I'm talking about small, small areas.
Another alternative that you can use is to inject a chemical.
One of those commonly used is called Ibotenic acid,
which is a very nice attribute, that when it causes a lesion,
the borders are nicely clearly defined.
So no matter how you do this, then once it
is done in a monkey, then you can study a monkey for months
on end to see what the vision is,
of how the vision is affected.
And then after you've done that, you then process the brain
and look at the lateral geniculate nucleus
to see what was the size and location of the lesion.
Now then, in some cases, it's "Oh, my god, you did both.
Nyah, nyah, nyah."
You screwed up.
So months and months of work goes down the toilet.
But in some cases, you get a good effect.
And that, eventually, if you do it
several times on several monkeys can
result in a solid publication.
So that is the basic process for making the lesions.
Now, let me then move on and broach
the next important topic-- namely,
what are you going to study?
So what you have to study since you want to have an open mind
and you don't want to say, "oh, yeah, everything in the brain
does color" or something like that,
and so instead of just studying color,
you have to study many other aspects.
So I'm going to tell you about several kinds of tests
that have the newest.
And I will explain each of those to you.
But first, I will list them.
The behavioral task that is used-- very important--
is that you've got to be able to confine the crucial stimulus
either to the area that you had blocked
or the area that is intact.
So one way to do that, which is the easiest way,
is to use a detection task.
We already talked about that briefly.
The monkey first fixates.
That confines his looking to that location.
And then you can present a stimulus like this.
And if he makes a saccade to it, he
gets a drop of apple juice for a reward.
Now, that is a procedure.
And then, of course, our next trial,
it appears someplace else.
On each trial, it's in different locations.
And on some trials, you can present the stimulus
in the area that had been blocked.
You get it from by magnocellular or parvocellular
lesions or infusions or in an intact area.
And that, then, enables you to compare performance
in regions where the monkey's performance is normal
because he's intact and in those regions where he lacks either
an input from the magnocellular or from the parvocellular
layers of the lateral geniculate nucleus,
meaning from the midget and parasol cells.
So now, another task which is used
to be able to carry out a more thorough examination
of visual capacities is his discrimination.
In which case, after fixation, you
have a whole bunch of stimuli coming on.
This is very effective for studying color.
And in this case, this discrimination task often
is called the so-called oddities task.
That's an easy way to remember it.
"Oddity" because this is odd.
All the others, the distractors, if you will, are the same.
Only one stimulus is different.
And, of course, the monkey has to make a direct saccade
to this stimulus to get a drop of apple juice for reward.
So that would be a so-called discrimination task.
So these are the two basic tasks that can be used.
And now, we can proceed and ask the question of what exactly,
what kinds of visual capacities should be studied?
So let me just say one more thing, by the way.
The way this is done in a laboratory
is that you have a performance monitor, so-called,
where the computer puts a square around each of the dots that
will have appeared-- in this case,
this should be discrimination-- or where
they will appear singly in the detection task.
And if the monkey makes a saccade that
lends the saccadic eye movement, which you are recording,
into the square area there, then automatically
a drop of apple juice is discharged.
But if he were to make a similar saccade to here,
he will not get rewarded because this
is the only correct position.
And on each trial, that's going to be someplace else.
Everybody understands the method?
It's fairly straightforward.
So now, we can move on and look at an example
of the kinds of lesions that this can create.
Here is a lateral geniculate nucleus again,
the six-layered portion.
And you can see this area here, that this is a lesion.
There are no cells functional here,
which affects only the parvocellular layers.
You see here the two magnocellular layers
are normal.
So this is the lesion area which affects
a few degrees of visual angle-- in this case,
in the lower part of the visual field.
Now, here we have a magno lesion.
If you just look at this quickly,
you say, what lesion are you talking about?
But if you look closely, can you see this here?
There are no cells here.
So this is the region where both layers, magnocellular layers
that get the input from the parasol cells,
had been blocked.
So that is the block there.
So this is, then, an example of a successful lesion.
And once you do these kinds of experiments--
some of these experiments can take a couple of years,
maybe longer-- you end up having some monkeys who
have neat lesions like this, then it's a control.
Let me just add that, which I'm not
going to show any pictures of.
But you can also make, on purpose, a lesion
where you block both of them-- both the magno
and the parvocellular layers.
You just block out a portion of the lateral geniculate
completely.
Now, that's an important control.
For all kinds of experiments, controls are essential.
Now, let me tell you-- this is available in the published
material that you have been asked to read--
that when you block both magno and parvo,
maybe a quarter of the lateral geniculate nucleus,
whenever you present stimuli in the area that has a topographic
correspondence to the lesion's region,
the monkey cannot see a thing.
He cannot perform any of those tasks at all.
So clearly, whatever effect one gets here
with these selective lesions can then
be ascribed-- if you see deficit after this one
or deficit after that one-- can be ascribed to what
the midget and the parasol cell systems do.
So that, then, is the procedure.
And now, we can move on and list the perceptual functions
that one wants to test.
Now, think about it for a minute, just quickly.
What kinds of functions would I want
to test if I'm running this experiment?
How can we break down the multitude of things
that we have to process into some basic functions?
Well, first of all, very important function,
even though it may have now [INAUDIBLE]
is called contrast sensitivity.
Because everything you look at, the light
reflects just about from everything that you look at,
and so the contrast of the stimuli that's
on a white sheet of paper or a gray sheet of paper
or when you look at photographs is highly varied.
And the question is, how well can you
see the different levels of contrast?
Another one, of course, that's obvious is color.
How well can you process color information?
And then another one is pattern.
We often talk about basic patterns.
And the one I'm going to tell you about mostly
would be checkerboards or something like that.
Then we talk about texture.
Most of the things that we encounter in the world
are textured.
And so it's important for us to be able to see texture.
Then, of course, shape, that's obvious.
Then stereopsis.
We will talk about stereopsis in much more detail in a bit.
What stereopsis involves, as I've mentioned to you already,
are the difference of the input in the two eyes.
And that difference is called disparity, which the brain then
interprets as depth.
Another one, very important because you often just see
things appearing quickly in very brief times,
is to study flicker.
And yet another one is to study motion
because that's so central to our existence.
And then to study brightness.
And one thing I haven't mentioned yet
is scotopic vision.
How well can you see on the photopic and scotopic
conditions?
So those are, then, the procedures.
And so let us now look at the first one of these-- contrast
sensitivity.
This has been extensively studied,
hundreds and hundreds of papers, many of them in humans.
And most commonly in these papers, what they did
was they used sinusoidal gratings.
And the way you do that, then, in similar experiments
as a detection experiment, you present sinusoidal gratings
with spatial frequency and whose contrast you systematically
vary.
And when you do that, you get what
is called a contrast sensitivity function.
And so the most common one that you read in many papers
is plotted this way.
This is spatial frequency low, high.
And this is contrast.
Low, high.
And then if you do that, then you systematically studied
this in humans, interestingly enough,
you get a function like that-- meaning
that in between levels of spatial frequency,
you see the best.
And extreme levels, you don't see quite as well.
So one could use sinusoidal gratings in animals.
But sinusoidal gratings aren't essential.
What you can do instead is you can present a checkerboard.
And so here's an example, same procedure as before.
The monkey sees this and makes a saccade to it.
It gets you water.
And then you vary the spatial frequency
and the contrast of it.
So here is one.
You can hardly see that because the contrast is low.
So now, to see this overall, here's an example.
Here, we vary the contrast.
And here, we vary the spatial frequency.
And if you look at that, you can see that in this region,
depending on how far back you are, this region,
you can see the best.
Here, it will be less so.
And here, of course, it drops off dramatically,
just like that curve I have drawn there.
So this, then, enables one to generate a so-called "contrast
sensitivity" function in a monkey
in those regions of the visual field that are intact
and in those regions of visual field
in which you have either magnocellular or parvocellular
lesion that selectively blocks the parasol
and the midget systems.
So that's the experiment, then, for just studying
contrast sensitivity.
And if you do that, this is the kind of result you get.
This is the monkey's normal performance.
In this case, of four spatial frequency levels.
And you go up and down with contrast,
just like that curve I drew there.
So this is your contrast sensitivity function.
And it shows that under normal conditions
and after magnocellular lesion that blocks the parasol system,
there is no effect, meaning that the parasol system doesn't seem
to be too important for contrast sensitivity.
By contrast, there's a huge effect,
especially at high spatial frequencies,
after a parvocellular lesion that blocks the midget system.
So that, in essence then, is what
happens with contrast sensitivity.
Now, let us move on and say, well, what about color vision?
So how do you do the color vision?
I already told you that before.
What you do is you present, in this case,
eight stimuli, one of which is different from the others,
and just have red and green ones.
This is the odd one.
The monkey makes a saccade to it.
He gets a drop of apple juice for a reward.
Now, if you want to be systematic about it,
you can vary the degree of color contrast.
But the effect is so dramatic that it was not
necessary to do that.
So let me show you what the effect was.
Here, we have a monkey's normal performance
when the test element is blue, red, and green.
This happens after a parvocellular lesion,
meaning when you block the midget system,
the monkey cannot see colors at all.
Just a total loss.
Whereas, after magnocellular lesion,
his performance is indistinguishable from normal.
So this, then, establishes the fact
that color vision is controlled by the midget system.
Now, the fact that this is the case perhaps
is not that surprising because I told you
that when you look at the cells in the midget system
in central vision, that most of them
get an input from just-- at least,
the red and green ones-- get an input from a single cone.
So just looking at the receptive field organization
tells you that that system is likely to be
very important for color processing.
So that, then, is confirmed by this kind
behavioral experiment.
So now, let us look at brightness perception.
Now, how is that different from contrast sensitivity?
It's different because, in this case, what to do
then is you use a discrimination task like this.
And I think most of you can tell that this one is
brighter than the others.
Purposefully, I made that a small difference,
so you can appreciate the fact that on each trial,
we can vary the difference between the distractors
and the target.
And you can generate a curve seeing
how much brightness difference do
you need to be able to perceive a brightness difference.
So if you do that kind of experiment,
one is in for a big surprise.
This shows here what happens after a parvocellular lesion.
And this shows here what happens after a magnocellular lesion.
So when you block the midget system,
the performance is unaffected as is the case with a magno
lesion, meaning that if you, obviously,
that both the midget system and the parasol system process
information about brightness, at least, at these low spatial
frequencies that we have used that I just showed you.
So now, the other surprise was that, then, the question
became, well, what if you do this not
under photopic conditions and do under scotopic conditions?
And again, there's no effect, meaning
that the unique inputs from the rods
and the unique inputs from the cones
must go into both of the systems.
Now, the reason that was surprising
is because a couple of papers have been published,
maybe about 15 to 20 years ago, that claimed that the rods feed
selectively into the parasol system,
not into the midget system.
So this totally disprove that.
And then subsequently, careful anatomical experiments also
established that both the small and the large cells,
magno ganglion cells, receive convergent input
from the rods and the cones as I had diagrammed
to you in the previous session.
So then, let's go on and look at pattern and texture perception.
In this case, let me show you the kind of experiment that's
done.
This is when you look at patterns.
One way to do it, go back to those same checkerboards,
but make them high contrast and have one
at a different spatial frequency than the others.
And then you can systematically vary the degree
of spatial frequency difference between the targets
and the distractors.
So that would be the method that is
used to study this kind of pattern perception.
The other one is to look at textures.
And in this case, those of you in the back
probably can't see this.
But those of you up front, can you see this little area here,
where the diagonal lines are reversed?
So what happens is, first, you just present this whole thing.
And then you present the reverse patterns and the surround.
And when you do that, the monkey has
to make a saccade to that location
and will get a drop of apple juice
again for that performance.
And then on each trial, this appears somewhere else
in one of the four to eight locations in the display.
So that's the procedure.
And then if you do this, you, again,
luckily get a very dramatic effect, apparently.
Here it is.
We have here normal performance.
Here's a parvocellular lesion, magnocellular lesion.
This is texture, and this is pattern.
Pattern tasks was, overall, much more difficult
than the texture one in this case.
Well, what you see here that is really dramatic
is that when you block the midget system,
there's a tremendous loss in your ability to see patterns
and in your ability to see textures.
So fine vision for detail seems to be
central for the processing of the midget system.
So that, then, is the effect that one
gets with texture and with pattern.
So now, let's move on and talk about stereoscopic depth
perception.
It's a topic we are going to look
at in more detail in a later session.
Let me now introduce this, first of all,
by telling you that stereoscopic depth perception resulted
predominately by virtue of the fact
that the eye is moving to the front
so that there was a major binocular overlap.
And if you talk about a monkey, for example, or even many,
many animals that do have stereoscopic vision, here's
an example of looking at a tree when just about the only cue
you have here would be based on stereopsis because all of them
are equally dark.
Which branch is in front of which one?
And it's very hard to tell.
If your monkey will jump from this branch to this branch,
if he can't tell where they are relative to each other,
the monkey is going to fall down and drop dread.
So it is very important for monkeys
to have a highly functional stereoscopic system, which
they do.
And so, how do we study this?
Well, the way we study this is to use
what is called a random-dot stereogram.
Random-dot stereograms were created
once computers became a reality many, many years back by Bela
Julesz.
And he came up with the idea that if you
use this kinds of random-dot stereograms,
there's no other depth cue.
So, in other words, you can study
just the stereoscopic depth perception aspect of it.
Now, why is this?
Because what you do here is you look at this two displays,
you present this to the left eye and this to the right eye.
The way this is done is that you use
what is called a stereoscope.
I bet you most of you have seen a stereoscope.
Everybody see a stereoscope?
No?
So a stereoscope used to be something
that was extremely popular starting in the 19th century.
They created these handheld devices with the two lenses
that you look through.
And then they created a camera that had two lenses in it
at the same distance, roughly, as your two eyes.
And so it took a picture, thereby,
creating two pieces, one by each lens.
And then, what you did, since the two have
a slightly different perspective of what you're looking at,
then the photographs are put into the stereoscope
to look at.
These two images are fused then.
Looks like a single image.
And due to their very disparities,
you see real depth.
It's really dramatic.
And when we talk about stereoscopic depth perception,
I'm going to actually bring some stereoscopes here
and some examples so you can see exactly what that is like.
But at any rate, in this case, what you can do
is you can take a little area here just like before.
And you can take the dots in this area.
You move them a little bit this way, a few pixels.
And you move this a bit this way, that way.
And then if it's a square area, you're
going to see a square sticking out.
And the monkey will then make a saccade to that.
But with one eye, he cannot do anything.
He can't see a thing because these random-dot stereograms
only give you information about disparity.
So if you do that, you're going to have
the monkey make a saccade to these.
You can vary the degree of disparity.
And when you do that, what you find is,
quite dramatically, is that after a parvo lesion, when
you block the midget system, there's a tremendous loss.
The monkey essentially, especially
at smaller disparities, has totally
lost his ability to use stereoscopic depth information.
So there is no deficit, however, after a magnocellular lesion.
So therefore, you can say safely that, especially at smaller
disparities, what you have is the midget system that
performs this remarkable task of seeing things in depth
by virtue of disparity in the two eyes produced
by stereoscopic vision.
So that's really a very dramatic effect.
Then the next thing we can look at is motion perception.
Again, this can be done in various ways,
but I will just show you an example of it.
So the monkey first fixates.
Again, use random-dot stereograms here.
And then you set in motion a small square area.
Ready?
I hope.
There we go.
Or you can do the high spatial frequency like that.
And then, of course, on each trial, that appears
someplace else.
And you can vary the velocity or you
can vary the contrast of the display
and see how the monkey performs in the intact portions
of visual field and how it performs
in those portions of the visual field that are blocked
either for the midget system or for the parasol system.
Clear?
So let's think about it for a minute.
What do you think you're going to get?
Here we go.
Here we are-- motion detection.
This is a parvo lesion.
This is a magno lesion.
And so what you get is a dramatic deficit, not
an all-amount deficit, but a dramatic deficit
in seeing motion after the magno lesion
but not after parvo lesion.
So this says that, indeed, the parasol system
plays a very important role in motion perception, not
an exclusive role.
There is still some performance there
at very, very low contrast here.
And there's a big effect at very high contrast,
and monkey does better.
So we can conclude that the parasol system
is very important for motion perception.
So now, the next thing we can look at is flicker.
And in this case, when you study flicker,
instead of using a monitor, people used LEDs.
Now, why do you think that is?
Why don't they just use monitors?
Well, I mean, the reason for that
is very straightforward, actually.
When you use a regular monitor, what
is the frequency of a monitor?
It's the same as the frequency of the alternating current
that you have, that shine the lights up here.
But what is that in the United States?
60 hertz.
And so that's what happens on a regular monitor.
And every 1 over 60 hertz is you shift the image.
In Europe, the frequency is actually 50 hertz.
So at any rate, because of that, there's
a rather limited range over which
you can vary the ON and OFF activity of a flickering spot.
So if you use any of this, however, you
can use it in a huge, huge range of small steps.
So, therefore, this is what the display
looks like that people use to study this.
First, the monkey fixates here.
And then one of these LEDs will start flickering.
And I'll show you the flickering, which
is not perfect here on this monitor,
but it will give you a sense.
Everybody see that flicker?
Now, the mean flicker value of that location
is the same as the yellow lights that you see there.
So if it flickers at a high rate,
you can't tell that it's flickering because it's
beyond the ability of the eye to resolve it,
and then you can't make a saccade to that location.
So if you look at that, what you find here, after parvo lesion
and after magno lesion, you get a gigantic deficit
after magno lesion.
And that fits with what I told you in the beginning--
namely, that the midget cells respond
in a fairly sustained fashion when the stimulus comes on.
Whereas, the parasol cells respond transiently,
which makes them much more readily available for motion
and for flicker.
So those, then, are the major arrangements
that we see with these various experiments.
And so we can summarize what happens after parvocellular
and magnocellular lesion and say what happens here.
So this one here is when you block the midget system.
This is where you block the parasol system.
And here are all the various test that had been used.
And you can see that for the parasol system,
the major deficit arises in motion perception and flicker
perception.
So those two are very important in the processing
of the parasol system.
Whereas, for the midget system, you
get lots of deficits in color vision, texture perception,
and fine pattern perception, fine shape perception,
in contrast sensitivity, and in stereopsis.
So this, then, gives you a sense of what these two systems are
important for in processing visual information.
And so, what you can do next is to summarize what I just
told you-- namely, that the midget system is
important for color, texture, fine form, and fine stereo.
The parasol system is important for fast flicker
and fast, low contrast motion.
Both systems are capable of doing brightness; coarse form;
coarse stereo; slow flicker; slow, high contrast
motion; and scotopic vision.
So it is not a simple arrangement.
It's a complex arrangement.
There is overlap in what both systems can do.
So now, the big question comes up.
Why was it so important to create both of these systems?
Well, the number of schemes that have evolved,
certainly, the motion is obvious.
But one thing one can come up with is
a scheme of this sort that has been proposed-- namely,
that what happened as a result of these two systems emerging,
your ability to process information has been extended.
And for the midget system, you expanded the ability
to see up to high spatial frequencies--
very, very important attribute.
And I should add, also for the midget system,
it became possible for you to see color.
Whereas, when you come to the parasol system,
it expanded the range of your ability
to process information in the temporal domain--
your ability to see very fast motion, to see flicker.
Now, let me add here that's a very important attribute,
by the way, for animals as well as humans because one
of the common things that has emerged
in the course of evolution is what is called camouflage.
I think I may have mentioned that once before.
That is that when you or an animal,
and the coloring of you, which is done in thousands
of animals, is made similar to the background, then
it's very difficult for you to see that particular animal.
So it has an excellent camouflage.
However, as soon as this animal begins to move,
the ability to camouflage itself disappears.
And animals have to move.
And that's because the parasol system
is extremely sensitive to motion.
And so whenever an animal begins to move,
even though it has excellent camouflage,
it is predominantly the parasol system
that will destroy the camouflage effect.
I'm not saying this is necessarily
the only hypothesis, but this is one hypothesis
that had been advanced to try to account for how sensible it
is to have these two systems.
Now, of course, you could ask, how
come this couldn't be just done in one system-- all of it?
Well, there are several reasons for that--
is that to combine a situation where you have
a sustained response and a transient response into one
is next to impossible.
And to have cells that are highly sensitive,
or the parasol cells, you need to have a convergent input
from several photoreceptors.
But as soon as you have that, you
lose your ability to see fine detail.
So these requirements to do this and this
are antagonistic to each other.
And it's not possible to do that in a single cell
at the retinal level.
So it was decided, inasmuch as they should decide,
that it will be best just to create
two separate systems however complicated that might be.
So that, then, brings me to the overall summary
of what I had covered today.
First of all, I told you-- that's
the obvious part-- are two major channels that originate
in the retina are the midget and the parasol.
I should add here that there are many other channels
in the retina, but the cells that
do that-- and we'll talk about some of those
later-- are much less numerous.
The overwhelming majority of cells in the retina
are either midget and parasol.
Then in central retina, the receptive field center
of the midget cells and parvocellular cells
is comprised of just a single cone.
The midget cells and the parvocellular cells--
meaning that the midget projects to the parvocellular layers.
And I told you before that the midget cells of the retina
have receptive fields which are quite similar to those, almost
identical to those that you see in the parvocellular
layers of the lateral geniculate nucleus.
Then the parasol cells have much larger receptive fields
than do the midget cells.
The cone input is mixed both in the center and the surround.
And that is the reason why this system, the parasol system,
cannot tell you anything about color,
but it is very sensitive and can tell you about any change that
occurs out there over time, irrespective of the kind
of color it has.
Now, the midget and parasol cell ratio from center to periphery
changes from 8 to 1 to 1 to 1.
Now, I should reiterate that in that
it is very important for us to be
sensitive to motion in the periphery.
That's if an animal is threatened by some predator,
it is highly desirable to be able to very
sensitive to any motion.
And because of that, you have a higher number
of parasol cells in the periphery than in the center.
And so the ratio changes to become equal in the periphery.
Now, the midget and parasol systems
converge on some cells in V1.
And the example, the prime example,
I've shown you when they were separately
blocked at the level the geniculate, that the cell
I showed you was one that did receive a convergent input.
But many other cells receive single input.
V4 receives inputs from both the midget and the parasol cells.
So it's not an area that only deals with color, obviously.
And what it will deal with, we'll describe in more detail
later.
The major input to MT is from the parasol cells.
And that, often, MT and MST have often
been called the motion areas.
But they also play important role, by the way,
in depth perception, as we shall see.
And then the midget system extends the range
of vision in the wavelength and high spatial frequency domains.
The parasol system extends the range
of vision in the high frequency domain.
And in the scheme that I showed you
is what leads to this particular conclusion.
So that, then, is the essence of what I wanted to cover today.
And I am now certainly open to any questions
that you might have about these two fascinating systems that
have evolved in the retina over the millions
and millions of years of evolution.
Well, I was so clear that there are questions, huh?
Well, I hope that you sort of gotten
a sense of what it is like to do these kinds of experiments
and how luckily, at least, in some cases, these experiments
can lead to nice discoveries as to the workings
of the visual system.
Now, last time when we talked about the APB, we did
have a "magic bullet."
This approach here is not as neat, really,
because you have to make lesions rather than specifically
affecting certain neurotransmitters.
And that could not be done because the neurotransmitters
for the midget and the parasol cells are similar.
So you can't use that kind of procedure
that we were able to use miraculously for the ON and OFF
channels.
So that, in essence, is what we are going to cover today.
Did everybody sign?
Any one of you not sign the attendance sheet?
If not, please come up here and sign it.
And then let me just say again that next time,
we are going to talk about color-- another fascinating
topic.
And we are also going to talk about visual adaptation.
And if you can, if you get a chance to do so,
please try to read the preparatory material which
should make it easier for you to not only
comprehend but, especially, to be
able to memorize these facts.
And the memorization is a very important part
of learning things in any course.
And it will, of course, be essential
when you get to the stage of having to take the exams.
Well, thank you so much.