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PROFESSOR: All right, so we'll go through the second part of
this class 23, and then we'll get started on the auditory
system today.
Now, I had just shown this picture of a very early stage
human, seven weeks after conception.
And you can see, even though the brain is tiny, you can see
how relatively advanced that forebrain is.
It's got a huge amount of neocortex, in relative terms.
The myelinated part there in the center is thalamus and
corpus striatum, and then midbrain and
hindbrain behind it.
Of course, the cerebellum there at the
back is part of hindbrain.
And then this just shows the brain is even relatively
smaller than that one.
These are done to scale.
There is the full-term brain here, the last one, so it's
even smaller than that.
And yet even at that stage, the human brain is a pretty
advanced mammalian brain.
Now, here's that human brain of the mature human, and we
have monkey, cat, and rat.
So what's happened between these brains that were smooth
like that, and the brains with all the gyri and sulci?
And one of the most obvious things, besides the fact that
it's got all the gyri and the sulci, is the information of
that temporal lobe.
So if we take an early brain, and say that this cortex here
has expanded relatively more than the rest.
And so here's what's happened, it's growing out this way.
Now, of course there's no room there in the skull for it to
keep growing downward like that, so what happens is it
folds up like that.
So it's this part here that's growing relatively
more than the rest.
It's not that the rest isn't growing, but in relative
terms, that posterior part of the hemisphere expands and
forms the temporal lobe.
So in the rat, this is temporal cortex down here this
area, and there isn't very much of it.
And we'll see a little more of that in a minute.
So now let's talk about a little bit of the
consequences of that.
One is changes in the white matter.
We talk about Meyer's Loop which is something that
happens, a distortion of the optic radiations that we
talked about before.
The pathway from genicular bodies up
to the visual cortex.
So let's look here at one of Naidu's picture's where he's
done a dissection showing the surface of
the internal capsule.
And in this one, he's shown in the background there-- the
corpus callosum-- and he's shown the caudate nucleus here
behind the internal capsule fibers.
And then back here he's shown the hippocampus.
Now, if we go back to this one I can show you where that
hippocampus is in the rat, the smaller brains.
It's an in-folding of the dorsal and posterior part of
the hemisphere.
That's where the hippocampus is located.
Well, when the temporal lobe grows, this
shifts down, too, see?
So the hippocampus then, in the monkey you will find
there, and in the human it's way underneath there in that
kind of position.
So we call this dorsal hippocampus, this ventral
hippocampus.
And we'll be talking more about that as
we go into the forebrain.
Here now it's taken away those other structures just to show
what's happened with the fibers of
the internal capsule.
And what's happened there is that the visual radiations
going up to the visual cortex back here have been pulled
into the temporal lobe.
And these fibers that get pulled most anteriorally, the
part that we call the Meyer's Loop, represent the upper
visual fields.
So a person with a temporal lobe injury, a lesion-- say, a
gunshot wound or a stroke that affected that part of the
temporal lobe--
can suffer an upper visual field defect.
Not because of the temporal lobe damage, but because of
the damage to the fibers that go up here
to the virtual cortex.
The upper visual field is located in the lower part of
the visual cortex.
Now, what's happening when that whole expansion that
we've just been talking about is occurring?
One of the things that's happened in the visual system
is not just the formation of more and more multi-modal
association areas, but more and more visual
representations.
More and more representations of the retina.
We saw this picture once before, the one on the right
here, of these many different representations of the retina
in the owl monkey brain.
And this is a picture from John Allman where he's just
summarizing the mapping of one of those areas, this area
here, Area M.
So here he's showing it in more of a close-up of the owl
monkey brain.
And here he's showing a visual field with the receptive
fields mapped for a series of penetrations in Area M. And
that's the method used for mapping out these areas.
Well, as the brain has grown in the primates especially, if
you plot neocortical surface area--
this is the linear scale down here.
Neocortical surface area there on the abscissa, and the
number of separate representations on the organ,
you can see what's happened.
As the brain gets bigger and bigger, you get more and more
representations.
Now it's true there aren't so many animals up here, but
there are enough.
Here he's done it in log log scales, and you can see it's a
fairly innate method of plotting, it's a
fairly linear function.
OK, now where would the human be?
This is the rhesus monkey, right up here, the macaque.
Humans would be up here, so we would predict that humans
should have just a few more.
And functional magnetic resonance imaging has been
done on humans, but they've not really tried to map out
all the visual areas.
Allman, in 2000, put one of the pictures done here in
Boston by Roger Tootell that revealed the similarity
between human and monkey and mapping, and just a few of the
visual field representations near V1.
There you see V1, V2, V4, and three other areas, he's got
area under T there as well.
OK, now here I have this picture from
Striedter, an owl monkey.
And then this is also the owl monkey, they've just flattened
it out to see more of the buried cortex, the cortex
buried in the cell side.
And then here you have the rat and hedgehog.
Hedgehog is relatively smaller neocortex than the rat.
And you can see in the hedgehog there's not much
cortex left after you've mapped out V1, V2, some meta
sensory areas, one and two, and the motor cortex, there's
really not a whole lot.
OK, this is all olfactory down here.
The rat has a little more left over.
Well, what's in those areas?
Well, it turns out that the rat does have several more
representations of the visual field, there's at least four
in the rat.
And remember the curve here, because this hemisphere is
relatively small, he's going to be way down here near the
shrew, if the rat fits that kind of scale.
And this was a study done by Rosa in 1999, who [? quip ?]
on a cladogram.
a depiction of the areas, because she wanted to show
which are the really old ones.
It turns out that even in the simplest marsupials, you have
a V1 and V2.
But in the animal that she was using, they
couldn't find [? MT, ?]
there wasn't much visual cortex beyond V1 and V2.
In all the others, all the placental mammals, they were
able to find at least three--
V1, V2, and MT.
Plus varying numbers of others, basically depending on
how big the cortex was.
The bigger it were, the more representations they had.
So now let's talk about the transcortical connections.
We know that V1, for example, has transcortical connections,
as well as connections back to the brain stem.
It projects the secondary optic radiations go from
visual area one--
as well as other visual areas-- back to the thalamus.
They also go a little further, to the midbrain.
But then they also go to the V2, and one or two other
visual areas.
But always nearby areas, they're not long connections.
The areas with the long connections we call
association [INAUDIBLE].
And I'm going to talk about the projections that go from
visual cortex involving some long connections where we know
something about important functions.
For example, starting with V1, the striate cortex, there are
connections to the pre-striate area, it's also called the
visual belt cortex.
It's a belt of cortex around the first visual area.
They talk about auditory belt cortex as well, somatosensory
belt of the cortex.
OK, so from this pre-striate area, meaning in front of the
striate, you have longer connections originating.
So this we call an association area, pre-striate areas.
And it's more than one area, there's several
representations of the visual field, it's
still unimodal though.
It then projects to a multimodal area.
It actually projects to a number of them, I'm only
showing one of them.
I'm showing the one that goes to the frontal lobes.
It goes right past the motor cortex into a pre-motor area
called Area 8, and that's the frontal eye fields.
The ventral pre-motor area's another one that has to do
with reaching movements that we think
is unique to primates.
Area 8 you find even in rodents, it
controls eye movements.
Here's another one that goes from a striate area to the
same pre-striate areas.
But they also have this more ventral connection that
reaches the input temporal cortex.
Now it's still unimodal, the association area here, and it
has a particular role in object identification, and we
know that from lesion studies.
We may not understand the details of object vision from
the physiological studies.
And Jim DiCarlo spends a lot of time working on that
problem here in this department.
And we've had a few talks on it recently.
It's a very complicated business.
And the details of how object vision occurs, and I think the
computational models are just beginning now to be integrated
a little better with those studies.
But anyway, lesions within pretemporal cortex wipe out
the animal's ability to discriminate complicated
patterns and distinguish them.
Even though he still has good reaching, the different parts
of the visual field, he has his basic
visual processes intact.
Humans depend on this kind of pathway, for example, for
distinguishing faces of people, and
monkeys do the same.
We know humans have a particular part of the cortex
near the hippocampus, the underside of the
[UNINTELLIGIBLE]
It's just around the bend there from the pretemporal
cortex, involved in the [INAUDIBLE]
department face area.
Well, if we look at the outputs then of the frontal
eye fields and then we'll do it for the intertemporal
cortex, you see some very clear differences that
correspond to their functions.
I know this looks a little bit like a bowl of spaghetti,
which anatomical diagrams tend to do, but I'm just trying to
pick up some principles.
And I've noted here that the striate area itself, and these
pre-striate areas, have overlapping connections.
This is part of the secondary visual radiations, projections
there to the pretectal area and the
colliculus, for example.
Especially the colliculus, because that's involved in
orienting [INAUDIBLE].
Well, if you look at the projections of frontal eye
fields, it also projects to those areas involved in
orienting, but then just like the striate area, it also
projects to corpus striatum, also projects to the
subthalamus and the ventral [UNINTELLIGIBLE]
Now to be sure, I've selected the connections--
there are more--
but these are major connections
through these areas.
Now if you look at the intertemporal cortex, you see
something different.
Only from the intertemporal, not from Area 8, do you see
connections to the amygdala, part of the limbic system in
the temporal lobe.
I call it a caudal output of the ventral striatum there, a
part of the striatum that's pushed back into
the temporal lobe.
And the amygdala has strong connections to hypothalamus
which defines it as a limbic system area.
It also projects directly to ventral pre-frontal areas
which then connects to the ventral striatum as well as to
the hypothalamus.
So very different kinds of projections.
And it's the outputs of structures that give you the
best clues to their function.
Let's just talk a little bit in theoretical terms about the
nature of all these interconnections.
If everything were connected to everything else, then if we
had just 16 neurons shown in the black there, we'd need 248
axons to get proportional connectivity.
Every one of these is connected to every other one.
And you don't have to look at these as neurons, you could
look at them as columns in the cortex, for example.
Or we could just maintain absolute connectivity, we'll
just connect to the nearby units, cells or columns.
And then, of course, we need a lot fewer axons.
So what does the brain do?
Well, it's a lot closer to this.
If you plot neocortical neuron density number and the amount
of white matter--
here's the amount of white matter--
you'll see that as the amount of gray matter goes up in
volume, the amount of white matter goes up
only a little faster.
It's certainly not growing this way,
from 12 to 56 to 240.
It's not growing like that, white matter is not
changing like that.
It's changing more like this, and yet we know we have those
long connections.
So what we call that kind of architecture is small world
architecture.
Here you have regular connections to nearby cells
that would be absolute connectivity, just as the one
on the bottom here.
Here you have the connections, not in any regular fashion,
they just connect randomly.
But we're not going to let axons increase so rapidly, so
we're just going to connect them randomly.
Or we're going to maintain the nearby connections, they
connect to all the nearby units, but then we'll just add
randomly a few longer connections.
And that we call small world architecture.
And they've plotted the amount of clustering which is what
you have in regular connectivity.
The moment of separation here plotted as a function of
degree of randomness.
And you can see that you can reduce the separation in terms
of numbers of synapses very markedly without going all the
way to complete randomness, and that's what
the brain has done.
If you take actual data from the visual system where we
have the most information, and take all these different areas
in the rhesus monkey--
30 different areas--
and look at their connections, it fits the predictions of the
small world architecture.
That's enough said, we're not going to go into
more detail than that.
But it's a very efficient way to prevent
growth of too many axons.
I can say this though, that in the more intelligent animals
with a lot more association areas with these long
connections, the amount of white matter has grown more
than the amount of gray matter, and it's very obvious
when you study the brain.
But it doesn't grow at all in the way proportional
connectivity would predict.
So now we have time to get at least maybe halfway through
the auditory system.
Actually, there's two auditory system classes.
There's only one chapter, but I combined them
when I wrote the book.
It took me a lot of editing, and I did eliminate a few
things that you'll see.
I may decide later to add some of those back in, but it's
always a tussle when you're teaching neuroanatomy, how
much you're going to throw at people.
Because it just gets overwhelming if you throw too
much, too fast.
So auditory system arose as one of the sensory systems of
what we call the dorsal lateral placodes.
Remember what placodes are?
Thickening of the epithelium in the head region that gave
rise to primary sensory neurons.
So it was one of those systems.
Then I want to ask why it evolved the way it did.
Two major kinds of functions.
Keeping the animal alive by anti-predator and defensive
behaviors, and then major impetus and evolution of the
auditory system especially was to improve predation.
And then we're going to look at some detail of the cochlear
nuclei and structures that it's connected with.
We'll talk about transduction and initial coding in that
pathway, and the various channels of conduction.
One of my diagrams, I admit, is a little too complex there.
But we'll get to that, and I'll go
through it with you carefully.
And then two functions that arose as probably the emphasis
was on the predatory animals evolved two clearly different
ascending pathways.
One more involved in localization, the other more
involved in pattern detection, which in the auditory system
means temporal patterns.
And we'll say just a little bit about animals with
specialized auditory systems, specialized for echo-location,
bird song, or of course, speech in humans.
So the dorsal lateral placodes, they gave rise to
multiple sensory cranial nerves, at
least eight of them.
The sensory categories, besides the eighth nerve
system that we're familiar with for mammals--
auditory and vestibular components
of the eighth nerve.
It's present in all vertebrate groups.
We have the mechanosensory and electrosensory lateral line
receptors distributed in a line along
the side of the animal.
We find lateral line systems present in the earliest
vertebrates.
It's absent in terrestrial vertebrates altogether.
The electrosensory lateral line system's present in fewer
species, they're all aquatic species.
And I'm pointing out here that the lateral line receptors are
innervated by up to six separate cranial nerves.
We only have one cranial nerve of this system of placodes
combined auditory and vestibular nerve.
The two branches of the inter-cranial nerve.
So now here's a much simplified diagram of the
auditory pathways to the endbrain.
Start here in the peripheral ganglia.
We call it the spiral ganglia, the eighth nerve.
They're bipolar neurons embedded in fibers that run
between the inner ear structures and the hindbrain.
They reach the hindbrain secondary sensory nuclei which
then project directly to the midbrain.
But they also project to other cell groups, several of them,
in the more ventral part of the hindbrain.
So I'm calling those tertiary sensory nuclei.
Both of these then project to the midbrain.
And there are projections.
They were discovered first in large primates directly from
the cochlear nuclei, right to the valves.
That would be more like the visual system,
the retina to tectum.
And retina to thalamus, and from there to the cortex.
Because, of course, the thalamic cell groups project
to the endbrain.
And endbrain structures here include both the auditory
cortex and the lateral nucleus of the amygdala.
I've given names here of the midbrain structures.
The main one that we talk about the most is the inferior
colliculus.
If we're not dealing with mammals it's called something
else, I've written it there, the torus and the circularis.
And there's other nuclei just below the inferior colliculus.
You can think of them as extra cell groups as part of that
system, and just call that the nuclei of that fiber bundle
which is called the lateral [? omniscus. ?]
So a very simple way to depict what can very easily seem like
a pretty complex system.
So why did it evolve as it did?
Did it start with anti-predator
and defensive behavior?
My favorite anti-predator behavior is shown by a little
insect, the moth.
When it picks up the cries of a hunting bat, it totally
changes its behavior.
It dives, and goes very rapidly right into the grass.
It's its only way of escaping that bat.
Because as long as it keeps flying, the bat's
going to catch it.
The bat's got very advanced sonar, and can localize them
very quickly and catch them.
So that's how the moths have evolved.
This particular auditory-triggered
anti-predator behavior.
And hindbrain circuits for invertebrates, it's been given
pretty high priority in evolution.
You take a look at fish and tadpole, we find huge cells
that originate in the hindbrain.
They get sensory inputs of various sorts.
They trigger rapid escape--
the moth, in their cells have very large actions.
They descend and trigger the contractions of the body that
turn the animal away from the predator.
And we know that amphibian hearing can very rapidly reach
the hindbrain.
You don't need forebrain, you don't even need midbrain to
trigger some of these behaviors.
It's a pretty primitive aspect of the auditory system.
And these animals don't have the kind of hearing that
mammals have at all, but they can detect these vibrations
indicating a predator.
We just take a few mammalian examples.
There, my favorite is the kangaroo rat, the way it
escapes from a rattlesnake attack.
How many of you know how the kangaroo rat escapes from a
rattlesnake?
You might remember.
Remember, the little kangaroo rat hears the rattle.
If he's hearing the rattle, he knows he's already within
attack range of that rattlesnake very likely.
So what does the kangaroo rat do?
He doesn't go running away.
Because if he starts to run, the rattlesnake attack is very
swift, he would probably get killed.
So what does he do?
He freezes.
He sits there.
And then the rattlesnake launches its attack.
The open mouth-- let's say this is open mouth of the
snake, here's the kangaroo rat.
Here comes the rushing movement of the rattlesnake.
This movement causes a slight noise because of the air.
I mean, it seems like impossible because I think we
would have trouble hearing it, but the kangaroo rat is
specialized to hear it.
That sound triggers a leap of the kangaroo rat.
He leaps up in air, he goes [SNAPS]
there the rattlesnake now missing him.
The kangaroo rat leaps backwards, does a somersault
in the air, lands and runs away.
It almost always works, so that's kept the
kangaroo rats alive.
A nice auditory-triggered escape behavior.
Hamsters respond to novel sounds.
I've kept hamsters in semi-natural environments and
observed this.
Any novel sound--
they've just emerged from their tunnels, and they're
starting to forage--
will trigger an alerting.
When they first hear a novel sound, if they're still near
their tunnel, you won't even see the details of the
movement unless you're filming at high speed.
Because hamsters don't seem to move very fast if we keep them
as pets, but in fact, in this situation they
can move very fast.
They're like that, they're in their tunnel.
They flee to their tunnel.
So the localization that the hamster has to do isn't
localization of the predator, it's localization of his
escape route.
And how is he doing that?
Visually.
He needs audition to trigger the fixed action pattern, but
then it's guided by his vision.
Many small mammals have responses of various sorts
like that that have evolved to keep them safe.
We know that rats have an aversion to loud noises.
I'm going to show you some information from experiments
that are done on the brain mechanisms to show you that,
in fact, again does not depend on the forebrain at all.
And then we'll talk about learned fear, which does
depend on the forebrain.
The aversiveness of noise that involves the limbic system.
If you start making lesions of the auditory system, you can
ablate this major auditory structure of the midbrain, the
inferior colliculus, the entire auditory cortex.
So he's got no audition endbrain at all anymore.
You ablate the inferior colliculus, arbitrary
intensity thresholds aren't affected.
He can still tell the difference of one intensity
from another.
If you have a situation where he's doing bar pressing and
all that, you can test for this.
You can train them to press a lever to turn off the noise if
he doesn't like it.
And they readily learn to turn it off when it gets too loud.
And they don't lose it by ablating the inferior
colliculus.
If you add the superior colliculus to it, you still
don't lose it.
Those rats can still discriminate different
intensities of sound.
If you just have them bar pressing for food,
you can test that.
But if the lesion goes more ventrally, and includes the
ventral part of the central gray area--
also called the periaqueductal gray, depending on which book
you're reading.
Central grey area, CGA, is the most common designation.
But if you ablate that-- of course, you can't avoid
getting a little of the adjacent reticular formation--
then you lose their aversion to loud noises.
Even though they can still detect sounds just as well,
you've preserved their auditory thresholds.
You've eliminated the aversiveness of noise by such
a midbrain lesion.
Here's a picture I've used a few times of the midbrain.
These are the limbic midbrain areas, the areas closely
connected to hypothalamus.
This is the central gray around the third ventricle
there, I've just marked it in the red.
And here is from a photograph, I've taken a photograph here.
I had some damage on the right side I've eliminated here.
I want to show here's the superior colliculus of the
hamster, a relatively large structure.
Here's the aqueduct, the ventricle,
going through the midbrain.
And it's this slightly darker stained area around the
ventricle, you can see the border there very clearly.
This is the third nerve nucleus controlling eye
muscles down here.
So the central gray is like that,
surrounding the ventricle.
It's when you make the lesion in the ventral part here which
they'll which lose the aversiveness of noise.
We can just say a little bit about learned fear.
It's often used in lab studies of learning.
There's a special role of a pathway to the
amygdala in the endbrain.
In two different groups--
I've listed them for you if you're interested in that.
LeDoux and Weinberger, they've both studied that, they're
both called discoverers of this
particular kind of learning.
It depends on the particular pathways to the endbrain.
And I've shown you there are pathways from the medial
geniculate body that gets that nucleus and cells just
surrounding it to get the auditory
input of the thalamus.
And they project up to the auditory
regions of the endbrain.
And what I'm showing here is, if you look at the opossum,
the hedgehog and the tree shrew--
and the tree shrew is by no means an advanced mammal in
the sense that monkeys and humans are, and apes.
All of them have a projection to the lateral amygdala, as
well as the neocortex.
Now, I didn't say much about projections to the amygdala
when I talked about the visual system.
They're not as well known, but I checked and found that yes,
there are cells in the lateral poster nucleus that we talked
about that project not just to the cortex, but they also
project to the amygdala.
The lateral nucleus amygdala gets quite a bit of input from
the thalus.
But the auditory system is more developed.
In fact, in the opossum I've just sketched in there, here's
the thalamus and where they put the
injections of a tracer.
And I've shown in blue here how the axons came out, and
then went forward, and then out laterally through the
internal capsule.
And they reach the amygdala and the neocortex.
And in the opossum, the amygdala projection's actually
larger than the neocortical projection.
In the hedgehog, the neocortical projection's a
little bit larger.
In the tree shrew, the neocortical projection is a
lot larger.
And the rat is like that, but it does have a direct
projection to the amygdala.
And it's that projection to the amygdala that's involved
in learned fear to auditory sounds.
You can train an animal to be afraid of noise.
How do you do that?
Well, you put them in a shuttle box where you can
shock their feet, and you give a certain sound, and they have
to run to the other side of the shuttle box.
And to learn that, to learn to be afraid when the certain
sound appears like that, they need this
projection to the amygdala.
Actually, that's a little bit too strong a statement, they
can still learn something.
But this seems to be the most important pathway, the one
directly to the amygdala.
So, next time we're going to talk about the things that
were more important to the predators.
Needing to identify prey animals, and to localize them
in order to be able to grab them.