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PROFESSOR: OK, I just wanted to go back over a few things
to make sure you're understanding it right.
When I talked about this anatomical plasticity
in the hippocampus, you just have
to realize that every one of these rectangles
represents the very same slice, just showing
different things in the same little bit of the--
as you see here.
It shows a slice in the dentate gyrus
but just through the dendrites of the dentate gyrus
from the peel surface down to the cell bodies.
So here it's showing one kind of connection,
here it's showing another kind of connection,
and it shows what happens if you remove one of them.
You get [? sprouting ?] of the other one.
Yes?
AUDIENCE: [INAUDIBLE]
PROFESSOR: It means that this particular projection doesn't
go there, but the projection here from the entorhinal cortex
doesn't terminate in the inner part
of the dendrite near the cell body.
It terminates in the outer 2/3 whereas the association
fibers coming from other parts of the hippocampus,
they terminate in that area.
So in that rectangle is white, the upper 2/3 is white.
So obviously there's some kind of specificity
in the way those terminals grow in.
Maybe in development they do overlap, but in the adult,
they don't.
But then if you remove one of them,
the other one will sprout.
And I'm only showing true projections.
There are other projections like the acetylcholine axons coming
from the septum.
They change too after you make one
or another lesions of these [INAUDIBLE].
OK and then the point about this more modulatory
states and how it changes with different stages of sleep
postulated to really change the flow of information
between the hippocampus and the neocortex.
I just wanted to point out that we
know that these are only three of the modulators that
can change the state of the brain.
So if this theory is correct, and probably
is at least partly correct, it just
indicates that when brain state changes, can pretty drastically
change the way connections are working
where the information is flowing in the cortex.
And remember when we-- in chapter 17,
I talked about how many different possible brain
states there are.
It means this kind-- this is just
the beginning of this kind of model
to represent information flow in neocortex.
AUDIENCE: [INAUDIBLE]
PROFESSOR: Sure.
AUDIENCE: [INAUDIBLE]
PROFESSOR: That's right.
AUDIENCE: [INAUDIBLE]
PROFESSOR: Yes, in fact, in REM sleep,
it doesn't mean there's nothing important going on.
We know that dreaming is occurring.
You know, people argue all the time
about what the function of that might be.
We also know that if you're in dream sleep,
when you're awakened, you tend not to remember.
You can train yourself to remember,
because if you keep it in mind, you
keep rehearsing after you get up, you can report a dream.
And that's why in studies of dreams,
it's not very reliable to talk about somebody a half hour
later after they get up, because they will forget most of it.
So that has something to do with these states too.
But there's really a lot that we just don't understand,
but we do know that there's different states
of our consciousness where we don't-- there's a lot
of dissociation between.
And in abnormal cases, you can get more than one
personality existing in the same person,
the same central nervous system.
That has to involve these different kinds of space,
but we don't understand the brain mechanisms
behind that kind of dissociation.
Yes?
AUDIENCE: [INAUDIBLE]
PROFESSOR: You would like to know
what the neurochemical coeruleus are, and I can't tell you.
You can look in the lecture to see if anybody's even tried.
And since you can get REM sleep in animals,
you can do these REM sleep deprivation studies in animals,
it seems to me that you could certainly
look for things like that.
There might even be changes in the cerebral spinal fluid.
As we know, you can inject cerebral spinal fluid
from one animal that's sleeping to an animal that's not,
and the animal that's not will go to sleep.
So we know there are effects even there,
but that kind of research is just not done.
One of the things that neuroscience like to-- people
work on what's popular.
It takes an enterprising graduate student to dive
into something like that.
These pictures of the human brain
are just to help orient you to these same structures
in our own brains.
You can begin to see why we use these rodents.
They're much more like the embryonic human brain,
because the human brains have grown so big
and the cortex, especially, has grown so big
that it distorts the whole appearance.
This here shows the hippocampal formation in fornix,
and the part of the hypothalamus memory body
where the fornix terminates.
And you can't tell from a picture like that,
but this is definitely the brain stem,
the upper brain stem and this is up in the hemisphere,
but in fact, that's what it represents.
And I just sketched here the hippocampus anterior,
posterior, and the fibers of the fimbria
in the fornix coming out of the hippocampus
and becoming the columns of fornix here.
I don't show the ones that go into the septal area which
would be right there.
I do show the commissure [INAUDIBLE].
OK and then this is a little more like a rodent,
but this picture was a reconstruction published
in a human neuroanatomy book by Nolte
which tries to depict the human hippocampus.
And it's not too hard to see the close relationship,
but the same structures we see in the rodent
we can find in a human.
I want to talk about the limbic-- other parts
of the limbic forebrain other than hippocampus
in the hypothalamus, especially the amygdala
and the basal forebrain.
They're closely related to each other.
This is Chapter 29 in the book.
Let's just review a couple terms to start with.
Where does that term rhinencephalon come from?
What does it mean?
It means nose brain.
Well that was an old term used for all these structures
that we now say are the limbric endbrain.
The term limbic system didn't start
to be used until after Papez's publication and then interest
that that engendered from other anatomists.
The neuron anatomists began specifically
studying these connections, especially with Nauta
introducing a more sensitive method
for studying connections in animals.
We talked about that in chapter-- way
back in the beginning, Chapter 2.
And now, of course, we have many, even more sensitive,
methods involving various tracer substances.
But anyway, this is the Papez story,
and I just point out here that some anatomy books, including
one that I've often made use of, [INAUDIBLE],
he-- in an earlier version of this book
he had this nice description of Papez's work,
and then in the third edition he eliminated.
The question is why?
Well he was trying to get rid of a lot of the history,
because he didn't want the book to be too long.
So lend it to what medical students will read.
But there are other reasons too.
There's different kinds of grandmasters.
Some of them are more interested in the structures, where
they live, how you can separate them.
But they don't focus on the connections as much.
Neurologists too.
We don't know enough about functions,
and they don't want to try to group things.
So it's really the people, the Nauta type of people--
and there's a lot of us, because now they
train a number of people, and we've
trained additional people-- that had led me and other people
to sort of talk more about [? Papez ?]
and the limbic system in general.
Remember that [? Papez ?] took that term,
rhinencephalon, and analyzed it and said
a lot of these structures aren't actually involved in olfaction
from the human clinical cases that he was familiar with.
This was back in the 1920s and 30s.
But he did find that all of these structures
were involved in seizures that affected
the motion and that autonomic nervous system.
So he said it seemed to be an interconnected-- he could
define what he called an interconnected serious of cell
groups that were concerned with feelings
and emotional expressions.
He emphasized that aspect of it.
He could have added autonomic changes.
But what it led to was new thinking about our ability
to group structures according to relationships
in their connections, and that led
to a colleague of Nauta's, Paul [? McCrane ?]
at NIH giving the system a name, the limbic system.
He based that on Broca's term from the 19th century.
We talked about the great limbic lobe.
And we've seen that in the medial views
of the human brain.
And more recently, the reason for a lot
of revival of interest, of course,
is because we know it extends-- the functions
of this interconnected system extends beyond mood and emotion
plays a major role in spatial cognition
and the formations of specific memory for places and events
in our lives, not just in humans of course but in animals too.
This is the Papez circuit, slide we saw before.
Papez described these structures that you see in red here
and the network diagram that I made up
where I was trying to include more recent findings of how
these structures are related to each other.
Some of them are exactly as Papez described, mammary bodies
to anterior nuclei to the thalamus
to the cingulate cortex.
Now in Papez's time, cingulate included
some of the more caudal areas that now are often
named differently, the retrosplenial cortex
and other paralimbic areas that extend
right down to the entorhinal cortex.
He, of course, separated the entorhinal area
from the cingulate, but what looks like posterior cingulate,
posterior, part of a singular gyrus
we now call retrosplenial cortex.
And there's some other names too used for components of it.
OK and then I'm showing how from the hippocampus itself,
there are connections, back to the mammary bodies
that Papez knew about.
Remember, he didn't have the methods to know what was direct
and what was indirect, but he did see that bundle.
You could even trace them into sections,
and you could follow that bundle all the way
to the mammary bundles.
But now we know there are many other connections
of those axons as I've shown here.
So what's dominant input if it's not olfaction
as Papez realized?
You can't just say, well emotions
are the dominant input.
Feelings are the dominant input.
That's crossing realms here from behavior to anatomy.
I want to know anatomically, what's the dominant input?
Well in mammals the dominant input is here.
It comes from the neocortex, because these association
areas, particularly the multimodal association
areas, the areas that have grown the most in the more
recent human evolution, and in that period
our brains have almost doubled in size.
They are closely connected to singular areas,
retrosplenial cortex and other paralimbic areas
and to the entorhinal cortex.
And often you will see in textbooks
that this projection of entorhinal area
into the dentate is the dominant input.
I point out here that there's connections to the subiculum
as well.
But the dominant input, by way of these paralimbic structures
comes from neocortex.
The
So now how do we get from neocortex to the hypothalamus?
I'm asking here, what are the most direct routes,
monosynaptic and disynaptic from neocortex to hypothalamus.
Well you can look at the page circuit diagram
and see their connections, but not so direct
between neocortex and hypothalamus
seen those diagrams.
But I've taken Mycelium's box diagrams
where he's depicting transcortical connections
from the most specialized cortical areas,
the primary sensory and lower areas,
to association areas which get connections
from those primary areas.
You have then the modality-specific association
areas and the multimodal areas.
Those are the areas closely connected-- adjacent boxes here
are interconnected, two-way connections
between those areas.
So for every one of these you could draw arrows like this,
and sometimes when I show this I do show that kind of arrow.
And then you have the paralimbic areas and then finally
the limbic areas which are the other cortex
and some subcortical regions, he calls corticoid
because they have some layering.
But I've drawn in there in red arrows direct connections
or disynaptic connections to the hypothalamus.
So, for example, we know the amygdala
which is directly connected to the hypothalamus
as well as through other areas of the limbic system,
the amygdala gets direct input from association areas,
multimodal especially, but even unimodal visual areas
project onto the amygdala as discovered by Nauta.
And then we also know that cingulate gyrus,
parahippocampal areas, they project
to hippocampus and to other of these limbic system
structures which are all closely--
we know by definition, these are the areas closely connected
to the hypothalamus.
So let's focus mostly on the amygdala,
and ask, what the heck is it?
What does amygdala mean?
Well it means almond.
It's got an almond shape.
Oh I shoot.
I already deleted one of the other slides.
I had a human brain there that shows--
I posted some slides somewhere online.
I'll have to find them.
You can see in a human dissection
how apt a name that is for the amygdala.
It's an almond-shaped structure that sits right
in front of the anterior pole of the hippocampal formation which
in a rodent would be the ventral pole.
You can think of it as kind of a modified
part of the corpus striatum.
In fact, we call, in the classical anatomy literature,
we call the basal ganglia the corpus striatum
and we the amygdala, all called basal ganglia.
Now actually, in embryological terms,
only part of the amygdala is striatal in origin.
Some of it's paleo in origin.
In other words, it's like a cortex.
But there's a very good reason-- some people have argued
though they're actually separate structures.
We should talk separately about them,
but I would say no, because connections
are what determines functions.
And the connections of the amygdala
indicate that it's one structure.
They are closely connected, and they have common outputs.
And as in the striatum, connections in the amygdala
are [? elastic. ?] Remember I made a big deal out
of that for striatum.
It had originally olfactory heads were formed.
It was the route through the ventral striatum, the oldest
part of the striatum to influence movement which
it did through the hypothalamus and midbrain.
Well this part of the striatum is not
concerned with the same kind of movements.
It's concerned with motivation, emotion, feelings,
if we talk subjectively about it.
So associations are formed between perceive objects
and sounds on the one hand and apex and autonomic changes
in the other.
It gives objects in the world valences or affected tags.
In other words, you can hang tags on things.
I like that.
I don't like that.
That makes me happy.
That upsets me.
But we'll all learn things or most of it.
There's argument about some of them like fear of snakes.
They might be at least partly inherited.
This is the collection of structures
that we lump together and call the amygdala
in a ventral view of a rabbit brain which
is very similar to rodent brains.
The connections are all the same.
So here's the olfactory bulb way up at the front,
but behind the olfactory bulb starts the olfactory cortex.
The first part of it we call the olfactory peduncle,
because it's sorts of a little stem connected
to the rest of it.
And you'll see they have these very widely projecting axons.
They're very widely branching axons of the olfactory system,
and they go back to this broadened part
of that cortex which is why it gets the name pyriform cortex--
it's P- Y- R, not P- I- R. It's not the [? piricortex ?] It's
the pear-shaped cortex, because this
is the pear shape like the Bosc pears you
buy in the supermarket.
That's the shape it is.
And this little special part of the olfactory bulb
the olfactory bulb projects directly
to the cortical nucleus to the amydala.
So that's in red here.
And medial nucleus connects to it,
also gets direct olfactory input.
That part, the cortical and medial nuclei
are often lumped together even though one of them
is paleo in origin and one of them
is striatal because of the similarity of connections
and because they get, not only direct olfactory input, they
also get some input from the brainstem from the taste
system, directly from brainstems from the parabrachial nuclei,
so you've got taste information.
It also gets pain input from the brainstem.
And the basal [INAUDIBLE] nuclei, they get input
from sensory systems like the visual system.
Some of it comes directly from the thalamas,
especially in the auditory system
but there are some visual pathways too, but even more,
especially for the visual system from cortical areas.
They also have projections to cortex, especially
to the prefrontal area.
So the prefrontal area recipricolly connected
to this, but all of these nuclei are
connected to the central nucleus and have some other connections
with each other.
That central nucleus which is a striatal structure, striatal
in origin, it gets input from all these different structures
and it connects directly to basal forebrain
and hypothalamus.
So we want to look at that.
So here I've just shown paleo and striatal [? derivatives ?]
separate.
I don't think it's such a big deal,
because [INAUDIBLE] connections.
It's really difficult to separate them in that way.
So let's describe the stria terminalis Its origins,
I just stated, comes from, mainly,
the central nucleus and the amygdala.
And then it's course in its major connections,
and you'll see that its course is very much like the fornix
fibers from the hippocampus.
It has to go around the internal capsule fibers.
And by going directly to the amygdala,
it pretty directly influences motivational states.
I want to start talking about it, just
by showing a section of the rat here.
This is the amygdala.
I put dotted lines around it.
This is olfactory cortex out here.
There's the rhinal fissure.
We look in the hypothalamus.
There's the fornix, and I pointed out
the ventral medial nucleus, because this central nucleus,
which is here, can you see my pointer here?
This area projects directly to the cells, the neurons,
of the ventral nucleus hypothalamus.
And we want to follow those.
Here's the stria terminalis.
I've outlined it for you.
And you'll say, well how do you know that?
Well If you look carefully here, you
will see-- you'd have to blow it up a bit
I guess to really see it, but let's do that.
These are neurons.
These little cells are oligodendro cells.
The basic dye will stain the region
of the nucleus in the oligodondron sites,
and you'll see these little tiny cells
all lined up along the myelinated axons.
You see them here too, but here they're going differently.
These axons here are going like this
and coming out of the thalamus or coming from cortex
and going down like this into the cerebral peduncles.
And this is the white matter of the cortex up here.
So all these axons are connected there.
We go right up here, and here they go.
This is white matter of the cortex.
So here then are the fibers that are--
you can see them here coming out of-- here they come here.
So now I've just drawn a line around here.
So why do you see two of them?
Because these axons go around the caudal end
of the internal capsule.
They go around.
They're the same axons you see here,
you're seeing again up here.
Just like if we were more caudal in the brain,
we would see hippocampus going all the way down ventrally
here, and with the axons coming out
of that hippocampus are mostly collected
in the fimbria of the fornix.
And there's the fimbria of the fornix up here.
And in this dorsal part of the hippocampus,
the fornix fibers are there.
So there's fimbria with the other fornix.
And all those fibers are collected there.
Where else do we see those axons in this section?
Yet those axons go around the internal capsule too.
But then where they go?
They come down in from of the thalamus,
they go into the septal area, but some of them
go more caudally.
Where are they going?
This is Papez circuit.
They're going to the hypothalamus.
Where in the hypothalamus?
I'm going to stop right here until one of you tells me.
Where's the hippocampus project in the hypothalamus?
It's Papez circuit.
Come on.
Mammillary bodies.
And there's the fornix fibers.
And then those fibers from the amygdala
are doing something similar.
Here they are.
There they are.
Where are those down here?
They're here in that light area around-- because the dendrites
of the cells in the ventromedial nucleus
protrude out into that light area where
you see the clumped cells.
So the cells here in central nucleus
go up, around the back of the internal capsule,
then they follow around, come down
through the basal forebrain, and run caudally just
like the fornix.
Here's our view of the-- medial view of the hemisphere where
I've pretended it was transparent,
so I can show you these structures.
There's the amygdala right in front
of the ventral end of the hippocampus in a rodent.
There come those axons.
They're going around the internal capsule
which I've cut off here.
I've cut them right there, but they're
terminating in the bed nucleus stria terminalis
By definition, that's why we name it the bed nucleus,
the stria terminalis, because those cells are
right among the axons of the stria terminalis
and they're getting connections from it.
And similarly, the hippocampal fibers-- you see there I
left those in black-- the columns of the fornix
are right there next to the stria terminalis.
They go to mammillary bodies, runs from the stria
terminalis, though mainly to the ventromedial hypothalamus.
There are other connections in the hypothalamus too
of both those bundles of axons, but the major termination
are in the mammillary bodies in the ventromedial hypothalamus.
So this whole area is basal forebrain.
We'll talk a little more about that.
In the frontal sections here, these
are the levels through the embryonic brain
and here we're in the mid thalamic region.
There's the amygdala down in the temporal lobe.
And there's the stria terminalis coming
around the internal capsule.
And there's the bed nucleus, the stria terminalis.
I cut it here right at the rostral limit of the bed
nucleus and the caudal limit of the nucleus accumbens.
Nucleus accumbens has become very big in humans.
It gets a lot of input from the amygdala and the hippocampus,
especially the hippocampus and other limbic system structures.
And if we go forward, we just see nucleus accumbens,
the major nucleus of the basal forebrain.
Accumbens means leaning, because it's
leaning against the septal which is here.
A couple more questions here.
What sensory inputs come to the cortical and medial nucleus
and the amygdala without passing through the neocortex?
We know they're very ancient from comparative studies.
We keep seeing it even in really ancient vertebrates,
vertebrates that is, that are still living
but are very similar to vertebrates
that lives hundreds and thousands of years ago.
OK olfactory is certainly one of them.
What's another one you'd expect?
What was really important in getting animals
to do one thing rather than another,
is a source of reward important in feeding?
Taste.
Yes.
And there are taste inputs directed from the brainstem
too.
Olfaction and taste and the other one
is pain-- all come in there.
Those are the ancient inputs to the cortical and medial nuclei.
And then the question for us is the lateral nucleus
the amydala receives various sensory inputs too,
but they come by way of neocortical associations
and a few of them directly from the thalamus
but not from more caudal brainstem structures.
And I showed you in the diagrams before those--
you think most about the visual system ones,
but we know auditory system ones and we will come back to that.
So here's what I just said.
I also pointed out that basal, particularly the basal nucleus,
the lateral somewhat, reciprocally
connected to prefrontal cortex.
This is that picture when we talked
about auditory system from experiments
where they labeled the cells in the medial colliculus body,
and they traced the axons not only to auditory cortex, there
here in the opossum but in the opossum very heavily
to that lateral nucleus in the amygdala.
But it also occurs in the hedgehog, and the treeshrew
and the rat and the mouse.
Probably in us although the connection to neocortex
in the primates is by far the most important.
I want to show you again what medical school
illustrations can look like.
To make it a little easier, just so
you understand what they're doing here.
They're trying to show too much, and because of the way
the human brain's developed it's very distorted.
This kind of picture is a lot easier to understand.
This is the human, and I've shown inputs
by labeling the cells red.
The outputs I've shown the cells in the amygdala with a green
dot so you can see.
But a lot harder to understand than the way I'm presenting it.
Here I'm in a dissection-- a big slice
so you can see the myelinated fibers really clearly.
This is from a book, beautiful book,
that shows-- I can bring it in class
and let you go through it-- showing beautiful dissections,
and then he also has some of these sections.
There you see the amygdala.
This has to be-- I'll ask you what level this cut.
This is thalamus here, and there's mammillary bodies
there.
If it were a rodent, this would be caudal thalamus,
but in human, the way it's arranged,
you can't count on that.
There's the putamen, the caudate nucleus,
but there's that big amygdala.
And you'll see it's a abutting the more anterior
parts of the corpus striatum right there.
That's all amygdala and if we went back just a little bit,
then we'd be in hippocampus, because that's
got to be the anterior most part of the temporal lobe here.
See there's the [INAUDIBLE], so this is all temporal lobe
down here.
This is parietal lobe up here.
Or if we're very far anterior, it
might even be coronal cortex.
Now some of the early functional information around the amygdala
functions came from electrical stimulation,
and it's been done a lot in monkeys,
but it's also been done in humans
during surgical procedures.
So I've taken this from human studies.
You stimulate the cortical medial area,
you get oral kinds of things, salivation,
smacking of the lips, licking, chewing,
and inhibitional involuntary movements as well.
You can also get elimination behavior.
If you stimulate the basal lateral nuclei
of the amygdala in a human you get arousal,
attentiveness, sometimes you get fear or rage,
or you get anxiety and another very strong emotions,
and you also get effects on memory.
The person will say, I've been here before,
and of course he hasn't been here before,
but it feels like he has.
It's an experience that many of us have when we're growing up.
It's called a deja vu experience.
How many of you can recall having such experiences?
You've been in a situation, you're
sure you were there before, but you
couldn't have been there before.
You know?
You're in a new place.
Well we think it probably happens
through a minor seizure.
It doesn't mean anything's wrong.
It doesn't.
Because these cells in the limbic system
are prone to getting overly excited.
People with temporal epilepsy can
have deja vu preceding an actual seizure.
But most of us, it doesn't go that far.
I kept having those until, I think I was 30 years old.
In the research, negative emotions have been stressed.
And when you hear talks about amygdala,
it used to be they would only talk about learned fears.
That's changing a bit now, and I know from the human literature
that it had to change because, in fact, positive feelings, as
well as negative, can be obtained
from manipulating that area.
If you take the amygdala out, there's not much on humans,
but occasionally there are humans with amygdala lesions,
generally not bilateral though.
It has been done on both sides with monkeys.
And the first thing you notice-- monkeys,
rhesus monkeys are pretty wild.
We were getting rhesus monkeys that were wild caught.
Then they started using only the ones that
are bred in captivity, but even the ones bred in captivity,
they grow up in these groups and they are not tame monkeys.
But after the amygdala lesions, they were remarkably tame.
They lost their normal defensiveness
and aggressiveness in social situations.
But the monkeys in social groups become socially isolated,
because they're not sensitive, the way they should be,
to dominance relationships.
So you now have this monkey who's not a dominant animal
at all, or he wasn't before the amygdala lesion.
He will walk right up to the dominant male
and get clobbered by him.
So they get injured, they become isolated
just because they lose their normal fears,
especially in response to visual inputs.
They show loss of autonomic reactions
that accompany fear and anxiety.
Also, you see some other types of effects like altered dietary
preferences.
And in the animal work, this was true also,
the cats get hypersexuality.
There's a famous picture that used
to be reproduced in all the physiological psychology
or brain behavior books of a animal
mounting another animal who's mounting another animal who's
mounting another animal because they had amygdala issues.
The amygdala, like the striatum is involved in habit learning,
but what kind of habits are we talking about now?
Well, I just described learned fears and other kinds
of learned [? effects. ?] That can be considered a habit.
Prejudices are learned.
That is an emotional habit, something learned.
It's a tag we put on certain things or even certain people.
That depends on the amygdala and basal forebrain, particularly
the amygdala because its close connections
to the temporal lobe.
This is from a study of fear conditioning
that was found to be dependent on the amygdala in rats.
So here you have a rat in a box with a grid they can electrify
and there's a speaker here and they're sounding a tone.
And you can see in response to the tone-- the left graph here
is blood pressure, doesn't change very much.
This is the time he spends resting
his behavior, freezing behavior, very little.
When the sound is [? novel, ?] you'll
get a little bit of increase in blood pressure, a little bit
of freezing right at the beginning,
and then he gets used to it and you don't get in anymore.
But now, when you get the sound, you electrify the grid,
as you'd expect, blood pressure goes way up.
He freezes a lot because he can't get away.
Of course, he tries to run, but he can't get away.
They don't shock them so much that they're really injured.
It's not a super cruel experiment,
and it's often been used to study fear condition.
But anyway, after they learn that association, now you just
give the sound, you don't electrify the grid.
Blood pressure goes up.
Freezing goes up.
That's learned fear, and that's how it's measured.
[? Ablation ?] amygdala or just damaged pathway
from the medial [INAUDIBLE] body of the thalamus
to the amygdala, you get rid of that.
There's pretty good evidence that
depends on that auditory pathway from the thalamus
to the amygdala to the lateral nucleus to the amygdala.
There's interesting lesion experiments
that have been done in monkeys.
I want to go through this quickly.
How do you produce a monkey that shows all these bizarre effects
of amygdala ablation only when he's looking with one eye
but not when he's looking with the other.
AUDIENCE: [INAUDIBLE]
PROFESSOR: Louder.
AUDIENCE: [INAUDIBLE]
PROFESSOR: So you do a split brain operation meaning
cut the commissures, cut the optic chiasm-- see,
if you cut the optic chiasm, you still
have ipsilateral fibers you haven't
cut, the ones that don't cross.
Like here, here's the chiasm, you cut around the midline.
So now the right eye goes to the right side of the brain,
the left eye goes to the left side.
Of course, each eye sees only half the visual field.
But to get this to work you start just
with the amygdala lesion in one side, the left hemisphere.
I'm looking at the top, but I'm showing where the amygdala is
down below in the temporal lobe.
So you have to not only cut the chiasm,
you have to cut the commissures, because otherwise
the visual input that reaches this visual cortex can
go from the [? juxtastriat ?] areas here
across to the other side, because these areas are
interconnected across the chiasm.
The reason they cut it all the way forward is they
actually have to cut the interior commissure
to get this to be complete, because the amygdala's
connected to the amygdala area.
Temporal lobe structures, even temporal unicortex
is connected across the interior commissure too.
So they cut these commissures and now the animal
has a totally different personality
with one eye than with the other.
We call that a disconnection syndrome.
Disconnection syndromes have become
well known in human neurology, because many lesions,
human strokes, can eliminate a particular group of axons,
a particular pathway.
So the person can lose his ability to read, for example,
but he can see perfectly well and he can respond to objects,
but if you've disconnected the pathway going
to areas, the Wernicke's area of the temporal and posterior
parietal cortex, then he won't be able to read.
You can read the rest of this, and I describe it
in the chapter.
Learn about how aggression-- these are all associated
with amygdala functions-- we know aggression
is also highly dependant on amygdala
even though it's also generated through the hypothalamus
of course.
The endbrain structure that's most closely connected to it,
in fact, it's a major function of that connection
from amygdala to the ventromedial hypothalamic
nucleus.
And you can stimulate the ventromedial nucleus
hypothalamus and get aggressive behavior,
but that is enhanced by testosterone.
This is just an experiment that shows males,
high aggressiveness-- it's low in females over here--
but if you castrate them, their aggressiveness goes down.
This is studies of rats, but it's
been done on a number of other species as well.
Then you start administering the testosterone
which affects the amygdala.
Then aggressiveness comes back unless you
drop the level of testosterone you're
administering to low levels.
Read about the basal forebrain.
I think that we will have time to go through basal forebrain,
and I want you to understand this hypothesis,
because it relates to Chapter 13, studies of plasticity.
| makes a prediction that has been verified indirectly
in studies of humans after Hurley temporal lobe lesions
in certain groups of schizophrenics.
This is from one of my papers, a paper published in 1979
I think.
We'll come back to that next time.