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PROFESSOR: The topic here is introduction to the forebrain.
It's really another introduction to the forebrain.
I do this on purpose, introduce it a number of times
in order to get enough redundancy so you can remember
the major points.
And last time, I was talking about the early influence of
olfaction on the development of the forebrain.
The endbrain, in particular, was totally dominated by
olfaction early on from the evidence we have
from existing animals.
And I had just mentioned that the early corpus striatum was
really what we now call ventral
striatum, part of the striatum.
The ventral striatum gets direct input from the
olfactory bulb.
Do you remember what that part of the
ventral striatum's called?
The olfactory tubercle.
It's sort of a little bump right on the bottom of the
base of the brain, right in front of the optic chiasm.
So it's just a little bit anterior to the hypothalamus.
But then olfaction also reached the pallium, of
course, not just initially, not just the lateral pallium,
but also the dorsal pallium, and the more medial structures
there also.
The pallium, of course, went all the way around.
At the base is where it became striatum.
And that's where the turbercle is.
But if you go up the medial side of the primitive
endbrain, you got to the medial pallium.
So it's another cortical structure.
It's dorsomedial to the striatal part
of the neural tube.
We know it gets direct olfactory inputs in primitive
vertebrates like the hagfish, but other animals as well.
Even some mammals like the hedgehog and the hamster,
there's an anterior part of the medial pallium that gets
direct olfactory input.
But the importance of this structure that I want to call
your attention to is what it became.
It became the hippocampal formation.
And it has this major function of memory per location in
space, in the world around us.
Let's see if I can get this to work.
And I think I showed this last time, one of the many
correlational studies that have been done on hippocampus.
And this one is on birds.
The volume of the endbrain plotted on the abscissa.
On the ordinate, they plotted the hippocampal volume.
And if you note two groups here, the corvids, including
the crows, some of hoard and some of them don't hoard.
And when they hoard, they have to remember place, because
they have to remember where they hid the food.
OK, there are a number of animals that do that.
You can see that the ones that hoard have larger hippocampus.
Anything more in this direction is larger with
respect to the rest of the endbrain.
And the same is true for titmice and
other birds that hoard.
And of course, there's a lot of experimental studies--
especially with mice and rats and monkeys, rhesus monkeys--
that have given us a lot more information about the role of
that part of the endbrain in remembering
places, memory for places.
And it's led to the importance of hippocampus in what we call
episodic memory.
OK.
Then there was a somewhat parallel evolution of both the
pallium and the subpallium.
Because each involved non-olfactory portions.
This is the invasion hypothesis.
There was an invasion of the non-olfactory modalities.
And the result was that the original olfactory parts were
still there.
But they don't occupy the whole region anymore.
For example, in the pallium, we call them limbic, because
they're at the edges, the fringes of the pallium.
A similar kind of thing was happening in the striatum.
In the striatum, the olfactory portions remained ventral and
portions that lost their olfactory input became the
dorsal part.
So it happened in both the striatum and the pallium.
And when we talk about striatum, we'll show you how
those different portions and how the
non-olfactory inputs came in.
They came in from the older parts of the thalamus,
probably much earlier than from the cortex itself.
These are the midline and intralaminar nuclei.
They give many sensory inputs.
They're multi-modal in nature.
And we can trace projections in modern mammals from that
part into both striatum and the overlying cortex.
And then later, non-olfactory inputs came
mainly from the neocortex.
And that is by far-- in the large primates especially--
that is the dominant input to the striatum,
coming from the neocortex.
And the striatal outputs, the early ones, went to the
hypothalamus, especially, and subthalamus.
They also went to the midbrain for controlling locomotion in
affecting, orienting, and grasping movements.
And with these non-olfactory inputs in the pallium resulted
in neocortex, which has expanded so tremendously in
mammals after that non-olfactory information
reached it.
The olfactory cortex is a somewhat simpler cortex.
It's usually four-layered cortex.
Neocortex is always at least six layers.
And when it has more than six, we just subdivide some of the
layers, call them sublayers.
Like layer four has expanded a lot in certain sensory areas.
So we talk about 4A, 4B, 4C, and so forth.
The same for layer 6 and layer 5.
And that, of course, brought with it a lot better sensory
abilities, sensory analysis, object discrimination.
And its outputs of that cortex went to the
striatum as I mentioned.
But they also went to the medial pallium, the
hippocampus.
They went to the tweenbrain and midbrain.
And then later on, as the cortex got bigger, as happens
with as many structures in the brain when they get bigger,
they develop more connections.
In the case of the cortex, it went everywhere.
It went to the hindbrain and spinal cord directly.
This is three modern mammals, all we
consider somewhat primitive.
Look at the Madagascar tenrec.
These are all insectivores.
Look at the relatively small neocortex at this
level of the brain.
This is all olfactory cortex.
There's the rhinal fissure way up there.
If this were a hamster, the rhinal fissure
would be down here.
And that would all be neocortex up here.
And the olfactory cortex would be down there.
It would come up the side ways.
In humans, it's all way under here.
Now here's the hedgehog, pretty similar.
There's the medial pallium.
It's now enfolded there.
Same here in the tenrec.
That's the hippocampus.
And it's pretty similar in the opossum.
This is a mouse opossum, but pretty similar to the Virginia
opossum or other opossums.
What they're calling olfactory tract here is
actually not all tract.
But it is all structures that also get input from the
olfactory system.
So in the tenrec here, everything from here all the
way up to there is getting olfactory input, even though
this is a mammal.
OK.
So let's go through these ideas about origins in a
series of pictures.
I divided it up into the stages that I've already
mentioned here.
In the beginning, the corpus striatum was a link between
olfactory inputs and motor control.
And that's what became the ventral striatum.
Here it is right here.
There's the primitive endbrain.
Olfactory bulb and the rest of the endbrain behind it.
And then, the tween-brain, midbrain, and the hindbrain.
And the primitive outputs, the earliest projections were to
hypothalamus and the epithalamus.
Hypothalamus here.
Epithalamus there.
As the striatum evolved and developed projections to the
ventral thalamus or subthalamus and more directly
to the midbrain--
now these midbrain structures were already there.
They were already important in controlling locomotion and
orienting for example.
But there weren't so many direct
projections from the endbrain.
OK.
So these are the functions we talked about before.
We talked about the midbrain and about the motor system.
And as I mentioned, one property that was so
important, and still is, is the plasticity of these
connections.
That was a modifiable link.
Now for that to happen, it required some feedback from
the responses.
When a response occurs, whether it gave a good or bad
result, had to affect the synapse.
And I've not drawn in those connections.
But we do know something about them.
They do come from the more response in the system here,
especially from the midbrain.
And these are--
at least now they appear to be mainly dopamine axons coming
from the ventral midbrain and hypothalamus,
depending on the species.
Many animals, they come from the posture hypothalamus here.
In mammals, they come from this region of the midbrain.
Well, that's what I see here.
And dopamine is about the earliest of the catecholamine
systems that you see.
Even in the most primitive chordates, you see dopamine.
Even though you don't see the other catecholamines.
You don't see serotonin and norepinephrine
in primitive animals.
That area in the hypothalamus that has the dopamine cells is
called the posterior tuberculum.
And it includes a lot of animals, as I mention there.
But in mammals, in all the amniotes, but also the sharks,
skates, and rays, it comes from the midbrain, the ventral
tegmental area and the nigra.
And I just point out here that there--
I had to look for this, because it seemed to me
obvious that if it's providing feedback for responses, one of
the most primitive kinds of feedback that would be
important would be from the taste receptors.
If they encounter something good to eat, they should learn
to do what they just did to get good food.
So I looked.
And initially, I didn't find it.
So I talked to somebody who had actually worked on it.
And they said, oh yeah, there actually is such projection.
It just hasn't been emphasized in the modern literature.
But I'm going to emphasize it.
Because the fact is, it is there.
And it needs to be studied a little more, especially in
animals other than mammals.
The studies I encountered were in the rat.
So this is the second stage then.
Non-olfactory inputs reach the striatum.
And here I show them coming by way of the midbrain into the
dorsal thalamus and then from there into the striatum.
And initially, I think these were overlapping.
There's examples of that in modern-- in development, if
you study development of brains.
There's a number of examples where
projections will overlap.
And then as they increase in density, you will get a
segregation.
I think that's what happens here in the case of the dorsal
and ventral striatum.
And then stage three, these
projections became more important.
They expand.
They resulted in an increase and an expansion of these
endbrain structures.
Both the pallium, which was also getting this dual kind of
input, and the striatum.
And then finally, premammalian and then mammalian expansions
went much further both cortex and striatum.
And I just point out that for the striatum the earlier
outputs and inputs remained.
They're still there, as the connections with
the neocortex expanded.
And I'm showing the most novel projection here that
increased the most.
This projection, this output of the striatum that went into
the thalamus that then projected to the neocortex,
especially the motor cortex.
All right.
So now we're going to go to our next topic.
We're going to start today by talking about hypothalamus and
limbic system.
And then we'll say a little more about the striatum,
especially the mammalian striatum.
And then finally, the last four or five classes we'll be
talking about the neocortex.
Which of course, because we're dominated by neocortex, that's
got to be the crown.
Well, it is in a sense.
It's the biggest.
It's right on top.
And that's the thousand-petal lotus.
Let's go to a slighter larger picture here.
This term, limbic system--
remember, you'll see exactly why it's called that in
pictures today.
But everything that we call limbic is always closely
related to that structure.
So we'll be talking mostly about hypothalamus today.
Why is that such a central structure
that led to this name?
The underlying motivational and emotional states as well
as endocrine and visceral control functions.
So again, we'll begin with evolutionary origins and
functions and give some definitions.
In the earliest evolution of the forebrain, that there were
areas there that controlled secretions into the general
circulation that were important for survival was
right there at the anterior end of the neural tube, part
of the forebrain vesicle.
That's the area that, of course, now is part of the
hypothalamus.
And it's actually where these functions are.
It's a caudal part of the hypothalamus, the ventral part
of tweenbrain.
And then, as we've already talked about, the
differentiation of the endbrain we think resulted
from the olfactory inputs, which through the striatum
were closely connected to the hypothalamus.
And not just striatum, the olfactory parts of the pallium
did the same thing.
I should have included that there.
The functions of hypothalamus and the structures connected
to it, the limbic system structures.
Sherrington, the famous physiologist, called it the
head ganglion of the autonomic nervous system.
We've talked about autonomic nervous system, the synthetic
and parasynthetic systems already.
But today, we'll talk less about the secretory
functions--
so I'll show you how that happened--
and the autonomic nervous system, and more about the
motivated behaviors that it controls--
ingestive, reproductive, defensive behaviors,
associated with what we call drives.
Or motivational states is another word for that, and
affects, which is the subjective component.
When we talk about affect, we're talking about feelings
associated with our drives and the consequences of our fixed
action patterns, inherited motivations.
Some people call them the basic biological drives.
And when we talked about the motor system, we pointed out
that these hypothalamic cell groups function as central
pattern controllers in that they connect to the lower
structures in the midbrain especially and also to the
hindbrain and spinal cord, controlling various action
patterns in the animal.
So limbic system is at the fringe of the hemisphere.
It came from a phrase used by this man.
You know Pierre Paul Broca because of Broca's area, the
language area in the frontal lobe, which controls our
ability to articulate speech.
He was a well-known neurologist.
And I've taken one of my pictures from the last
lectures here, a picture that I've altered quite a bit to
divide it up for both human and here the rodent picture,
the entire brain stem and spinal cord--
minus, here's the hemisphere up above.
So you can imagine to make that an entire brain now, you
just take that put it down on top of that.
And I've shown the lateral view and the medial view.
And here is for the human.
OK.
Now the structures closely connected to the hypothalamus
that are all involved in some way in motivation and emotion
are these structures from the red stripes.
And you can see it.
It forms what you could call a lobe.
It's that medial fringe of the hemispheres.
You go anyplace in the neocortex here and then keep
going and follow that surface around, you'll get to that.
Here it comes out a little bit on the lateral surface.
That's the only place anterior to the temporal lobe.
In the same picture here--
well, you can see the same thing in the rodent brain.
In the same picture here, I've shown primary sensory areas in
the orange color or yellow color.
So visual, auditory, and somatosensory, so-called
primary sensory areas.
And then right in front of the somatosensory,
primary motor cortex.
And then I've shown areas which are involved in more
organized patterns of behavior, like the premotor
cortex, parts of the brain stem, the brain stem core.
These are the areas when you place electrodes can elicit
patterns of behavior rather directly.
You can elicit them also from stimulating the areas in red
there, the limbic system.
But you do it for different reasons.
You're changing their motivational state, their
likelihood of responding to stimuli with a particular kind
of behavior when you're stimulating here.
If you're in the, what I label, behavior areas, you're
directly causing the behavior regardless of their
motivational state.
All right.
Now, I'm going to approach the limbic system from below here
by talking about the midbrain, as I did when I talked about
motor system.
I introduced it through the subdivisions of the midbrain,
controlling different kinds of movement.
Here, we're going to talk about two different kinds of
activating the entire brain, arousal systems, because
there's a limbic type of arousal and a nonlimbic type
of arousal.
The nonlimbic type, we associated with
the reticular formation.
And it's called the ascending reticular activating system,
because when you stimulate it, you activate the entire brain
in front of it, the tween-brain
and the whole endbrain.
And if you're recording from say, an electroencephalograph,
which the potential that you can record from the scalp, by
little currents induced in the scalp by the underlying
electrical activity, you see changes that are very
characteristic of an aroused state, very fast and low
amplitude?] activity.
If you stimulate the limbic areas, you get a different
kind of arousal.
Although the electroencephalographic change
is the same.
They're very similar.
In both systems, it causes sympathetic
nervous system arousal.
I think I noticed this last time.
It cuts off part of my picture there.
I just note here about the discovery of that ascending
reticular activating system.
In the mid '50s, these two men--
everybody knew their names.
And everybody was talking about the ascending reticular
activating system.
It was a new concept then.
The limbic system was extended into the midbrain by the
neuroanatomical studies of Nauta as I pointed out before.
He did more than anyone else to make the concept of the
limbic system a rational one.
He has shown that in fact there were consistent
properties in terms of connections to hypothalamus
you could use to define it.
And people who aren't very anatomical in their thinking
about brain still reject the idea of the limbic system,
because they don't think anatomically.
Needless to say, I do so--
And I'm a student of Nauta's.
OK.
So here's the midbrain.
As we've seen several times.
And here I've shown that division, the same one we had
before, the somatic parts and the limbic parts.
So now we're going to talk about the effects of
simulating it artificially.
You put electrodes in there, anywhere in those regions,
what happens when you apply stimulation?
You get somewhat similar things, but a little bit more
specific, less general when you're in the tweenbrain in
the corresponding or closely related areas.
So they have different effects of stimulation
and different anatomy.
Let's just go through those.
The first type of arousal from stimulating the ascending
reticular activating system.
As I pointed out, you get the EEG arousal.
And if you stimulate repeatedly, you get less and
less effect.
It's a habituation.
Same as if you're using a novel stimulus
to cause the arousal.
You often get forced turning.
That depends on where your electrode is.
Even if you're avoiding directly stimulating the
output of the tectum, the superior colliculus, you can
still get force turning in many cases.
And what do I mean by this--
self-stimulation affects our slight?
I mean they're not rewarding or punishing.
Self-stimulation is the method you use to test for
motivational effects of the stimulation.
You give the animal control of it.
Rats very quickly learn to control a bar that changes the
stimulation through an electrode in his brain.
If he doesn't notice it very much, of course, he's not
going to change his behavior much.
And that's true for this type of arousal.
If you look at the kind of connections there, you find
they're sensory in various types, coming from below you
get vestibular, somatosensory, auditory, and visual inputs,
especially from the colliculus.
You also get cerebellar inputs.
And the descending connections come from corpus callosum--
I'm sorry, neocortex and corpus striatum.
But they also come from older parts of the thalamus and the
subthalamus.
OK.
The other type, the limbic areas--
and you can be either in the central gray there or in the
ventral tegmental area--
you still get the EEG arousal.
But now these in bold here, I've shown where the biggest
differences are.
They don't habituate.
Every time you stimulate, you get the arousal even if you've
done it many, many, many times.
And yet, if you give the animal control over the
stimulation, the effects are very strong.
The animal will work to turn it off if it's
in that dorsal part.
He doesn't like it.
If it's in the ventral part, he loves it.
And he will turn it on again and again.
Often preferring to turn on that stimulus to eating.
In fact, animals will stimulate in preference to
eating to such an extent that they can even die.
From more caudal structures it gets connections that are
especially dominated by visceral sensory inputs.
But from rostral structures, the main inputs are coming
from hypothalamus but also structures of the limbic
system rostral to hypothalamus-- septal area,
basal forebrain, and medial pallium or hippocampal
formation, and the amygdala in the temporal lobe, which is
really the more caudal part of ventral striatum.
So these structures here are closely connected to these
structures.
And I've not shown the more rostral endbrain here.
We did show that when we-- and we will show
it again very shortly.
But first, I want to talk now about the specific functions
of the hypothalamus.
Control the autonomic nervous system and the endocrine
system first.
And that happens by way of the control secretions.
It happens primarily by way of the pituitary.
And this is the picture from [? Rodale. ?]
I like Nauta's picture better.
But I don't have it scanned.
And I couldn't find my picture of it.
So I took the one from [? Rodale ?] which is fine.
Here he shows two groups of neurons in the hypothalamus,
paraventricular nucleus and super optic nucleus.
And they have many axons.
[? Rodale ?] says there's about
100,000 of them in humans.
They're very small axons.
And here they come into that little protrusion that we call
the neurohypophysis, or neural pituitary,
the posterior pituitary.
These are all synonymous terms.
It's part of the brain.
What's unique about it is these endings
aren't on other neurons.
They're on capillaries.
And when these neurons are activated, they release
specific substances that we call neural hormones directly
into the bloodstream.
We call them hormones, because that's the way hormones work.
They go into the bloodstream.
Otherwise, it's like release of a neurotransmitter.
But this isn't affecting a neuron directly.
It's affecting the whole body through
the circulatory system.
And here he shows an ending of a neuron
like that on a capillary.
And you see molecules of these neural hormones going directly
into the capillary.
Now there are also endings in the capillaries further up,
not in the neuron hypothesis, not in
the posterior pituitary.
They're in this region here that we
call the median eminence.
And here he shows some neurons of another part, more
posterior part of the hypothalamus, right at the
base there called the arcuate nucleus.
And there's other groups that do this too.
They terminate capillaries.
So here is the blood from the artery coming in.
There it ramifies in the capillary bed.
It picks up hormones being secreted there.
In this case, they're not--
It's a different kind of hormone.
They're called releasing hormones.
Their function is to continue through the circulation.
They go through a portal vein and into another capillary bed
here in the anterior pituitary.
And there those hormones, the releasing hormones cause the
release of specific hormones, like growth hormone,
gonadotrophic hormone, adrenal corticotrophic hormone.
So that's how the endocrine system is control by way of
the pituitary.
Next major function, homeostatic mechanisms.
Good example--
and I asked you a couple questions about that here.
But first, let's talk about
temperature regulation briefly.
And temperature regulation depends partly on input from
hypothalamic neurons that are changing their firing rate
with body temperature.
So they're directly detecting our core temperature.
But temperature regulation is also controlled directly in
the spinal cord.
It's also controlled by hindbrain mechanisms, midbrain
mechanisms.
The finest control over temperature is caused by this
region of the brain, the hypothalamus, even though it's
a very redundantly represented system.
How did Nauta and [INAUDIBLE] define that term, homeostasis?
What is it?
What does the term mean, homeostasis?
Same state.
OK.
But it's not really the same.
It allows--
it's controlling a certain parameter in each case within
a certain range.
So your body temperature is always able to fluctuate a
little bit.
But if it gets too high, what happens?
It activates various patterns of behavior and reflex
functions that cause body temperature to be lost--
heat energy to be lost so that body temperature will drop.
And similarly, if your body, your core temperature gets too
low, it's detected by those neurons in the hypothalamus,
it causes the opposite kinds of behaviors that cause
raising your body temperature, like it causes shivering.
It will be involuntary.
And of course, there's many activities--
it changes your motivations as well.
You'll put on more clothes.
So your body temperature will fluctuate.
But it doesn't fluctuate too far in endothermic animals.
It fluctuates a lot more in exothermic animals.
But they also have to regulate the body temperature.
They have to do it more through their behavior.
So they have different kinds of behavior.
Lizards lie out in the sun to gain body heat.
And they actually can't function very well.
They can't attack their prey very well if their body
temperatures too low.
So in real cold weather, you're pretty safe from
snakes, because they really can't do much
when it's so cold.
They're too slow if they can respond at all.
All right.
This function, this term, diabetes insipidus, I like you
to know, because it's what happens if this is cut.
There's other causes of diabetes insipidus.
There's genetic diabetes insipidus, where there's a
degeneration of these cells in the brain.
But anything that compromises the secretion of these neural
hormones into the blood stream--
there's actually two of them, oxytocin and vasopressin.
And vasopressin is also called antidiurectic hormone, ADH.
And it's that one that, when it's missing from the
bloodstream, it causes diabetes insipidus.
OK.
Because you cannot retain body fluids.
You lose a lot more body fluid through the kidneys.
And to compensate for that, to maintain blood volume and so
forth, you have to drink a lot.
So it's like diabetes--
acute onset diabetes mellitus in that you drink a lot and
urinate a lot.
But it has a very different cause from diabetes mellitus.
In diabetes mellitus those symptoms are caused by acidity
of the blood, which is caused by inability to get enough
glucose into the cells.
So you're using other energy pathways that are generating
ketone bodies to make the blood acid.
So that's diabetes insipidus, which just to help you
remember about the antidiurectic hormone that's
secreted by these neurons directly into the blood.
So control the endocrine system, homeostatic
mechanisms.
Now regulation of cyclic behaviors.
We're going to talk about cyclic behaviors and then
episodic behaviors.
Examples of cyclic behaviors are things like sleeping and
waking, feeding, drinking, predatory attack.
These things fit into a daily cycle of activity.
And that cycle is regulated by another function of the
hypothalamus, this endogenous clock, where our activity
changes depending on time of day, synchronized by the daily
light dark cycle as we talked about when we talked about the
visual system.
And all these cyclic behaviors show species typical pattern.
So the details of the behavior will differ a little bit from
one species to the next.
And then we get to episodic behaviors,
also species typical.
And they also have a lot of learned components.
Two major ones are agonistic and reproductive.
And the agonistic behaviors are fighting,
fleeing, and defending.
And reproductive behaviors are sexual and parental.
Reproductive behavior was regulated by hormones
controlled by pituitary secretions.
And of course, they're heavily influenced by hypothalamus.
In the case of agonistic behavior, there's an initial--
very early it was dominated in mammals, in many animals by
olfactory sense, it played a particularly important role.
But other senses also played a very important role.
And you get some agonistic behavior,
even without an endbrain.
At least, the more automatic components.
So the hypothalamus, we sometimes call it a center for
the basic drives.
And just to refer you back to class 15, this was a slide
from class 15 on the hierarchic controlled
locomotive behavior.
And here at the top of the hierarchy in Swanson's picture
was the locomotor pattern controller.
And they call that region the hypothalamic locomotor region.
And he's really talking about how the basic drives can cause
locomotion.
If you're very hungry, you're very sexual, you have a high
parental drive, or your babies are being threatened in some
way, the drives change.
Your motivation changes.
And that's what these neurons at that level of the brain are
doing in the hypothalamus.
And yes, they control locomotion too.
And I, at that point, in the motor system, I was adding how
the influences from the forebrain occur--
especially the earliest one here,
olfaction through the striatum.
So when we're talking about this part of the brain, we're
talking about changes in what we call appetitive behavior,
which we can distinguish from consummatory behavior.
You'll remember the effects of forebrain removal in cats.
You take out the whole cerebrum, you get a lack of
normal appetitive behavior.
That means no seeking of food, no seeking of a mate.
Actually, they don't even show much motivation to change
their body temperature.
They have more automatic temperature regulation.
But their body temperature now will also fluctuate a lot
more, because they don't show normal appetitive behavior,
motivated behavior.
But they retain a lot of consummatory behavior.
And this is the specific movements involved in the
endpoint of any of these drives--
mouth opening, chewing, swallowing in the case of
eating; the aggressive responses
caused by painful input.
If you take a cat that doesn't show any normal aggressive
behavior at all, but you grab its tail and pinch it, you
cause pain, he will turn around and bite and claw.
These are what I mean by the pain
elicited aggressive responses.
And you could also elicit sexual postures and reflexes
even though they don't show normal sexual motivation.
Now most people leave this study out because it's been
difficult for people to understand.
But if you go back to this picture, what he's talking
about is a section here between the hypothalamus and
the midbrain, where he partially severed these
connections.
He didn't affect how the endbrain is connected directly
to the spinal cord and hindbrain.
But you eliminate a lot of the connections between
hypothalamus and the midbrain.
And he did it by making lesions at the midbrain,
partially disconnecting the forebrain motivation systems
from the control of the fixed action patterns of the
midbrain and hindbrain.
So these animals with these large lesions in the caudal
membrane showed really bizarre behavior.
They could regulate food intake.
But they showed very abnormal execution of the various
feeding behaviors and attack behaviors.
In fact, they couldn't eat without constantly treating it
like prey, even if they were animals being kept
as pets in the home.
And each mouthful of food they would
treat like a prey object.
And they couldn't eat unless they first carried the food
around as if they had caught prey and killed it.
So they would show the killing bite.
Some of them would, any water they found, they would
immediately show fishing behavior.
And yet they didn't show all aspects of
their attack behavior.
They wouldn't position themselves for an ambush.
They wouldn't pounce.
After they finished eating, they wouldn't groom as a
normal animal would.
They lost a lot of the behaviors associated with
elimination.
Of course, they would still eliminate.
But they wouldn't search, dig, scratch, and do the things
that a cat would normally do.
So you have a disorganized system for regulating these
fixed action patterns.
They've lost higher control.
Swanson put it a little differently.
He said the behavioral pattern controller's been partially
disconnected from the midbrain pattern initiator.
But that's perhaps a little more abstract way to talk
about the very same thing.
All right.
I just want to mention that these kinds of behaviors have
been simulated.
That is we understand enough about the logic to
be able to do that.
That started in 1990 with Randall Beer who simulated
cockroach neural control of feeding, where he had to
distinguish appetitive and consummatory components.
And my favorite is Bruce Blumberg's work here at the
MIT Media Lab.
One of our students, Jung, did a thesis with him, where she
characterized a lot of the work in terms of brain
mechanisms.
And I just want to point out that there are characters, if
you've never seen them, you should visit Blumberg's lab
and take a look.
The characters are very human-like or animal-like.
They run a simulation.
And they're never completely predictable
what's going to happen.
It's not like a cartoon that's been written and
scripted by an author.
These characters are actually controlled by their
motivational state and by how much the motivational state
builds up over time, the deprivation.
And it decreases when they encounter what they're looking
for, and so forth, just like real animals.
Even though they don't have what we would call higher
cognition, they do have striatal-like habit formation.
They respond to feedback and reward and so forth.
This is a picture--
I was involved in one of these studies of effective synthetic
characters, because I was Jung's
adviser and so was Blumberg.
And I, together advised her-- these are three characters.
And she was able to create three different personalities.
Of course, she made them look different by the way they
appeared on the screen too.
But the important point was they behave slightly
differently.
They had different habits, just by the way she had set
the parameters.
And we did a psychological study of them.
We asked groups of people to