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PROFESSOR: So we've been talking about the hypothalamus
and its role in motivated behavior patterns, and
motivation itself, and the nature of
motivation a little bit.
To go further with that, today I'll talk a little bit more
specifically about hunger, and feeding, and also behaviors we
often associate with hunting and cats.
And that'll finish the topic that I started with last time.
So if the mid-branch is the highest level, meaning we've
done a decerebration, and we've cut off the hypothalamus
from the lower brain stem, you could still get eating
reflexes, and what we call consummatory behavior
patterns, that is, animals will pick up food, can eat it.
But they really don't have regulation, and they don't
show hunger.
That is, they don't regulate their eating.
They'll show these behavior patterns as reflex patterns.
There's very little regulation.
You'll get chewing and licking and swallowing reflexes.
They're hind brain reflexes really.
Hind brain, and of course, spinal cord
is involved as well.
So they won't show active seeking behavior.
We need four brain mechanisms to get that kind of
motivational control.
It's been like that since pre-ancient times.
In the case of humans, sometimes we get humans born
without much of a forebrain at all.
The hemispheres don't develop because the neural tube fails
to close at the end anterior end.
They don't live very long, but while they do live, they can
be fed, they'll eat reflexively.
They'll show the rooting response, looking for the
nipple, they'll show sucking and swallowing.
But it's only normal babies that you get signs of when
they're too full, they'll stop,
they won't keep suckling.
They respond to stomach distension.
And of course later, as they mature, they respond to other
cues as well.
But not early on.
A lot of the queues for hunger and satiety come through the
vagus nerve.
If I can get my pointer here.
The 10th cranial nerve.
For example, inputs from mechanoreceptors of the
stomach, and also the throat.
What are the mechanoreceptors in the throat doing to
regulate feeding?
Do you remember anything about that?
If you take an animal and let him eat, but have the food not
reach the stomach, you put a tube here and a sack so the
food comes out, never makes it to the stomach,
falls into a sack.
And you can prepare such animals.
They will still eat meals of a certain size and
then they'll stop.
Well, how do they know they've had enough food?
Yes?
AUDIENCE: Don't we have mechanoreceptors tell them how
much food they intake?
PROFESSOR: Yeah, just so throat sensations, exactly,
without actual filling of the stomach.
So there's two separate kinds of
mechanoreceptor inputs there.
Each play a role.
Meal size is largely determined by the these throat
sensations.
And of course, there's blood factors.
And blood factors, especially blood glucose levels, are
detected by hypothalamic neurons.
And there's other blood factors too, some of which are
detected by hypothalamic neurons, but others by
secretions that occur in the digestive tract, especially
parts of the stomach.
So we have various factors that are pretty redundant,
actually, but they serve both short and long term
regulation.
Short term, meal size, the timing of meals.
And long term, what your total food intake is over the day.
I mentioned here that we always talk about feeding the
hypothalamus, and the importance of hypothalamic
regulation.
There are a number of studies by psychologists interested in
brain function that have also implicated subthalamic
mechanisms.
These are closely tied.
And the subthalamic involvement in these things is
less studied than the hypothalamic.
OK.
Now we can get hunger, just like I've been talking about,
you get hunger by just depriving an
animal of food, right?
Well, you can also make an animal hungry by putting an
electrode in his lateral hypothalamus.
And if you get the right places, you can, just by
turning the current on, and you can use just 60 cycle
current, and stepped down house current and use it, and
you'll get animals that behave in every respect
like they're hungry.
Even though they might be full of food, so
they should be satiated.
You can overcome that just by stimulating the hypothalamus.
You can also elicit other motivational states.
There were early studies done in chickens by von Hoist and
von St. Paul that became pretty well-known.
There was an interesting Scientific American article
about it a number of years ago.
They'd found certain sites that when they turn the
current on the animals would eat.
And other sites that he would stop eating.
Instead he would look as if there's a bird about to attack
him from air.
Or they would respond as if there was a
ground predator near.
It's like they were hallucinating these things.
So they could vary the motivational state quite a bit
just by where in the hypothalamus they were
stimulating.
And of course, there were effects of the intensity too,
because when they raise intensity there's a greater
spread to more axons themselves and the
hypothalamus, and they could get to
other drives to dominate.
Some of the most interesting studies of this nature were
done at Yale University by John Flynn and his students.
They focused on electrically elicited aggressive responses,
which are pretty prominent in cats.
They found that they could, just by where in the
hypothalamus they were, and it wasn't always clear exactly
what the localization was, except that the more lateral
components would often get predatory aggression.
Whereas defensive aggression they would get from more
medial placement.
So what's the difference?
Well, how many of you have had a pet cat?
OK.
So what's a cat's defensive aggression in a cat?
That's when the cat arches his back, the hair stands up, he
hisses, and he will strike out with his claws.
That's defensive aggression.
They show the same thing if you pinch them, like if you
grabbed them by the tail.
If you were a nasty little kid who did that you would know.
Well, predatory aggression is very different.
When you find a site that elicits that motivation, just
different groups of axons in the lateral hypothalamus, all
you will notice about the cat is that his ears perk up, he
becomes much more alert.
If he was a little sleepy beforehand, now he becomes
wide awake and alert, his eyes widen, and
he's looking around.
What you've done is elicit predatory aggression.
What he's looking for is mice or birds,
whatever he likes to attack.
Now, the interesting thing here is that cats,
some cats will hunt.
If they had a mother who hunted, they imitated her and
they will hunt mice.
Other cats won't.
If they didn't grow up with that kind of mother, they may
never hunt.
You could have a pet mouse and it could play with your cat if
he was a cat like that.
But if you stimulate this area in the hypothalamus, even if
he's a cat that's never attacked in his life, you will
get predatory attack.
And so much for the pet mouse.
They'd show all the normal behavior.
They will find, they look for the prey animal.
When they find it they will crouch, and even hide if
that's the way they're hunting.
They will then pounce, grab the animal, and elicit a
killing bite, which is very characteristic of
each species of cat.
But they're pretty similar across different cats.
Almost the same and the lion or a tiger as they
are in a house cat.
Very similar behaviors.
That's predatory aggression.
So if you turn the stimulation off, that motivation
disappears.
Now, have we just elicited hunger in those animals?
How could you test for that?
Well, cats love certain foods like tuna fish, and you might
be feeding the cat tuna fish, say, once a week as a
treat he loves it.
OK, so we'll put a can of--
well after he's already eaten now, we'll put the tuna fish
there, and we'll put a mouse in the background, turn the
stimulation on.
What does the cat do?
If you elicited hunger he'd go eat the tuna fish.
But that isn't what he'll do.
He will leap right over the tuna fish in order
to get at the mouse.
This just illustrates that these are
innate behavior patterns.
They've inherited them, and they depend on motivational
mechanisms controlled by this part of the brain.
And there's many other examples of different
motivations.
They've been studied most extensively in the rat.
You can stimulate certain areas that, instead of making
the rat want to attack anything or wanting to eat, he
wants to gnaw.
It's just a slightly different drive state, just showing they
have an innate drive to gnaw.
They need to gnaw, actually, to keep their teeth short
enough, otherwise the teeth just would keep growing.
All right.
So there's been many experiments on
the cat on this behavior.
And one of the questions was how necessary is the
hypothalamus?
They found sites, they would implant the midbrain area,
especially the central gray region, and the limbic
midbrain areas that we've talked about before.
And they could elicit these behaviors, these motivational
states from there too.
So they tried actually eliminating the connections
between the hypothalamus and the midbrain.
They did just a certain section of the hypothalamus.
So all the fiber connections are gone.
Now the hypothalamus can still communicate with the
pituitary, and influence secretions, the endocrine
system, by way of the pituitary glands.
But they couldn't influence the motor system at all
through the midbrain, lower brain stem.
And they found that they could still elicit this behavior
from the midbrain.
Without the hypothalamus, there was reduced initiation
of these kinds of behaviors when the cat wasn't being
electrically stimulated.
Presumably, the fore brain now couldn't influence the brain
as it would normally, since a lot of the influence is by way
of the hypothalamus.
Now, I just want to briefly mention this because we know
the hypothalamus and the axons running through the
hypothalamus are--
we've mentioned two kinds of things they're important for,
drive and reward.
To get habit learning, which is a special role of the
corpus striatum, you need feedback from the response
that indicates that the response
worked, it was rewarding.
And this involves axons, the dopamine axons, that run
forward in the medial forebrain
bundle to the striatum.
They come mainly from the ventral midbrain.
But then we also know you can stimulate that area and get
these drive states, which we think involves mainly
descending connections.
And you can separate the drive and the reward
aspects of the behavior.
You can prove that they, in fact, involve different axons.
And that was done in a very interesting way using the
different refractory periods and different sizes of axons.
What we mean by the refractory period?
Any of you physiologists?
If you stimulate an axon, it won't respond for a very brief
time after you stimulate it.
That's called the refractory period.
It recovers pretty fast.
But how fast it recovers depends on the size of the
axon primarily.
So if the axons are a different size, they'll have a
different refractory period.
Here's where I need my Tablet PC.
So let's say here's your line you're recording.
And you stimulate with pairs of pulses--
I'm, of course, slowing it down a lot here--
you're stimulating with these little pulse pairs.
Now, if those two pulses are acting like a single pulse,
you'll get a very different affect than if they're
interacting like two separate pulses.
Well if they're real close together, they second might be
within the refractory period of that axon.
So we can separate different axon populations by using
pulse pairs.
We'll make them very close together, and they we'll
gradually separate them.
And they find that if the intensity of the drive
elicited that it will suddenly change when you separate the
pulses by a certain amount.
The amount of reward the animal gets in the learning
experiment will change with a slightly different interpulse
to interval, indicating different axon populations.
They're a different size.
Basically, the reward depends on one's projecting forward
from the midbrain, drive is mainly to the descending axon,
we go into the midbrain and lower down.
So class 28 just continues with that.
Now I'm going to talk a little bit more specifically about
cell groups in the hypothalamus.
And then the Papez circuit in the limbic inbrain.
We've mentioned limbic inbrain structures a number of times,
so you've certainly been introduced to these things.
But some of this will get a little hairy because there's a
lot of structures.
So if it's something I've mentioned many times before,
you should start to learn it.
If it's something I mention for the first time, just try
to follow it and you will know by later on which are really
important enough for you to remember.
Eventually, if you stay with a topic like this and you study
it, you get familiar with all of it.
I'm also going to talk about the connections between limbic
and non-limbic system structures.
We'll talk about limbic forebrain activity and mental
states in human beings.
And we'll then review some of the major pathways.
Now, part of the hypothalamus can be divided into multiple,
distinct cell groups.
That's the medial part.
The lateral part is very different.
It's all the axons in medial forebrain bundle with cells
scattered among those axons.
Now we can separate functionally these different
groups of cells in the lateral hypothalamus too, but it's
much harder to do anatomically than in the medial
hypothalamus.
And this fellow, a biologist, Le Gros Clark, was the first
to do this for humans in 1936.
This is from one of his pictures.
He's taken really a sagittal section through the human
hypothalamus.
Now, it doesn't look too much like the brains we've been
looking at.
This is thalamus up here, hypothalamus down here.
There's the stock of the pituitary, which he's cut off.
And sort of scrunched up there next to it is showing the
optic chiasm.
And he's shown mammalary nuclei,
there's a number of them.
He's grouped them together here.
Mammory bodies, its protrusion of the caudle end of the
hypothalamus.
And then going forward near the
pituitary, the arcuate nucleus.
And then just above the optic chiasm, supraoptic nucleus.
And then the more dorsal part, austerior hypothalamic
nucleus, ventral medial nucleus,
paraventricular nucleaus.
Now, these two nuclei, paraventricular supraoptic are
the nuclei that their axons secrete neurohormones into the
bloodstream, and they release from here in
the posterior pituitary.
Now, this is a lot easier to understand.
This would be one of these small rodents, another
parasagittal section.
Here's the posterior pituitary, the anterior
pituitary would sit under here like this.
This is the position of an antromedial hypothalamic
nucleus, mamillary body in back.
The optic chiasm there.
The anatomy is a lot easier.
The ventral tegmental area where those dopamine cells are
that send axons forward into the ventral striatum,
especially, and also into the parts of the cortex.
That's right here.
That's the base of the midbrain.
And this is a picture I showed you a long time ago.
So you can see here how the medial hypothalamus looks.
In this case in a rat, you see how some of these cell groups,
there's the arcuate nucleus.
There's the ventral medial hypothalamic nucleus.
It stands out very clearly.
Whereas here, the lateral hypothalamus just cells
scattered out among the axons there traveling in the bundle.
That little white area there is a bunch of axons that are
coming from this structure up here.
Here's the same axons up here.
This is the campal formation.
Many of these axons are going to cross to the other side,
others are going to go forward down through in front of the
thalamus, then they will continue back again, and many
of them are terminating right here.
But the ones that are still up there in that bundle are going
to terminate in the mamillary bodies and in the midbrain,
the limbic areas of the midbrain.
Now, we've mentioned how things in the bloodstream can
affect hypothalamus.
And there's a hormone related to blood volume, or state of
hydration, called angiotensin II, that
circulates and affects--
has to reach cells in the hypothalamus.
But we also know it's a protein, and it should be too
large to go through the blood-brain barrier.
And in fact, it is.
It doesn't get through the blood-brain barrier.
And yet, it influences the brain.
So how can this happen?
It happens in this region called the subfornical organ,
and this is an illustration from the Nolte textbook on
human brain.
And he's shown here a midsatchel section.
Here's the ventricle, ventral coming through the midbrain,
into the hindbrain, here's the third ventricle.
And then the lateral ventricles would
be out to the side.
Here he's showing this very thin membrane that's become
choroid plexus here, at the top of the diencephalon.
And the blood-brain barrier's very weak there.
It's also very weak in one little region here, right
below the fornix fibers, fibers coming from the
hippocampus.
There's another area here, and it's also true in the area,
this area called the--
well, the choroid plexus, the fourth ventricle, and then
further back, the area postrema.
This is where toxins in the blood that can reach the brain
and elicit through hindbrain circuits, they can elicit
vomiting by a pretty rapid effect that depends on these
toxins getting through the blood-brain barrier.
Now, there are experiments on this.
This is a section from the median eminence region in the
hypothalamus.
It's this region right here.
I don't know if he labels it here.
Well it's this region here.
So this is the median eminence, right near the stock
of the pituitary.
And this is a frontal section.
And the experiment was to inject horseradish peroxidase,
which is a fairly large molecule, a protein, from the
horseradish plant.
And they inject it in the blood, and here you can see
it's all through the capillary system here.
But it's not coming out into the brain because of the
blood-brain barrier.
But right there on the median eminence it is coming out.
It's leaked out into the tissue, it's filling the
interstitial fluid of that region.
And that kind of experiment is a very simple experiment to
reveal these areas that I was talking about.
So that's how the selective, weaker areas of the
blood-brain barrier, or how it works, to get the brain to
respond specifically to certain kinds of molecules.
Just a little more about sensory inputs to the
hypothalamus.
We've mentioned how these limbic system structures get
visceral afference.
They also get inputs that signal pain, taste inputs
reach the hypothalamus.
There's a pretty strong projection from the nucleus of
the solitary tract in the main brand.
And we know that that nucleus gets a lot of afference of the
vegus nerve.
So the vegus isn't just a parasympathetic nerve that
carries output from the brain to the various
organs of the body.
It actually distributes very widely to structures of the
thorax and the abdomen.
But it carries input going in the opposite direction too,
carrying afference from the stomach, for example, and from
the intestines, from the heart region.
Well it turns out, there are more direct pathways carrying
input directly to the hypothalamus.
And some of this has been discovered by physiologists.
This paper, I put there, Geisler, very simple study
using physiology primarily, and then it was followed up
with anatomy showing these kinds of projections.
The hypothalamus has developed a number of direct connections
with the spinal cord going in both directions.
We're talking here about the afference, the sensory inputs.
There's also inputs going from the
hypothalamus down to the cord.
For example, control urination depends on a direct pathway.
How does that give us
voluntary control of urination?
Probably by way of connections from the prefrontal cortex to
the hypothalamus.
That's the only area of our neocortex that connects
directly to hypothalamus.
And now we know that there's a direct pathway from that
region, hypothalamus, to the cord.
I'm going to talk now about a pathway that was first found
by a guy named James Papez.
I'll give you that story in a minute.
He described an interesting circuit that starts with--
you could start various places in it-- but if you start with
a singular cortex, which projects the hippocampal
formation, we know the hippocampal formation projects
to the hypothalamus.
And the caudle end of the hypothalamus, mamillary
bodies, project back up to the cortex by going to the
anterior thalamic nuclei, which then project to the
singular gyrus.
So it forms a complete loop.
And this is how it was first described.
Papez was a neuroanatomist.
In 1937 he published this paper called "The Proposed
Mechanism of Emotion." And it's interesting because it
was a pretty accurate paper, even though many of the
connections he was talking about weren't very certain
because we didn't have very good experimental techniques
to demonstrate them at that time.
That was before Nauta invented the silver stains for tracing
axons by following degenerating fibers.
Here was Papez's argument.
He pointed out, first of all, that even though we called a
group of structures in the inbrain, the rhinencephalon,
the nose brain, associated with the olefaction.
He said, in fact, they're not dominated by olefaction in the
higher primates, including humans, and he presented some
evidence for that.
These are mostly medial structures in the hemisphere.
He said they were associated with feelings and emotions,
and he cited a number of clinical cases.
People with lesions, people with seizures that affected
those regions.
But with changing isn't their olefaction all the time.
Sometimes olefaction is affected.
But what dominated these cases was changes in emotion.
He also noted that a number of people had pointed out that
the threshold for seizures is lower in those structures and
in other regions, and that he mapped out an entire circuit
involved in such seizures.
So we assume these structures had to be highly
interconnected.
And that became known as his Papez circuit.
And that circuit, which we'll review right now, it's been
expanded to include other structures.
We now group into the so-called limbic system, which
was a term based on Paul Broca's term, the
great limbic lobe.
And then brought back into modern neurology by this
fellow Paul MacLean who was working at the NIH in the
middle of the last century.
So why do I even bother with such an old
thing as Pepez circuit.
There's been a revival of interest in this circuit
because of the importance of the hippocampal formation and
spatial memories.
And in humans, that role in spatial memories, extends to
the formation of long-term memories for specific events,
not for habit memories, procedural memories that
depend on corpus striatum.
But when we remember that a certain thing happened
yesterday at a certain time, I mean that depends on--
this structure plays a critical role in the formation
and recall of that memory.
So that gave a special importance to the anatomical
studies that I'm going to describe now.
This is a medical school text--
sorry--
this is a medical school thing.
It's easy to get upset by these medical school texts.
This is a schematic picture of the human brain.
I wouldn't expect it to be very clear to any of you.
This is obvious.
There's spinal cord, there's the pons.
And that sort of looks like midbrain.
But what is all this stuff?
Well, the hemisphere, remember, has
become huge in humans.
And so they tried to make these illustrations that are
half way realistic, and so they're showing hemisphere
pictures, hemisphere sort of superimposed on the upper
brain stem.
And yeah, the whole Papez circuit is there, but not too
easy for you to figure out.
So I want to go back to something closer to these,
easier to understand schematic diagrams.
I'm going to show you how now I'm going to get a more
realistic sketch.
Here's what I'm going to do.
First I'm going to turn around, so
rostral end is this way.
And now I'm going to cut off the two hemispheres where I
show the red mark.
And then I'm going to throw this one away.
And this one I'm just going to pick up above.
Pull it up towards you, because we're going to look at
it from the left side.
You can do it for a hamster or mouse brain.
Now, it looks a little complex, but you can forget
about all these words right now.
Just imagine now, here's the hemisphere, there's the
olefactory bulb.
Here's the hemisphere.
Here's where the internal capsule is.
So remember, I cut it off here--
sorry, right there.
So now all these fibers going between thalamus and
hemisphere are just cut off there.
So that's what that is right there, it's cut off.
And these are all up in the hemisphere.
We had to sever the two hemispheres from each other
along the base here.
That's basal forebrain.
Everywhere else, we can sort of pull the hemispheres apart.
They're separate.
One there, one there.
But at the base there they're together.
And there I'm showing the hippocampal formation where it
sits in these rodent brains, sort of an infolding of the
caudle and dorsal part of the hemisphere.
If you ignore the corpus callosum there which forms
later, you can treat all of this as an infolding of the
hemisphere.
And there you see fibers from the hippocampus
coming to this region.
And then in order to cut the hemisphere off, I had to cut
this bundle of axons, so right there I've
severed that bundle.
That's the fornix fibers coming from the hippocampus
and going into the hypothalamus.
There you see the connections in the hypothalamus.
There's the mamillary bodies, the longest connections.
Now we can trace all of Papez circuit, as I've done here.
So let's start down here.
Here's the fornix fibers.
Here they're coming into the mamillary bodies.
So I'm ignoring the other connections here.
It connects heavily into the hypothalamus.
Now, the mamillary bodies have a projection into the brain
stem, but the one we're interested in here goes to the
thalamus, the anterior thalamus.
Those cells send their axons out through what we call the
anterior thalamic radiations, and they go right up into the
singular cortex.
To all this cortex.
Different parts of these nuclei connect to all of this
cortex, from way up here, all the way to this posterior part
that we call a retrosplenial cortex back here.
These structures there project to the hippocampus,
hippocampal formation.
Now, a lot of those come by way of the entorhinal cortex.
This more ventral part here.
Some of them come from further up the retrosplenial area.
The hippocampus then has a major root that goes out
through these fibers, and there's where I've cut if off.
So you can pick these axons up again here, right back to the
mamillary body.
So there's your simple circuit, Papez circuit.
Notice all these structures here, cingulate hippocampus,
you can all see on a medial view of the hemisphere.
So this whole region here is the limbic system.
When you get further from the area, we're up
in neocortex there.
Now, let's show it in a circuit diagram.
Here's our mamillary body, so this is hypothalamus.
There's the rest of the hypothalamus there, heavily
connected with the septal area right in front.
There's the septum in between the two hemispheres there.
Here's the projection into the brain stem, the hindbrain.
And here's the projection up into the thalamus which then
goes to singular cortex.
Now, Papez just showed singular cortex projecting the
hippocampus.
Actually, that connection goes by way of what we call
paralimbic areas, especially in humans, the one that's most
important is the entorhinal cortex, which in our previous
picture is this.
That's the most important one in humans.
And some people would include these as part of the
hippocampal formation.
I've shown here this is hippocampal formation that
includes the hippocampus cells themselves, the parametal
cells, the hippocampus, is just a one
cell layered cortex.
And the subiculum is really part of it.
It's the output part.
The dentate gyrus is another part of it.
And the dentate is so important because it gets a
lot of this input from the entorhinal area.
But so does the subiculum, which is a two-way connection.
Now, and then that then projects the most direct
connection back to the hypothalamus is this one, the
long fornix fibers.
And then here are the shorter connections through the septum
and hypothalamus.
So there's Papez circuit.
I've underlined in red Papez's orginal structures.
Just want to point out that there's two major inputs and
outputs in that circuit.
One is down here in the brain stem.
The other one is up here, and there are a number of others,
but these are the ones I think are the most important to
discuss, the tegmentum nuclei, the midbrain.
And here, two-way connections between the cingulate and
other paralimbic areas, including entorhinal cortex.
And the association areas of the neocortex, which are
critical for our highest functions, like language, for
example, and many other cognitive functions.
So now this starts to look a lot more interesting, and we
can talk a little more now about the
functions in these areas.
I want to ask what's the functional significance of
this pathway coming from the hypothalamus
back up to the cortex?
A discovery by physiologists, and this discovery has
happened since I first learned about all this.
I first learned Papez circuit from Nauta and discussed the
anatomy without knowing what these axons were doing coming
from mamillary bodies.
In fact, I wondered what is this connection?
It's a two-way connection between the mamillary bodies
of the hypothalamus, and [INAUDIBLE] hindbrain.
That has become clear from physiological studies that
they signal direction of the head.
So why is that so interesting?
Well we know the role of the hippocampus in spatial memory.
I've got a map, it's there in my hippocampus, of this room,
and all of you, and the windows, and the door.
I have a rapid escape route if I need to get out.
It's all there in my hippocampus, right?
Now, if I turn my head in any way, I'm shifting my position
in that map.
The map is staying the same, but where I am and what I'm
going to do in it is shifting every time I turn my head.
For the animal to be able to do that, he's got to know the
direction of his head.
So how is he getting that information?
How's he learning about the direction of his head?
Part of the information here comes from the vestibular
system, signaling the direction of a head.
And we can record cells here that signal head direction,
cells here.
We can find them in the singular cortex, we can find
them right in the hippocampus.
So I think it's a way to anticipate
direction of movement.
All you need is head direction and information about
locomotion, and you can update your map to the environment.
So you need head direction.
It's critical information there.
Beyond that, it's a little more speculative.
The role of the hypothalamus in updating this internal map.
I think the hypothalamus probably adds an activation
component that affects the priorities we get for what
we're doing in that environment.
And I'm just pointing out here that the hypothalamic cells
that receive the hippocampal output might be separate from
the ones that project to the anterior nuclei.
These are details that--
a lot of details like this remain to be worked out.
And of course, the hippocampus is sending information there.
Not just to the mamillary bodies, it's sending
information throughout the whole hypothalamus.
And it could very well be altering the level of various
drives, depending on the location.
This is I'm going to show you some sections of the brain,
and we'll find out where these structures are.
But time isn't here.
I think we're right at the end of the hour.
You can look at these.
They'll be online.
These are sections of an embryonic human, or a rodent.
Most my knowledge comes from rodent.
And I've drawn the midbrain.
And then these levels in the embryonic brain, remember,
this is a top view of the brain stem here, and then a
horizontal section of the inbrain, and I've shown five
levels of section.
And then I've pictured what they look
like in these pictures.
And the abbreviations for all those occurs in this here.
Do I expect you to memorize it?
No.
But if you read it, get familiar with the names, you
will start, some of the major ones you will get to know.
Some of these, for example, hippocampus, pay attention to
where that is.
There it is up there.
There it is back there, the caudle into the brain.
Of course, neocortex.
Neocortex and the hippocampus you should certainly know.
Major picture here, between brain, hypothalamus below,
thalamus up above.
Then basal forebrain below.
The more dorsal striatum above.
Basal forebrain includes the ventral striatum.
And then the more dorsal striatum there.
That's the septal area right on the midline, getting--