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PROFESSOR: All right, today we're going to talk about the
corpus striatum, and we will finish that next time with
some discussion of the treatment
of Parkinson's disease.
And then finally we will be going through the neocortex.
I want to say something important, especially for the
people listening to this and not coming to class that--
and I know you've depended on the chapters that I've written
for the book, and they are fairly close to the lectures.
So there is some material in the lectures
that doesn't overlap.
The main things are covered in both.
I haven't written the neocortex chapters yet, so I
will probably finish the first one and it will be posted
since I'm more than halfway through it right now.
So after that, you'll have to come to class in order to
learn the material, although we will post the notes as
before on the web.
To talk about striatum, I like to start with the evolution,
beginning with the position of the early striatum as a link
between the olfactory system and motor control.
In this diagram here I show it, the olfactory bulbs here
is one of the two new inputs that came in at the very head
end of the animal.
They both came into the forebrain.
Detection of light, detection of odors and there were
probably other chemical senses that came in through the
terminal nerve that are less important for
most mammals now.
Here I show in this little neck between the olfactory
bulbs and the diencephalic region and originally that was
mostly the pituitary and the hypothalamus attached to it,
and also the epithalamus at the thalamic region where the
pineal was located.
You see those kinds of things even the
most primitive chordates.
There was a link in this region.
The olfactory bulbs had a few projections right into the
hypothalamus and between brain, but most of them went
through a link in this region.
And I think that was of great important, because
of what it led to.
I show it here following a polysynaptic route into the
hypothalamus, which then projected into the midbrain.
That would correspond to what physiologists call the
hypothalamic locomotor region, controlled approach and
avoidance movements.
I also show a link going through the epithalamus.
I point out here that the function of these projections
into that hypothalamic region were of course in inputs,
influences on the endocrine system, motivational states of
the animal.
It controlled the inherited action patterns of the
animals, the fixed action patterns, the instinctive
movements and controlled those kinds of movements through its
connections to the midbrain.
And that's still important in most animals.
It's only more recently among the mammals that connections
bypassing the midbrain have become so important.
So the outputs to the midbrain were very important, though
most of them probably went through hypothalamus and
epithalamus originally.
And these controlled locomotion, they influenced
orienting movements which didn't really depend on those
inputs, but they modulated those inputs.
What the animal was smelling would affect what it was
sensitive to in its environment.
And similarly what it would grasp--
now I said that later they're grasping
with mouth or forebrain.
You don't need to control grasping by the forebrain.
The animal will grasp with its mouth in response to inputs
coming through the hindbrain, the meta sensory inputs
through the trigeminal nerve.
And grasping similarly is affected by its meta sensory
inputs and of course by visual.
But why then were the links through this striatum, why did
they evolve at all if you didn't need
them for those things?
I think it was this reason.
That that link was modifiable.
Weren't the links through the tectum modifiable?
If you get input from the tectum that causes orienting
movements, was that a modifiable link between the
input and the output?
Can anybody say anything about that?
What kind of learning can we show if
we just have a midbrain?
Remember you can take out the forebrain on a pigeon and it
can still fly, it can still land on things.
It shows its instinctive movements, it orients, avoids
vertical stems and tree limbs and so forth, and yet lands on
the horizontal ones.
It will do that just by its midbrain connections and
connections from there to the motor system.
What was different about the learning here in the striatum?
That was a big issue.
It was different because it was an involved feedback from
the consequences of action that could change a connection
that had been activated a little bit earlier.
When you get a reward, it affects the probability that
you'll repeat something that was caused by input that
happened earlier, before the reward occurred.
That's called reinforcement learning and that was quite
different from the kinds of learning that was happening in
the spinal cord, in the brain stem and midbrain.
At least that's what we think.
And these reward mechanisms, in most animals that have been
studied, used dopamine pathways.
It's interesting that you find dopamine as the only one
monoamine in the earliest chordates, like amphioxus, is
you don't find norepinepherine, you don't
find serotonin in those most primitive animals.
So where were the dopamine neurons that could respond,
that could provide that feedback into the endbrain?
They were, in most animals, in the posterior tuberculum
That's part of the hypothalamus.
We don't have that in mammals.
We don't have many dopamine neurons there, because they're
just caudal to that now in mammals.
And it's a little bit uncertain relationship between
the ventral tegmental area and the substantia nigra, where
you find all the dopamine neurons in mammals and the
posterior tuberculum of the fish, and also amphibians as I
point out here.
It's sharks, skates and rays, it's in the midbrain just like
it is in mammals.
And here I point out the finding that, when we
mentioned this, we mentioned that when we studied the
gustatory system, the taste system.
Inputs come directly from the hindbrain into that region
from the taste system, even though they haven't been
emphasized in modern studies.
You don't find what you don't look for.
So let's look at connections that support this story that
I'm talking about.
Here's the diagram that shows cortex up here, here is the
caudate and putamen, the outer part of the corpus striatum.
Here's the output side of the corpus
striatum, the globus pallidus.
This is the part of the thalamus that projects to
motor cortex.
And here in the midbrain in the ventral midbrain where
those dopamine cells are located.
Of course there's a lot of cells there besides the
dopamine cells.
And in red there, they show the dopamine axons diagrammed.
They also show other outputs of the nigra there, going into
the thalamus, going to the superior colliculus.
We'll talk more about these other pathways in a minute.
Now that picture is a medical school text picture, the one
I've given a few readings from, by Per Brodal.
The next big step in striatal evolution was non-olfactory
inputs coming in.
And in the diagram, which you can sort of see there, I show
inputs coming from the dorsal midbrain.
The midbrain tectum coming into the dorsal thalamus and
projecting from there in the striatum.
And along with that, this is more than just
a little neck now.
It's becoming a bigger bump.
This is the endbrain starting to expand.
And it wasn't just striatum.
There were inputs going to the pallium, too.
So are there connections like that in
modern mammalian brains?
That's the question here.
There should be.
I mean, I've made up this story from evidence.
Here is a picture again from Brodal showing one of the
nuclei of the old thalamus, the parts of the thalamus that
have the more diffuse projections, called the
centromedian nucleus.
It's the largest part of the so-called intralaminar nuclei
of the thalamus in large primates.
The next picture will show a similar nucleus in rats.
And it shows this cell group projecting main forward
projection into the caudate and putamen.
It also shows the nigral projections there, the
dopamine axons coming into the caudate and putamen.
And then it shows the cortical projections that came into the
caudate and putamen.
Well in this earliest period we're talking about, the
cortex wasn't very big.
It wasn't very specialized.
It was mostly sort of this dorsal cortex we call it, you
still see that in fish and other non-mammals.
It tends to be polymodal, not very big.
But this projection and the old thalamus coming into
striatum is probably more important, but only early on.
In modern mammals and in us, it's this projection from the
cortex that's become the most important in the inputs into
the caudate and putamen.
I brought a few pictures of what these neurons look like.
This is a neuron labeled there, PF.
It means parafascicular nucleus, which is similar to
that centromedian.
It's the [UNINTELLIGIBLE]
intralaminar nuclei in the rat.
And it shows its axon going out of the thalamus, through
the internal capsule that's the axon here.
And it's got a lot of termination in
the caudate and putamen.
You also see collateral branches here and in the
globus pallidus, and some of them even coming back into the
subthalamus and the substantia nigra in the midbrain.
But note also that the same axon has a branch going right
up into the cortex.
So it went to both pallium and subpallium, although the more
important projections of many of these axons is the one to
the caudate and putamen.
Here's another one in this particular picture, they
weren't able to draw the cell body, so they just indicated
where it was, where it would be if they could see it.
It's very difficult to do these studies because these
are from Golgi preparations or sometimes they filled this
cell with a dye and these axons cover
many different sections.
So it's very difficult to cut one section, even if you make
it very thick and get that whole axon.
It's possible to reconstruct it, but that can require so
many sections.
Without special software that's very difficult.
Such tracing has never been made automatic.
But there you see the axon coming out of the thalamus,
arborizing a little bit in a nucleus that surrounds the
thalamus called the reticular nucleus that has feedback
connections into the thalamus, and there it is arborizing in
the caudate or putamen.
In the rat, we just call it the caudate putamen or the
caudal putamen, because there's no real internal
capsule in those animals.
The axons coming through the corpus striatum are sort of
scattered in a lot of little bundles going through.
So here it is our rising in the corpus striatum and then
it continues right up into the cortex.
In this case, the motor cortex, where it arborizes in
the cortex.
So again, both pallium and subpallium coming from this
older part of the thalamus.
I just want to point out--
I just added this this morning, that both of those
cell groups with those axons that go to both the striatum
and the pallium, the neocortical part of the
pallium, in mammals receive inputs from
the midbrain tectum.
I've traced them myself in the hamster.
Especially the deeper layers of the tectum project pretty
strongly to these parts of the thalamus.
Now here's another neuron--
one more picture here-- a neuron in the thalamus that's
not in the intralaminar, it's in part of the newer thalamus.
But it's a part that adjoins the ventral nucleus that gets
some meta sensory input, and then just caudal to adhere the
medial geniculate body and up here, the lateral geniculate.
It's right next to those cell groups that get single
modality input.
These neurons tend to get multiple modality inputs.
You record from them, you tend to get at least two, sometimes
three modalities that they respond to.
They have similar axons, axons that arborize in both the
caudate and putamen.
And up in the cortex in this case, in the parietal lobe, in
between visual and semi-sensory areas.
All right.
So the next stage then was with this new input, there was
further expansion of the endbrain.
And I'm showing that as an enlargement here of the
striatum, and now the pallium is thickening, too.
And as those developed, their outputs became more important
in controlling behavior and then finally as you got into
the evolution of mammals, that expansion continued and became
very massive.
And what I'm showing here is a projection we'll consider
further later in the class.
An output of the striatum, and now we're talking about
striatum, not the olfactory parts of the striatum, the
non-olfactory parts projected into the thalamus, a part of
the thalamus that projects up to the motor cortex.
So now the outputs of the striatum are changing too, not
just those inputs.
In the previous stage I'm showing the old outputs were
still the most important, but in mammals, they're not as
important anymore.
Now the main projection of this of the corpus striatum in
order to control output is through the cortex.
The cortex has become the dominant structure in
controlling movement, particularly fine dexterous
movement for actions where learned habits are important.
So let's see where these things are.
I've taken a little rodent brain here and here's the most
rostral section.
You see the ventricle in the middle there.
So there's the pallium around the outside, and you can see
the ventral part has thickened a lot.
That's the striatal part.
You see where the hippocampus or medial pallium is in these
sections, there, there, and there, on the medial side.
And in blue and in red I've outlined the dorsal striatum
and the ventral striatal structures.
That ventral striatum was the earliest in evolution.
That was where the olfactory inputs came in.
And in fact, the olfactory bulbs still project to the
surface layers down here and here.
And then here's where the non-olfactory inputs came in,
initially from the thalamus, as we've seen, but now even
more from the cortex.
And here we go caudally, here we are in the temple lobe,
that's position of the amygdala, which can be
considered part of the striatum
in the way it functions.
Here we are at the very caudal pole of the hemispheres
related to the amygdala.
And if we look at the hemisphere from the medial
side, here we sectioned all the axons connecting that
hemisphere to the brain stem.
So here's the hippocampus, with its fibers going out.
Here's where we've cut them off.
And that would be the position of the
striatum, the dorsal striatum.
There's the ventral striatum in the amygdala area.
And by comparing the hemisphere, here's the three
levels in that hemisphere picture that correspond to
those three sections.
I've also indicated there where various parts of
neocortex, where the edge of the motor cortex would be.
Most of it would be not seen from the medial side.
You'll see a little bit of it, same for somatosensory and the
visual cortex.
Auditory cortex would be completely on the other side
there, on the lateral side.
That's all important because the important inputs coming in
to the striatum is from those cortical regions, also
important inputs into the hippocampus.
OK, so when Nauta points out that a major output at the
extrapyramidal motor system is the pyramidal system, all he
means is that the striatum which is a major part of the
extrapyramidal motor system.
Actually its major output now reaches the pyramidal system
by way of that connection through the thalamus to the
motor cortex, which we're going to take a look at.
And we'll look at the other connections.
Here I've got a very simplified diagram that shows
neocortex up here.
Then we have the limbic endbrain and the dorsal
striatum, and how they each connect to the neocortex, the
dorsal striatum by way of the thalamus as a major connection
to neocortex.
And then the very different kinds of outputs--
the neocortex has the most extensive outputs directly to
the spinal cord and brain stem.
The limbic structures have shorter connections, mostly
the longest connections are to the hypothalamus, not many
further down, a few to the midbrain.
That picture is really based mostly on
neuroanatomy of primates.
It doesn't represent earlier stages of chordate evolution
and has nothing about ventral striatum really, which is just
lumped here with the limbic endbrain.
That characterization of ventral striatum--
I may have pointed this out before--
wasn't really conceptualized until about 1975, when people
realized that these more ventral structures were really
part of the striatum.
It was called the ventral striatum by Heimer and Wilson
here at MIT in 1975.
So I've presented here another diagram.
It looks pretty complex, but I've simplified it as much as
I can, separating the whole system into limbic and
non-limbic.
So I've got limbic cortex at the top and neocortex at the
top, separating them by the colors.
And then below it I've got the major subpallial structure,
the dorsal striatum on the left and the ventral striatum
on the right there.
And then the major inputs coming from thalamus and from
hypothalamus.
Now notice the outputs, how different they are.
Neocortex, with the long outputs to spinal cord,
hindbrain, midbrain, and also to the thalamus, which I don't
show, because these are two way connections between
thalamus and neocortex.
And then here's that major connection to the striatum
from neocortex, and from striatum to thalamus, which
then goes back to cortex.
But now look at them from the limbic system.
It's dominated by these shorter connections.
You don't have any connections from limbic cortex down to the
spinal cord.
The longest connection would be from hypothalamus to the
spinal cord.
I don't even show it here, because these aren't major,
dominant connections in most animals.
In fact, they've only been known in recent studies.
The dominant type of connections are the kinds that
I'm showing here.
I've indicated there that there are some polemic
structures where these two are not so clearly separated.
That's because the parts of the thalamus, the medial
dorsal nucleus, also the anterior nuclei have
connections.
They're limbic in many of their inputs but they project
to neocortex.
Also the neocortex does have some connections to
hypothalamus.
So that's where I'm indicating the cross talk.
Do you remember which part of neocortex has these
connections to the hypothalamus that sort of
violates this separation?
The cortex just above your eye sockets, the prefrontal cortex
just above the eyes there.
The orbital frontal cortex.
That would this cortex that projects directly there.
OK let's look at how we've see these kinds
of connections before.
We've talked about lateral and medial forebrain bundles.
It's really the same thing.
This is lateral forebrain bundle here on the left, these
are the medial forebrain bundle axons on the right.
So here are some pictures of the endbrain and the
'tweenbrain.
There you see the origin of the medial forebrain bundle,
the limbic system components, and here it's getting
connections from the olfactory cortex.
Here it's getting connections from the ventral striatum and
from hippocampus.
And then here's dorsal striatum, and it's as well as
both dorsal striatum and neocortex are contributing
there to the lateral forebrain bundle.
And I'm consistent there in using the
blue color for those.
And then here in the 'tweenbrain, I've outlined on
one side here the medial forebrain bundle related to
the limbic system in red.
I've not used the blue there, but these are the lateral
forebrain bundle axons up here.
We've seen this before, I'm just summarizing major origins
in the major course of these two pathways.
From lateral forebrain bundle, from the corpus striatum, the
outputs to the corpus striatum, the
dorsal part at least.
And then through the internal capsule coming from the
neocortex, and then enters the cerebral peduncle and follows
the pyramidal tract all the way down to the cord, but on
the way projecting to all level.
Then the medial forebrain bundle from olfactory cortex,
various cortical areas we call limbic.
And then the subcortical limbic endbrain structure is
the amygdala and the basal forebrain.
The outputs come from the pallidal components there
which we'll talk about a little more in a minute.
And then of course from the lateral hypothalamus and
limbic midbrain areas.
Now some textbooks have tried to simplify that a lot more by
not considering the connections except the most
dominant ones in the primates.
So they just omit many of the diencephalic connections to
the hypothalamus and the ventral thalamus.
They focus on neocortex, striatum, and midbrain.
And in fact, I've added the midbrain connections here, and
I've added the dopamine axons.
So there's the cerebral cortex, there's the striatum,
and I've added dorsal striatum, because many
textbooks don't even consider the ventral striatum in these
kinds of pictures.
Why is that?
Because the dorsal striatum is dominant for the kinds of
movements that usually get disturbed in human
pathologies.
So they focus on that.
And there you see the outputs to the pallidum, that means
globus pallidus, then to the substantia nigra.
Pallidum is actually a more general term, and we'll see
here in a minute, there's a pallidum part of the ventral
striatum, too.
In fact, there's several different palladial
components.
And then you see the pallidal input to the thalamus, which
goes up the motor cortex.
And there's also connections like that from the nigra.
And both the pallidum and the nigra have connections into
the midbrain.
The pallidum to the caudal midbrain.
The nigra gets input from the striatum and projects to the
superior colliculus.
That's how the striatum is affecting orienting movements
and locomotor movements most directly.
It doesn't need the cortex for those influences.
The ansa lenticularis is a term you encounter when
reading about the striatum.
That's just the name for one of these connections that
we're talking about.
It's the name for this connection here, that goes
from the pallidum to the thalamus.
So we'll see why it's called that.
Ansa means handle, and it's the handle of
the lentiform nucleus.
Well, what the heck is the lentiform nucleus?
Well, it refers to the way the thing looks in a cross-section
or in a dissection of the human brain.
So let's just look at that.
It's really just more names for things we've already
talked about here.
OK here, I'll make that a little bigger
so we can see it.
This is human brain.
What kind of a stain is that on the right side?
What are we staining for?
The cells?
Fibers.
What are we staining for to get the fibers so black?
We're staining for myelin.
So this is a myelin stain, commonly
used in human pathology.
In fact, they often use a stain that stains both one
color for cell bodies and one color for axons.
Neither of them are very sensitive but they're good
enough for picking out major problems in the brain.
Here is the lentiform nucleus, the lens shaped nucleus.
This is the putamen.
Here's the internal capsule there, as we pointed out here.
So this is all internal capsule, these fibers coming
through the striatum.
There's the putamen.
There it is there.
These cells out here actually are not part of the putamen.
There's a fiber layer between the putamen and most cells
that's called the claustrum.
They're sort of cells that form like the deepest layer of
cortex except they're below a part of the white matter.
They tend to get polymodal inputs, a pretty primitive
part in the brain, and still understudied.
This is the cortex of the so-called insula, the island
of cortex that you can't see at all from the lateral
surface of the brain because it's buried
inside the sylvian fissure.
That's the sylvian fissure there.
So the ansa, the handle, here is the internal part of the
globus pallidus, there and there.
Axons go like this through the peduncle and then they come
back and terminate there in the ventral thalamus.
So I've drawn a whole bundle of them
there, by my thick line.
That looks like a handled in its shape.
Well, that's what it's called.
The axons actually when they turn are turning a little
rostrally also and going back forward.
That's the ansa lenticularis because it's coming from
lenticular nucleus which is just a name for the putamen
plus the globus pallidus.
Its meaning simply refers to the way these are grouped and
they're of course closely connected structures, because
the caudate part of the corpus striatum is separated there by
the internal capsule.
It's up there, and down here by the way also.
We'll see in a minute how part of it got down there.
This is Nauta's shmoo diagram and here he shows a neuron in
the [UNINTELLIGIBLE] motor cortex with a long axon coming
down all the way to the spinal cord, and here's one
projecting to the striatum, because a major output of the
cortex is to the striatum.
Here he shows the striatal projection to the globus
pallidus, and there's the pallidal axon coming out,
going down to midbrain, but here's its branch that goes
back into the thalamus and turns forward.
That's the ansa lenticularis, that part right there.
And here it is in the Brodal picture of the main
connections of the basal ganglia.
Now, this is an interesting picture.
I'll point out what I think is interesting about it.
First of all, there's the projection
from cortex to putamen.
There's the putamen projection to the
pallidum, or globus pallidus.
And there's the putamen connection to
the substantia nigra.
So there's the pallidal output by the ansa lenticularis into
the thalamus with the thalamus, that's a part of the
thalamus that projects up to the cortex.
And I've added to it these connections to the midbrain.
Outputs to the subthalamus and caudal midbrain controlling
locomotion, and outputs to the superior colliculus
controlling orienting movements.
It's not the only pathway controlling orienting
movements, but its influencing them.
Now the other thing about this picture, it shows you
something really important to understand striatal
pathologies in humans.
Namely, that these connections aren't all excitatory.
In fact, many of them are inhibitory.
This connection from cortex to putamen is excitatory.
I know that by their label here because they've put a
plus sign by it.
All the other connections in red that don't have that plus
sign are inhibitory.
They're using gamma aminobutyric acid as a
transmitter.
So note the putamen is
inhibiting the globus pallidus.
The pallidal cells, projecting by way of the ansa
lenticularis into the thalamus are also inhibitory.
So you're inhibiting an inhibitor.
So what happens?
If you get a lesion up here, you remove this inhibition,
what's the effect on the thalamus?
If you have a lesion of the pallidum here, you remove this
inhibition to the thalamus, those thalamic cells are now
going to respond more to their other inputs, coming in from
cerebellum, for example.
And you're going to get movement abnormalities, which
is what happens.
Similarly there are inhibitory inputs into the substantia
nigra and these projection of the superior colliculus is
also inhibitory.
So because of all the inhibitory connections, you
can't simply predict depression of function.
In fact, what happens to the notion of diaschisis When
you're dealing with these, in most parts of the brain the
long connections are not inhibitory.
They're excitatory.
And the short connections are inhibitory.
In the striatum, it's just the opposite.
So when you remove a large inhibitory connection that's
as dominant as these tend to be, you're going to get
increased excitation.
The excitatory connections will start to dominate.
That's the diaschisis effect.
See diaschisis simply means a separation into two.
You're cutting off one structure from another.
And when I first started to realize this, I was writing it
in my chapter I of course decided I better look on the
web to see if somebody else has the same notion.
I found out of course, that they do.
Fairly recent, but it is well recognized by neurologists
that this is the kind of thing that's happening.
This isn't just to make your life difficult, but to
understand the striatum adequately you need to know
that not only the substantia nigra is a close satellite of
the caudate and putamen, but so is the subthalamic nucleus.
So I've shown just how.
Here's the neocortex and thalamus with the kind of
connections we've just been talking about.
Here's those two outputs to the midbrain.
To the colliculus, by way of nigra and subthalamus, and to
this midbrain locomotor region, the part there that
gets the input is the peduncular pontine nucleus.
It's part of the midbrain reticular formation.
It gets an input from the globus pallidus.
Well note here, the nigra is reciprocally connected with
caudate and putamen, dopamine axons coming back.
And then the axons coming into the nigra from the caudate,
whereas the subthalamic nucleus is reciprocally
connected to these compliments of the globus pallidus.
They are also reciprocally connected to each other.
So lesions that affect the nigra, like the loss of cells
in the nigra in Parkinson's disease will
cause striatal diseases.
Lesions of the subthalamus, which also occur in humans
often on one side, will also affect the way the striatum is
functioning.
I've shown in the green line there, the whole striatum,
caudate and putamen and the globus pallidus.
I'm just dealing with the dorsal striatum, because
that's the important part for movement control.
This is the Brodal picture of the subthalamic nucleus, with
it's reciprocal connections to the nigra on the one hand and
to the globus pallidus on the other.
Also showing that it gets input, excitatory input from
the cortex.
So I'm just pointing out these behavioral disorders, and
we're at the end here of Parkinson's disease.
These are all disorders that show some effect of removing
inhibitory connections.
So you're getting over excitation of cells.
So in Parkinson's disease, you get the resting tremor, but
you also get a lack of initiation of movement.
That's the akinesia part of Parkinson's disease.
In Huntington's, chorea.
The word chorea means a dance-like writhing movement.
And with cell loss in the striatum, you can get these.
It's a genetic disease, you get these peculiar movement
starting to occur.
Sometimes it appears to occur spontaneously.
Hemiballism is also a very strange movement disorder, in
that the person starts to make a movement, he can't just make
a controlled movement.
Instead his arm just flings like that and he
loses control of it.
This particular syndrome, I have sympathy for because I've
had it as a consequence of low blood sugar.
A couple times, my blood sugar gets very low, I get some
striatal sign.
And one thing is if I start to make a movement, I can only
make the flinging movements, I can't make
the controlled movements.
I mean, I've gone through this for so many years, and being
trained in neuroscience, I began to
understand what was happening.
And that's actually helped me a lot.
I don't have these problems anymore because I recognize
much earlier now what's happening.
But I sympathize with people that go through this.
The big advantage of having it due to low blood sugar is you
get over it as soon as you control the blood sugar.
These poor people get it because of a lesion, and they
can't control it.
Unless there's other ways to treat it, and that's what I
want to talk about next time.
We'll finish these slides and then we'll be able to finish a
discussion of treatment of Parkinson's.
And it's related to the treatments that are being
worked out for these other conditions, as well.
That double inhibition is important to know in
understanding just what's happening when you get a
disorder where you get too much activity.
And you might want to think about, is there anything like
that affecting the limbic system, which would affect
emotion and motivation.
And I think the answer is yes, there are things like this.
But they're not as well recognized as being related to
these diseases.