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PROFESSOR: We were talking about how we know what's
connected to what.
This is where we ended last time.
And we know that doing the sections, we can see major
fiber bundles, but we can't really see where they connect.
Some of them are pretty clear.
We could follow the optic tract, for example.
We can follow it to the surface of the midbrain.
So we can be pretty sure it connects there.
But many connections are not so obvious.
And even that, we still don't know--
it doesn't tell you much about how it
connects or exactly where.
And we know we have various staining techniques.
You've seen some of those pictures.
We can stain for cell bodies, we can stain for fibers.
The Golgi go method does show individual cells, including
the enlargements at the end of axons, but we often don't see
the cells that those are touching.
And we can't follow things very far
with the Golgi technique.
The brain's just too complex for that.
And I mentioned how that's led to some beliefs in the history
of the field that were just wrong and that had to be
corrected by the use of experimental techniques that
were better than what came before.
So today, I won't to talk anymore about
electrophysiology, but I will talk about experimental
methods of tracing the pathways.
The first experimental neuroanatomical method or
technique for tracing pathways was called the [? Marquis ?]
stain.
You produce a lesion.
For example, you can oblate the motor cortex of a primate,
and you'll get degeneration of the pathway for motor cortex
down to the spinal cord.
And you can trace it because the stain is selective for
degenerating myelin.
The only trouble with that is the myelin doesn't actually go
all the way to the endings.
An axon will lose its myelin when it gets in
the terminal region.
So you're still limited.
In fact, there are some pathways and have very little
or no myelin.
So for those, we would be totally
unable to trace anything.
And it was Walle Nauta, who ended his career as at MIT
professor in the last decade of his career.
He came to MIT in the mid 1960s and retired in the '70s.
He recognized this problem with the [? Marquis ?]
techniques, and he also knew that there were silver stains
for staining axons that were capable of staining
unmyelinated fibers.
So he started working with colleagues, particularly
Gygax, on a method that would not stain the normal fibers,
suppress the staining of normal fibers, but lead the
staining of degenerating fibers.
And the way they did that was use an oxidizing agent that--
the more you oxidize the tissue, the more it gets rid
of the staining.
But the degenerating tissue was less reactive to the
oxidizing agents that they ended up using.
So if you time it right, you can get the normal fibers to
be relatively suppressed, and the degenerating ones still
still stain, will still pick up the silver.
And the Nauta methods and derivatives of the original
Nauta-Gygex method became the most sensitive methods for
tracing pathways for a number of years until tracing methods
that used axonal transport.
That is, you inject something or you get something that the
cells will take up and transport.
And then we add various methods of
looking for those axons.
The labeled amino acids were the first technique like that.
How would you label an amino acid and use it to trace an
axon pathway?
Why does it work?
Somebody?
Can you guess?
STUDENT: Isn't it some sort of radioactive thing?
PROFESSOR: You can make them radioactive in
order to trace them.
That's what the autoradiography is about.
But why does it work?
How do you trace axons with that?
STUDENT: [INAUDIBLE]
PROFESSOR: Talk a little louder.
STUDENT: [INAUDIBLE] an x-ray or something of that sort to
trace the pathway as it comes back down.
So it will be transported from [INAUDIBLE].
PROFESSOR: Actually, the amino acids won't go very far.
It's only when they get incorporated into proteins
that they'll be transported.
So what you do is inject them in the vicinity of the cell
bodies whose connections you're interested in.
So let's do the motor cortex again.
Let's inject that-- some [? are ?] labeled proline and
labeled leucine.
We can even just use tritium.
And inject them the motor cortex.
Those cell bodies, those large pyramidal cells in layer 5 in
the motor cortex will take up the amino acids.
And many of those amino acids will get incorporated into
proteins, being synthesized in most cell bodies, and they
will be transported down to the terminals.
That's what we're using in order to trace.
The proteins then become radioactive with the tritium
label, on the leucine or proline.
Those proteins will collect in the terminal.
And if we don't wait too long, so they disappear, we can see
them there by--
we'll cut the brain into thin slices.
We'll coat the sections in a dark room.
These are the Dark Ages in the neuroanatomy.
We did a lot in the dark.
And we coat the sections with the photographic elmusion.
And keep them in the dark.
And we do some extra ones so we can test to see when the
photograph elmusion is beginning to be exposed by the
radioactivity.
Of course, it doesn't show you too much detail, but at least
we'll see the silver grains over the areas where there's a
lot of radioactivity.
So that was--
we just call the autoradiographic method.
And those are still used sometimes, but not very much
because it's so easy to use other methods.
But the reason--
the biggest advantage of that method is that if the amino
acids are injected into a pathway, into the fiber
bundle, they don't go anywhere, except maybe very
short distances.
So you don't have a fiber-of-passage problem.
If you're using the degeneration as a tracing
technique, you damage an axon, those will degenerate, too.
And they will mess up your findings.
It won't just be the cells in the region of your lesion
whose pathways you're tracing.
So other techniques--
the first was HRP, horseradish peroxidase--
a plant enzyme.
It's taken up by endocytosis, when you
inject it into the brain.
If you inject it, say in the spinal cord, it's taken up by
the endings of corticospinal axons.
And transported all the way back to the cell bodies that
gave rise to those axons, that are terminating in the cord.
If you inject it in the cells up in the cortex that are
giving rise to those axons, it will be endocytosed by the
cells and, some of it will be transported down the axons.
So it can be used for anterograde tracing and
retrograde tracing.
And initially, HRP was used as a retrograde tracer.
But then the techniques for visualizing it, which were
histochemical techniques, to visualize
where the HRP was located.
They became more sensitive and people were able to use it as
an anterograde tracer as well.
And then later on., various fluorescent molecules were
discovered that acted as good tracing molecules.
And so pretty soon, you didn't have to use histochemistry.
You could just look for fluorescent lights.
And the microscope companies all started producing good
fluorescent optics, so we could use different
wavelengths of light to excite the tissue, and we could see
the fluorescent.
You illuminate with the light at an oblique angle so that
doesn't reach your eye.
But then when the cells fluoresce, you can see the
fluorescent light that's given off it still.
And some of the substances that are taken up act as very
good tracers.
They don't fluoresce.
We can link a fluorescent molecule to them.
Or we can make an antibody to them.
And those antibodies will bind to the substance--
a very sensitive way.
So if we have a way to find those antibodies where they
stuck, we can use both things as a tracer, too.
Then we're using immunohistochemistry as the
method of visualization.
This is just a little bit about Nauta.
I've written it in the chapter.
He became an institute professor in 1973.
And I said '70s, actually until the mid
'80s, he was here.
The interesting thing about Nauta is something about MIT
and in this department.
It was the department of psychology and brain science
at that time.
In fact, it was just called psychology department for a
while, even though half of what we did was brain science.
It was the first place like that in the country, to
appoint a neuroanatomist to the faculty.
Psychology departments didn't do that.
So other universities were watching MIT--
what are they up to?
And basically, the vision of the field that was being
formulated by Teuber and others at MIT became what we
now know as modern neuroscience.
So Teuber and Nauta both played important roles.
And Teuber was the head of the department.
This is a picture of Nauta.
And there are tapes by him on now dissecting the human brain
that are available at MIT.
You can borrow those tapes, look at them.
You probably won't understand too much right now, but
they're very useful as you're learning more
neuroanatomy to do it.
One of Nauta's students, Lennart Heimer produced a
shorter version of that that's more accessible
for beginning students.
It's often used in medical schools of showing the section
of the human brain.
This is just a picture of a section that I produced many
years ago and studies of visual system.
I would remove an eye to cause degeneration of all of the
axons coming from the eye.
And I was studying hamsters with early
damage to the brain.
And what do you see here?
You see all the little black grains there?
Those are degenerating axon terminals, or butons,
degenerating butons, that we could see with a modified
Nauta technique, produced here at MIT by two men--
Lennart Heimer, who was the research associate of Nauta's,
after coming here from Sweden.
And Robert Fink, who later got a degree, but at that time he
was working as a technical assistant in the lab, but he
was very inventive.
And the two of them each invented a version of a stain
that was based on the Nauta method that made it more
sensitive, and both of them could stain these terminals.
And what you're seeing here is an abnormality in the visual
system produced by the early lesion.
That was one of the early discoveries produced by the
sensitive method.
The picture of the--
we call this dark field microscopy because the tracer
can be seen as the glowing things there in the picture.
And the very bright area here is bright because it's filled
with labeled axons.
Axons labeled as HRP from the eye.
I was using HRP as an anterograde tracer here.
The optic tract travels over the surface, and then you can
see fibers penetrating in this direction, coming in from the
surface here.
Most of them are ending right here.
That's the edge of the lateral geniculate body, a few of them
[? in the baby ?] go further, which is what you see there.
And here, I've injected a fragment of the
cholera toxin molecule.
You wonder why anatomists use such dangerous things like
cholera toxin.
Actually, we used a fragment of the molecule.
We still were pretty careful with it.
But then using antibodies to it--
it was a very sensitive way to visualize the entire axon that
was labeled right up to terminals.
And here, it shows you the difference between a bright
field picture and a dark picture.
Here's the bright field picture.
You see normal axons that just look lighter there.
Here you see the edge of the brain.
There is the optic tract, at the edge of the 'tweenbrain.
Here's the hippocampus overlying.
And there you see the label, axon and axon terminals side
in the geniculate body, coming from just of the retina that
had picked up the cholera toxin fragment.
And here, you see them in dark field, where you don't see
much else, but you do see the axons.
Here's a picture where I injected a retrograde tracer
that, in this case, was fluorescent--
a molecule that is easy to get the fluorescence, it's called
floral gold.
I injected it into the midbrain tectum, one of the
places that the retina projects.
I waited a little while, and this molecule was transported
back to the retina.
And then I took out the retina, I flat-mounted it on a
slide, and I looked at it through the fluorescence
microscope with particular wavelengths of light that
could see the floral gold fluorescence.
And there you see retinal ganglion cells.
Some of them, very intensely labeled, some of them less
intensely, depending on how much of the molecule it had
picked up, their axons had picked up, a couple of
centimeters away in the brain.
Now, here, different labels are being used.
The bright label here, in this case, is
called nuclear yellow.
It's concentrating in the nucleus, but it's coming from
the optic tract in the brain.
So similar to the other picture, they're coming into
the retina from axons.
In this case, not the axon terminals, but the trunk of
the axon that had been severed when we made the injection.
And this one in the center, the nucleus is labeled with
the nuclear yellow, but the cytoplasm has HRP in it.
As we've also done an HRP process to visualize the HRP.
So why would it have two labels?
We didn't inject the same place.
We injected the other side of the brain with HRP.
So one side was injected with nuclear yellow, the other side
was injected with HRP.
And a few cells have both labels.
So it's an experimental methods to discover when an
axon is branching.
And I had another picture of that where I--
after that, we used that method, we found other methods
that were easier to use.
Using, for example, floral gold for one injection, and
florescent beads, with tiny beads that contain fluorescent
molecules in the other end.
So here, I've injected two different optic track terminal
areas with pretty precise tiny injections.
And I had to hit equivalent parts of the two structures.
So what I did was one of the structure, I made a much
bigger injection and the other one's smaller.
Now, I wanted to see--
do any of the cells project to both places, indicating
branching axons?
And you can see here, there's two axons.
This is equivalent, that we're looking at the same piece of
retina with two different wavelengths of light.
So there you see these two cells, here.
They are there.
One fluorescing because the presence of one molecule, one
with the other molecule.
So we know that some of those cells in that region project
to both structures.
They have branching axons.
Whereas others project only to one of them.
I want to say, we skipped over endogenous activity as a
primitive cellular mechanism.
I believe when I wrote it in the chapter, I put it earlier.
But I didn't do it here.
I just want to say a little more about it here.
It was neglected early on.
People love the reflex model, and all behavior has to start
with a stimulus, so they sort of neglected endogenous
activity as a method of generating behavior.
And another reason that I can discern for why it was
neglected--
it was not actually neglected in invertebrate organisms, but
in mammals, it was.
People didn't like to deal with things where we did not
understand what was going on.
Now we do know a little more about the molecular mechanisms
generating activity that can change within a single cell.
And some of the early studies were done by this fellow,
Felix Strumwasser, in the '60s and '70s on the sea slug.
The same animal that Eric Kandel has
used in learning studies.
And let me show you just some of his results here.
He was recording from the abdominal
ganglion of sea slugs.
And he would keep all the electrodes in the neuron for a
long period of time.
And what he saw was fluctuating membrane
potential, an oscillation of membrane potential that had a
period of about 40 seconds.
And as the state of the depolarization of the
membrane, which is going in the upper direction there.
Depolarization increased.
The cell would fire action potential.
So you'd get this periodic burst of action potential.
So if you're recording, you could hear the action
potentials because you amplified them, you would hear
[MAKING NOISE].
At a period, in this case, of 40 seconds.
So not as fast as I just did.
He then tried blocking the action potentials with the
dendrototoxins.
When he used dendrototoxin, he found that the oscillation of
the membrane potential continued.
It was not dependent on those action potentials at all.
If he blocked the sodium pump in the membrane, then this
oscillation would be stopped.
So those were the early studies of Strumwasser.
And that led to later studies on the molecules in the
membrane that are showing these changing processes that
could generate such a rhythm.
I wasn't totally convinced of it, but he claimed he could
hold those cells--
they stayed in the lab day and night to do these studies for
days at the time.
And they claimed--
they were big cells, and they could hold them for long
period of time-- and he said there was evidence that they
in fact, had a circadian rhythm in addition.
That is a rhythm they've changed with a
period of about 24 hours.
And that when the animal was exposed to light, you could,
in a daily rhythm, you could synchronize that
rhythm to the light.
We call that entrainment by the light.
The same way our biological clock--
that is, of the most people anyway-- is entrained by the
sun or by alarm clocks, where we get up.
Most animals, actually, it's light that's very
effective for that.
One mammalian study that I found curious that was done in
that early period.
They gave mice, that they were following the circadian
rhythm, keeping them isolated from all indications of time--
that is, they were in steady light conditions.
So they could see the free running
rhythm of their activity.
And they found out that that rhythm would slow down when
they fed the mice heavy water, D2O instead of H20.
In fact, it slowed down proportionately to the amount
of the D2O they were fed.
Let's talk now about evolution of multicellular organisms.
I'll review briefly the behaviors most fundamental for
survival because it is those behaviors that have driven
evolution and resulted in the changes as multicellular
organisms have evolved.
Studies of this group of animals, [? chilenterates, ?]
also ctenophores, have seen what must be the earliest
stages of nervous system evolution.
We can look at the sponge, and we see cells that do have
membrane potentials, and they do conduct potentials.
But they're not really neurons.
Structurally, they're not like a real nervous system.
Whereas in these animals, you see real neurons.
And studies of those animals lead to a very simple
generalized conception for the central nervous system.
And that allows us to define some terms we will use
throughout the class.
And then I want to go through the body plan of the most
primitive chordates.
For example, the example we use is the amphioxus, one of
the cephalea chordates, they're called.
They're the most primitive group.
And when you look at a cladogram of relationship of
different species, this is an invertebrate chordate.
A member of our phylum, but it doesn't have
the bones we have.
And that, then, sets the stage for what happened in evolution
as this neural tube-- that that simple coordinate has was
elaborated.
So the most basic actions of organisms that enable survival
are these, in my view--
approach and avoidance.
And, in fact, we look at the midbrain, we will see later,
as we study the midbrain of mammals, we will see these
behaviors all controlled from the midbrain.
Not that they are mainly controlled by the midbrain in
us, but in evolution, it's very important to see
because that was--
we didn't initially have any endbrain.
Amphioxus has no endbrain, in fact, to speak of.
So approach and avoidance orienting, which is not the
same as a different kind of orienting.
Approach and avoidance--
going towards or away from something.
Orienting means turning towards it in response to
stimulation, or turning away from it.
And finally, if you add a motivational component, you
give a goal to the orienting.
Then we're talking about exploration or foraging.
Foraging for food, for example or seeking for food.
So those are the most basic action patterns.
We call them multi-purpose actions because they're used
by the various goal-directed activities that organisms
depend on for their survival.
And that's leaving out all the background activity that has
to go on all the time-- that the nervous system is also
important for.
Things like respiration, temperature regulation, blood
pressure control, heart beat regulation, and so forth.
That's controlled by a whole host of reflex-type activities
that we will mention.
How that has evolved in evolution, control of those
kinds of things.
It's evolved at all levels of the central nervous system,
from spinal cord right up to the endbrain.
I already mentioned this-- sponges and the
[? chilenterates. ?]
These are pictures from studies of George Parker, a
Yale, published in 1919.
Nauta likes to cite them in the beginning of his book.
He used to talk about them in his lectures.
Parker was able to see the simplest possible nervous
system of one neuron chain.
There's a sensory neuron in the surface
layer of the animal.
My red arrow there is pointing to it.
It connects directly to contractile
cells, to the muscles.
So this is the doorbell nervous system.
Triggers the action directly.
And then when he studied jellyfish and animals like
hydra, [? chilenterates ?]
like hydra.
He saw elaborations of that very simple plan, he found in
the sea anemones.
He found, for example, interposed neurons--
where the sensory neuron is still there, looking pretty
much like in the sea anemone.
But now it's contacting a sub-epithelial neuron, and
that sub-epithelial neuron contacts the muscle cells.
This sub-epithelial neuron, we would call a motor neuron
because it contacts the muscle cells.
In this case, the sensory neuron is
also the motor neuron.
And then, finally, and you do see this even in hydra.
But you see this second
arrangement in hydra [? too. ?]
You see the primary sensory neurons contacting these, we
could call secondary sensory neurons, that then contact
motor neurons.
So these are the beginnings of an
intermediate network of neurons.
These are types of interneurons.
So the motor neuron is defined as the cell with the axon that
contacts the muscle, or the effector, if we want to use a
more general term, because then we can use gland.
Glandular secretions is another kind of output.
And we're separating them from the primary sensory neurons.
And we can go a little bit further.
We'll call the cells that receive input from the primary
sensory neurons--
we'll call them secondary sensory neurons. and separate
them from the rest of the intermediate network of cells.
And then we have the motor neurons that send their axons
to the muscle cells.
They're contacted by some of these neurons in the
intermediate network.
The central nervous system will include all of these
cells, including the secondary sensory neurons, all the way
to the motor neurons.
But not the muscles and not the primary sensory neurons.
That's how we'll define it.
And notice here that interneurons there, in this
intermediate network--
some of them are a long ways away.
So here, I show axons coming in, say from another ganglion.
Or if it's a mammal, say, from the brain.
And we also have some of the secondary sensory cells giving
rise to long axons, going to other structures because this
intermediate network became more and more
elaborate in evolution.
So many long connections were developed.
So those definitions are important and I'll review
them, and they're reviewed in the book chapter.
I wanted to mention one thing about hydra, so we don't need
just Strumwasser's recordings to talk
about endogenous activity.
This was from a paper published in American
Zoologists back in 1965.
Some people had studied hydra in the most homogeneous
environments they could create, where there were no
disturbances.
Everything was as quiet and uniform as possible.
They assume that if particular stimuli were needed to trigger
hydra's behavior, the hydra would just sit there.
Is that what the hydra did?
No.
The hydra showed periodic movements.
It generated movements on its own, which indicates that the
S-R model, again, have to be modified by
endogenous this activity.
We could say the hydra was motivated to move periodically
in specific ways, related to his foraging for food.
So here's some of the feeding behavior
movements he's showing.
The hydra can also locomote by this particular
somersaulting movement.
They saw both of these kinds of behaviors appearing
periodically, even in the most homogeneous environment,
indicating that it was endogenously generated.
I took the picture from Swanson, 2003, but it was
originally published in that earlier
study of American Zoologist.
So these are the terms you should know.
They're here on the slides, which will be posted online.
They're also in the book chapter.
I will just note here--
collections of neurons have particular names.
We talk about the ganglia, if they're in the peripheral
nervous system.
We talk about cell groups or nuclei.
Sometimes a few of the names will arise, too, in the CNS.
These are the terms over here, on the left,
that we defined already.
If we talk about a collection of axons in the PNS, we call
them nerves.
In the CNS, we call them tracks, central
nervous system tracks.
Or sometimes we call them fascicles.
Or a singular word, the fasciculus.
We use the Latin, fasciculi, plural, in the CNS.
We also sometimes just call them bundles, bundles of axons
in the CNS.
And now I want to talk about the nodal cord and neural
tube, which are terms that are applied specifically to
chordates, our phylum.
So we can define them even in amphioxus.
This is from the Striedter book.
This is a drying of amphioxus.
And you'll see, it looks pretty similar at the two ends
that you'll see in the silhouette.
It's difficult to tell which is the front and
which is the back.
And if we look inside the animal, we'll see that he's
got a nervous system going all along the back.
And here's what it looks like, this top picture here, is what
it looks like up near the head end.
How do they know it's the head end?
Well you'll see, just because of the direction the animal
locomotes and because of some specializations that have
appeared at the front end of the animal.
And this is the animal we sometimes call the simplest
living chordate.
There are others that are closely related amphioxuses
that have also been studied a little bit.
They're not easy to study.
These are tiny little worm-like animals.
I've diagrammed it in a different way here because I
just want to show you two characteristics of all the
chordates, including us.
Another chord, which is a cartilaginous rod that
stiffens the animal, that goes along the back.
We have that, too, when we're embryos.
Then our vertebrae, the vertebral canal formed around
the nodal cord.
And above the nodal cord is where the central nervous
system develops as a tube of cells.
It develops from the surface, epithelium, by an infolding
process that we'll see.
Some of you have seen this before--
infolding of the surface layer early in development.
It forms a tube of cells, on cell thick initially.
And then that tube thickens and forms the entire central
nervous system.
And you can see that connected to that central nervous system
are the peripheral nerves.
Going out, carrying sensory input into the central nervous
system and also carrying axons and motor
neurons out to the muscles.
So if we take a cross section right through there, we'll get
this kind of picture.
Again, simplified in order to show you specific things.
There's the nodal cord.
There's the gut below it.
So here's the wall of the animal.
There's the neural tube.
And I'm showing there, coming into the dorsal part.
This is the back, up here.
So this is a dorsal root carrying mostly sensory
information into that central system.
Just like the dorsal roots in a mammal.
And here's a ventral route on the other side that mostly
carries neurons axons out to contractual cells.
Now I know it looks a little odd--
the dorsal root on one side and the ventral on the other.
I didn't do it in order to simplify it, I did because
that's the way the animal actually looks.
You go a little further forward and you would see the
dorsal root on the other side, and the ventral root on the
other side.
So they alternate sides.
We have a pair of dorsal roots at every level and a pair of
ventral roots at every level.
And most vertebrates have that.
And we can't be real purist about the sensory being in the
back, and more dorsal and motor being more ventral
because there are a few exceptions to that rule.
But that's probably true even in mammals.
So there's been a number of recent studies of that very
primitive chordate that are of interest to anyone interested
in evolution of the chordates.
They found that most of that neural tube
at the rostral end--
well, most of the neural tube is just spinal cord, but at
the rostral end, its most behind hindbrain and also a
tiny bit of midbrain and 'tweenbrain.
There are no cerebral hemispheres
at all in this animal.
In our molecular studies that support the structural
studies, they do have the three primary brain vesicles--
hindbrain, midbrain, forebrain.
Just not much of the forebrain, or
midbrain, in fact.
The forebrain that's there is mostly like our 'tweenbrain.
They do contain some cells that are like an infundibulum,
that is, the pituitary gland, and the [? phulip. ?]
The other side, more [? dorsaly, ?]
that are like the pineal.
And he's got visual input coming into that--
we think is equivalent to the pineal.
He's also got-- that is some light detection, also some
light detection stimulating cells in that rostral end of
the nervous system.
There's no proof, even of an olfactory nerve, for sure, but
in pretty recent studies, they have discovered
two nerves up there.
At least one is probably an olfactory nerve.
The other may be, what we call terminal nerve, which
innervates the nasal septum in vertebrates.
So the Allman book, which I don't remember if this this
page is included in what we posted.
I think it probably is.
So you can read some of Allman.
He summarizes some of the work of the [? Licchelli ?]
on structural studies of amphioxus.
And one of the interesting things they found was that the
little pigmented area of the 'tweenbrain of that animal has
a cell arrangement which seems to match the cell arrangement
of the early developing eye in
vertebrates, including mammals.
And that's what he's summarizing here, with neurons
with axons going out, pigmented cells, which are
like the cells of our pigment epithelium and
then receptor cells.
This shows a sagittal section of the spinal cord and brain
area of amphioxus.
It shows that area of the visual optic detection, like a
retina of the anterior.
But he also shows structures that indicate a little bit of
a midbrain there, in green, and the gene expression
studies to verify that.
And they've also verified the rest of the tissue is mostly
like a 'tweenbrain.
This area's the end brain here of an early development of a
vertebrate, and they didn't really find tissue that
matches that for sure.
It's that very simple neural tube that's just beginning to
be elaborated in an animal like amphioxus.
That's because of the behavioral demands that led to
better survival of creatures, especially as they increased
in size in evolution, that led to the elaboration of the
neural tube.
H. Chandler Elliot has this nice phrase he
published back in 1969--
every brain system grows logically from the tube.
By logically, he meant it had to
happen that way in evolution.
So basically, what I do here, early in the course is to show
you what he meant--
what had to happen.
So I have a little bit about what I meant by evolution.
You can read this.
It's in the book chapter.
I don't have time to talk a lot about evolution now.
But remember that what causes evolution, what is natural
selection--
whatever results in more genes surviving and being passed on.
And of course, these are genetic changes.
It depends on gene variation.
It's enhance by sexual reproduction.
And of course, some of the gene variation in any species
is caused by mutations.
It could be very tiny, and once in a
while, bigger changes.
Most of which are detrimental, so they don't survive.
But a few of them, in fact, are beneficial and they
increase in frequency in the gene pool.
I've summarized that right on the assignment sheet there for
this class.
So the basic behavioral demands there are the demands
critical for survival and reproduction.
And, at the same time, the animal is to maintain itself
vis-a-vis background support.
They need the interfaces with the outside world in order to
function so we can go through all of these things.
We elaborate a little bit what enables an animal to survive
and reproduce.
He's got to have these approach and avoidance
actions, and the underlying motivational systems.
A major one is always anti-predator behavior.
I'm always a little frustrated by an animal behavior book
that puts in anti-predatory behavior way buried in the
middle some place, as if it's not so important.
They often even put feeding light--
sorry, these are so basic to evolution, they should be
right at the beginning.
So I put anti-predatory behavior first because if the
animal doesn't survive, then that's it.
Feeding and drinking-- and I put next
reproductive behavior.
So these are all extremely important.
And to do those things, you need to control the endocrine
regulatory systems.
You have to have hierarchies of goals-- like flight from a
predator gets priority, even over eating and mating.
And that has to be represented in the nervous system, as the
nervous system control of those functions evolves.
These are what I mean by the ongoing background support.
I've already mentioned these things.
But it also includes stability and space.
And for that, we've evolved vestibular system, visual
motor reactions that maintain stability,
proprioceptive reflexes.
And they depend on these reflexes that are always going
on, whether we're aware of it or not.
I'm up here talking, and yet all those functions are
happening in me-- keeping me from falling all over, keeping
me alive, and so forth.
And the same thing is true for you.
So you can review this--
the interfaces with the outside world.
I just want to point out that eventually it led to what we
call cognitive functions, which I define
in very simple ways--
the ability to anticipate what we're going to sense, not just
what we're sensing now.
But what we're about to sense.
We can anticipate events.
And what we're going to do.
In fact, I think a neglected area of study is constant
formulation of what we're just about to do.
Not just what we're going to do tonight or tomorrow or in
an hour or after the class, but I'm always anticipating
what I'm about to do-- a very important part in the nervous
system evolution.
And that's a cognitive function.
And these are just-- you can read this-- all of the things
that the nervous system had to do to do all those things.
So that will lead to the speculation, which we'll go
through next time about the basic steps and the basic
changes that begin to happen to that very
simple neural tube.
And I want to give you a little evidence, too, that
this isn't just speculation.
These things really happened this way.
So it's a good place to stop.
We'll start there next time and we'll start talking about
real nervous systems.
Especially, we'll use a lot of comparative neurology here at
the beginning, to talk about simple nervous systems that
represent some of those early changes in the evolution of
the chordate animals.