The following content is provided under a Creative
Commons license.
Your support will help MIT OpenCourseWare continue to
offer high quality educational resources for free.
To make a donation or view additional materials from
hundreds of MIT courses, visit MIT OpenCourseWare at
ocw.mit.edu.
PROFESSOR: This is class six.
In the previous class, we were talking about the brain of the
ancestors of mammals.
Mammal-like reptiles that I suggested were, and many
people have suggested were, the cynodonts.
We know from endocasts of the skulls of these animals quite
a bit about the brain shape.
And we know that the brain couldn't have been too much
different from the brain I've outlined as the Shmoo 1.
The major connections are fairly certain because there's
so much conservation across vertebrate brains.
Brains are so similar.
The same basic structures and the same connections.
So we can be fairly certain what they were like.
We went through major subdivisions and different
types of neurons in those brains.
Then we were talking about the sensory channels of
conduction, the reflex channels.
I defined local reflex and the dermatome.
And then the lemniscal channels.
We mentioned the spinoreticular pathway as the
oldest lemniscal channel, that is a ribbon of fibers starting
in the spinal cord proceeding up to the brain, the
encephalon.
Mostly ending in the reticular formation.
It was mostly an ipsilateral pathway, mostly uncrossed.
And this is where we ended, with a medical school
illustration of a human brain section showing that
spinothalamic pathway.
So I want to show you a little bit of data on the most
primitive living vertebrates.
There's our amphioxus at the top, a cephalochordate, an
example of the animals we can still find that are the
simplest of the living chordates, Even though they
have a head end, and we can define structures there that
are like a brain.
That's not really enlarged, as you can see
right in this region.
Pretty much the same at both ends.
But then we have the hagfish, another slightly larger
worm-like animal.
This is a 1 centimeter scale here.
There's a 5 centimeter scale.
So the hagfish is considerably bigger.
And the brain is considerably enlarged in this animal.
Although the endbrain is not really much bigger than the
tweenbrain or the midbrain behind it.
And then here's a sea lamprey, similar
in size to the hagfish.
It also has some brain enlargement.
So these animals, if we put them on a cladogram showing
what paleontology, and there's also some genetic data,
indicate are the relationships, evolutionary
relationships.
You can see that amphioxus, hagfish, and lampreys, the
ones I've marked with the red arrows there, have not changed
that much since they branched off from
the earliest chordates.
Amphioxus is not a vertebrate.
The other two are vertebrates.
But they're not jawed vertebrates.
So these are the unjawed vertebrates.
These animals had spinoreticular pathways.
And I mention that here on amphioxus.
First of all, just mentioning the gene studies showing that
it does have some brain structures.
And there had been some recent studies that followed some
inputs from body's surface into the CMS.
They found that the secondary sensory cells distribute axons
to both sides, mostly on the same side.
So not very much unlike the spinoreticular pathways of the
vertebrates.
In the hagfish and sea lamprey, there are also
secondary sensory neurons that have axons that extend
rostrally, mostly on the ipsilateral side, reaching the
brain stem.
We can call it a spinoreticular pathway.
There's nothing like the spinothalamic tract.
Some textbooks talk about the spinothalamic pathway as the
oldest pathway.
But now that we have a few studies on these very
primitive vertebrates, we know that that's not
likely to be true.
Of course, it's always possible that in evolution,
more recent evolution, these animals have lost pathways.
But the loss of structures doesn't occur
so much in the brain.
It's mostly in additional structures.
But there was pretty early evolution of a cross-pathway.
And that's the one we call the spinothalamic tract.
We call it spinothalamic.
These are axons of secondary sensory cells that cross right
in the spinal cord.
So the secondary sensory cells are in the dorsal horn of the
spinal cord.
You'll see them in pictures in a minute.
They send their axons through the floor plate of the spinal
cord across to the other side and then they ascend.
And the anterolateral part of the cord, towards the
hindbrain and midbrain mostly, a few of them make it all the
way to the tweenbrain.
And we've talked a little bit before about
why pathways decussate.
And that's a subject we'll take up again later.
Now, here on the Shmoo brain, I show these axons.
Here's two secondary sensory neurons receiving input from
the ganglion cell's axon.
And they ascend up the cord, with branching to termination
points in what we call the reticular formation, here in
the hindbrain and in the midbrain.
And a few of them probably even in primates, no more than
20% of them are making it to the tweenbrain.
There they contact cells that project into the forebrain, to
other parts of the forebrain, the endbrain.
The dienchephalon is of course part of the forebrain too.
And here, I'm showing them projecting into this
structure, the subcortical part of the endbrain, the
corpus striatum.
The connection from thalamus to corpus striatum is probably
more primitive than the connection to the cortex
overlying it.
That's not absolutely certain because in fact there is some
cortex, even in these very primitive animals.
It's not neocortex.
It doesn't have the laminar pattern of neocortex.
But even in fish, we do see some cortex that we call
dorsal cortex.
So there could have been axons going there.
And that's a subject that will come up.
So if we look at this view, the more realistic view,
where's the spinothalamic tract?
I want you to know this.
I want you to be able to take that top view and say, I'm
going to show you the spinothalamic pathway.
And then we'll do the same thing for dorsal column,
medial lemniscus pathway, a faster pathway.
Now, we could draw all those in.
I've turned it on its side here to show
you a similar drawing.
So here's the primary sensory neuron.
There's the cell body and the dorsal root ganglion.
It enters the cord and branches, contacting some
cells there that send their axons
right across the midline.
Then they ascend.
And I show them terminating there in the hindbrain and the
midbrain and a few making it into the tweenbrain.
That's the spinothalamic tract.
That's its characteristics in all the vertebrates.
And in the tweenbrain, there's the cell that's projecting to
the cortex if this is a mammal, although there are
connections.
It's probably a little bit inaccurate there, because I
should show connections also to the corpus striatum.
They still exist in mammals, though they're not the same
parts of the tweenbrain that have those kinds of
projections.
And we'll see pictures of them later on.
So you can take this picture, go back to this picture if you
have a print-out of it, and just draw it.
See if you can.
I find that students in this class have great difficulties
in memorizing even the simplest possible pathways.
And I appreciate the difficulty.
I was a student of neuroanatomy once too.
Didn't find it very easy, especially when it was novel.
So I will repeat it various times.
But eventually, hopefully, you can do that.
You can draw the cell, show an axon coming in, show the axon
going across.
The same thing as far as the tweenbrain, with branches
there at the midbrain and hindbrain.
That's the spinothalamic pathway.
And then in the tweenbrain, you would find cells that
project to the corpus striatum and up into the cortex.
And we could show exactly where those things are on the
cross-sections too.
We'll do some of that later.
So remember, we're not representing the earliest
chordates at this point.
You may remember that I said those earliest chordates
didn't even have a cross-pathway like this, a
spinothalamic pathway.
Here we're talking about the mammalian brain.
There was a very long period of evolution between those
early chordates and the ancestors of mammals.
Those cynodonts were pretty advanced creatures in
comparison to the animals that looked like amphioxus.
It seems likely that the spinothalamic tract simply
evolved as the specialization of a portion of that more
widely branching spinoreticular pathway.
There must have been some advantages, functional
advantages.
I'm not going to try to spell out functional advantages in
every case.
It's amazing how many things we don't know in neuroscience.
And here's some basic questions.
Now, what can vertebrate animals do if none of the
somatosensory pathways even reach the forebrain?
There aren't many studies like this.
In fact, I have trouble thinking of any.
Or what if they had no cross-ascending pathways from
the spinal cord?
What if only the spinoreticular
pathways were present?
It's a doable study with animals, especially with the
animals with a fairly small neocortex.
Yes?
AUDIENCE: It's a little hard to hear you.
PROFESSOR: Could you come up?
Come on up.
Sorry about that.
Is it nosier in here that before or am I just
talking less loud?
Because nobody had trouble last week.
AUDIENCE: [UNINTELLIGIBLE].
PROFESSOR: I can ask them for an amplifier
if it's real problem.
But I encourage you to come closer.
It's not too helpful to you if can't hear me.
And I'm not a very loud speaker, but I'll try.
So if you're having trouble, there's a chair here.
There's chairs on the side.
A second kind of lemniscal pathway was the
spinocerebellar.
And there is several spinocerebellar pathways.
In particular, there's a crossed pathway and an
uncrossed pathway.
And just to introduce it, this second kind of lemniscus
ascending into the brain, there was a problem when you
had multiple sensory inputs, multiple pathways coming from
the spinal cord, but other pathways that originated with
cranial nerves, all concerned with the same outputs, the
same movements, orienting movements, escape movements,
locomotor movements of various sorts.
It's a problem with timing.
If they're going to influence the very same movements, it's
very important that the timing be coordinated.
And that problem increased with increasing size of the
body and increased role of head receptors in the control
these movements.
And it increased further with the need for precise
coordination of large numbers of muscles, especially these
distal muscles of the limbs.
And one major reason the cerebellum evolved was
to deal with this.
It's not clear that it was the only reason it evolved.
There is evidence that some of those very earliest
vertebrates had electroreception.
And it plays a special role in analyzing
electrosensory inputs.
Allman has a somewhat more specific suggestion
there in his book.
But I'm going to give the more general problem that the
cerebellum is dealing with.
Here on Shmoo brain, here's a secondary sensory cell and the
dorsal horn of the spinal cord.
Here's a pathway of secondary sensory cell axons that goes
right up to the cerebellar cortex, a simple example of a
spinocerebellar pathway.
And as I mentioned, there are both crossed and uncrossed
pathways like this.
I say a little bit here on evolution.
There's been remarkable conservation, although its
size and form vary a lot.
And the biggest expansions occur first of all, in the
weakly-electric fish that use electroreception to localized
objects, detect the presence of objects and to localize
them around their bodies in the ocean.
This one part of the cerebellum, the valula, has an
enormous expansion.
And I'll show you a picture that.
Maybe later, we'll get to the today.
And as locomotor and manipulatory abilities
increased in tetrapods, especially the land mammals,
the growth of the cerebellar hemispheres and the associated
deep nuclei provided the output for those level
hemispheres.
They increased enormously.
So it's very big in humans, what we call the hemispheres
of the cerebellum.
So it had sensory functions in animals, especially animals
with lateral-line receptors, electroreceptors.
We know it plays an important role in the motor system, in
the coordinated timing of outputs.
Those pathways can be adjusted through feedback, so the
connections change.
And that's a major way the cerebellum works.
And we also know now, in more recent studies, that there are
some cognitive functions.
Exactly what they are is not clear.
I suggest they function in the coordinated timing of the
representations of our inner model of the world.
Let's just take a break here and talk about some
specializations in different animals.
We already mentioned the electroreception in some fish
and the big cerebellar expansion.
Let's look at that.
Other specializations were using infrared to detect the
presence of potential prey in the pit vipers.
They developed a specialized trigeminal nerve, the fifth
cranial nerve, to innervate those infrared detectors.
With echolocation in bats and porpoises, that led to another
kind of specialization, especially in
the auditory system.
And then we have the primates, including us.
High visual acuity and learned object recognition, which led
to a great expansion of especially the neocortical
areas concerned with vision.
And there's been a similar expansion, a related
expansion, for the whisker senses of rodents, a very
specialized somatosensory system.
Here's a Mormyrid fish brain.
There's the cerebellum.
You see it in the drawing up there.
We'll look at this one.
This is secondary sensory cells of the
lateral line lobe.
Remember that huge vagal lobe, the animals with specialized
taste, the buffalo fish.
Well, these animals have their lateral line lobes receiving
electrosensory inputs in large.
And this structure projects into the cerebellum.
And there's this part of the cerebellum that has grown so
enormous that when you open up the skull, you find nothing
but cerebellum when you look at it from the surface,
because its grown out over the hindbrain
and the entire forebrain.
Here's a pit viper, like a rattlesnake.
And it shows here the position of the pit viper, of the pit
organ and his face, innervated by the maxillary branch of the
trigeminal nerve.
This nerve that innervates the face areas.
It's got three main branches, which is why we call it
trigeminal.
And the same branch of the nerve that innervates in the
area below the eye including the lower lid,
innervates the pit organ.
We don't know much about the central representation there.
But it would make an interesting study to look at
that in these brains.
And I mentioned echolocation.
Here at the top, this is the brain of two echolocating
animals, the echolocating bat and a dolphin.
And if you look down on the surface of the brain, here in
the bat you see this greatly expanded midbrain surface.
The more anterior part of the superior colliculus, better
known for its visual input.
But the more caudal part, the inferior colliculus is a major
structure in the auditory brainstem pathway.
Information goes from there up into the thalamus, from there
to the cortex.
And there's been a number of studies of this structure and
the cortical areas that get that input in the bat.
Look at it in the dolphin.
Now, here it's a very different kind of picture.
Because they've actually dissected away for this
picture the entire telencephalon.
Because if they had included that, you wouldn't see the
midbrain at all.
So it's like human in that respect.
They have a very large midbrain.
Now, if you look at the corresponding nerve, which
would be eighth nerve, the auditory component of the
eighth nerve, and I've done this with Eric Montie, we've
done studies using magnetic resonance imaging of dolphin
brains, the Atlantic white-sided dolphin in
particular, they have an enormous auditory nerve.
And the pathways leading from the cochlear nuclei up into
this inferior colliculus are likewise huge.
So it's no problem to see them in our
magnetic resonance images.
Now, look at these animals below, that don't have
echolocation.
Look at the difference in their midbrains.
It's these animals, it's the superior
colliculus that's huge.
The ibex or wild goat and the tarsier, which is a prosimian
primate, both use midbrain.
You could say midbrain vision is very important to them for
orienting and escape movements.
The tarsier is a little prosimian that can, very
accurate in his orienting.
And he can catch flies on the wing with his hands.
Try it sometime.
It's very difficult.
Humans can learn it.
But we're not nearly as good as an animal like the tarsier.
Now, the wild goat doesn't do that.
He's not using it for these kinds of
built-in grasping movements.
But he's using it to detect predators and to guide rapid
locomotion.
OK, now, I said vision has become a very specialized
sense in the pri--
Yes, in the back?
AUDIENCE: Yes.
Do all wild goats, so like gazelles and things, in
predators, do they all have inferior colliculi?
PROFESSOR: It's superior colliculi.
Yes.
We do a sheep brain dissection.
Maybe we should do that sooner rather than later.
Once we just survey the whole brain, we can do a sheep brain
dissection.
You'll see that in the sheep, pretty
large superior colliculi.
I would say the sheep isn't so different in relative size of
the colliculi as this brain.
This is from John Allman's studies, the fellow that wrote
the book I'm getting you to read a little bit of.
This is from his studies of the owl monkey.
And here, V1, is the primary visual cortex.
It gets input directly from the thalamus, the thalamic
structure, the lateral geniculate body that gets
input from the retina.
But then look at all these additional areas.
Every area with a line around it there has a different
representation of all or most of the visual field.
And that continues all the way down through the ventral
portion of the temporal lobe.
So it's probably a third of the entire neocortex in the
owl monkey is taken up by this visual areas.
And they in turn project into the frontal lobe and to parts
of the parietal lobe.
So it's a very dominant sense in these animals.
So the last specialization is the brains of small rodents,
like mice or rats.
They have specialized areas, a specialized somatosensory
system getting input from the whiskers.
And if you look, here in the cortex, what they've done is
taken the cortex before it's well-fixed fixed and they take
it out and flatten it.
They remove it from underlying structures and
flatten it on the slide.
And then they embed it so they can cut it tangentially and
stain it for cells.
And that's what they've done here.
And you can see there they look like
adjacent little rings.
Can you see that?
Well, each of those little rings, the cells form the
darker areas around the side.
This is through layer 4.
And then the lighter areas are areas with few cells.
If you did a fiber stain, you'd find a lot of fibers
there coming through the core there, the
area with fewer cells.
And they're terminating on the cells around it.
Well, each one of those barrels represents just input
from one whisker.
So it's a highly specialized structure.
And they use those whiskers to detect the texture of
surfaces, to detect object location, and many details.
Of course, they're also using their olfactory sense in
situations where vision is of not much use to these animals
because they're in dark areas.
Let's talk about a few other behavioral specializations
that have led to brain expansions.
The hand in apes and raccoons and certainly humans, very
high tactile acuity, especially the fingertips.
And going along with that, very fine motor control.
That has led to expansions of somatic sensory and motor
areas of the cortex and of the related areas in the
cerebellar hemispheres.
Those cortical areas actually project to the cerebellum by
way of the pons, that is as a synapse in between.
And these have become quite large.
The raccoon for example, well, I think I have
a picture of that.
This one.
Here's a picture of a raccoon on the left and the coatimundi
on the right.
They're showing different body areas.
But look here at the representation of the hand in
these two animals.
They've outlined it in the red there.
Much larger in the raccoon than in the coatimundi.
And if you look closely at the area representing the digits
in the raccoon, you'll see that there's a separate little
gyrus for each digit.
And primates with highly developed tactile sense have
something similar.
Well, there are similar specializations in the spider
monkey, in which case it's the prehensile that's involved.
They have an expanded tail representation in the sensory
and motor cortex.
And then we can mention the elaborate social organization
in the higher primates especially.
That requires a lot of planning and problem solving.
And it's believed now its provided a large impetus for
expanded prefrontal neocortical areas, very
important in strategizing, planning of actions.
And then of course, language in humans led to specialized
parts of the association cortex.
We call it polymodal association cortex.
It gets input from various senses.
We find these in three different major regions of the
cortex, parietal lobe, temporal
lobe, and frontal lobes.
And then in addition, the two hemispheres have specialized,
with language dominating the left hemisphere in most
people, and the right hemisphere concerned with
other functions, spatial functions in particular.
Those are all examples of specializations, not so
unrelated to the specializations in fish that
we mentioned earlier.
I want to now give an overview of the forebrain structures in
the vertebrates and introduce the neocortex.
Let's start by asking this question.
What can an animal do without a forebrain?
If you look at studies that have made animals chronically
decerebrate, that is they remove the forebrain, that's
been done in older studies in cats and in rats and in
pigeons primarily.
And we'll mention contributions of these
different major components of the forebrain.
There's been major species differences.
And that's been a huge problem in interpreting brain lesion
effects generally.
The functions an animal shows after brain lesion, especially
soon after a brain lesion, can be very different
from animal to animal.
And so the question is why?
There are both qualitative and quantitative reasons for that.
And I want to review that right now.
First, let's deal with the cat studies.
Bard and Macht did this back in '58.
And they claimed that cats which had the whole forebrain
removed were a purely reflex animal.
They said they didn't do anything that required the
performance of a series of reflex-like actions in a
proper sequence.
So let's look a little more at what these animals could do.
First of all, the forebrain gets both
olfactory and visual inputs.
That's where the cranial nerves are attached.
So without the forebrain, these animals are anosmic and
blind, the first big problem.
Well, an anosmic and blind animal can still do a lot,
after a little time to adjust.
But these animals showed a lot of problems besides that.
They didn't eat spontaneously.
They would show licking and chewing responses if food was
placed in their mouth.
And they had to be hand fed like that, otherwise they
wouldn't eat.
They wouldn't initiate eating, even after a long, long
periods of recovery.
They didn't groom themselves.
Grooming is a complicated sequence of movements too.
They would show reflexes, like the withdrawal reflex.
For example, they'd pull away from a painful stimulus.
But they didn't show the more complex actions.
They showed no spontaneous sexual or
other social behaviors.
But you could illicit sexual reflexes by genital
stimulation.
They would stand, sit, right themselves if
you push them over.
They could walk.
Even though they would walk, they didn't initiate walking.
But if you nudged them, they would show some walking.
Their posture was abnormal.
And their gait, they often didn't reposition their limbs
the way normal animal would.
They showed some sequence of responses by showing rage if
you'd pinch their tail.
But on the other hand, they didn't bit or strike out the
way a normal animal did and carry through the rage.
People called it a sham rage, like they
are not really angry.
They're just showing a reflex.
And that's what it seemed like to the investigators.
They showed a lot of autonomic responses, like things
involved in thermoregulation, piloerection, standing up of
the hairs on their body, thermoregulatory responses.
But temperatures had to be more extreme
than in a normal animal.
So their body temperatures would fluctuate more than in a
normal animal.
Remember, I said that autonomic control developed at
all levels of the nervous system.
Well, these animals still had their spinal cords, their
hindbrains, the midbrains.
So they had still a lot of temperature control, but not
the finer temperature regulation of the forebrain.
And the investigators learned that because of autonomic
functions, it was almost impossible to keep animals
alive because of this.
So they left a hypothalamic island.
Even though they could cut off that island from the midbrain,
they left the island attached to the pituitary, which left
them with some crucial visceral regulation, like
regulation of water balance.
They showed very little learning.
But they could get conditioned eye blink responses or
respiratory changes.
They didn't retain very well, but they did
show some simple learning.
So that was a pretty sorry state of these cats.
They were really like a reflex machine.
When Woods did the similar types of studies, published in
1964, he did on rats.
Now, rats have a relatively smaller forebrain.
The cortex is mostly a smooth cortex, unlike the gyri and
sulci of the cat.
They were similar to the decerebrate
cats in some respects.
But they showed a lot more rapid recovery of their
righting reflexes and their locomotion.
And they showed more eating and drinking.
They still didn't seek food.
So again, they had to be fed in order to keep them alive.
But now these animals unlike the cats,
would actually groom.
So the cat, the conclusion of Bard and Macht, that they
don't show any series of reflexes, wasn't entirely true
of these animals.
I wouldn't call them really reflexes.
But they used that term to include a
broader group of responses.
We would call many of these fixed action patterns, things
with an innate program that the animals inherited.
And the rat showed a lot more of the fixed action patterns
of grooming.
They also showed more defensive behavior.
It was more typical of a rodent.
They could scream if you pinched their
tail, try to escape.
They would claw and bite more than the cats.
And they even showed some turning towards
sounds, novel sounds.
So why did the rat show more recovery than the cats?
Why is their recovery faster?
Is it because the forebrain in the cat does a lot more?
Its taken over functions.
Whereas in the rat, that's happened less.
Or is it something else?
That something else we're going to call diaschisis,
something that happens to structures that are connected
with structures that you've damaged or removed.
And we're going to define that.
But first, I'll mention the pigeon results.
Because they were so different.
Now, the pigeon has relatively speaking even a smaller
forebrain than the rat.
Well, they showed a lot of behavior.
Now when they did this, they left the optic nerve and tract
connected to the midbrain.
They removed all the forebrain they could.
But they left the optic tract.
It's possible to do that.
It's very large.
It's easy to see.
And they found they wouldn't initiate flying, but they
would fly if you through them into the air.
And they would avoid vertical sticks, land
on horizontal sticks.
But they also landed on the back of a dog or cat.
So they obviously weren't normal.
And yet, they were showing some basic instinctive
behaviors involving flying.
They lost everything that seemed to depend on learning.
Now, there weren't extensive studies of exactly what was
learned and unlearned.
But I'm giving you the impression these people got.
Notice that these were done a lot earlier.
Most people didn't know about them.
But I had the advantage in my early years in this field of
being able to read the German.
So that's how I know about this work.
It's too extreme to say that they lost learned behavior and
retained unlearned behavior, although they do lose many
learned responses.
And I say that because even spinal animals you can get
conditioned leg withdrawal and other types of conditioning
that involve the spinal cord or brain stem, including the
cerebellum.
One hypothesis in what's going on here is that the forebrain
is important somehow in linking together by learning
different species' typical action patterns, which are
built-in and genetically determined.
But they're often individually inherited and they have to be
linked together to function normally.
These animals seem to have lost a lot of that.
Nauta put it this way.
He said that animals without a forebrain maintain good
stability in space.
They also had pretty good stability of the internal
environment.
They had very poor stability in time.
Their behavior is determined by just the current inputs.
So they have little or no motivation-initiated behavior,
little or no long-term memory.
And I should add that we know from a lot of studies done
since that early period that these animals lost a lot of
their acuity, sensory and motor acuity.
Some investigators, including Bard and Macht, went on and
they just took out the cortex.
They left the corpus striatum underneath.
And they found that the cats with that, showed a lot more
behavior sequences.
They were more like the rats without the forebrain.
They showed some grooming, some
spontaneous eating and mating.
But remember, the rats did this even
without a corpus striatum.
So again, why this species difference?
Another quantitative effect when you use very large
lesions is that the more neocortex you remove, the
longer lasting the defects are.
For example, you can get rid of orienting to visual stimuli
by just a visual cortex lesion in a cat.
But then, they gradually come back.
Well, if you just make a bigger lesion, get outside the
visual cortex, say you remove the visual and auditory and
somatosensory, then it doesn't come back right away.
In fact, when you remove enough posterior cortex in the
cat, the orienting never comes back.
So we might have species differences all right.
But some of these may just be quantitative.
And we explain it in terms of this.
Diaschisis refers to quantitative
effects of large lesions.
We define it as deafferentation depression.
What does that mean?
What does it mean to deafferent something?
It means remove the inputs.
So if you remove the inputs, you can make the cells that
have lost all their inputs depressed in the sense that
they can't reach threshold for firing action potentials if
they've lost so many inputs.
An example, and we can see this in many different
species, is spinal shock.
You transect the spinal cord, even in a frog.
And for a while, he loses his spinal reflexes.
Local reflexes, segmental reflexes like the stretch
reflex and the withdrawal reflex, they just disappear.
And then they come back.
And they come back faster in the frog that they
come back in a rat.
And faster in the rat, than they come back in a cat.
They're very slow to come back in humans.
If we just make a large cortical lesion, we get
corticospinal diaschisis.
You lose some spinal reflexes just from
removing cortex up here.
Why?
Because in animals with a large cortex, there's a big
projection from the cortex down to the spinal cord,
without any intervening synapses.
That didn't exist in those primitive brains that we've
been talking about.
But it exists in many mammals.
And we'll talk about two kinds of recovery from that
deafferentation.
One is a sprouting of remaining
inputs on the same cells.
And the other is changes in the receptors.
So they develop more receptors to the same neurotransmitters
and become more sensitive to the remaining inputs.
I'm going to go through diaschisis
with some simple diagrams.
So if you don't understand it now, don't worry.
You can read in the chapter.
And then we'll go through it in class.
Right at the beginning of the next class, chapter.