This video is going to be all about sensory processing,
how autistics learn, the fast rates of information
coming in. We'll talk a little bit about sensory
processing, but we'll talk a lot about many columns.
We've mentioned many columns in the visual thinking
episodes, so this is just drawing these things
out, because I know the episodes are very dense.
I want people to follow along though. I want
it to be easy to understand, because I want the
autistic phenotype to be understood. because
these are real benefits what the biology of autism
gives us if understood and if put into environments
and situations where they can utilize the autistic
phenotype. So this is all about many columns.
Over the recent few episodes, we've covered A
lot of things regarding the autistic phenotype
and the ability to learn and sensory processing,
the fast sensory processing. I know it's pretty
dense and so forth. We talk a lot about excitation
and inhibition. The last three episodes were
about excitation and inhibition more specifically.
Episodes four and five way back were about excitation
and inhibition as well and throughout many different
episodes. We've kind of woven in the excitation
and ambition kind of phenomena with autism But
since we've detailed it more and more and we've
talked about sensory processing those high rates
of information more and more There's some things
here that maybe can help us understand What is
happening with the autistic phenotype? Okay,
so there's some recent episodes that are kind
of regions of interest for us. That's visual
thinking part one which is mostly the neurobiology
of visual thinking, and visual thinking part
two, which is how autistics learn. We talk about
the machine learning, similar to AI, and how
we build up different categories for different
catalogs. We have massive amounts of databases
to pull from. And in large part, that's because
of what we're going to kind of get into today
with the intense detail. And a large part of
our learning is paying attention to the information,
kind of time on task. With autistic phenotype
and these high rates of information coming in,
we'll talk about the gamma waves briefly before
we talk about, we're really gonna talk about
many columns, okay? That was mentioned in, I
think, visual thinking part two episode, but
we'll really draw them out and understand them
a little bit better. But. One thing with the
autistic learning style is it's very structured
and that's huge for learning, right? That's when
we're learning something we have to have kind
of an order To go about doing this. Otherwise,
it's friction a lot of friction inside and it's
very unstructured The autistic phenotype learns
in a very specific and accelerated accelerated
way And that's because the sensory information
coming in allows us to not scan the information
so much, but pay specific attention on the detail,
on a specific detail. You'll hear about Temple
Grandin talking about churches, and she'll talk
about the different types of blocks or doors
or something specific. And then from there, just
with those databases, just massive amounts of
imagery comes across. Okay. This is another part
about accelerated learning as well, because there's
an added layer of visualizing. And this is massive,
because we are not only taking in the sensory
information from the outside, but we're pulling
from many different types of sources, if you
will. And this is huge, because This is increasing
time on task and attention to detail. If you're
thinking about learning, you have to learn the
detail. It's not that complicated. So the biology
that gives us autism really allows us to be here,
and this is huge. So some of the episodes recently
about excitation and inhibition that are kind
of a region of interest is Sonic Hedgehog. Sonic
Hedgehog. Inhibitory. Neurons and Autism. Okay,
and let's see. Dilemmic reticular nucleus. Sensory
gating. And Autism. And the excitation episode.
Goal signals. And Autism. These are the last
three episodes that we've done. This is inhibition
here because inhibition is more of a region of
interest for us. And then excitation here, which
are mostly the pyramidal neurons, which we'll
map these out in the many columns here shortly.
So a way of thinking about excitation inhibition
is our default is go. The whole reason we have
a central nervous system is to move the living
organism. So our default is go. We can't just
always go though. We need some sort of pull.
And this is what inhibition cells are doing.
It's kind of pulling back into an optimal range.
If you think about excitation and inhibition,
it's kind of like a seesaw, okay? Excitation
here, inhibition here. You want a healthy balance.
It's context dependent, depending on the activity.
But the default for the autistic phenotype is
here. High excitation. And in large part, from
what we've covered, is we have low inhibition,
especially the parvalbian interneuron. This is
the most dense GABA cell that we have in the
human body, parvalbumin interneuron. Remember,
these are very fast acting. We have a whole episode
on this maybe six or seven weeks ago about parvalbumin
interneuron and the autistic phenotype because
autistics lack these, especially in key brain
regions like the insula, the medial prefrontal
cortex is lacking. kind of all throughout though.
So this is the very fast acting GABA. This works
on GABA -A. Remember the different here we talked
about the different GABA receptors. We only have
three GABA receptors. A and C are kind of fast,
but GABA -A is more dense. We have more GABA
-A. These are ionotrophic, which means they activate
within two to 10 milliseconds compared to GABA
-B, which is metabotrophic. anywhere from 10
to 50 milliseconds. So there's a big difference
there with the different types of inhibition.
But this is our most dense one, parvalbum interneuron.
So the autistic phenotype, there's not enough
pullback from that go system. So there's always
massive amounts of go. And that is a big benefit
for learning though. However, the outside world
Doesn't really go like we go. So there's a big
contrast. Okay, it's a it's quite the conundrum
with the autistic phenotype and the same the
classroom or the society at large remember the
examples of B movie how the cameras zooms out
and you can see the hive and there's thousands
upon thousands of bees swarming around at high
rates very efficient like so We've also covered,
and this is relevant, the waves. The inputs coming
in with the sensory processing. So different
waves. So we have high gamma, and this is 80
plus Hertz. Low gamma. So 30 to 80 Hertz Yeah,
it's showing up Beta So let's say 12 to 30 Hertz
Alpha 8 to 12 Hertz Theta is 4 to 8 Hertz and
then delta, which you're probably sleeping or
some sort of psychedelic maybe in that state.
But we also know from people like Earl Miller
at MIT that we kind of have theta ranges going
on in the background to help us task switch and
modulate our attention. But not to get sidetracked
here, The autistic phenotype, when we're processing
sensory information, we live mostly here. That's
because the rates of information are coming in
at mass scales compared to kind of the normal
typicals, if you will, which live mostly here
with a little spike into low gamma. So with the
sensory processing, for instance, vision, okay?
So you have the retina to lateral geniculate
nucleus, and this is a little relay station on
the thalamus. All vision will hit here, and from
here, it kinda just branches off. So each stop
is just recruiting more and more brain regions,
essentially. It's a good way of looking at this.
So from here, we can go from to the superior
colliculus. We've covered that in the Autism
in Eye Movements episode. This is a very cool
region. It's a very fascinating, powerful region.
We'll talk about the inferior colliculus soon
with auditory. And then V1, the visual cortex,
V1 through V4, making sense of what is being
seen. And then things like the amygdala for the
low row. and also the thalamus. It'll hit the
thalamus. But it hits these regions. So let's
say the eye, the retina here sends it back to
the thalamus. And on the back part is the lateral
geniculate right here. That will geniculate and
then the superior colliculus is down here It's
like a little noodle shape and the midbrain the
mesencephalon is here. Okay, so we kind of have
the pons The brainstem it's at the top of the
brainstem And this is the thalamus kind of in
the middle of the brain so it will also go to
the superior colliculus will Recruit back up
to the frontal eye fields which are up here So
if we had the brain here, cerebellum, sorry,
Dr. Reza Shatner, that's a bad drawing of the
cerebellum, right? And then if we just outline
the brain here, the temporal lobe, we're coming
in here like this, so forth. And then back here
is the occipital lobe, right? So V1 through V4,
it's kind of hitting here really fast. And then
up through here is the parietal. And remember
the visual thinking episode, there's a little
nucleus here about right here called the pretenus.
Pretenus. In visual thinking, this is lit up.
In the default mode network, this is lit up,
especially in the autistic phenotype. And here
are the frontal eye fields. It's right here with
the sensory motor, but the front, the anterior
part of the sensory motor. So the superior colliculus
here has to reach all the way up to here. And
that's a distal connection. And that's what I'm
talking about. This is where we lose eye gaze.
Eye contact and eye gaze for the autistic phenotype
is not that difficult to understand because remember
the analogy. If we have a destination and there's,
let's say there's five stops. From point A to
point B, you make five stops, and essentially
this is what this is. Stop one, stop two, stop
three, stop four, and so forth. The autistic
phenotype hits these early spots really fast,
much faster than normal processing because that's
the the high and low gamma in comparison to the
beta and alpha. So the autistic phenotype is
just getting blasted with these early sensory
processes and then by the time it has to recruit
these distal areas which is more cortical it's
challenging because there's the delay now because
of this myelination here that connects these
so right here is the medial prefrontal cortex
we talk a lot about that this is huge this is
adaptive responses when you're navigating the
world and you're making good decisions and healthy
decisions and you can fit in with the ever -changing
flow of society your medial prefrontal cortex
is leading the way and also the dorsal lateral
which is more up here and the orbital prefrontal
which is right here just right here so orbital
kind of medial in the middle and then this outer
surface is the dorsal lateral this leads the
way and it will instruct the subcortical areas
on what to do how to respond and so forth okay
that's a long wind about the sensory processing
but the thing to know here is these early regions
of the sensory inputs coming in are just so fast
for the autistic phenotype in comparison to so
-called the normal or the typicals okay that's
a big thing and that's one of two things that
is about this accelerated learning type of thing.
And the second thing is going to be the many
layers or the many columns. So remember the myelination
is a problem with the autistic phenotype. Huge
problem. Things like speech and language with
the arcuate fasciculus. We also have another
fasciculus called superior longitudinal. fasciculus
so now research is kind of thinking that the
arcuate is just a type of superior longitudinal
fasciculus but regardless fasciculi are nerve
fibers that connect distal regions okay and with
autism you just think about myelination right
we've talked about the comparison of driving
on an interstate versus a gravel road Good myelination
is like an interstate where you can have optimal
rates of speed. The gravel road from point A
to point B is going to be different. And that's
a big part of this. So the many columns. Let's
talk about the many columns. And we have many,
many columns. These are layers in our cortex.
And our cortex is layered, kind of like crepes.
So they just kind of they just kind of stack
onto each other like this This is exactly what
they they kind of are layer 1 2 3 4 5 and 6 Which
is I have laid out here because they all have
different roles So we can draw this out They
will look like this This is just a representation
of it there's different areas of many columns
have different amount of cells so like the cortex
has So I don't 100 neurons per this a little
slice of area like within microns So we'll draw
it like this as well see We'll go like this,
because two and three is going to be crucial.
Layer four is going to be something like standalone
thing. And layer two and three are full of pyramidal
neurons. They look like pyramids. Remember? They
look like pyramids. This is our goal signal.
These are excitation. And then also in here,
you have parvalbium. So they're kind of stopping
unwanted signals too. There's this PARP albium
here. Layer four is huge, because this is the
input area. These are stellette neurons. They
look like stars. We also have them in the pancreas
and liver, but they have different functions.
So these kind of star -like things right here.
And then layer five and six as we're working
down, it kind of looks like layers two and three.
Okay, and there's also some part of albumium
here. There's also other types of GABA. Um, somatostatin
is a little bit. Remember, those are the second
most dense. They're kind of here. Uh, carotidin
can be here, but these many columns are found
all throughout, like the each cortex, like the
visual cortex, the auditory cortex, the somatostatin
cortex, all of these things. The cerebral cortex
has their own and they all have different roles.
So there are some inhibitory neurons down here
as well. then these are columns so they're like
this and you can just stack different columns
together so you can also have I mean these are
just spatially represented like the same okay
then you have this starlet And then down here,
same thing. Some inhibitory, okay? So each one
of these, this is one mini column. And as you
stack some, if you just have a slice or splice,
That's called macro columns, but we're just talking
about one. But I also want to talk about the
space in between. Nerve pill. This is where there's
no cell bodies here. There's actually no cell
bodies here. These are all axons and fibers and
so forth. OK, for the connections. With the autistic
phenotype, this is big. This space here. Let
me clean this up a little bit. This space right
here, if you ever look at drawings, diagrams,
blueprints, or so forth, you might see some measurements
that kind of look like this. This inside diameter,
okay? In autism, this is smaller versus typicals.
The density of these macro columns because of
the stacked and close together of the many columns
is so dense. you can just find research articles
and images just having a spice and it's just
full. The autistic phenotype is just loaded here
with different cells and remember there's a decrease
in inhibitory and that's a big part of this as
well so there's massive amounts of pyramidal
neurons here for the autistic phenotype and this
closeness together It makes it hard to kind of
shut off and remember the the role of the so
excitation to go and then the inhibition the
the thing that pulls us back down into healthy
states healthy ranges Keeps us out of GABA and
so forth. This is huge in autism The density
here with the autistic phenotype a lack of cell
pruning remember The Autism, Century Map, and
Serotonin episode. Serotonin's role in development
is pruning the thalamus and these cortical areas
of dendrites. And also in the autistic phenotype,
the dorsal striatum has massive amounts of dendrites.
Dr. Hannah Stevens at University of Iowa has
studied that. She's a previous guest. I was going
to say something, but I know what I was going
to say. So you would think how the brain functions
and how Mother Nature just allows us to evolve
to be optimal. You would think these would be
linear, either starting from one to six or six
to one. Okay, that's not the case. Inputs come
in to layer four. These are mostly inhibitory,
depending on where you are. Definitely in the
cerebellum, they're all inhibitory. All stellate
neurons are inhibitory. In other areas, the different
visual, auditory, somatosensory, I should say,
and the cerebral cortex, they're a combination
of excitation and inhibition. Now you probably
know that autistics have fewer. inhibitions here
so it's hard to kind of dictate and determine
where signals go and that's the big part so after
inputs come in to layer four inputs are sent
up to layer two and three and then so one two
three essentially this is the process so why
two and three Why not go here and down? Layers
two and three is where you can say This is where
our intelligence our memory our ability, our
experiences live. So inputs come in from the
thalamus. It will check layers two and three
so that the specific living organism can draw
from its database and go down to layers five
and six. Now you notice there's a 5a and 5b and
a 6a and 6b. 5ab is mostly regular spiking. We've
talked about tonic, phasing, and burst firing.
This is a lot to do with the brain waves mentioned
earlier. Layer 5A is regular spiking. 5B is intrinsically
burst firing. Where we need to really activate,
we burst fire. So these action potentials will
burst like this. Let's just draw this out right
now. So this is tonic. This is just your baseline,
okay? And this is also time. Time and baseline.
So this is activation. This is like gamma, way
up here, way up here at the top. So burst firing
will go boom, boom, boom, and then drop off,
boom, boom, boom, spike. Drop off boom boom boom
like such Now the Delta is if there's more increase
than decrease. It's going to stay higher Now
as you relax calm down time passes and so forth
The burst firing can start to drop You see that's
how that's our molecules work essentially things
like dopamine and so forth. Dopamine nation is
good on this from Dr. Anna Lempke. It's easy
to read information. If I can read it, you can
read it. I promise you. So this is what layer
five is doing. Regular and burst firing. Layer
six, or it's kind of the output area, okay? Layer
6a is corticothalamus. This is huge for the thalamic
reticular nucleus. Remember, remember the thalamus
is a shell over it and it's all GABA. And a large
part, it's part of albium. So 6a is speaking
back corticothalamus. Thalamus. 6b is cortex
to cortex. Cortico... Oop. Cortex. So it's just
speaking back and forth throughout the areas
of the cortex. So the thalamus is huge. Every
sensation runs through there and all of our models,
how the living organism acts and lives, will
run through the thalamus. because that's our
sensory information. It's recruiting. Remember
the basal ganglia. Maybe we'll do a drawing of
basal ganglia, too, and more detail about the
sensory processing. But just a side note, at
Stanford, Karl Deisseroth and a neurosurgeon
named Jamie Henderson, this isn't autism -related,
but they found in humans that when people disassociate,
or, you know, they're having seizures or, you
know, people that have bad trauma will disassociate.
They found that the timing from these layers
and information coming into layer five is off.
Layer five and timing looks like to be the spot
for when and why people disassociate. Remember,
all of this is about time, space time. We covered
space -time so much in this little rant that
I'm doing in these awful drawings, maybe. I hope
you can follow along. But these are many columns.
I think I'll do a solo episode just about many
columns now that we've talked about the excitation
inhibition in more detail. And we've covered
a lot about the sensory processing because the
many columns are huge because of the amount of
density. and the inability to shut off. But there's
huge benefits to that with learning. Much different
than other people. So, many columns.