There it is. Okay so we're going to cover the
thalamic reticular nucleus. Okay I'm going to
map out some episodes here that kind of hits
on this. We talk about it a lot though because
it's going to have to do with the EI imbalance
and this is the protective shell that surrounds
the thalamus. We talk about this a lot so it's
going to be nice just to see it all laid out
and understand its functions. The main episode
that we'll cover is episode 83 so not long ago.
delimic reticular nucleus, trigating, and autism.
Episode 82 will also hit on this. And that's
Sonic Hedgehog. Let's see. An inhibitory, neurons,
and autism. So we had back -to -back episodes
on this inhibition. This is all inhibition. This
ERN is all inhibition. And then episode 60 or
76 kind of covered this because this is part
of albium interneuron. We'll talk more about
this specific interneuron, this inhibitory interneuron,
a lot. Because it makes up the most of this.
Parv -albium interneuron and the autistic phenotype.
Episode 84 is the opposite side of this. And
that is all about excitation. The goal signals.
Excitatory. Excitatory neurons. The brain's goal
signal. I don't want to say something. Okay.
Showing up. Nah, not bad. Okay. and then back
way back episode let's see three and four touched
on it was like a two -part excitation inhibition
episode back -to -back episodes episode four
would have touched on more inhibition but very
it wasn't very specific as these episodes are
these are really dialing in to specific aspects
of the excitation and inhibition especially for
this one right here The thalamic reticular nucleus.
Now, science. Because people are kind of career
-driven, the TRN, you can see it abbreviated
and named many different things. Just for the
sake of this, just to keep it standard here,
keep it similar, we're going to say it's TRN.
You can see it probably three, four, five different
names. It's all the same thing, though. We love
to identify. and then name things and then rename
things and then rename things that's just the
that's just the culture and the kind of the atmosphere
of science because people want to kind of make
a buzzword create this new idea and have it captured
have it gain momentum for funding purposes for
citations just for the publicity of it it's irrelevant
so let's talk about the thalamic reticular caniculus.
Remember it's the shell. So let's just draw it
out the thalamus. Remember the thalamus is a
workhorse. That's why it has kind of these assistants.
Remember the basal ganglia episodes. The subthalamic
caniculus which just sits posterior and inferior
to the thalamus and it helps relay the go -no
-go signals in the basal ganglia. So let's just
draw this out the thalamus because we're going
to cover hopefully eventually the different subdivisions
of the thalamus because there's a lot. The thalamus
is a lot to parse out. And there's a good drawing
of this. And you can see right here on the daylight,
this is, you can get this image on the internet.
It's very, it's a very good image of it with
this shell right here. And then this is helping
you parse out the different subdivisions because
remember this trn just surrounds the thalamus.
And then here's a different view of it. You can
see the trn. is all around the outside. Prevents
signals from coming in. So I'm going to draw
that top one out though, just because I think
it might help. It might help us understand it.
Remember, at the bottom here, you have the medial
geniculineculus. Right here, remember the, um,
the auditory. This is the relay station for audition.
Remember the, um, the auditory brain stem response,
A, B, R. This is, this is the... the kind of
the last stop this is where all relay for the
auditory happen and then right next to that laterally
is the lateral geniculate nucleus this is the
same thing but for vision this receives roughly
80 percent maybe 75 percent of the retinas fibers
all vision will eventually come here but the
other 10 to 15 percent gets the superior colliculi,
which is in the mesencephalon, which is just,
they're all right here. There's spatial relationships.
They can just reach out and high five each other,
which is what I said in the autism and eye movements
episode, all about the superior colliculus. So
we have the medial and the lateral here. The
thalamus is kind of egg shaped. It's deep in
the brain. Remember this area right here, the
third ventricle is right here. And then the lateral
ventricle. um vitricles are up here there's a
lot of water here there's a lot of electrical
power and things just surrounding this different
nuclei surrounding these areas deep in the brain
stem or the brain just above the brain stem so
the the trn as you see in that picture this kind
of just imagine this is kind of this cut out
and then it's just a shell it's a shell over
it and then we're going to talk about We're going
to break this shell down a little bit. Hopefully
it helps make sense of it because there's a lot
of cool stuff here. At least I think it's cool.
I love this stuff though. So in like the bottom
picture here, okay, you got this on one side
and then you got the thalamus on the other side.
Now remember one side of the brain or the hemisphere
is ipsilateral. Both sides is called contralateral.
this is just the contralateral so this is one
hemisphere this is the other hemisphere and the
trn would be actually i think it might look better
if it just had if it just had some color in it
like bob ross let's just do it we're going to
get through this i promise you see just basically
just basically like this so yeah like the third
ventricle will be right here Before we parse
this out, remember the sonic hedgehog. Remember
we talked about the sonic hedgehog a lot. Several
different episodes. Remember, in neuroscience,
in things like rodent studies, you can have these
things. So S -H -H is sonic hedgehog. And then
you can see in neuroscience papers where you
can knock out the gene, protein sequencing and
so forth. So it will look like this. That's a
knockout, double knockout. So the animal, the
subject, doesn't have this at all. Then we can
see what happens. What is missing? Or what kind
of behavioral effects does this have? It's basically
like a lesion, okay? Remember in the neurolation
episode, when we are kind of subdividing the
neuroepithelial cells, we have the four cells
in the neuroepithelial, three of them for the
brain. And we kind of start looking like this,
right? We have the tail encephalon and the diencephalon
here, the mesencephalon, and then the things
like the my and met encephalon. I think I have
those backwards. Met and my encephalon. Remember,
this one does not subdivide, but these are subdividing.
So this is the big subcortical area and the cortex
right here. And then this is just a little brain
stem area. It's a very small area here. And then
this is more of the pons and the cerebellum and
then the medulla and then the spine. If you knock
out the sonic hedgehog, it's responsible for
this area right through here. So in a rodent
model with this knocked out sonic hedgehog, you
don't get this. This does not. form. It doesn't
really do much for the human autistic phenotype,
but at least it provides information on what
is causing abnormalities with the thalamic reticular
nucleus. Okay, so it's kind of unimportant for
this episode learning about the TRN, this gel,
but it's huge. It's a good finding in neuroscience
and with the knocking out of that gene and the
protein sequencing. So what is the overall function
of this and what makes this? Remember the parvalbium
interneuron. Okay we had that specific episode
on that because there was a lot there was a great
paper published about how autistics have kind
of problems in a couple of different brain regions
with the parvalbium interneuron. Remember parvalbium
interneuron is the most abundant GABA in habition
neuron that we have okay and this is acting on
GABA -A which is very fast acting receptor this
ion trophic i mean these are happening within
one two milliseconds and then the parv albium
interneuron makes up the majority of the shell
the second type is somatostatin this is the second
most abundant GABA cell. Neuron. And this works
on GABA B receptors. These are metabotrophic.
These are a little bit slower. These are roughly
20 to 50 even longer milliseconds. It takes longer
for these to act. Now what are these two roles
in this thalamic reticular nucleus is the parvalbium,
which is most of this nuclei. It's acting on
specific inhibition. The somatostatin is more
like globally. It's just kind of sprinkling the
area just to help maintain balance. Remember,
we talk a lot about the EI balance. With the
autistic phenotype, there's a lack of inhibition.
There's problems with inhibition. Not only a
reduced number of cells but the cells on board
are kind of abnormal. This is a great finding.
Two decades ago, even maybe longer, something
caused Rubenstein and Mike Merzenek to study
this. They don't study autism. They study things
like neuroplasticity. But something caused them
to study this. I don't know what, but it's a
good paper. 2003. So what about this TRN? What
else besides these two specific cells make up
this? we talked about in the episode of the thalamic
reticuloniculus about the different sectors okay
so the first sector is sensory the thalamus receives
all sensory information coming in even things
that we don't really pay attention to things
that we're not perceiving that's because of this
so with this we obviously have visual so the
lateral geniculate is going to be involved We
might as well just, let's see if this will work
out. We'll just try this. Auditory. The orange.
It's not bad. Looks like Miami hurricanes. I
don't know about that. I don't know about that
now. And then somatosensory. Remember somatosensory
is right here. It's kind of sandwiched in between
the sensor - the sensory motor area and the parietal
lobe the parietal lobe is back here kind of talk
about the parietal lobe here because it's going
to be involved it's very involved in visual thinking
and this is very involved in visual thinking
as well so now the somatosensory doesn't have
its own little relay station like vision and
audition does these are huge sensory processing
kind of mechanisms here especially vision right
remember A lot of our brain is for vision. And
then with the auditory, remember, this is another
fascinating thing with the endocochlear potential.
Remember, this is the highest DC voltage in the
human body happening in the stria vascularis.
I was thinking of stria terminalis, but that's
a brain region. So anatomy, man, it's tough.
So what are some of the inputs coming in? And
then what's the little crosstalk? Because all...
pretty much all regions this is a we can call
this a region it's the thalamus all regions will
have crosstalk they will cross and talk within
each other it's very much a thing so let's talk
about the afferents signals coming in and the
efferents the signals going out remember with
the basal ganglia episode though the thalamus
is the main goal everything from the basal ganglia
is working to modulate dictate what the thalamus
is doing and that will determine our goal our
activation and our no goal or inactivation the
whole basal ganglia is for this and then remember
the mini columns that's it let's just draw the
mini columns again remember the mini columns
which are everywhere Remember layer four. Remember
the many columns. It puts command from the thalamus
to layer four and layer four will kind of start
these many columns. Remember this is a many column
and then this is a many column. And as you build
many columns, they're macro columns. And then
the space in between are neurofills. In the autistic
phenotype, they're about half the size of typicals.
So they're roughly 40 to 60 microns, which is
about, if you shape the thickness of a piece
of paper in half, the autistic's neurofill is
about that thickness, whereas typicals are closer
to the full sheet of paper thickness okay but
the thalamus remember after it runs through the
basal ganglia and we decide to go and no go because
they're simultaneous actions the thalamus will
then speak up to layer four remember and then
that will jump start and go to two and three
next because everything about the living organism
as far as like intelligence and memory and ability
experiences um our skill sets and so forth basically
live in layers two and three of the mini columns
and then it will go down to five and six both
five and six remember five a and five b and then
six a and six b five a is for tonic firing it's
just basically firing based off of the inputs
and signals coming in it kind of just is a baseline
activation to keep the living organism present,
to keep them active and appropriate in large
part here. 5b is more that burst firing. Remember
what we're talking about is these first signals
they fire and then they drop and then and then
they drop then they drop right so we get these
bursts right here and then they're working its
way up this is more activation and then over
time or you can use like physiological tools
breathing exercises etc these will start to drop
and this is in large part You can think about
this on a seesaw because somewhere through here
is tonic. Somewhere through here is baseline.
You're like resting state. So that's what layer
five is kind of doing. So how is this involved
with the thalamic reticular nucleus? Well the
shell is help determining. It's helping regulate
this and the actions coming out of the thalamus.
What does the thalamus want to pay attention
to? What does the living organism want to pay
attention to? That way the thalamus can do its
work. Remember, it's a workhorse. So let's keep
in mind the basal ganglia and these many columns.
I don't have the basal ganglia mapped out here,
but the end target is the thalamus. Okay, so
the connections coming in. A lot of them are
that crosstalk within the thalamus because the
signals will eventually, well actually, let's
talk about Because in the episode of the episode
83, I think it was the one that's specific to
the Salamic Reticulonucleus, we kind of outlined
it as like guards. These are like guards and
kind of providing protection. So let's map out
what has access and the level of security that
this shell is providing the thalamus. What kind
of security? About this information coming in
So just remember this is a large part sensory
processing over here Okay, what how much access
okay, so the sensory vision auditory touch and
so forth how much access or Said differently
how much security so I have to make a decision
here. Do we want to go how much access? or how
much security? Let's just say access. Very little,
no access. These signals coming in from either
vision, auditory, touch. Let's just say the retina
is sending some fibers to the lateral geniculate
nucleus and then some fibers up. to the thalamus,
it's going to be regulated by the salamic reticular
nucleus. And then it's also going to send signals
back to the visual cortex. So if we want to draw
that out real fast, here we have the retina.
So signals will come in to the lateral geniculate
nucleus, roughly 80%, and then about 15, well,
85%. 15 % to the superior culliculus. the lateral
geniculate nucleus will send some to inside the
thalamus, especially this area right here, which
is pulvinar. This is a lot of sensory, but this
islamic reticular nucleus will determine how
much and what kind is going to be able to go
from the lateral geniculate nucleus to inside
the thalamus. And then it will also, the lateral
geniculate nucleus will also send fibers projections
however you want to say it to the visual cortex
V1 through essentially V5 right and then it'll
just kind of work its way through the occipital
lobe and then the parietal lobe will be up here
so like the brain is kind of like this and you
got the eyeballs right there the temporal lobe
so you can kind of see this cartoon drawing of
retina to the lateral geniculate nucleus here
The lateral geniculus will send some information
to the thalamus. Most of the information back
to the V1. We also have the superior colliculus
processing vision. And remember, a large part
of this is going back up to the thalamus and
to the frontal eye fields. Frontal eye fields
are up here. There's a little subdivision of
the thalamus right here, medial dorsal, and that's
getting a lot of the information from the superior
colliculus. It's a lot. I know, but... Just to
understand this visual information and the processing
of it, just kind of follow along here with what
this thalamic reticular nucleus is trying to
do because there's a lot of information. Just
imagine if you don't have this or if it's abnormal
and you're processing all the sensory information.
It's a lot. But you know, it's easy for you to
say that the autistic phenotype can be overstimulated.
You can understand that easily. this is what's
going on that's why i want to cover this stuff
that and i love it okay so the sensory it has
little access into the thalamus this layer right
here remember 6a and 6b one is cortico bless
it remember the white fibers right through here
too like the fasciculi um and so forth so cortico
cortex or cortico cortical. So this is just speaking
back and forth through the cortex like the parietal
lobe will be heavily involved, the sensory motor
in the prefrontal. That's what this is. After
layers come down from two and three, sending
signals down to these cells and then the white
matter tracks here, there's a lot of crosstalk
between the cortex bringing other subdivisions
on board helping the living organism adapt. responsibly
and then the other one is corticothalamus or
thalamic this is a big one here okay because
the minicons are already receiving information
from the thalamus into layer four with these
stellette cells and then it goes up to layer
two and three to gain information about what
the living organism knows everything the living
organism knows is basically receiving a summary
here okay this is what's happening from the environment
as far as sensory processing. What do I do? Remember
in the background the basal ganglia is working.
to help determine movements because the basal
ganglia is movements and this is the living organism
that's the role of the central nervous system
is to move the living organism we're mapping
out how it happens so the thalamus is sending
cells or information to layer four and then it
goes up to layers two and three to receive information
and then that information is carried down to
layers five and six and from five and six it's
kind of being a completion but it's never complete
it's just updating because it's a constant loop
man it's just constant and what's allowing the
thalamus to be updated here is this layer cortical
thalamic or thalamic because based off of everything
coming in it's getting updated how is it doing
what does it need to do how is it making adjustments
and that's in large part what this is doing too
so let's just imagine this is the parietal lobe
where sensory integration is kind of happening
higher order sensory integration making meaning
making sense of the things in the environment
and then it can send signals to either the sensory
motor because maybe you just have a habit based
off of this information that habit will then
send information down to the dorsal striatum
remember the pertainment remember we mapped out
we extracted a specific cell from the pertainment
because this is where habits happen sensory motor
to to the putamen that's very lateral in the
dorsal striatum and a specific cell spine will
hit remember these are medium spiny neurons we've
mapped this out and then it will orchestrate
based off of the basal ganglia those other relay
stations and output areas and it will inform
the thalamus okay what am i doing remember the
habits though you don't have to think about things
You just automate responses. That's why we have
habits. If it's a habit, this is just an example
of a habit. Let's say it's not. So this corticocortical
could send information to the prefrontal cortex.
Maybe it's parts of the dorsal lateral, which
is this superior colliculi will update the dorsal
lateral early. Well, let's just map it out because
I really want to talk about the prefrontal cortex
now for sure. So we have the eye again, OK? and
then the thalamus here. And then we'll do the
brain stem here. You know, remember we have the
pons, a little football shape, and we have the
cerebellum, inferior coeliculi, inferior coeliculi,
right? And then we have the occipital lobe, the
parietal lobe, sensory motor. We're up through
here now. The dorsal lateral, we're getting into
the dorsal lateral area. This is going to be
more of the orbital frontal. And just to make,
help us make sense of where we are, okay? Remember
the the basal ganglia is right through here.
Remember it's all surrounding this ventricular
area. The third and the lateral ventriculars.
Okay a lot of electrical signals here because
there's a lot of water. There's a lot of freaking
water there. Low blood brain barrier too. So
let's just map out this prefrontal cortex. Let's
go blue right here. Dorsolateral. Use these colors
if I don't have to. I don't know if that shows
up much different than black. It kind of does.
Orbital frontal cortex. This is why I'm wearing
parts of the south because this is a lot of sensory.
It gets fast acting things from the environment.
About 90 % of the things in the orbital frontal
cortex, which is just right here, just right
on the other side of your eyebrows, is sensory.
It's very specific as well. And then deep inside,
on the inside of this area is the medial prefrontal
cortex. We've talked a lot about that, especially
the anterior cingulate cortex. Okay. We'll do
an episode all about this because these are heavily
involved, especially the medial prefrontal cortex
and maybe more so the orbital frontal cortex
and the dorsolateral prefrontal cortex, more
than what people might consider. I know the medial
prefrontal cortex is heavily involved with autism
because there's a lot of studies done because
this is where adaptive responses happen. This
is where, as we're navigating the world and we're
mapping this out neurally with these connections,
the medial prefrontal cortex leads the way. And
in large part, it's these other subdivisions
of the prefrontal cortex are helping out. Yeah,
the anterior cingulate cortex. Remember they
have the spindle neurons and the the lack of
parv albium. So the medial prefrontal cortex
is there's a lot of different abnormal cells
neurons here. That's that's why it's really known.
And in addition the adaptive responses because
everybody knows that the autistic in a social
situation lacks kind of skills because this is
being suppressed and the other subcortical areas
down through here and the habit formation with
the rigid thinking, repetitive behaviors are
acting more than here. This is more habit. This
is more goal directed. This is more being able
to adapt in the environment based off of useful
skills. So that's big. Okay, let's just get back
to what has access now. Trying, we're getting
through it though, because we were talking about
the layer six. So this information coming back
down here, back down to the thalamus is no, not
very good access, little access. Okay, so we
just map all this out. receiving sensory information
from the environment, which is that that's what
sensory processes is doing. It's extracting physical
information and phenomena from the environment.
So the living organism knows what to do. We mapped
all that out and then we sent it up to the many
columns, whichever cortex or whichever area you
want to think about. They're all slightly different.
In large part, what's different is the layer
four. And then what kind of cells make up layers
five and six and two and three? A lot of pyramidal
neurons and then inhibition neurons are making
up layers two and three and five and six. And
then you have things like microglia, like the
little support cells, which we haven't spent
a whole lot of time on that. So layer six has
very little access. Layer five has a lot of access.
Remember this is more firing rates. Good access.
Lots of access. Not bad. Okay. This tonic and
burst firing will help determine because this
is kind of providing some modulatory impact.
Some intensity. How much intensity? So that's
valuable information. Then we have some access
from the brainstem, especially remember the auditory
brainstem response. But there's other things.
Remember, with the, um, right here, with the,
with the brainstem, there's a, there's a network
called the reticular formation, not reticular
TRN. It's just the repurposed word reticular.
um reticular activating system is one where it
has ascending and descending fibers and just
the reticular formation or just a collection
of these brainstem areas used for arousal used
to go activate the sympathetic nervous system
so this is kind of involved with that so it has
some brainstem arousal get up and go the access
here with this reticular activating system is
context dependent. So it's hard to say if it
has easy access, you can just get right in, no
security, or if it's heavily guarded. It's context
dependent. Okay? Okay. And then there are things
like with this crosstalk, how much does this
shell have to be involved with this crosstalk?
Maybe it's talking back and forth to these different
subdivisions here. there's a lot of different
subdivisions in the thalamus. It's a heavily
studied area here. So this kind of helps with
what has access. The big thing to remember here
is just the raw sensory input here has very little
access. Now one thing that I should mention is
things like pain, things coming up from the body,
that intensity is also more context but mostly
pain has pretty strong access, so there's not
a lot of regulation control by the TRN. And here
with this pulvinar, which is heavily involved
in sensory information here, but the difference
between the sensory sector of the shell and the
subdivision with the sensory processing, inside
the thalamus is this provides more attention.
So remember the salience network, remember the
superior colliculi reaching up to the frontal
eye fields and then back down to the thalamus
and back down to the... superior colliculi. This
information here regarding the sensation isn't
so much raw anymore. The living organism is making
sense of it. So that visual input has little
impact for the thalamic reticular nucleus. It
has direct access to go back into the thalamus.
Why? Because it's determined. Something's made
the determination that that's valuable because
that's what i'm spending my spotlight of attention
to remember we've talked about signal to noise
and this is what i want to talk about kind of
right now because of um how important this is
with the signal to noise because that's a lot
about what we're talking about so i'm just going
to go ahead and erase some of this stuff here
so we can talk about We can talk a little bit
about some of the functions and goals here since
we're getting It's already covered. We already
did a pretty good job of covering that Okay,
and then the brainwave generation remember the
layer five the layer five helps with this and
something that's Pretty good is alpha band MIT
does good work on um alpha or the brain waves
and it should probably have a little bit more
traction i think in research is the brain waves
but i don't know i don't know the brain wave
is very functional especially alpha in this regard
which is 8 to 13 hertz remember we've we kind
of covered that you could probably pick up based
off of what we've talked about attention modulation
this is helping so it's unclear to me if this
is if this process is helping attention modulation,
or if... I think it's probably bidirectional,
especially if you think about the Autistic Phenotype.
It seems like it's bidirectional. Things that
are irrelevant are very much irrelevant to the
Autistic Phenotype. Things that are salient are
very much salient to the Autistic Phenotype.
So I think this, and with that lack of adaptive
responses and so forth... and the habits and
the restricted fixated interests that are abnormal
in intensity or focus. This is kind of helping
explain why the autistic phenotype has that.
What is really a big wow factor here for the
autistic phenotype and this so -called sensory
gate is regulating sleep -wake states. This is
not talked about enough. in the autistic phenotype.
But every autistic phenotype, every person with
autism, has sleep -wake dysregulation. These
things, 100 % of the autistic phenotypes have
sensory processing problems, which we're covering.
In large part, this is the core of it. Two is
speech -language problems. Three, GI problems.
Fourth, an underrated one, circadian rhythms.
E or no E. I don't know. Could be an E. But these
four, 100 % of autistics have 100%. 100%. I don't
care what the research suggests. Like this 50
to 80 % of autistics have a sleep -wake disorder.
No, it's not. It's 100. I promise you. NGI and
speech and language and sensory processing. promise
and a fifth thing would be mitochondria but semantics
i'm not going there the sleep wake regulation
remember in a large part because of this area
right here the reticular activating system is
involved with that this brain stem here is a
super highway man and it's got a lot to do with
balancing the brain and physiology okay so sleep
wake Not bad. And another one is just overload
protection. It's just that protection. Like especially
said the same as I think maybe one in three.
But it's a big deal. It's a very big deal. Another
thing that I want to talk about while we're talking
about this is back to the rodent knockout model
is because this right here is heavily involved
in autism. CNT -NAP2. You can double knock out
this. and you're going to have hyperactivity
because this is going to be abnormal. This is
very well studied in autism. I don't mind this
as like one of them so -called gene things. I
think genes are... broken. But, you know, there
are some. Like this one is Shenk 3. Neuraligen,
Neurexin are good ones. P10, good one. It's more
of an enzyme, whatever, but... some good stuff
there. So whenever this is knocked out you get
the hyperactivity. You get seizures and poor
socialness. Poor socialness. Wonder why? Or this
is um under -regulated. This is there's a lot
of information coming in and through this. Makes
it hard for the environment. Makes it hard to
interact. Remember listening to sonnets. Remember
the processes with the auditory brain. stem response
with wave five and the vision aspects of it there's
a lot happening here that's abnormal for the
autistic phenotype so there's isolation in a
rodent knockout of this right here and also repetitive
behaviors so what does repetitive behaviors look
like for a mouse or rat a lot of saying like
a lot of licking doing just a lot of the same
kind of behavioral activation the same action
just abnormal than what they were doing or what
their peers are doing so this is a pretty good
finding too what's different about this and the
sonic hedgehog i think is because this is this
comes on early with like the neuralation this
is more downstream this is more after So it's
not likely that the human living organism is
going to just not have the shell. That's not
likely to happen. That's not likely the case.
But it is likely because we know that. Remember
from the parvalium even that we can have a shell
but it's just not functioning properly. So this
is more in line with that. And based off of these
kind of phenotypes from this double knockout,
it's pretty good data. So what happens? This
is in on what are some of the strengths of this
kind of abnormal shell? So if you think about
it, if you think about what we've been talking
about, there's a lot of information coming in.
So what is a lot of information? What could that
mean? Well, we know that accelerated learning,
okay, so strengths of a poor TRN, it's accelerated
learning. Why? Because of that attention modulation
is inner, we're inward. The autism, look here.
Autism comes from the word autos. Autos, like
automatic, automobile. This means self. Too few
people know this more people need to know autism
means self So accelerated learning because if
you think about learning you need time on task
you need access to the information This actually
provides more. So this is a huge thing. We talk
about these splinter skills and so forth I don't
necessarily know if I like the term of that but
with having a poor thalamic reticular nucleus
we can accelerate the exposure and this is good
for learning and it's not difficult to see especially
if you read the early Cantor papers from 1943
or Asperger's paper from 1944 he's Asperger spent
a whole lot of time those are large long papers
by the way Asperger spent a lot of time on autistic
intelligence and Cantor did too he just didn't
frame it with that those words Asperger called
those little kids little professors this was
happening this was happening back then so this
accelerated learning is a very thing it's a very
functional thing the second thing i don't want
to say too much about this right now because
it's a whole at least one episode this is very
hard to explain if it's not you but that is visual
thinking this it's almost like this is bi -directional
here too and then you can lump things like this
on but remember right here is the parietal lobe
and then there's a little nuclei here called
the precuneus the precuneus is involved in the
default mode network as well where am i right
here the default mode network okay and visual
thinking this is imagination when sensory information
the sensory processing is such it's heightened
in the autistic phenotype remember because there's
a lot of brainwaves being responsible here and
even independent from this shell independent
of it with the the retina to the lateral geniculate
and the superior colliculus and the lateral geniculate
and the superior colliculus both are sending
fibers to the visual cortex, right? Because the
retina, it's split between receiving, sending
some projections to the lateral geniculate and
the superior colliculus. So there's like two
distinct pathways here, but each of these two
will send some information up to the visual cortex.
We'll parse this out. The visual cortex is being
bombarded and it makes it hard to. kind of flow
through the process and that's why you hear things
like bottom up or details first this is so huge
with learning this is so underrated and this
is a big benefit this is just such a huge benefit
i can't speak enough on visual thinking and accelerated
learning or even the default mode network because
that that's a big misnomer science and people
think The autistic phenotype has an abnormal
default mode network. No. This is our default.
The default is the default mode network because
it's all inner. Remember the salience network
as well. Inner. Autism means autos, which means
self. It's not complicated stuff. People researching
autism are not autistic. People researching autism
are just viewing it from the outside. The weaknesses
though, we kind of talked about this. The weaknesses
is the hyperactivity and just the lack of being
able to filter out properly. So there's like
anything in life. There's some benefits and some
struggles with the thalamic reticular nucleus.
But if you have the thalamus like this, the shell
over it for protection. Thalamic reticular nucleus.