Defining the autistic phenotypes is not difficult.
Understanding it and bringing real -life data
and experiences can bring these autistic phenotypes
into power. For today's episode, we will cover
inhibitory neurons and the autistic phenotype.
You likely know about the excitation and inhibition
imbalance. In the autistic phenotype, this push
-pull tactic the central nervous system uses.
Today's episode is all about those inhibitory
neurons. In addition, we've discussed the thalamus,
our major hub for sensations, awe. Sensations
will hit the thalamus and it will continuously
provide information in a feed -forward feedback
loop. to the rest of the brain. The thalamus,
because of its massive role, has a specialized
shell evolution has equipped it with. Imagine
perceiving every sense coming in. You can't.
You don't. And I suspect you wouldn't want to.
The thalamus has a special feature that appears
to evolve alongside with more complex behavioral
species. In humans, this is called the dynamic
reticular nucleus, or TRN. Now, because humans
are humans and scientists are scientists, you
can see this abbreviated slightly different,
but it is the reticular nucleus. Don't get this
confused, however, with areas of the brain stem
that create the so -called reticular formation.
These are two different things here. The thalamic
reticular nucleus is a shell, a thin layer of
inhibitory neurons protecting what enters, what
signals enter the thalamus. It's a sensory gate
system. Now hopefully you can understand the
connection of schizophrenia and autism. The visualization
and these heightened senses that we have both
have both schizophrenia and autism. have an excitation
and ambition imbalance. The outside world is
chaotic and understanding eye gaze is not complicated.
Once you understand how those early eye areas
for visualizing are in heightened waves such
as gamma compared to so -called normal that are
in alpha and beta and slight transient shifts
into gamma, all while being able to inhibit noise
from the background, which is theta. Theta helps
kind of regulate, it scans the brain and kind
of helps regulate these waves. See Earl Miller's
lab at MIT for some of that. Today's episode
is all about autistic brainwave phenotype. and
the gamma power, synchrony, with this EI imbalance,
and the sensory -cognitive disassociation with
the autistic phenotype. So let's get into the
types of inhibitory neurons and their characteristics
and roles. But first, what do the inhibitory
neurons do? Where do they go? GABA has three
receptor types. GABA A, which is ionotropic,
which is fast. These occur within milliseconds.
GABA B, which are metabotropic. These are slower.
These are so -called G -coupled protein receptors.
These occur, these act within hundreds of milliseconds,
so they are slower. And a more rare, but still
important receptor type here is GABA C. which
is another ionotropic, and these are for sustaining
the inhibition response, that inactivation, more
in a tonic -like flow, tonic -like activation.
These receptors hyperpolarize neurons and modulate
neural activity with hopes of maintaining EI
balance. The goal is a balance, but with the
autistic phenotype. There is a known imbalance.
Now hard stop here. I said tonic -like. And this
is true. This is definitely a thing happening
in the background. Now more recently, we've began
to talk about waves, these oscillations and frequencies.
And all of these molecules, these modulators,
dopamine, serotonin, these excitation inhibition,
et cetera, norepinephrine. All of these are released
in different types of kind of frequencies outside
of the alpha, beta, gamma, and so forth. These
are called tonic firing, burst firing, and phasing.
Now tonic is more regular single isolated spikes
that are in proportion to signals coming in.
It's a steadier state in the background. and
this can be used to track changes and reward
value such as those internal calculators anytime
you expose or experience a stimuli how does these
things kind of shift the delta of these so you
can track the tonic burst and phasic along with
the the beta gamma and so forth the other one
is burst firing It is just exactly what it sounds
like it is. They are bursting high frequency
and rapid succession. They are short clusters
of action potentials and they are stronger with
more potent effects. Now an easy example here
is like doing a drug. If you do like let's say
methamphetamine or something you're going to
get a high bursting action of dopamine. Don't
do that though. Phasic. is more of a pattern
of firing that alternates bursts and pauses of
activity. These signals are transient or more
so -called moment -to -moment changes. And this
is also used to allow those internal calculators
to evaluate things that are happening in the
environment, like reward or value, conflict,
and certain outcomes. More event -related than
tonic. these are all very fascinating things
and very relevant okay we'll hit on those a little
bit as we move through the episode but remember
we have GABA A which are very fast acting GABA
B slower acting still fast but slower and then
GABA C which is kind of rare so in the autistic
phenotype these dysfunctions will drive sensory
hypersensitivity, cognitive and social deficits,
and repetitive behaviors. Things that you understand
about the autistic phenotype. But we're going
to help explain these so -called phenotypes a
little bit better. With the specific neuron type,
certain brain regions and receptor interactions,
and then just general autistic phenotype problems.
Now I want to go back before even the central
nervous system is created and maybe go upstream
here and something that we've mentioned before
in the two part neural relation episodes and
that is a fun sonic hedgehog gene and protein.
It's called sonic hedgehog not sonic the hedgehog.
Before the central nervous system is forming
sonic hedgehog and it's Mesodermal cells will
signal to the ectoderm to create neuroepithel.
Neuroepithel is the action by which the central
nervous system will kind of come in, kind of
be formed here. This is the process of the central
nervous system. Sonic Hedgehog is very responsible
for differentiation and migration. So remember
the differentiation. Cells become specialized
cells. and then they migrate to similar cells.
They migrate to their area of operation, kind
of. See also P10, SHNK3, and fibroblast growth
factors and WNT proteins on this kind of epoch
that we're talking about. All of those things
that I mentioned are regions of interest for
the autistic phenotype during this early embryonic
development. Now I say most of that to say this
because this is huge. Sonic hedgehog is critical
for developing inhibition type neurons and an
area that we're going to discuss a little bit
in detail later with that thalamic reticular
nucleus. Sonic hedgehog is responsible for progenitor
proliferation here that guides in the cortex
and the thalamus and it supports maturation and
synaptic integration here this is huge for the
thalamic reticular nucleus specifically here
it is sonic hedgehog established the ventral
domain and it enforces GABAergic identity which
are patterns if you knock out sonic hedgehog
you will see this in research paper they'll have
two minus signs. It'll say SHH minus minus. The
rodent or the living organism, whatever they're
studying, will not develop part of the thalamic
reticular nucleus. The sonic hedgehog gene and
protein is responsible completely for developing
the ventral part of this shell. But it has no
role with the adult formation. Meaning you can't
knock it out in an adult model and do anything
to this reticular nucleus. It's already established.
So for development, this is vital. And if it's
impaired, the thalamic reticular nucleus and
these inhibitory neurons, two different things
there. are going to be impaired or even missing,
completely missing. And this is shown with models
for epilepsy, the autistic phenotype, and schizophrenia.
One additional thing before we get into the specific
neuronal types of the inhibition. A former guest,
Ezekiel Ben Ari, had discovered that GABA during
embryonic and fetal development during gestation,
GABA is excitatory. It's not until the birth
that is shifted to inhibitory. There are certain
sodium and chloride and potassium, I believe,
if I remember correctly, interactions that kind
of guide this. You can check out the episode
I did with Ezekiel Ben Ari. And in the show notes
of that episode are all those papers. He explains
it well and uses a PowerPoint for easy understanding.
So the first inhibition neuron, we've talked
about it. We have a whole episode on it and it's
called parvalbum interneurons. These are the
most dominant type of inhibition that we have
in the brain. These are fast spiking and expresses
Parv albium for rapid calcium buffering. Brain
regions here for the parv albium interneurons
are the cerebral cortex, specifically the dorsal
lateral prefrontal cortex. Remember the spindle
neuron episode. Humans have, we found clusters
of spindle neurons. They're very few and hard
to pick up in the dorsal lateral, those spindle
neurons. and also the ventromedial prefrontal
cortex. This is a huge region of interest because
of its massive connections, bi -directional connections
to all the neuromodulatory nuclei here, such
as the acetylcholine, serotonin, dopamine, epinephrine,
norepinephrine, and so forth. And there's also
a lot of connections with the subcortical areas
here. This is a big hub here. And also the orbital
frontal cortex. primary visual cortex, and the
primary somatosensory cortex, primary auditory
cortex, so V1, S1, and A1. Huge, huge for sensory
processing. In addition, parvoalbum, which is
an area that we covered in the episode about
parvoalbum, the interior insula, which is emotional
interoception. understanding what you're doing
in the environment, how you're feeling. And also
the posterior insula, so the insula is loaded
here. And the ACC, anterior cingulate cortex,
which is kind of like a similar hub to the ventral
medial prefrontal cortex. It's a huge internal
calculator here. The superior temporal gyrus,
remember the decoding the brain? how reading
works in autism and dyslexia. We talked a lot
about the superior temporal gyrus. And lastly,
the inferior temporal cortex. So, within the
cerebral cortex alone, parvoalbum has massive
roles. It's also involved with the hippocampus,
both CA1 and CA3, and the dentate gyrus, and
also the striatum, the caudate and putamen, and
also the nucleus accumbens, so both the dorsal
and the ventral striatum. We talk a lot about
the striatum because of the basal ganglia. It's
a major network here. Parv Albium is, of course,
involved with the thalamus, the thalamic reticular
nucleus, and the amygdala. You mostly or probably
know about the amygdala for fear. Well, I have
news for you. The days of certain regions responsible
for certain states, emotions, feelings, and so
forth is over. We're over that. The amygdala,
yes, is very involved with fear, but it's also
involved with much other different opposing types
of emotions or feelings and actions. It's more
about neural correlates and pathways and connections
and networks instead of certain regions. That's
a very bad misnomer. And hopefully that will
continue to shift. We'll shift out of that. And
also, finally, the cerebellum. We've had an episode
about the cerebellum with Reza Shadmir. And the
parv albium is helping to modulate purgenji cells.
So the parvalium will hit on all three of those
receptors A, B, and C. It will hit GABA -A to
help modulate pyramidal neurons, which is our
most dominant excitation type. We'll do a whole
episode on that. GABA -B receptors for a slower
inhibition for potassium -calcium channel modulation,
and the prefrontal cortex, hippocampus, and the
thalamus. And then finally, and this one will
make sense, it hits GABA -C for sustained inhibition
and the thalamic reticular nucleus and the lateral
geniculate nucleus, one of the first stops for
vision, and the amygdala and cerebellum. And
it has a high GABA affinity in these areas. So
what roles do these have in typical brains? Parvalbium
drive gamma oscillations for sensory integration
and attention and working memory, providing somatic
inhibition to prevent hyper excitability. And
this is critical for the TRN sensory gating.
So what is happening with the autistic phenotype?
The reduced density and function in that dorsolateral
prefrontal cortex, the anterior insula, which
is mainly what that episode is about, and V1,
visual cortex 1, and the TRN impairs gamma oscillations,
leading to sensory hyper sensitivity. The lack
of parvalbium here cannot regulate this push
-pull system. So it creates that imbalance and
it has massive implications to cognitive integration
and social deficits. Last thing for now on the
part of Albion, enter neurons. This imbalance
contributes to that elevated EI ratio, amplifies
this brain -derived nootropic factor, excitatory
enhancement. Okay, this is studied in molecular
psychiatry in 2017. Decent paper about this.
We'll say a little bit more about brain -derived
nootropic factor or BDNF in the excitation episode
more so. But to recap, the parvalbium interneuron
is the most dense, should be the most dense of
all the inhibition type neurons, the inactivators.
The second most is somatostatin expressing interneuron,
SOM for short. These are slower firing and provides
feedback inhibition that target the pyramidal
neuron dendrites. Brain regions here are the
cerebral cortex, the dorsolateral, that ventral
medial, and the orbital frontal in addition to
the V1, S1, and A1, so those three main sensory
processing cortexes as well. Anterior and posterior
insula, and the ACC, the superior temporal gyrus,
just like the parvoalbeom, but they're less,
and they're also found in the hippocampus CA1
and CA3 as well, and the amygdala. More so for
the social behavior, the basolateral and the
cortical amygdala. We haven't really parsed out
these different subdivisions of the amygdala
too much. Receptors, so it works on all three,
GABA -A, and depending on which one, A5 or A1,
A2, it's kind of helped modulating the tonic
inhibition or the phasic on the dendrites. It's
mostly acting on dendrites here. GABA -B for
slow dendritic inhibition, and GABA -C has a
minor role in the amygdala and hippocampus for
sustained inhibition. The somatostatin helps
modulate AMP -A and NMDA activity. Those are
excitation receptors, the post -synaptic. We
talked about those in quite detail. in an early
episode of the podcast, episode four or five.
I can't remember which one, but those are receptors
that excitation, excitatory neurons will park
on, they will connect to. Some general roles
here for the somatostatin and so -called typical
brains is regulate dendritic excitatory inputs.
and modulates synaptic plasticity, for instance,
long -term protetiation. So we've talked about
the hippocampus there. That's something that
it does. And it supports, the somatostatin support
sensory adaptation. Remember, an overarching
theme of the autistic phenotype is a lack of
adaptive responses. We talked about the anterior
cingulate cortex and the ventral medial prefrontal
cortex. These are major regions major hubs for
applying adaptive responses. Remember the social
world is the most unpredictable and most chaotic
thing that we do especially for the autistic
phenotype. The role here for the somatostatin
in autism what it looks like for the autistic
phenotype is impaired function in the interior
insula, hippocampus, and V1. In visual cortex
1, it reduces tonic inhibition, an amplified
sensory input that contributes to repetitive
behaviors. And this is also linked to the brain
-derived nootropic factor, which helps drive
the excitatory imbalance. So the third inhibitory
type of cell here, neuron, is vasoactive intestinal
peptide VIP interneuron. Some characteristics
of this is mediates disinhibition by inhibiting
the SOM and the parvalbium so it inhibits inhibitory
neurons. Does that make sense? We have this inhibition
as well. So it shuts off somatostatin neuron
and the parvalbium neuron. And this will enhance
the pyramidal activity. Now the pyramidal neuron
is going to be the major region of interest for
the excitatory cells. So we'll have a whole episode
on that. But this is going to be huge for sensory
integration, sensory processing as well. Some
brain regions of the VIP, the cerebral cortex,
the same areas. These are all in the same areas.
Dorsolateral, ventral medial, visual cortex 1,
somatostatin 1, and the auditory cortex 1. The
anterior insula and the ACC, anterior cingulate
cortex. superior temporal gyrus. The hippocampus
this time only CA1 for those that really want
to know and the amygdala the basolateral again
and this time we're going to find that the vasoactive
intestinal peptides are also in the central amygdala.
Now evolutionarily the central amygdala is kind
of It predates the more lateral areas. It's kind
of home to innate type of fear. The receptors
here, GABA A. And this targets the interneurons
for disinhibition, like we talked about. GABA
B has a little bit of a role here with indirect
modulation. And GABA C. It has a minor role,
again, with the amygdala and hippocampus. Another
role that it has is expression of VIP receptors,
which are G -protein coupled, and nicokinetic
acetylcholine receptors. Now, nicokinetic acetylcholine
receptors are very, very fascinating. Acetylcholine,
you might know, is a neuromodulator. It has two
receptors. Nicokinetic and mucicarnic. The nicokinetic
receptor, just similar as nicotine, right? You
know about the nicotine. These are very excitatory.
These are very excitatory type of excitation.
So the vasoactive intestinal peptide row in so
-called typical brains is to facilitate selective
circuit activation for attention and sensory
processing. We kind of made sense with that,
with this inhibition role here, and then how
it's interacting with the excitation parts. The
role of the autistic phenotype is an altered
function in the dorsolateral prefrontal cortex
in the interior insula disrupts attention and
social processing, which will then, of course,
lead to social deficits. And this is a good study
in Cell Reports. One of my favorite journals
is Cell Press. And this was done in 2019. Okay,
so a fourth type of inhibitory neurons. It's
kind of a two -in -one. Calbindin and calretinin
expressing interneurons. So why the two -in -one?
Well, I... Just assume that these are very rare.
They're not real known. Not studied that much.
But the characteristics here is the calbindin
provides dendritic inhibition, which is pretty
common theme here. Calritinin mediates that disinhibition
and it targets those interneurons as well. Brain
regions here for the calbindin. is pretty similar.
Dorsolateral prefrontal cortex, orbital frontal
cortex, V1, various layers of S1, layers four
through six, so very detailed location here for
S1. Calbondin is also in CA1 and CA3 subdivisions
of the hippocampus and the dentate gyrus. and
the amygdala, the basolateral amygdala again
and the cortical amygdala. The chalretanin is
in the ventral medial prefrontal cortex so we're
kind of separating here finally. Visual cortex
1 and auditory cortex 1 and also the anterior
insula. and the ACC anterior cingulate cortex,
and the superior temporal gyrus. There's not
a whole lot of information to provide on the
receptors, what they're acting on, why they're
acting on it. These are not well -known cells
here that we're talking about. But the roles
in the typical brains is fine -tuning local circuits
for sensory and emotional processing and neuroplasticity.
The role in the autistic phenotype is shown to
be reduced functioning in the interior insula
and hippocampus contributes to sensory and emotional
deficits. Though this is kind of not well studied.
They're just not well known kind of cell types
here that we're talking about. But we'll wrap
it up with the purgenji cell, which is well studied.
especially in the autistic phenotype. There's
a major deficit of progeny cells in the autistic
phenotype. The whole episode with Dr. Reza Shadmir
is so fantastic. He's such a great human being.
The characteristics here are these are GABA -urgent
neurons in the cerebellum only and they provide
primary inhibitory output. It's for precise motor
control. Very precise. detail here, fine -tuning
these purgenji cells are doing. Brain regions
are the cerebellar, the cortex of the cerebellar,
and lobules one through five, and they project
to deep cerebellar nuclei. Receptors here are
GABA -A for fast inhibition into deep nuclei.
And then GABA -B for the slower inhibition. Remember
these are slower type G protein coupled. And
GABA -C for a sustained inhibition. So more of
that helping sustain and tonic flowing of granule
cells. And it also helps receive AMPA and NMDA
inputs. The role in the typical brain is refined
motor coordination and cognitive timing in cerebellocortical
loops. The Burgenji cells here are vastly underrated.
One of the most underrated cells in the entire
human brain. And if you don't know, the cerebellum
is kind of like that miniature brain in the back,
the posterior ventral back. of the brain. And
most species have them. If you look at like a
rat or a mouse, it's at the top. But that's because
the mouse and rat brain isn't as developed. So
anatomically, the cerebellum and the rat or mouse
brain is identical. If you think about the growth
and evolution versus the human cortex, it's all
structured the same. just less. For the autistic
phenotype, the cell loss in vermis. Dr. Shadmere
talked about this a lot, and Lobules 6 and 7
disrupt motor and social behaviors and contributes
to serotypes. So we covered six inhibitory pepsi
neurons there, quite dense, and the nomenclature
and roles, brain regions and so forth. So it's
pretty dense stuff here but very important because
of the roles of this push -pull tactic system
that the central nervous system uses. So let's
talk a little bit more about this push -pull
system. An EI balance is dynamic interplay between
activation and inactivation. We use excitatory
like glutamatergic and these pyramidal neurons
and inhibitory the GABAergic that we've just
talked about and this is regulating neural circuitry
the push side this excitation side the pyramidal
neurons in the cortex and the thalamus drive
activity with those AMPA and NMDA receptors and
this is promoting things like learning and promoting
sensory and cognitive processing, we must be
activated to process things. The pull system,
the inhibition, the things that will help keep
us in check here, are here to prevent overload,
hypersensitivity, hyper excitability, and ensures
precision. This is all about a balance, a healthy
movement of a seesaw or the bumper rails down
a bowling alley. This is what excitation inhibition
is doing. It's trying to keep everything in check,
in line, in optimal ranges. Okay, before we wrap
up, I like to think about things from an evolutionary
standpoint. Why do we have the things that we'd
have and what are they trying to accomplish?
What are we supposed to be doing with them? So
the parv albium interneuron, this is mostly responsible
to drive gamma oscillations for sensory and cognitive
synchronization. And it gates sensory inputs
for that thalamic reticular nucleus, especially
in the visual somatosensory and auditory sectors.
We'll parse that out in a different episode now.
It's too much to add in the thalamic reticular
nucleus for this episode. It's just too much.
And it also provides somatic inhibition in the
cortex and hippocampus. So this is the most dense
interneuron, inhibitory interneuron I should
say. The somatostatin interneurons is mostly
responsible to regulate dendritic inputs. So
it kind of regulates where cells park on dendrites.
modulates plasticity and supports sensory adaptation.
This is a big thing that humans do is adapting
but specifically in the cortex and the hippocampus.
The VIP interneurons VIP this facilitates that
this inhibition for helping to select attention
in the cortex signal And noise is how neuroscience
looks at this. Signal to noise ratio. What can
you quiet? The cow binding and cow retaining.
These are more for the fine tuning of local circuits
for the sensory and emotional processing. For
Genji cells, refine cerebellar motor and cognitive
output. Remember this is all about precision
control here. especially with reward, Shadmere
said. They're mostly involved with highly rewarding
things. So some evolutionary aspects. In early
vertebrates, GABAergic interneurons, the parvalbium
and somatostatin, emerge to stabilize neural
circuits and prevent seizures even. Now you know
about autism and epilepsy, for sure. This was
reviewed in Nature Reviews neuroscience. Mammalian
expansion. The increased, should be increased
parvalbium interneuron density. In the thalamic
reticular nucleus and the cortex support complex
sensory cognitive processing. Everything we're
doing in the environment is pretty complex. Primate
specific. increases in the dorsolateral prefrontal
cortex and the anterior insula. And this enhances
social and cognitive functions. That whole episode
was essentially about this. So lastly, if you
think about developing, learning to navigate
the world, learning your environment, how this
is interacting here and interfering, the translation
of autism or autist Autistic is autos, A -U -T
-O -S, which means self. Do you understand why?
The self is much calmer and even a lot more entertaining
because of our ability to be present inside.
The biology that gives us autism allows us to
be comfortable within our self. And this promotes
accelerated learning as well. This is very fascinating
with those visual thinking processes here, which
is in large part due to that heightened gamma
activity in those early visual processes. Retina,
the retina ganglion cells, lateral geniculate,
and then the superior colliculus and the visual
cortex V1 through V4. These are all gamma waves.
These are all heightened. in the autistic phenotype,
you know about the attention to detail, the inability,
let's say, to shift off of something. It's not
that difficult to understand, is it? It's not
that difficult to understand the autistic phenotype.
The major problem here is environmental insults.
People are not understanding it, not understanding
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