Today's episode is all about the thalamic reticular
nucleus or TRN. In the previous episode about
sonic hedgehog and inhibitory neurons, we mentioned
this nuclei that surrounds the thalamus for inhibiting
signals or noise. The TRN is a shell designed
to quiet unnecessary noise coming in to the thalamus.
Remember the thalamus receives all sensory inputs
and it's on a constant feed -forward feedback
loop with other areas of the brain. We'll review
this nuclei in good detail and use a security
guard analogy for each type of sensory processing
and nuclei. that makes up this shell known as
the thalamic reticular nucleus. This is all GABAERGIC
or inhibition. The more I think about it, the
more the TRN is like a shield or armor. The TRN
is a critical brain structure composed of GABAERGIC
neurons that envelopes the thalamus, acting as
a gatekeeper. I know, another analogy here, but
it all fits, they all make sense. For this thalamocortical
communication, the TRN modulates sensory processing,
attention, memory consolidation, sleep -wake
transitions even, and brain wave generation,
with a significant implication to the autistic
phenotype, where its altered function contributes
to cognitive strengths such as strong learning
ability. Remember the biology that gives us autism
allows us to be comfortable inside of ourself.
This shell, this t -r -n with the autistic phenotype
prevents all of that outside noise, all of that
outside external insults and care. It's also
responsible for some of the visual thinking.
However, It also implicates some challenges such
as sensory hypersensitivity as discussed in the
previous episode and impaired integration. The
TRN is a very thin sheet -like layer of GABAergic
neurons that surrounds the lateral and anterior
thalamus and it forms a reticular shell between
the thalamus and the cortex. Remember from last
week's episode in a previous episode all about
the parv albium interneuron. This is the major
neuron here within this TRN shell. Remember the
parv albium interneuron is very fast acting,
fast spikes for precise inhibition. Remember
the GABA -A receptor in comparison to GABA -B.
And a small subset of the somatostatin, SOM,
neurons for a more broad modulation. The receptors
here are the GABA -A for the fast inhibition
and GABA -B more with the somatostatin for the
slower inhibition. Let's review some functional
goals of the TRN. One of course is sensor gating.
This is the major one. So enhancing signal to
noise ratios. inhibiting irrelevant activity,
and even prioritizing salient stimuli. For example,
visual patterns over the background noise. So
different sensory organs there. Attentional modulation,
brainwave generation, sleep -wake regulation,
Cross Modal Integration. So coordinating activity
across sensory and limbic circuits for integration
of perception and behavior. It's kind of helping
coordinate or bridge the limbic areas in the
cortex. We'll talk more about that later. Neuro
overload prevention. This is huge. We'll use
a little security guard example at the end of
the show. And it's also a support for the thalamus.
The TRN helps the thalamus by sharpening signals,
coordinating timing, preventing overexcitation.
And this is enabling flexible processing. So
it enhances the thalamic efficiency. And that's
a big part. So what signals come in to the TRN?
The afferents, or inputs. Well, it receives inputs
from the thalamus itself. excitatory glutamatergic
inputs from relay nuclei such as the lateral
geniculate nuclei remember for vision and the
medial geniculate nuclei which is for auditory
and the ventral basal and the medial dorsal via
AMPA and NMDA receptors. which is organizing
for modality -specific processing. We'll have
a whole episode on those excitation neurons,
just like we're doing for the inhibitory neurons.
It receives cortical inputs, again more excitatory
inputs from cortical layers, especially six for
the sensory and prefrontal cortex, enabling top
-down control of attention and sensory gating.
We'll talk a lot about the sensory gating. It's
a good overarching theme and description of this
shell. And also, a favorite of mine, the basal
ganglia inputs. Inhibitory GABAergic inputs from
the Globus pallidus external GPE and the substantia
nigra pars reticulata. Remember in the basal
ganglia episodes, these two little nuclei the
GPE and the SNR are pretty similar in function.
And this modulates motor and cognitive processing.
Now the basal ganglia is a major region of interest
for us here. Remember when we discussed the basal
ganglia nuclei? There's five different nuclei
there. And there's an additional assistant for
the thalamus, which is sort of like the TRN.
the subthalamic nucleus. This is another assistant
to this thalamus. The basal ganglia role here
with the TRN is some of the functions or action
selection and suppression. So a normal role,
a normal brain, let's say the basal ganglia disinhibits
the thalamus and the TRN will send tonic releases
of the neurons for sustaining adaptive behavior.
However, in the autistic phenotype, there's an
excessive TRN burst. So a difference between
tonic firing and burst firing. And this oversuppression
will lead to repetitive stereotypies. You know
that with the autistic phenotype. Sensory motor
gating. The TRN here in a normal brain filters
the limbic input. Let's say from the ventral
anterior or the ventral lateral. But for the
autistic phenotype, the TRN is hyper excitability
and sensory overload. And under filtering causes
this so -called hyper and hypo sensitivity, well
known and understood in the autistic phenotype.
The basal ganglia to the thalamic reticular nucleus.
is also involved with cognitive flexibility.
You know about this with the adaptive responses.
We talked a lot good detail about this. Major
regions of interest here are the medial prefrontal
cortex sending signals to the input areas of
the basal ganglia called the dorsal striatum
and this will orchestrate the basal ganglia for
the no no -go areas and it's kind of conducting
what we do next. This is huge in the autistic
phenotype, a so -called lack of adaptive responses.
Remember the medial prefrontal cortex is essentially
conducting these movements and our healthy responses
to this very unpredictable and chaotic social
world. So depending on the projections coming
in, from the prefrontal cortex especially the
medial part and even the dorsal lateral part.
We talked about these two regions in great detail
last episode. These connections here will determine
where the cells and signals will connect to the
dorsal striata and this provides meaning. Okay
this is happening because these cells are active
So this is what I do in response to that. These
specific signals and connections from the prefrontal
cortex to the dorsal striatum will house our
movements. What we do, remember the prefrontal
cortex is a rule setting machine. And we want,
we need a flexible rule setting type of machine.
having different skills available to us for different
situations. Now you know about this with the
autistic phenotype, very rigid. So these signals
coming into the dorsal striatum is also very
rigid. We only have these limited amounts of
kind of response types. And this is very big
here. These are the neural correlates and the
cellular functions of the lack of adaptive responses,
the rigidness, the black and white thinking,
and so forth. This is all happening here. So
with this cognitive flexibility, for the normal
brain, let's say, the TRN switches thalamic output
so it can just... Remember, we talked about action
selection. This is all coming together here.
For the autistic phenotype, we have those rigid
routines and the poor task switching. This is
why this basal ganglia to dilemmic reticular
nucleus connection is just downstream from those
prefrontal cortex to the basal ganglia inputs.
So salience, remember we've discussed the salience
network as well. I know a lot of different kind
of nomenclature and terminology here but... It's
really not that difficult. So what is salient
to us? Where do we want to spend and send our
attention for the so -called normal brain? The
TRN is helping mark social and reward cues. This
is very big in how mammals, complex living organisms
kind of navigate the society based off of cues.
In the autistic phenotype, there's this so -called
blunted social motivation here and very abnormal
kind of reward processing for the outside world.
In addition, this TRN here, as we just described
it over the last couple of minutes, it can cause
us that so -called stuck feeling or repetitive
actions. So maybe a lot there about the basal
ganglia and the thalamic reticular nucleus connection
and interaction. So let's get back to the afferents.
There's interactions with the major neuromodulation
inputs, the neuromodulators that we talk about
and you probably know about, such as cholinergic
acetylcholine from the basal forebrain. Remember
the Nucleus basalis of Minert is a hotspot for
acetylcholine. And serotonin from the raphe nuclei.
And norepinephrine from the locus coeruleus.
And dopamine from the ventral tegmental area,
VTA. And the substantia nigra pars compacta.
Remember, this is different than pars reticulata.
Reticulata is all GABAergic. that's helped modulating
the basal ganglia no -go area. The substantia
nigra pars compacta is a seat of dopamine. Remember,
it's in the midbrain, the mesencephalon. This
house releases excitatory and inhibitory dopamine.
And these inputs from these neuromodulators regulate
firing modes, such as tonic, or burst firing.
This is very huge. This is at the at the heart
of how we operate or these firing modes and brain
waves. It's really underrated here in my opinion.
So some of the efferents, the outputs, what does
the TRN do? Where does it send information to?
One, there's a feedback inhibition. This is a
so -called closed loop control of the cortico
-thalamic axons. Excitatory neurons, pyramidal
neurons to be exact, project to both the relay
nuclei of the thalamus such as the lateral geniculate
and the TRN. So the excitatory neurons coming
in from the cortex is received by various areas,
various nuclei within the thalamus. such as the
lateral geniculate and other subdivisions here,
and the TRN. And these nuclei within the thalamus
itself are interacting. They're sending information
back and forth to each other. And the TRN will
receive that information and then decide to shut
it off. It just turns it off. It's disinhibiting.
And this is purposeful for sharpening sensory
tuning. regulating attention, suppressing noise,
and promotes oscillatory rhythms. This is huge
for sleep spindles and gamma waves. In addition,
another efferent interaction here is a phi -forward
inhibition or a so -called open -loop modulation.
There are some ascending sensory pathways here
from the brain stem or the retina. that sends
collaterals to the TRN before reaching relayed
nuclei. So it's kind of privileged here. The
retina, of course, massive amounts of visual
input and sensory coming in from the retina.
And also the brainstem, the so -called major
highway. The brainstem is very underrated as
well. It's major highway here of information
from the brain, from the body, and just interacting
here. It's just making sense of so much. We'll
talk more eventually about the reticular formation.
Remember, this is different than the thalamic
reticular nuclei, but the reticular formation
within the brainstem has two major pathways,
ascending sensory pathway and descending sensory
pathway. But for this example, The region of
interest for us is the ascending sensory pathway
and the trn will then inhibit relay neurons and
it delays or sculpts the sensory interaction.
The function here is controls gain timing and
salience of the incoming sensory input. It's
kind of like it's privileged here it's getting
first privilege information of what is happening
so we can stay ahead of any unwanted stimuli,
unwanted things from the environment or signals
from within ourself even. Another major efferent
and role of the TRN for the outputs is regulating
burst versus tonic firing. And this is huge as
we just discussed earlier. The TRN neurons switch
between burst mode which is for strong inhibition
promoting sleep seizures or sensory suppression
or tonic mode sustained inhibition which helps
fine -tune attention and sensory discrimination.
What do you want to pay attention to? Remember
just imagine if the thalamus had to discriminate
all of the sensory inputs coming in from the
environment, vision, hearing, taste, touch, etc.
There is no way that you'd want that. In short,
and in summary, the TRN is a major dynamic gate
that is central to state -dependent processing,
meaning between sleep and wake, or something
like attention. versus distraction. Signal to
noise. So you might ask, and you ought to ask
maybe, what is the thalamic reticular nucleus
made of? I know I'm not saying GABA -ergic, but
let's zoom in to the thalamic reticular nucleus.
What is it made out of? What is each area trying
to accomplish? That's a good way of asking yourself
a question about our biology. Why is it there
and what is it trying to accomplish? Well, the
TRN has different sectors. We are going to say
it has four major sectors here, four major kind
of hubs or responsibilities. One is the visual
sector. The second is the somatosensory sector.
The third is the auditory sector. Remember last
week we talked about V1, S1, and A1. This is
what's happening here. This is where we're going
into. And the last and the fourth sector is the
limbic sector. So the visual sector is located
in the rostral, the limbic reticular nucleus,
and it's adjacent to the lateral geniculate nucleus.
which is the major relay station here, one of
the first stops for vision. And this is using,
no surprise, the parvalbium interneurons, and
it's also using the VIP interneurons. Remember
the vasoactive intestinal peptide. And it's using
all three of the GABA receptors, A, B, and C.
A for the fast inhibition of the lateral geniculate
nucleus. So it's just kind of quieting visual
distractions. Gaba B for the slow inhibition,
for the sustained modulation, trying to help
you maintain attention. And Gaba C for sustained
tonic, like inhibition, for fine tuning that
visual gating. How long can you sustain your
attention on a visual input? Think about children
doing the staring contest. This is a good example
here. Children doing the staring contest will
utilize probably gaba B and definitely gaba C
in order to just quiet themselves while they're
staring at you. How long can you sustain that
without being uncomfortable? Functions of the
typical brain is the sensory gating. No surprise,
we just talked about the staring contest. The
gamma oscillations. This visual sector helps
drive gamma power in the lateral geniculate loop.
Lateral geniculate to visual cortex one loop.
And this supports visual feature integration.
And synchrony. Facilitates gamma synchrony between
V1 and downstream dorsal lateral prefrontal cortex.
for visual cognitive integration. What's happening
in the autistic phenotype is a reduced inhibition
here. So the decreased parvalbium interneuron
with especially GABA A and GABA C receptors impairs
lateral geniculate gating. And this increases
excitatory input to visual cortex one and elevates
gamma power. We talked about this a lot and I
hope people have a good takeaway here. The sensory
processing is mostly gamma, even higher gamma,
and this is one of the mechanisms by which that
happens. Remember visual thinking and attention
to detail. This is huge here. You know about
how eye contact is a pretty much a no -go for
the autistic phenotype. especially for me and
as I've learned about others and talked to others
during speaking. Eye contact during speaking
is a huge problem. There's so much happening.
Remember the B -movie example. The sensory processing
in the outside world is chaotic. Carl Dyseroth
calls it a fire hose of information, a torrent
of information. It's like a machine gun, a torrent.
This is very accurate. If that's not you, you
will have no idea what it is or what it feels
like. In addition, there's a disrupted synchrony.
So that reduced gamma synchrony between V1 and
the dorsolateral prefrontal cortex impairs the
visual cognitive processing. We just kind of
discussed that. But V1 to the dorsolateral prefrontal
cortex is very long distance. The dorsal lateral
prefrontal cortex is essentially at the very
top, as far out as you can go. And V1 is at the
very bottom back of the occipital lobe, right
above the midbrain. It's a very long distance
there. And also there's a disruption in the autistic
phenotype with brain -derived neutropre factor
influence. This is mostly excitatory. We'll talk
a lot about this in the excitation episode. But
this really amplifies that hyperactivity and
sensory processing. And you should also remember
the social cues now that you think you know about
autistic phenotype and the social cues. This
is all happening here as well. So the somatosensory
sector, S1. This is in the central. to lamic
reticular nucleus. And it has connections to
other areas of the thalamus, excitatory inputs
from a so -called ventral basal complex and gabaergic
projections back to the ventral basal complex.
In the cortex, there's a bidirectional with S1
and the secondary somatosensory areas. It also
uses inhibitory neurons, of course, parvalbium
interneuron and somatostatin and the VIP. So
it's using three of the inhibitory neurons we
discussed before, parvalbium, somatostatin and
the VIP. And the major region of interest here
is kind of modulating and gating tactile, filtering
out irrelevant touch stimuli. And it's also helped
driving gamma oscillations to the VB, the ventral
basal, and the S1 somatosensory sector loop.
These are communicating back and forth for tactile
discrimination. And it supports gamma synchrony
with anterior insula for sensory emotional integration.
The big part is that insula, especially the anterior
insula. major region of interest with the parvalbum
episode. It's the anterior insula. So what about
the autistic phenotype? There's an impaired parvalbum
inhibition so that increases the ventral basal
activity and elevates gamma power and the S1.
So you're thinking about touch responses. Reduced
synchrony with the anterior insula impairs sensory
-emotional processing. And because of the lack
of inhibition, this will amplify excitatory inputs
from the S1. So tactile hypersensitivity is huge
here, with downstream deficits, which impair
synchrony with the anterior insula, affecting
emotional processing of touch, impacting social
interactions. discomfort with physical contact,
if you will. The third sector, auditory sector.
This is in the caudal trn and it's adjacent to
the medial geniculate nucleus. You should probably
have guessed that because of its auditory roles
here. So the connections to the thalamus, excitatory
inputs from the medial geniculate nucleus and
then The TRN will send back GABA -ergic projections
to help balance the auditory stimuli coming in
and also to the cortex as a bidirectional with
the auditory cortex 1 and the superior temporal
gyrus. We will talk about autism and the auditory
cortex. We'll do a whole episode on that soon.
This sector uses the parvalium interneurons.
Remember, these are the most dense. These are
the most common type of inhibitory neurons. So
no surprise there. And this also is modulated
by the somatostatin interneuron and the VIP interneuron.
In typical brains, this inhibition of the medial
geniculate nucleus is for the auditory sensory
gating. filtering out irrelevant sounds and drives
gamma oscillations in this medial geniculate
nucleus to A1 cortex loop for auditory featuring
and integration. And it supports synchrony with
the dorsolateral prefrontal cortex and the superior
temporal gyrus for auditory social processing.
In the autistic phenotype, that reduced parvalbum
inhibition increases the medial geniculate nucleus,
so it cannot have that push -pull tactic. And
this will elevate gamma power in our auditory,
auditory cortex one. This disrupted synchrony
with the downstream or distal connection, I should
say, and downstream. Actually, that works. Which
are distal connections and remember these are
all distant and this is that impairing that auditory
social integration So you should be thinking
about the elevated gamma power and auditory cortex
one Enhances auditory detail processing and sensitivity
to loud sounds very good hearing Because of this
though downstream deficits that reduce synchrony
with those distal connections and processing
speech in noisy environments. This is me. Remember
I used the example of the later Beatles songs.
At the end of the songs they're experimenting
with different types of musical instruments and
things that aren't musical instruments. They're
just making noises out of like whatever they
can find around the recording studio. This is
me. This is clusters of noise and conversation
and social settings are really amplified. I can
pay attention to different clusters of conversations
happening around me and it's very difficult.
It's very heightened and tough to sustain. So
the last sector, the limbic sector. This is in
the anterior, so the front of the the limbic
reticular nucleus and it's adjacent to the mediodorsal
nucleus and the anterior nucleus. I know a lot
of language there about the different subdivisions
of the thalamus, but very relevant. Connections
here with the thalamus. The thalamus will send
excitatory inputs from these regions, the mediodorsal
and the anterior nuclei, and the TRN will send
back GABA -ergic projections into the cortex
as well. Bidirectional with the dorsolateral
prefrontal cortex and the anterior insula and
the orbital frontal cortex and the ACC, the anterior
cingulate cortex. So the limbic sector here is
responsible for a few additional major hubs,
major nuclei here with the anterior insula, the
orbital frontal, and the ACC. The inhibitory
neurons here are similar, but we're going to
add that two -for -one from the previous episode,
parvalbium, no surprise, and then it's modulated
by the somatostatin and the VIP, and we finally
introduce again the calbindin and the calretinin
in the dorsolateral prefrontal cortex and insula
connections. Remember those last two that two
for one are very, very rare. In functional brains,
the limbic sector is responsible for inhibiting
the medial dorsal nucleus for attention and emotional
regulation. And this drives gamma oscillations
in the medial dorsal to the dorsal lateral prefrontal
cortex loop for cognitive processing. And it
supports synchrony. with the interior insula
and the ACC for emotional integration. Now remember,
an early episode of the podcast, Autism and Adaptive
Responses and how the medial prefrontal cortex,
ACC, and insula are in play here. When we are
adaptive responding, when we are applying adaptive
behaviors in society as we navigate life, the
medial prefrontal cortex and the ACC lead the
way. About minute 15 of that episode that I just
mentioned really highlights this. It's there's
a time stamp. MPFC, ACC lead the way. This means
it's regulating those downstream behaviors. Remember
the basal ganglia conversation that we just had.
These inputs lead our responses, the skills that
we have available to us. Whenever we are kind
of heightened or hijacked, people will call it
hijacked. The insula, because it's receiving
so much, it receives inputs from the brain, brain
states, what's happening in the brain with thought,
and it's receiving inputs from the body, and
it's receiving inputs from the environment. It
has three sources, the three main sources there.
The anterior insula is kind of privileged for
that. This will lead the way and allow the subcortical
areas, areas like the amygdala and all of these
things that are kind of making us be physiologically
out of control, will start paying attention to
the heartbeat, the heart rate, the rate of speech,
our phase locking. and we will just kind of panic.
Remember the para -aqueductal gray in the mesencephalon,
the midbrain. There's different areas there with
that happening here as well. It's what is regulating,
what is controlling these circuitries, these
neural correlates. This is a good example of
this because you've probably even heard of the
limbic system. which is mostly subcortical or
all subcortical. And we can get hijacked with
this. So some inputs or some functions of the
autistic phenotype is impaired and or a lack
of parv albium inhibition reduces the gamma power
and synchrony in the dorsolateral prefrontal
cortex and the anterior insula. And this will
cause over excitation inputs from the dorsal
lateral prefrontal cortex and amplify dysfunction.
So with the autistic phenotype implication, there's
a lot of cognitive and social deficits happening
here. In addition, there are some OCD -like behaviors
here because of the dysfunction of the medial
dorsal and the orbital frontal cortex circuits.
that contributes to repetitive behaviors. So
how strict is this TRN? What can get in and what
has a more challenging time of getting in? The
security guard examples. So with normal senses
like sight, sound and touch, the TRN exhibits
strong control over these. It's like a guard
checking every bag at an airport. Very detailed
and deliberate checks. Can things bypass? Not
easily. No. It's fully filtered. Thoughts and
plans. The TRN has a kind of a weaker control
over this. The TRN barely touches it. The guard
waves, the VIP enter neurons through. And there's
just a little delay. Can things bypass this?
Can thoughts and plans bypass this? And the answer
is yes, quite easily. If you think about evolution,
the thoughts and plans aren't really an external
insult. So evolution doesn't equip us with protecting
it, protecting ourselves from thoughts and plans.
Evolutionarily, these are very critical and productive
and necessary things. However, now, But the human's
infinite capacity to just think will spend all
of our time occupying our time thinking about
maybe good things, maybe bad things. Loud and
painful shocks. Well, this is dependent. The
TRN is a little limited here. It tries to, but
it can fail. The guard can only stop so much.
Too much input overwhelms it. Can things bypass
it? Yes, it can break through. Wake -up chemicals
from the brain stem. Remember the sleep -wake
cycles? Well, the wake -up signals modulates
the TRN. It's kind of dependent. It can be strict
or it can just be laid back. There's a lot going
on here. There's a lot of variables with the
sleep -wake. So there's a rule changes. It's
just too dependent pain and danger alerts Well,
this is kind of minimal the TRN is minimal here
because there's we have to kind of bias towards
safety and Another way of looking at this is
high -intensity stimuli Well, this can bypass
the inhibition if there's life threatening if
there's one trial learning type of things going
on. The TRN is very limited at this point because
remember the evolution example, security and
safety typically wins. Visual attention can be.
There's a lot happening with the visual inputs.
So that's it's kind of dependent but it's mostly
yes especially in the typical brain. Now the
autistic phenotype will pick out kind of subtle
things in the environment without people even
knowing that it's happening. That's a huge benefit
and that has a lot to do with the the high gamma
and the lack of gating here. So the the security
guard can just kind of depends on Maybe they
have a buddy and they let them in. Nobody knows
it. They just got this secret message or whatever.
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you for listening. to From the Spectrum Podcast.