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 explore the basal ganglia and the specific subdivision within the basal ganglia, the dorsal striatum.
Already, lots of biology here and may be confusing and even uninteresting to the listener.
However, it is my goal to explain this in a way that connects the Autistic Phenotypes, explain the behaviors and implications from these regions.
And I can do that. We will do that today.
The basal ganglia is a collection of subcortical regions, which means they are ancient and below the cortex, the area that gives humans our higher functioning and abilities to be dominant species.
If you draw a line from the eyes to the back of our head, our head extends up and like any other species.
In addition, for the ratio relatively speaking, our eye diameter in relationship to the size of the brain, our eyes are likely to have a larger ratio than any other species.
Now this is quite fascinating because of the eye development, predicts the brain development. At least it helps it. Remember the eyes are a highway and interstate to the brain and very crucial for development.
Evolutionary. You can think about the lower areas of the brain or older.
Loosely and generally speaking, the basal ganglia are where motivation and movements converge.
Motivation in no way should be defined as actions we want to do.
Don't define motivation from your perspective, such as I'm motivated to do better. I'm motivated to lose weight. I'm motivated to read this book, etc.
Define it from the nervous system's perspective.
Remember the nervous system does not like to work. It wants to conserve energy and respond to what and how it knows.
And it biases us towards safety, but it takes an account of what it knows over safety.
And even based off of what it knows over fear, meaning, you can provide fear into somebody.
And that doesn't mean that they will change, or their nervous system will change specifically.
Addictions is the best example of this.
This is why everything I just said about motivation and the nervous system responding.
This is why change is hard.
The basal ganglia is known as our go, no-go area.
And it operates best when projections, or you can say signals or connections, are coming down from our cortex.
The go side is connected to excitation dopamine.
The no-go side is connected to inhibition dopamine.
This is simple to connect because of the excitation inhibition phenomena with autism.
Remember Mike Mersenex, wonderful paper back from 2002.
Excitation is activating. Inhibition is inactivating.
Now you know the mechanisms by which this occurs.
With autism, this EI imbalance is well established.
Also, some well-known genetic implications is shank 3, which are mutations or deletions, are frequently understood in autism.
Its roles include, synaptic formation, maturing dendrites, synaptic transmission, and plasticity of synapses.
Neurolegin 3, this is more synapses formation and plasticity, and neuronal communication, meaning forming of the cleft, the space in between the synapses.
Now this space is roughly 10 nanometers.
And for reference, there are 1000 nanometers and 1 millimeter, sometimes called micron.
And a sheet of paper, the thickness is roughly 80 to 90 microns.
CNT NAP2 for axonal guidance and myelination and some more synaptic functioning.
Some other genetic studies for these areas include 16p11.2.
Remember the conversation with Dr. Hannah Stevens, MD, PhD.
Towards the end of the episode, she mentioned the dorsal striatum and studying this, this is enlarged in autism.
And it's unclear if the number of dendrites are a factor, connections and axons and so forth.
All of these genetic identifiers mentioned are well understood in autism.
So if interested, seek that data.
In episode 3 of the podcast, way back then, I covered these in more detail.
For today's episode, I just want to briefly mention them for their roles with the autistic phenotype, especially in the basal ganglia.
The basal ganglia, we can break these regions into three different roles.
Inputs, or they receive signals, relays, or connects regions within the basal ganglia.
And outputs, or sends signals outside of the basal ganglia.
A region that receives most of these outputs is the thalamus.
We will talk more about the thalamus in a little detail shortly.
The inputs are the cadet nucleus and putamen.
These are known as the dorsal striatum.
The cadet is involved with motor learning, movement planning and execution, various cognitive functions with decision making,
cognitive flexibility, more so with reasoning and evaluating and problem solving, working memory,
focusing our attention, reward processing and emotional regulation.
You can see sensory, motor and cognition are involved.
Remember the signals coming in to the cadet and from the cortex, remember the orbital frontal cortex, the medial prefrontal cortex.
So the prefrontal is orchestrating here and as we review those items,
you can remember the roles of various prefrontal and cingulate cortex as having the same roles,
such as the interior cingulate cortex and the medial prefrontal cortex.
These things work in concert with one another.
The other input region, the putamen, plays parts with motor, especially with skill acquisition, fine tuning movements.
If you think about catching a ball or reaching out for something, especially if you are passively attending to the object,
you can still grab it. You can successfully grab it with precision.
Okay, how about learning to type or learning to walk?
Imagine being a child and learning to walk versus walking now.
Imagine being an Olympic hurdler, the motor control and the learning.
When we were learning to walk, it was very much different than passively just walking now.
There was a lot of deliberate action needed and this is mainly areas of the dorsal anterior cingulate
projecting down to the dorsal region of the striatum, so more cadet than putamen.
As we learn to do this skill, becomes a habit.
That is more from the so-called infralimbic or sometimes called the ventral medial prefrontal cortex
projecting down to the more lateral side of the dorsal striatum, which is the putamen.
These signals are orchestrating our ability to learn and have memory and be able to perform the skill.
So as it comes into skill development or learning, it passes it off to more habitual or habit forming.
And I think this is because it frees up those learning mechanisms needed for future skills.
The putamen is involved with inhibiting inappropriate movements.
Of course it is. We've learned to do it. This is where habits reside.
You can start to understand some connections with autism here.
Some dyspraxia, lack of motor control, flappy hands and stimming.
The putamen has a huge part in habits.
Habit formation, the transition to go directed to automatic.
We no longer need that deliberate effort when we know how to walk versus when we were learning how to walk.
Now walking is the easy example that we can all make sense of.
This is procedural learning and action selection.
That area, the ventral medial prefrontal cortex, sometimes called infralimbic and rodents.
This is a toggle. It toggles through action selection based off of the habit.
It's providing context.
It also integrates sensory information and reward prediction.
So you can see the dorsal striatum is huge in our previous discussion on internal calculators.
The role, why learning and guiding rewards and future behaviors.
Soon we will discuss the substantia nigra and the role of dopamine.
Remember our episode on internal calculators and what makes autistics innate.
Stuck in our inner world.
And being comfortable, being comfortable with inside of ourselves and preferring our inner world.
Think about motor control and speech as well.
This is within these regions, the broca area projecting to these dorsal striatum areas.
If you think about, sometimes people just talk. They talk a lot quite frankly.
This is habit formation. This is them action selecting to comfort them.
They have something to say. Something on the external world is not quite satisfying them.
And they must speak to calm themselves.
It's habit.
It's returning their nervous system to that homeostasis.
That's not all speech, but it is in play.
In learning and memory, zooming into the dorsal striatum and the cadet is more action and go based.
The putamen is more reflexes and habits.
The putamen receives signals from sensory motor regions as well.
Towards the middle and the top of the head. It's a big sensory motor region.
After the input areas receive these signals.
The dorsal striatum, those regions just covered, orchestrate downstream behaviors.
Remember each connection. Each synapses. Provides a brief summary.
Each connection is conveying a story.
This whatever this is, that specific cell activation means something.
It builds a story and the basal ganglia, based off of these, the summary,
orchestrates downstream behaviors. Based off of that story, it is completely subjective to the living organism.
This is why we are all essentially have the same regions, molecules and chemicals, but are very much different.
Before we get into the relays and outputs, I want you to think about the substantia nigra here.
A place of dopamine.
We can think about substantia nigra as a relay and an output.
Autism or not, the substantia nigra is vital for humans.
Remember dopamine is much more in humans than just wanting and liking and motivation.
However, remember you don't define motivation. Our nervous systems define the motivation for us.
If you look at it from this perspective, you can start to understand dopamine and drive and motivation and how people are so unique, a little bit better.
Also a big topic for us, the neuro melanin. Much more than what people consider.
This is crucial for energy. Melanin plus water.
Remember, cytochrome c-oxidates. So dopamine is a modulator.
Okay, that's easy to understand. If you think about regions, modulators, networks, etc.
Activating and inactivating. In the basal ganglia, as the go, no go area, you can see dopamine is crucial.
In a quick review, dopamine has two receptor types. Of course those are excitation and inhibition.
You can see how much of our brain are involved with conducting movements.
The role of the central nervous system is to move the living organism.
While allocating as little energy as possible. So those internal calculators are here.
And in case you are wondering, every aspect discussed so far are implicated and involved in autism.
So the receptor types, D1 like, are excitatory. And those are DR1 and DR5.
Inhibitory receptors are D2 like. And are DR2, 3, and 4.
So 5 total receptors for dopamine broken down into two types. One for excitation.
Two for inhibition. Soon we will cover autism and Parkinson's.
In that episode, we will go more into the so called direct pathway and indirect pathway.
The two most common conversations when talking about the basal ganglia.
For this episode, we will cover all of those components just not in detail.
We will cover the regions, but we won't specifically go into detail on the direct pathway and the indirect pathway.
Dopamine orchestrates those pathways. At minimum, dopamine has a huge involvement in them.
Just think about it as precise movements based on precise signaling and instruction.
You can see the connection here. Why? Artistics are vulnerable to Parkinson's.
For the substantia nigra, it has two main subdivisions. The pars compacta, abbreviated as SNC.
This area sends signals. Remember this is information. The summaries to the dorsal striatum.
That work in concert with those other signals coming into the dorsal striatum.
This is called the nigrotriatal pathway. The second subdivision is the pars reticulata, shown as SNR.
This area is crucial for inhibiting and is an output area.
Other areas involved in the basal ganglia include the globus pallidus, which has two parts as well.
This forms a triangle in the basal ganglia. The two nuclei forms a triangle.
The globus pallidus internal, so closer to the center of the brain, receives inhibitory signals from the striatum.
It also receives excitatory signals from the subthalamic nucleus.
The GPI will then send signals to the thalamus and areas of the brainstem, midbrain area, including the substantia nigra and superior colliculus.
The superior colliculus is crucial here for an upcoming episode on autism in eye contact.
The GPI and substantia nigra reticulata are essentially the same functions for the basal ganglia.
The GPI is both a relay and an output.
The globus pallidus external receives inhibitory signals, so GABA are the inhibitory neurotransmitters from the striatum.
Then the GPI sends inhibitory signals to the subthalamic nucleus and the globus pallidus internal.
The GPI is a relay, meaning it only sends signals within the basal ganglia.
With the subthalamic nucleus, remember the GPI sends signals here.
The subthalamic nucleus will send signals back to the GPI as a feedback loop.
This communication is providing updates, asking for guidance.
What do I do? Are we good? Etc.
And if you zoom out and think about how many movements the human being is conducting over space and time, it's extraordinary.
These circuits right here are in constant loops.
Now imagine if these signals, these loops, have a delay they lack behind.
Imagine what that's going to do for activating and inactivating our movements.
Remember the go, no go areas.
And remember, everything here is clocked timed and we need specific and efficient energy flowing through these cells, these connections, these regions and pathways and so forth.
So when we think about a future episode, autism and Parkinson's, or when we think about autistics and these kind of erratic and uncontrollable movements,
and stemming and the neuroplasticity, doing this out of comfort or to satisfy the living organism, our nervous system and these habits,
all of this is happening here.
So if this is kind of abnormal circuitry, you can begin to understand this. Why? It's hard to control.
So the subthalamic nucleus. Remember the thalamus from episode 1.
This is where all sensations are processed.
In episode 1, I gave a kind of an analogy of a big skyscraper in a big metropolitan area, a big building, and it has revolving doors.
And people are coming into the revolving doors from the outside world and they go up into this building and they all have different roles.
They go to different areas of the building and at the same time, people are leaving the building.
And they all came from different areas of the building. They all have different roles.
And as they exit the building, they're going to different areas of the world or the city.
Maybe it's local or maybe it's distal.
Anyway, I like to think about the thalamus in this manner because of the amount of signals running through the thalamus.
Essentially, you can think about every region or nuclei that we talk about in this analogy.
But because of the inputs and outputs of the thalamus, it gets this special visual representation in my mind.
So if you imagine how many sensations our body is going through,
even right now, the thalamus needs help.
Sephthalmic Nuculus is a major relay center.
It receives excitatory inputs from the cortex and the globus pallidus external,
and relays to the globus pallidus internal and the substantiate nigra.
Why? Imagine processing all of those sensations coming through the central nervous system.
All of those smells, sounds, visual inputs, taste, pressure points.
We have a lot going on with the sensations.
A big factor of this nuclei is it is a break, an emergency break,
an assistance of processing the information.
You can think of the septalamic nucleus as a personal assistant to the thalamus.
So it inhibits.
Remember autism and the EI imbalance, where most data, the data are impressive on too much excitation,
lacking inhibition.
If it was a seesaw, we want this pretty balanced, but the excitation is always high.
And we can measure this in neuroscience with the Raskoerler-Wagner model.
We can put numbers to actions and learning, and then we can test them from memory and habits and so forth.
This nuclei is a major controller of movements.
The signals coming straight from the cortex are interesting whereby it provides faster responses and bypasses those connections,
those regions and relays and so forth.
If you think about autism and motor control, movement, motivation and so forth, many concerns arise.
Think about criteria B1, stereotyped, repetitive motor movements, use of objects and speech.
Soon we will cover autism and speech and language.
Also think about B4, hyper or hypoactivity, of sensory.
Hopefully you can start seeing why this is covered and connect the autistic phenotype to these areas.
With autism research, it is well understood that the cod debt nucleus is enlarged.
What is happening here? Is it more dendrites? More connections going in? Is it a loss of thermodynamics?
Is it a loss of energy? And with a loss of energy, things get larger.
Remember the conversations about obesity and losing energy to the environment.
This isn't that difficult to understand. The cod debt is larger.
So the inputs and outputs coming in and out are going to be compromised.
In addition, cognitive control and the B3 restricted fixated interest that are abnormal in intensity or focus.
And the insistence on sameness, the B2, so we've covered all four of the criteria B symptoms.
This so-called lack of cognitive flexibility.
Think about penmanship and handwriting, those precise motor movements and how this is implicated in autism.
Think about some of the treatment options with autism, such as occupational therapy.
What do you think it is, these therapy types are trying to change based off of the neuroplasticity?
This is all about changing the living organism to fit into something that will be satisfying and acceptable to the social norms.
And if you think about ABA therapy, controversial or not, occupational therapy and ABA therapy,
it's trying to train the nervous system to change into a manner that other people have constructed based off of how autistics should be.
Now, I'm not saying that this isn't needed, I'm just providing the data behind what is happening here.
Think about how so much repetition or in play with autism and the connectivity of these regions.
In neuroscience, it's morphology, it's when signals grow in size based off of the connections and frequency and intensity.
These connections are shown to even double in size.
Now, this could explain the enlarged cadet nucleus as well.
This makes us who we are, autism or not.
This is how the living organism's nervous system is operating.
Our nervous system and changes.
The more it prefers specific connections, the more the living organism becomes that.
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