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Defining the Autistic Phenotypes is not difficult.

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Understanding it and bringing real-life data and experiences can bring these Autistic Phenotypes into power.

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For today's episode, we will explore the basal ganglia and the specific subdivision within the basal ganglia, the dorsal striatum.

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Already, lots of biology here and may be confusing and even uninteresting to the listener.

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However, it is my goal to explain this in a way that connects the Autistic Phenotypes, explain the behaviors and implications from these regions.

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And I can do that. We will do that today.

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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.

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If you draw a line from the eyes to the back of our head, our head extends up and like any other species.

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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.

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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.

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Evolutionary. You can think about the lower areas of the brain or older.

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Loosely and generally speaking, the basal ganglia are where motivation and movements converge.

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Motivation in no way should be defined as actions we want to do.

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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.

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Define it from the nervous system's perspective.

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Remember the nervous system does not like to work. It wants to conserve energy and respond to what and how it knows.

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And it biases us towards safety, but it takes an account of what it knows over safety.

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And even based off of what it knows over fear, meaning, you can provide fear into somebody.

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And that doesn't mean that they will change, or their nervous system will change specifically.

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Addictions is the best example of this.

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This is why everything I just said about motivation and the nervous system responding.

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This is why change is hard.

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The basal ganglia is known as our go, no-go area.

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And it operates best when projections, or you can say signals or connections, are coming down from our cortex.

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The go side is connected to excitation dopamine.

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The no-go side is connected to inhibition dopamine.

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This is simple to connect because of the excitation inhibition phenomena with autism.

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Remember Mike Mersenex, wonderful paper back from 2002.

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Excitation is activating. Inhibition is inactivating.

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Now you know the mechanisms by which this occurs.

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With autism, this EI imbalance is well established.

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Also, some well-known genetic implications is shank 3, which are mutations or deletions, are frequently understood in autism.

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Its roles include, synaptic formation, maturing dendrites, synaptic transmission, and plasticity of synapses.

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Neurolegin 3, this is more synapses formation and plasticity, and neuronal communication, meaning forming of the cleft, the space in between the synapses.

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Now this space is roughly 10 nanometers.

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And for reference, there are 1000 nanometers and 1 millimeter, sometimes called micron.

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And a sheet of paper, the thickness is roughly 80 to 90 microns.

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CNT NAP2 for axonal guidance and myelination and some more synaptic functioning.

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Some other genetic studies for these areas include 16p11.2.

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Remember the conversation with Dr. Hannah Stevens, MD, PhD.

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Towards the end of the episode, she mentioned the dorsal striatum and studying this, this is enlarged in autism.

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And it's unclear if the number of dendrites are a factor, connections and axons and so forth.

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All of these genetic identifiers mentioned are well understood in autism.

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So if interested, seek that data.

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In episode 3 of the podcast, way back then, I covered these in more detail.

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For today's episode, I just want to briefly mention them for their roles with the autistic phenotype, especially in the basal ganglia.

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The basal ganglia, we can break these regions into three different roles.

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Inputs, or they receive signals, relays, or connects regions within the basal ganglia.

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And outputs, or sends signals outside of the basal ganglia.

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A region that receives most of these outputs is the thalamus.

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We will talk more about the thalamus in a little detail shortly.

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The inputs are the cadet nucleus and putamen.

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These are known as the dorsal striatum.

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The cadet is involved with motor learning, movement planning and execution, various cognitive functions with decision making,

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cognitive flexibility, more so with reasoning and evaluating and problem solving, working memory,

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focusing our attention, reward processing and emotional regulation.

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You can see sensory, motor and cognition are involved.

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Remember the signals coming in to the cadet and from the cortex, remember the orbital frontal cortex, the medial prefrontal cortex.

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So the prefrontal is orchestrating here and as we review those items,

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you can remember the roles of various prefrontal and cingulate cortex as having the same roles,

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such as the interior cingulate cortex and the medial prefrontal cortex.

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These things work in concert with one another.

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The other input region, the putamen, plays parts with motor, especially with skill acquisition, fine tuning movements.

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If you think about catching a ball or reaching out for something, especially if you are passively attending to the object,

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you can still grab it. You can successfully grab it with precision.

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Okay, how about learning to type or learning to walk?

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Imagine being a child and learning to walk versus walking now.

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Imagine being an Olympic hurdler, the motor control and the learning.

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When we were learning to walk, it was very much different than passively just walking now.

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There was a lot of deliberate action needed and this is mainly areas of the dorsal anterior cingulate

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projecting down to the dorsal region of the striatum, so more cadet than putamen.

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As we learn to do this skill, becomes a habit.

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That is more from the so-called infralimbic or sometimes called the ventral medial prefrontal cortex

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projecting down to the more lateral side of the dorsal striatum, which is the putamen.

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These signals are orchestrating our ability to learn and have memory and be able to perform the skill.

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So as it comes into skill development or learning, it passes it off to more habitual or habit forming.

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And I think this is because it frees up those learning mechanisms needed for future skills.

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The putamen is involved with inhibiting inappropriate movements.

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Of course it is. We've learned to do it. This is where habits reside.

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You can start to understand some connections with autism here.

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Some dyspraxia, lack of motor control, flappy hands and stimming.

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The putamen has a huge part in habits.

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Habit formation, the transition to go directed to automatic.

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We no longer need that deliberate effort when we know how to walk versus when we were learning how to walk.

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Now walking is the easy example that we can all make sense of.

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This is procedural learning and action selection.

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That area, the ventral medial prefrontal cortex, sometimes called infralimbic and rodents.

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This is a toggle. It toggles through action selection based off of the habit.

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It's providing context.

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It also integrates sensory information and reward prediction.

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So you can see the dorsal striatum is huge in our previous discussion on internal calculators.

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The role, why learning and guiding rewards and future behaviors.

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Soon we will discuss the substantia nigra and the role of dopamine.

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Remember our episode on internal calculators and what makes autistics innate.

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Stuck in our inner world.

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And being comfortable, being comfortable with inside of ourselves and preferring our inner world.

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Think about motor control and speech as well.

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This is within these regions, the broca area projecting to these dorsal striatum areas.

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If you think about, sometimes people just talk. They talk a lot quite frankly.

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This is habit formation. This is them action selecting to comfort them.

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They have something to say. Something on the external world is not quite satisfying them.

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And they must speak to calm themselves.

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It's habit.

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It's returning their nervous system to that homeostasis.

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That's not all speech, but it is in play.

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In learning and memory, zooming into the dorsal striatum and the cadet is more action and go based.

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The putamen is more reflexes and habits.

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The putamen receives signals from sensory motor regions as well.

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Towards the middle and the top of the head. It's a big sensory motor region.

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After the input areas receive these signals.

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The dorsal striatum, those regions just covered, orchestrate downstream behaviors.

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Remember each connection. Each synapses. Provides a brief summary.

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Each connection is conveying a story.

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This whatever this is, that specific cell activation means something.

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It builds a story and the basal ganglia, based off of these, the summary,

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orchestrates downstream behaviors. Based off of that story, it is completely subjective to the living organism.

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This is why we are all essentially have the same regions, molecules and chemicals, but are very much different.

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Before we get into the relays and outputs, I want you to think about the substantia nigra here.

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A place of dopamine.

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We can think about substantia nigra as a relay and an output.

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Autism or not, the substantia nigra is vital for humans.

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Remember dopamine is much more in humans than just wanting and liking and motivation.

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However, remember you don't define motivation. Our nervous systems define the motivation for us.

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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.

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Also a big topic for us, the neuro melanin. Much more than what people consider.

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This is crucial for energy. Melanin plus water.

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Remember, cytochrome c-oxidates. So dopamine is a modulator.

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Okay, that's easy to understand. If you think about regions, modulators, networks, etc.

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Activating and inactivating. In the basal ganglia, as the go, no go area, you can see dopamine is crucial.

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In a quick review, dopamine has two receptor types. Of course those are excitation and inhibition.

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You can see how much of our brain are involved with conducting movements.

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The role of the central nervous system is to move the living organism.

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While allocating as little energy as possible. So those internal calculators are here.

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And in case you are wondering, every aspect discussed so far are implicated and involved in autism.

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So the receptor types, D1 like, are excitatory. And those are DR1 and DR5.

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Inhibitory receptors are D2 like. And are DR2, 3, and 4.

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So 5 total receptors for dopamine broken down into two types. One for excitation.

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Two for inhibition. Soon we will cover autism and Parkinson's.

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In that episode, we will go more into the so called direct pathway and indirect pathway.

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The two most common conversations when talking about the basal ganglia.

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For this episode, we will cover all of those components just not in detail.

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We will cover the regions, but we won't specifically go into detail on the direct pathway and the indirect pathway.

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Dopamine orchestrates those pathways. At minimum, dopamine has a huge involvement in them.

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Just think about it as precise movements based on precise signaling and instruction.

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You can see the connection here. Why? Artistics are vulnerable to Parkinson's.

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For the substantia nigra, it has two main subdivisions. The pars compacta, abbreviated as SNC.

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This area sends signals. Remember this is information. The summaries to the dorsal striatum.

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That work in concert with those other signals coming into the dorsal striatum.

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This is called the nigrotriatal pathway. The second subdivision is the pars reticulata, shown as SNR.

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This area is crucial for inhibiting and is an output area.

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Other areas involved in the basal ganglia include the globus pallidus, which has two parts as well.

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This forms a triangle in the basal ganglia. The two nuclei forms a triangle.

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The globus pallidus internal, so closer to the center of the brain, receives inhibitory signals from the striatum.

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It also receives excitatory signals from the subthalamic nucleus.

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The GPI will then send signals to the thalamus and areas of the brainstem, midbrain area, including the substantia nigra and superior colliculus.

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The superior colliculus is crucial here for an upcoming episode on autism in eye contact.

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The GPI and substantia nigra reticulata are essentially the same functions for the basal ganglia.

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The GPI is both a relay and an output.

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The globus pallidus external receives inhibitory signals, so GABA are the inhibitory neurotransmitters from the striatum.

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Then the GPI sends inhibitory signals to the subthalamic nucleus and the globus pallidus internal.

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The GPI is a relay, meaning it only sends signals within the basal ganglia.

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With the subthalamic nucleus, remember the GPI sends signals here.

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The subthalamic nucleus will send signals back to the GPI as a feedback loop.

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This communication is providing updates, asking for guidance.

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What do I do? Are we good? Etc.

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And if you zoom out and think about how many movements the human being is conducting over space and time, it's extraordinary.

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These circuits right here are in constant loops.

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Now imagine if these signals, these loops, have a delay they lack behind.

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Imagine what that's going to do for activating and inactivating our movements.

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Remember the go, no go areas.

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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.

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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,

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and stemming and the neuroplasticity, doing this out of comfort or to satisfy the living organism, our nervous system and these habits,

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all of this is happening here.

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So if this is kind of abnormal circuitry, you can begin to understand this. Why? It's hard to control.

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So the subthalamic nucleus. Remember the thalamus from episode 1.

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This is where all sensations are processed.

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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.

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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.

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They go to different areas of the building and at the same time, people are leaving the building.

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And they all came from different areas of the building. They all have different roles.

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And as they exit the building, they're going to different areas of the world or the city.

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Maybe it's local or maybe it's distal.

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Anyway, I like to think about the thalamus in this manner because of the amount of signals running through the thalamus.

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Essentially, you can think about every region or nuclei that we talk about in this analogy.

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But because of the inputs and outputs of the thalamus, it gets this special visual representation in my mind.

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So if you imagine how many sensations our body is going through,

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even right now, the thalamus needs help.

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Sephthalmic Nuculus is a major relay center.

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It receives excitatory inputs from the cortex and the globus pallidus external,

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and relays to the globus pallidus internal and the substantiate nigra.

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Why? Imagine processing all of those sensations coming through the central nervous system.

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All of those smells, sounds, visual inputs, taste, pressure points.

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We have a lot going on with the sensations.

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A big factor of this nuclei is it is a break, an emergency break,

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an assistance of processing the information.

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You can think of the septalamic nucleus as a personal assistant to the thalamus.

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So it inhibits.

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Remember autism and the EI imbalance, where most data, the data are impressive on too much excitation,

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lacking inhibition.

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If it was a seesaw, we want this pretty balanced, but the excitation is always high.

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And we can measure this in neuroscience with the Raskoerler-Wagner model.

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We can put numbers to actions and learning, and then we can test them from memory and habits and so forth.

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This nuclei is a major controller of movements.

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The signals coming straight from the cortex are interesting whereby it provides faster responses and bypasses those connections,

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those regions and relays and so forth.

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If you think about autism and motor control, movement, motivation and so forth, many concerns arise.

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Think about criteria B1, stereotyped, repetitive motor movements, use of objects and speech.

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Soon we will cover autism and speech and language.

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Also think about B4, hyper or hypoactivity, of sensory.

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Hopefully you can start seeing why this is covered and connect the autistic phenotype to these areas.

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With autism research, it is well understood that the cod debt nucleus is enlarged.

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What is happening here? Is it more dendrites? More connections going in? Is it a loss of thermodynamics?

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Is it a loss of energy? And with a loss of energy, things get larger.

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Remember the conversations about obesity and losing energy to the environment.

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This isn't that difficult to understand. The cod debt is larger.

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So the inputs and outputs coming in and out are going to be compromised.

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In addition, cognitive control and the B3 restricted fixated interest that are abnormal in intensity or focus.

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And the insistence on sameness, the B2, so we've covered all four of the criteria B symptoms.

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This so-called lack of cognitive flexibility.

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Think about penmanship and handwriting, those precise motor movements and how this is implicated in autism.

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Think about some of the treatment options with autism, such as occupational therapy.

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What do you think it is, these therapy types are trying to change based off of the neuroplasticity?

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This is all about changing the living organism to fit into something that will be satisfying and acceptable to the social norms.

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And if you think about ABA therapy, controversial or not, occupational therapy and ABA therapy,

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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.

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Now, I'm not saying that this isn't needed, I'm just providing the data behind what is happening here.

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Think about how so much repetition or in play with autism and the connectivity of these regions.

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In neuroscience, it's morphology, it's when signals grow in size based off of the connections and frequency and intensity.

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These connections are shown to even double in size.

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Now, this could explain the enlarged cadet nucleus as well.

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This makes us who we are, autism or not.

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This is how the living organism's nervous system is operating.

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Our nervous system and changes.

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The more it prefers specific connections, the more the living organism becomes that.

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If you are listening to the podcast or listening to the episode, please feel free to leave a review or rating.

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In podcasting, reviews, ratings and downloads are huge and I very much appreciate your feedback.

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You can contact me on X at RPS 47586 and we can have conversations about autism.

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You can check out the YouTube channel and you can check out the Hop link for links to all other show platforms and contact information.

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You can email me info.fromthespectrum.com

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Thank you for listening to From the Spectrum Podcast.

