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Speaker 1: Back. Today, we're gonna be studying dopamine and serotonin, so

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let's look at these neurotransmitters. So neurotransmitters is how neurons

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communicate with each other. We're gonna be looking at dopamine, serotonin, neuropinephrin, gabba, glutamate, acelocholon,

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and neuropeptides. But we're gonna look at them in parts.

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So today, dopamine influences reward movement and psychosis, and it's

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connected to schizophrenia and Parkinson's. This is when you hear

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high levels of dopamine has been associated with park with schizophrenia.

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So high levels of dopamine has been associated with schizophrenia

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and low levels with Parkinson's. The drugs are used for

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Parkinson's or aldoba el dopa to try to increase the

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levels of dopamine. If it schizophrenia, obviously you're using antipsychotics

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to reduce the amount of dopamine. Serotonin reg relates mood, anxiety,

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and sleep, central and depression and anxiety treatment. Neuropinephrine supports attention,

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arousal and alertness implicated in depression and ADHD. So of

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course with serotonin which you're looking for there is anti

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depressants right, SSRIs, selective serotonin reuptake inhibitors, and then neuropenephron.

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You're thinking of things like atomoxetine, adderall or riddlin for

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helping attention if you have low levels of noperneferne. And

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it's more complicated than that, but I just wanted to

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get you thinking about those things. GABBA is the primary

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brain's primary brake systems. This function is tied to anxiety

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and it's an inhibitory neurotransmitter, while glutamate is the main

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excitatory neurotransmitter involved in learning, memory, and neurotoxicity. Acetylcholine shapes

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memory and attention, and it's linked to Alzheimer's and movements.

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So I remember there's two linquid movement here. Dopamine and

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acetyl col lead. Neuropeptides modulate pain, emotion, and stress responses.

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So when someone walks into therapy saying that they feel off,

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something that is happening under the hood thought, movement, mood, whatever,

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it's not abstract. They're actually biological signals. Traveling across SIT

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and APS is a lightning speed shaped by tiny molecules

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that decide how neurons talk to each other. These molecules

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are the neurotransmitters. But remember you don't want to just

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memorize them. It's really understanding how the varying builds these

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behaviors and how psychotropic medications aim to adjust the volume knob.

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So let's get into the first two. We're gonna go

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a little deeper in each one, and that's why I'm

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only doing two today, and then we'll do again, probably

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four tomorrow, because they're not as big. So start with dopamine.

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It's one of the ones that a lot of times

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we see blame for because when things go too fast

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or too slow, especially too fast in psychosis too slow

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in Parkinson's. Dopamine's story begins in the substantia nigra and

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what they call the ventral tegmental area the vta V

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as in Victor. So make sure you know those two

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names for sure. For the structure brain structures substantia nigra

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and the ventral tegmental area where its synthesized from the

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amino acid tyrosine. There are multiple pathways. There are four pathways.

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The most unfamiliar for people is tubua infinnibular, which regulates

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prolactin block this pathway and you get a side effects

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such as lactation or menstrual disruption. Yes, if men have

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an issue with this area, it could actually cause them

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to create milk in their chest. Nigro striata controls movement

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in that pathway. Low dopamine here can you equal something

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like Parkinson's disease, especially for the movement area you see

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slow gate, shuffling of the feet, pill rolling with the fingers,

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the thumb and the index finger. Antipsychotic medications that block

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dopamine can cause tremors and rigidity by interfering here, so

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you talked about that earlier. They have low levels of dopamine,

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so if you're blocking more, it'll cause more issues. And

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we'll talk about a little bit of the side effects

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of antipsychotics, because think about this for a second. If

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you have somebody who has too much dopamine and you

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give them an antipsychotic and it's too strong and it

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drops it too low, what would you create. You would

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create Parkinsonian symptoms, so they can start getting the physical

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movement symptoms of somebody with Parkinson's. If you give somebody

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like el dopa for Parkinson's and it's the dosage is

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too high then, which could create they're psychosis for the

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person who has Parkinson's right to just think of it

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that way. Mesocortical, it's tied to motivation and executive function.

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Low activity here is linked to negative symptoms like a

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flat affect or abolition. And then lastly, as mesolymbic think

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rewarded pleasure. This path light's up when someone wins money,

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uses drugs, or falls in love, and that pathway, the

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meso olymbic pathway, is connected to the nucleosiccumbents and the

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prefunnel cortex in other areas. So again mesolymbic reward and

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pleasure mesocortical tied to motivation and executive function, which is

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also the prefunal cortex. Nigrostraatal controls movement, and tubero infundibular

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regulates prolacted. Now the other one of mesolymbic that's in

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the olympic system, so remember that it's also where you'll

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see hallucinate hallucinations and delusions. This is part of the

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dopamine hypothesis of schizophrenia, and the key word that is hypothesis.

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So there's nothing conclusive here about the dopamine levels in schizophrenia.

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So once dopamine is released into the synapse, AD bindes

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to what they call D one through D five receptors,

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and they all have different functions and locations. So after binding,

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it's either reabsorbed through reuptake or broken down by MIOS.

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So it's monamine oxidemos or cmt enzymes. Remember mzi's break

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down things, right, They break it down either for energy

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to get rid of drugs like MAO inhibitors and antipsychotics

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manipulate these processes. Now we're switching to finally to serotonin

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or five HT. It starts, sets the name for it,

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and it's in the raphi nuclei r A phe nuclei

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in the brain stem fans across the brain. So let's

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revisit the brain stem and continue to drow this in

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your head. You talked about the brain stem yesterday, so

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it helps you stay alive. The breathing controls breathing, heart rate,

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and consciousness damage here of course, can it cause mild

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dysfunction including sleep issues, vertigo, or cranial nerve symptoms. There

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are twelve cranial nerves. I'm sure everybody's aware of the

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famous one. The vegas nerve is a cranial nerve, so

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let's go back again. The serotonin synthesized from the amino

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acid trip to fan, which will all heard, of course,

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trip to fan. That comment about trip to fan in

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Turkey or chocolate, it's oversimplified, so we have to be

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careful with that. This neurotransmitted transmitter has we talked about

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modulates mood regulation, So low cerintene levels are associated with

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depression part of the monamine hypothesis, and this has been

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challenged for a while. There's a lot of debate about it,

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which suggests the deficits and serotonin r opineprin and dopamine

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underlined depressive disorders. Anytime you heard the words association link,

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correlation hypothesis, that's what it is. It's an educated guess.

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There's nothing definitive here. Sleep cycles, especially the regulation of

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rem sleep, appetite and unfels control, seen and eating disorders

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and impulse related behaviors. And then finally, this neurotransmitter and

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modulates anxiety. And this is where SSRI is like prozac

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or zoloft or first line treatments for both depression and anxiety.

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Prozac also the name is phylaccotine and then searchilene for zola.

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Serotonin binds to a large family of receptors five HT

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one to five HT seven. After its release, it's mostly

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taken back up into this presynaptic neuron for reuptake transporters,

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the same ones targeted by SSRISE. We're gonna wrap up

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there and next time we'll start talking about nora penephyrin,

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and I've seed a coline and if we have time, fallably,

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gabba and glue tomacers are shorter. The big ones here

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A dopamine serotonin for sure, just because you'll see them

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a lot with SSRIs and other medications. So we'll continue

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with that. So remember again, dopamine influences reward movement and psychosis,

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tied to schizophrenia and parkinson Serotonin regulates moon, anxiety and sleep.

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It's one of the key features of depression and anxiety treatment.

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The dopamine has four pathways mesolymbic, mesoportical, nigrostraato, and tubero infunibular,

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and then serotonin has five hts also known as edits

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in the raphi, nuclei and the brainstem that allows us

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to survive. Thanks for listening,