Speaker 1: Back. Today, we're gonna be studying dopamine and serotonin, so
let's look at these neurotransmitters. So neurotransmitters is how neurons
communicate with each other. We're gonna be looking at dopamine, serotonin, neuropinephrin, gabba, glutamate, acelocholon,
and neuropeptides. But we're gonna look at them in parts.
So today, dopamine influences reward movement and psychosis, and it's
connected to schizophrenia and Parkinson's. This is when you hear
high levels of dopamine has been associated with park with schizophrenia.
So high levels of dopamine has been associated with schizophrenia
and low levels with Parkinson's. The drugs are used for
Parkinson's or aldoba el dopa to try to increase the
levels of dopamine. If it schizophrenia, obviously you're using antipsychotics
to reduce the amount of dopamine. Serotonin reg relates mood, anxiety,
and sleep, central and depression and anxiety treatment. Neuropinephrine supports attention,
arousal and alertness implicated in depression and ADHD. So of
course with serotonin which you're looking for there is anti
depressants right, SSRIs, selective serotonin reuptake inhibitors, and then neuropenephron.
You're thinking of things like atomoxetine, adderall or riddlin for
helping attention if you have low levels of noperneferne. And
it's more complicated than that, but I just wanted to
get you thinking about those things. GABBA is the primary
brain's primary brake systems. This function is tied to anxiety
and it's an inhibitory neurotransmitter, while glutamate is the main
excitatory neurotransmitter involved in learning, memory, and neurotoxicity. Acetylcholine shapes
memory and attention, and it's linked to Alzheimer's and movements.
So I remember there's two linquid movement here. Dopamine and
acetyl col lead. Neuropeptides modulate pain, emotion, and stress responses.
So when someone walks into therapy saying that they feel off,
something that is happening under the hood thought, movement, mood, whatever,
it's not abstract. They're actually biological signals. Traveling across SIT
and APS is a lightning speed shaped by tiny molecules
that decide how neurons talk to each other. These molecules
are the neurotransmitters. But remember you don't want to just
memorize them. It's really understanding how the varying builds these
behaviors and how psychotropic medications aim to adjust the volume knob.
So let's get into the first two. We're gonna go
a little deeper in each one, and that's why I'm
only doing two today, and then we'll do again, probably
four tomorrow, because they're not as big. So start with dopamine.
It's one of the ones that a lot of times
we see blame for because when things go too fast
or too slow, especially too fast in psychosis too slow
in Parkinson's. Dopamine's story begins in the substantia nigra and
what they call the ventral tegmental area the vta V
as in Victor. So make sure you know those two
names for sure. For the structure brain structures substantia nigra
and the ventral tegmental area where its synthesized from the
amino acid tyrosine. There are multiple pathways. There are four pathways.
The most unfamiliar for people is tubua infinnibular, which regulates
prolactin block this pathway and you get a side effects
such as lactation or menstrual disruption. Yes, if men have
an issue with this area, it could actually cause them
to create milk in their chest. Nigro striata controls movement
in that pathway. Low dopamine here can you equal something
like Parkinson's disease, especially for the movement area you see
slow gate, shuffling of the feet, pill rolling with the fingers,
the thumb and the index finger. Antipsychotic medications that block
dopamine can cause tremors and rigidity by interfering here, so
you talked about that earlier. They have low levels of dopamine,
so if you're blocking more, it'll cause more issues. And
we'll talk about a little bit of the side effects
of antipsychotics, because think about this for a second. If
you have somebody who has too much dopamine and you
give them an antipsychotic and it's too strong and it
drops it too low, what would you create. You would
create Parkinsonian symptoms, so they can start getting the physical
movement symptoms of somebody with Parkinson's. If you give somebody
like el dopa for Parkinson's and it's the dosage is
too high then, which could create they're psychosis for the
person who has Parkinson's right to just think of it
that way. Mesocortical, it's tied to motivation and executive function.
Low activity here is linked to negative symptoms like a
flat affect or abolition. And then lastly, as mesolymbic think
rewarded pleasure. This path light's up when someone wins money,
uses drugs, or falls in love, and that pathway, the
meso olymbic pathway, is connected to the nucleosiccumbents and the
prefunnel cortex in other areas. So again mesolymbic reward and
pleasure mesocortical tied to motivation and executive function, which is
also the prefunal cortex. Nigrostraatal controls movement, and tubero infundibular
regulates prolacted. Now the other one of mesolymbic that's in
the olympic system, so remember that it's also where you'll
see hallucinate hallucinations and delusions. This is part of the
dopamine hypothesis of schizophrenia, and the key word that is hypothesis.
So there's nothing conclusive here about the dopamine levels in schizophrenia.
So once dopamine is released into the synapse, AD bindes
to what they call D one through D five receptors,
and they all have different functions and locations. So after binding,
it's either reabsorbed through reuptake or broken down by MIOS.
So it's monamine oxidemos or cmt enzymes. Remember mzi's break
down things, right, They break it down either for energy
to get rid of drugs like MAO inhibitors and antipsychotics
manipulate these processes. Now we're switching to finally to serotonin
or five HT. It starts, sets the name for it,
and it's in the raphi nuclei r A phe nuclei
in the brain stem fans across the brain. So let's
revisit the brain stem and continue to drow this in
your head. You talked about the brain stem yesterday, so
it helps you stay alive. The breathing controls breathing, heart rate,
and consciousness damage here of course, can it cause mild
dysfunction including sleep issues, vertigo, or cranial nerve symptoms. There
are twelve cranial nerves. I'm sure everybody's aware of the
famous one. The vegas nerve is a cranial nerve, so
let's go back again. The serotonin synthesized from the amino
acid trip to fan, which will all heard, of course,
trip to fan. That comment about trip to fan in
Turkey or chocolate, it's oversimplified, so we have to be
careful with that. This neurotransmitted transmitter has we talked about
modulates mood regulation, So low cerintene levels are associated with
depression part of the monamine hypothesis, and this has been
challenged for a while. There's a lot of debate about it,
which suggests the deficits and serotonin r opineprin and dopamine
underlined depressive disorders. Anytime you heard the words association link,
correlation hypothesis, that's what it is. It's an educated guess.
There's nothing definitive here. Sleep cycles, especially the regulation of
rem sleep, appetite and unfels control, seen and eating disorders
and impulse related behaviors. And then finally, this neurotransmitter and
modulates anxiety. And this is where SSRI is like prozac
or zoloft or first line treatments for both depression and anxiety.
Prozac also the name is phylaccotine and then searchilene for zola.
Serotonin binds to a large family of receptors five HT
one to five HT seven. After its release, it's mostly
taken back up into this presynaptic neuron for reuptake transporters,
the same ones targeted by SSRISE. We're gonna wrap up
there and next time we'll start talking about nora penephyrin,
and I've seed a coline and if we have time, fallably,
gabba and glue tomacers are shorter. The big ones here
A dopamine serotonin for sure, just because you'll see them
a lot with SSRIs and other medications. So we'll continue
with that. So remember again, dopamine influences reward movement and psychosis,
tied to schizophrenia and parkinson Serotonin regulates moon, anxiety and sleep.
It's one of the key features of depression and anxiety treatment.
The dopamine has four pathways mesolymbic, mesoportical, nigrostraato, and tubero infunibular,
and then serotonin has five hts also known as edits
in the raphi, nuclei and the brainstem that allows us
to survive. Thanks for listening,