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<v Speaker 1>Cook back everybody. Today, we're going to start our last

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<v Speaker 1>redode here. This is the fixed audio version of the

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<v Speaker 1>neurotransmitter systems we split the last time the neurotransmitters. Today,

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<v Speaker 1>we're gonna just combine them all so hopefully you can

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<v Speaker 1>hear this better. And now you don't have to listen

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<v Speaker 1>to two different podcasts with the neurotransmitters. You can get

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<v Speaker 1>them all here and this will complete our redo of

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<v Speaker 1>the messed up audio versions we had in the first

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<v Speaker 1>five episodes that we recorded, and I apologize for that.

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<v Speaker 1>So neurotransmitters once. We're going to be learning about today

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<v Speaker 1>is dopamine, which influences reward movement and psychosis tied to

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<v Speaker 1>schizophrenia too much dopamine or Parkinson's too little. We'll look

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<v Speaker 1>at serotonin regulates mood, anxiety, and sleep, central and depression

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<v Speaker 1>and anxiety. Right SSRIs serotonin selective reuptick inhibitors. No upernephrine,

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<v Speaker 1>which supports attention, arousal, and alertness implicated a depression at ADHD. Yeah,

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<v Speaker 1>but the brain, the brain's primary break system. It's dysfunction

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<v Speaker 1>is high into anxiety. Glutamating is the main excitatory neurotransmitter

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<v Speaker 1>involved in learning, memory, and neurotoxicity. Acetocholine, which shapes memory

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<v Speaker 1>and attention. Also connected to Alzheimer's and movement neuropeptides, which

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<v Speaker 1>is something you don't hear very often about. They modulate pain,

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<v Speaker 1>but also deal with emotion and stress. That's why they're

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<v Speaker 1>connected into our world. See when you see someone that

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<v Speaker 1>goes into your office and they feel kind of off,

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<v Speaker 1>something could be happening and in their brain maybe thought

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<v Speaker 1>mood movement. They're not abstract, they're biological signals. So traveling

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<v Speaker 1>across synapses at lightning speed, right, this is a neurotransmission.

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<v Speaker 1>This is where neurotransmitters travel is through neurons. They communicate

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<v Speaker 1>with each other, and these molecules are neurotransmitters. Knowing them

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<v Speaker 1>isn't just about memorizing what they are. It's about how

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<v Speaker 1>they understand, how they build behavior, and how they operate

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<v Speaker 1>in the brain to build behavior. So we'll be looking

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<v Speaker 1>at that also, how psychotropic ments can adjust them, modulates

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<v Speaker 1>what they usually say, modulate the amount of this particular neurotransmitter.

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<v Speaker 1>Remember this, neurotransmitters travel through neurons, hormones through the bloodstream

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<v Speaker 1>much more specific. When it comes to neurotransmitters. Hormones are

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<v Speaker 1>slower and not as specific. So the first one out

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<v Speaker 1>of the get go is dopamine. It's the one that

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<v Speaker 1>gets blamed for a lot of things, going too slow

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<v Speaker 1>or too fast for instance, or too much really so,

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<v Speaker 1>high levels of dopamine have been associated with psychosis and schizophrenia.

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<v Speaker 1>It's really a strong theory, but it has not been

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<v Speaker 1>proven to be always the case. But for now, also

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<v Speaker 1>too low of levels for Parkinson's disease, this is caused.

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<v Speaker 1>This has caused a lot of movement issues for people

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<v Speaker 1>with Parkinson's. A side note, if you have somebody that

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<v Speaker 1>has psychosis and you're trying to reduce the levels of dopamine,

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<v Speaker 1>if you reduce the levels too low in certain areas

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<v Speaker 1>of the brain, you can cause what they call Parkinsonian symptoms. Right,

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<v Speaker 1>they start moving like a person with Parkinson's, they have

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<v Speaker 1>shuffling gait, they could have pill rolling with their thumb

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<v Speaker 1>and index finger. Because it's causing issues because now the

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<v Speaker 1>dopamine levels are too low, and in the same case

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<v Speaker 1>happens with people with Parkinson's if you raise their dopamine

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<v Speaker 1>levels too high, guess what now? They have psychosts. Dopamine

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<v Speaker 1>is located a lot of it in the substantia nigra

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<v Speaker 1>and the ventral to mental area. This is where it's

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<v Speaker 1>synthesized from the amino acid tyrosine, and then it travels

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<v Speaker 1>from there to different areas. It's got four different pathways mesolympic.

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<v Speaker 1>The mesolimbic is about reward and pleasure. This path lights

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<v Speaker 1>up when someone wins money or uses drugs. Two metch

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<v Speaker 1>activity here hallucinations and delusions. This is part of the

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<v Speaker 1>dopamine hypothesis of schizophrenia. Remember, hypothesis is an educated guest.

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<v Speaker 1>The theory is when you have a lot of studies

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<v Speaker 1>that kind of supportive, but sometimes have mixed results, so

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<v Speaker 1>it's not solid either. So in this case, this is

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<v Speaker 1>where they're getting this theory from. So hallution, nations, and

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<v Speaker 1>delusions is in the mesolimbic system. This is important to

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<v Speaker 1>know for the E triple P. Mesocortical is tied to

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<v Speaker 1>motivation and executive function. So low activity here is linked

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<v Speaker 1>to negative symptoms like flat affect abolition. Member negative here

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<v Speaker 1>means things that are taken away, so they don't have emotions,

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<v Speaker 1>they don't have motivation, so that's the mesocortical mesolimbic. You're

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<v Speaker 1>talking hallucinations and delusions. Those are the positive symptoms, and

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<v Speaker 1>schizophrenia the negative. Located in the mesal corticle. The nigro

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<v Speaker 1>striatal controls movement. Low dopamine Parkinson's disease. Antipsychotic meds that

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<v Speaker 1>block dopamine can cause tremors and rigidity by interfering here

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<v Speaker 1>tubero infantibulary area, that pathway is called. It regulates prolactin.

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<v Speaker 1>And block this pathway and you get side effects like

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<v Speaker 1>lactation or menstrual disruption. Yes, even men can lactate from

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<v Speaker 1>their breasts with issues here in this part picular region

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<v Speaker 1>of the brain. Once dopamine is released into the synapsid

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<v Speaker 1>binds to what they call D one through D five receptors,

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<v Speaker 1>each with different functions and locations way over the top

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<v Speaker 1>for this particular licensing exam. After binding, it's either reabsorbed

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<v Speaker 1>through reuptake via dopamine transporters are broken down by monamine

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<v Speaker 1>oxidase MAO or c MT enzymes. Drugs like MAO and

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<v Speaker 1>ebitors and antipsychotics manipulate these processes. And remember anything that

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<v Speaker 1>ends with asee is an enzyme so monamine oxidase, which

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<v Speaker 1>means they're broken down. Now we head to our next neurotransmitter,

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<v Speaker 1>serotonin SO serotonin or at five HT as it's known

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<v Speaker 1>though the receptors starts in the raphie nuclei in the

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<v Speaker 1>brain stem and fans out across the brain. It is

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<v Speaker 1>synthesized from the amino acid trip to fan. Remember that one.

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<v Speaker 1>This has led to very popular stuff in society today.

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<v Speaker 1>But again, like usual, anything you learn from societies usually

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<v Speaker 1>over simplify, so be really careful with that. Make sure

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<v Speaker 1>you always focus on research textbooks professors try to stay

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<v Speaker 1>away from with social media or even the news articles

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<v Speaker 1>tell you about something in world psychologies, a lot of

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<v Speaker 1>times it's oversimplified and it's mostly done for clickbait. Back

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<v Speaker 1>to this, so yes al tryptfan, which we know we

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<v Speaker 1>get from turkey and dark chocolate boost serotonin. By the way,

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<v Speaker 1>the levels of eltryp defan turkey are not the only

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<v Speaker 1>thing that makes you tired later. A lot of it

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<v Speaker 1>is actually coming from the high carbs that you're taking.

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<v Speaker 1>The newer transmitter, serotonin modulates mood regulation, so low levels

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<v Speaker 1>are associated with depression and this is part of the

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<v Speaker 1>monamine hypothesis. There it is again hypothesis for this theory

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<v Speaker 1>which suggests that deficits and serotonin are up anefferent and

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<v Speaker 1>dopamine underlie depressive disorders. Hence, when you take an SSR,

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<v Speaker 1>you're trying to increase the levels of serotonin. That's the

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<v Speaker 1>rule of thought. They estimate about forty fifty of antidepressants

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<v Speaker 1>will work sleeve cycles, especially the regulation of rem sleep

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<v Speaker 1>is also involved with serotonin appetite and impulse control seen

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<v Speaker 1>in eating disorders and impulse related behaviors. And believe it

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<v Speaker 1>or not, there are a lot of serotonin receptors in

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<v Speaker 1>your gut. Anxiety is dealt with SSRISE I like the

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<v Speaker 1>serotonin reuptake inhibitors like fluoxetine which is prozac, or sertraline

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<v Speaker 1>which is zoloft, and these are usually the first line

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<v Speaker 1>treatments for both depression and anxiety disorders. Serotonin binds to

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<v Speaker 1>a large family of receptors we mentioned earlier, five HT

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<v Speaker 1>one all the way to five HT seven. After its release,

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<v Speaker 1>it's mostly taken back up into the presynaptic neuron through

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<v Speaker 1>reuptake transporters, the same ones targeted by SSRIs. When you

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<v Speaker 1>block the reuptake, you leave more serotonin in the synapse,

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<v Speaker 1>increasing its effects, and that's what you're hoping to help

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<v Speaker 1>the individual with. The next neurotransmitter is neu upineffort, which

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<v Speaker 1>is alertness, arousal, and depression oropenneferent also known as nora.

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<v Speaker 1>Adrenaline is made in the locus curiolis in the ponds

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<v Speaker 1>and plays a key role in your fight or fly response,

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<v Speaker 1>but its everyday function is more subtle. It's fine tunes, attention, vigilance,

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<v Speaker 1>and wakefulness. Psychologically, this means low epineffrin is associated with fatigue,

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<v Speaker 1>core concentration, and low energy of major depressive disorder. I

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<v Speaker 1>think you see where we're heading. High or openefferent agitation,

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<v Speaker 1>hyper arousal and raising racing thoughts seen in mani our

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<v Speaker 1>anxiety states. It's also targeted in ADHD treatments like atomoxetine stratera,

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<v Speaker 1>a nor epinefern re uptake inhibitor to try to calm

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<v Speaker 1>down those racing thoughts. Once released, nor epenefferent binds to

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<v Speaker 1>alpha and beta a drenegic receptors that like dopamine and serotonin.

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<v Speaker 1>It's taken back up were broken down by MAO TCAs

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<v Speaker 1>tricyclic antipress, and it's not commonly used anymore, but they

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<v Speaker 1>are used with treatment resistant clients like no. Tripolene work

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<v Speaker 1>by blocking the reuptake of both serotonin and nora penefphrin,

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<v Speaker 1>making them more available. Our next neuro transmitter is gabba.

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<v Speaker 1>Gabba is kind of like stepping on the gas. I mean,

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<v Speaker 1>glutamate steps on the gas and gabba pulls the brake.

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<v Speaker 1>I'll repeat that again. So gabba is like pulling the

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<v Speaker 1>putting on the brake. It's the brain's primary inhibitory neurotransmitter.

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<v Speaker 1>It's a calming neuro neuron and preventing and prevents over stimulation.

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<v Speaker 1>Gabba is synthesized, believe it or not, from the most

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<v Speaker 1>excitatory neuron, glutamate. That's what I got mixed up earlier

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<v Speaker 1>because glutamate steps on the gas pedal, while gabba puts

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<v Speaker 1>steps on the brake. So low GABBA activities associated with

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<v Speaker 1>what well generalized anxiety disorder, panic attacks and seizures when

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<v Speaker 1>an inhibition is lost and neurons fire excessively. Because GABBA

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<v Speaker 1>isn't controlling that. Benzodiazepines like lorazapam and dazepam remember pam

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<v Speaker 1>and LAMB. They work by enhancing GABA a receptor activity.

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<v Speaker 1>By the way, lorazepam also known as atavan and diazepam

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<v Speaker 1>is value. They increase inhibition and producing sedation, muscle relaxation,

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<v Speaker 1>and reduced anxiety, but tolerance and dependence are major concerns,

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<v Speaker 1>so highly addictive. GABA does not get reabsorbed like de monomines.

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<v Speaker 1>Instead is broken down by GABA transminaise. There's the a's again.

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<v Speaker 1>Another target for seizure medications. Another neurotransmitter is glutamate. Glutamate

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<v Speaker 1>is everywhere. Over ninety percent of excitatory synapses in the

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<v Speaker 1>brain uses it. It powers learning, memory, and synaptic plasticity,

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<v Speaker 1>especially in the hippocampus and cortex. Which makes sense right

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<v Speaker 1>because we learn and remember things in our hippocampus as

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<v Speaker 1>well as our cortex. Member a working memory or short

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<v Speaker 1>term memories located in that frontal lobe, and it binds

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<v Speaker 1>to multiple receptor sites, including NMDA, which is involved in

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<v Speaker 1>long term potentiation. That's the mechanism behind learning something. You

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<v Speaker 1>need that long term potentiation. AMPA receptors for fast synaptic

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<v Speaker 1>transmission and kN eight receptors for modulating signals a MPa

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<v Speaker 1>for fast synaptic transmission KNATE, which is kai NATE receptors

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<v Speaker 1>from modulating signals too much Glutamate causes extotyxocity, excitotoxicity. I'm sorry,

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<v Speaker 1>excito toxicity. These are neurons firing themselves to death. They

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<v Speaker 1>can't stop. This happens in a stroke, a TBI and

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<v Speaker 1>also Alzheimer's disease. Medications like Memantine block NMDA receptors and

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<v Speaker 1>this reduces the data of this damage in dementia. So

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<v Speaker 1>remember that Memantine dementia also blocking NMDA receptors. We're heading

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<v Speaker 1>over to now to acetocholine. If you're a fitness person

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<v Speaker 1>or a personal trainer in the past, you'll probably remember

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<v Speaker 1>this neurotransmitter. It's central to learning and memory and as

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<v Speaker 1>early decline as a whole of Alzheimer's disease. It's made

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<v Speaker 1>from coline in a cetolchola and released widely in the

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<v Speaker 1>cortex and hippocampus, as well as a neuromuscular junction for

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<v Speaker 1>voluntary muscle movement. This is the one for the fitness people.

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<v Speaker 1>In psychological terms, loss of colonegic neurons colononergic neurons is

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<v Speaker 1>called equals memory deficits in dementia, right, because you're gonna

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<v Speaker 1>need a seal colone as well for learning and memory

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<v Speaker 1>medications like aerocept or donapizila. Sorry about that. My dog

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<v Speaker 1>was going crazy there for a second. We're back at it.

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<v Speaker 1>So we're in aerocept which is one of the medications

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<v Speaker 1>that they'll use for dementia. Blocks. Acetyl colonist RaSE Acetyl

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<v Speaker 1>colonis torase is what that's right, The enzyme that breaks

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<v Speaker 1>down AH which increases availability. So again these asse always

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<v Speaker 1>enzymes and the periphery AH plays a role in autonomic

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<v Speaker 1>nervous system function also helps with salivation, digestive digestion, and

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<v Speaker 1>heart rate. Member the autonomic nervous system are things that

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<v Speaker 1>we're not controlling consciously. Are just happening, right. Our heart's beating.

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<v Speaker 1>We don't have to worry about that part. Lastly is neuropeptides.

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<v Speaker 1>This is what you don't hear much about, but they're

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<v Speaker 1>associated with pain, stress, and attachment. Neuropeptides are slowly acting,

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<v Speaker 1>longer lasting molecules will modulate rather than directly excite or inhibit.

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<v Speaker 1>They control the amount. They often travel alongside traditional neurotransmitters

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<v Speaker 1>and effect mood, pain, and interpersonal bonding. You've heard of

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<v Speaker 1>some of these for sure. For instance, the first one

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<v Speaker 1>is endorference, which is the body's natural form of opioids.

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<v Speaker 1>It reduces pain and enhances pleasure, released a lot during trauma,

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<v Speaker 1>intense exercise, or even laughter. Substance P involved in transmitting

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<v Speaker 1>pain signals to the brain. By the way, substance P

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<v Speaker 1>is one of the key neuropeptides involved in transmitting pain

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<v Speaker 1>signals like I mentioned, and this is what pain medications

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<v Speaker 1>and experimental therapies aim to block or modulate to reduce

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<v Speaker 1>pain perception. So it's again a neurotransmitler also a neuromodulator.

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<v Speaker 1>So if you're taking something and some pain strategies they'll

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<v Speaker 1>target substance P, especially in chronic pain, neuropathic pain, and

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<v Speaker 1>inflammatory conditions like capsacan creams. You remember probably use some

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<v Speaker 1>of those capsacan creams like Cutenza. They'll actually deplete substance

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<v Speaker 1>P from nerve endings over time. Used for a localized

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<v Speaker 1>neuropathic pain like diabetic neuropathy, but certain antidepressants and anti

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<v Speaker 1>convulsants like deloxitine, symbalta, or gaba pedtin. They don't directly

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<v Speaker 1>block substance pe but they modulate the pain transmission at

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<v Speaker 1>higher levels, indirectly affecting its pathways. It's a kind of

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<v Speaker 1>interesting side note there for you, and you can see

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<v Speaker 1>why those drugs can actually help relieve a little bit

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<v Speaker 1>of pain if you have some from some kind of injury.

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<v Speaker 1>So now we go back again. The last one is

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<v Speaker 1>oxytocin vasopressing. You've probably all heard of oxytocin. It's known

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<v Speaker 1>for its properties for attachment, trust, and social bonding, as

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<v Speaker 1>well as vasopressin too. They're also studied in autism and trauma.

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<v Speaker 1>These aren't first line targets of psychiatric medication though, these neuropeptides,

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<v Speaker 1>but they do shape how people feel in deep embodied ways.

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<v Speaker 1>So it is key to remember these when you're exploring

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<v Speaker 1>trauma or chronic pain. Each neurotransmitter that we've talked about

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<v Speaker 1>today acts like a lens on the world. Having too

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<v Speaker 1>much or till little of these neurotransmitters can affect how

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<v Speaker 1>we perceive the world. It can alter our energy levels

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<v Speaker 1>and rewire our behavior. They won't the E triple P

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<v Speaker 1>won't ask you to draw synapses from memory, but it

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<v Speaker 1>will expect you to reason through a taste where an

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<v Speaker 1>antidepressant isn't working or a new medication triggers tremors. So again,

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<v Speaker 1>if you're taking a medication and it increases dopamine levels

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<v Speaker 1>too high and causes psychosis, this is what it is. Right.

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<v Speaker 1>It also hinges a lot on whether them stem from

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<v Speaker 1>a gabba imbalance or serotonin drop. So you need to

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<v Speaker 1>think like a system analyst and know the multiple transmitters

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<v Speaker 1>and multiple levels. This is why when it comes to psychopharmacology,

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<v Speaker 1>it's a very difficult process. It's not so easy targeting

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<v Speaker 1>these neuro transmitters. Well, there you go, folks. This is

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<v Speaker 1>the last fixed audio version. We'll continue through our journey.

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<v Speaker 1>I believe we're heading into culture in our more recent

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<v Speaker 1>updates soon