Speaker 1: Cook back everybody. Today, we're going to start our last
Speaker 1: redode here. This is the fixed audio version of the
Speaker 1: neurotransmitter systems we split the last time the neurotransmitters. Today,
Speaker 1: we're gonna just combine them all so hopefully you can
Speaker 1: hear this better. And now you don't have to listen
Speaker 1: to two different podcasts with the neurotransmitters. You can get
Speaker 1: them all here and this will complete our redo of
Speaker 1: the messed up audio versions we had in the first
Speaker 1: five episodes that we recorded, and I apologize for that.
Speaker 1: So neurotransmitters once. We're going to be learning about today
Speaker 1: is dopamine, which influences reward movement and psychosis tied to
Speaker 1: schizophrenia too much dopamine or Parkinson's too little. We'll look
Speaker 1: at serotonin regulates mood, anxiety, and sleep, central and depression
Speaker 1: and anxiety. Right SSRIs serotonin selective reuptick inhibitors. No upernephrine,
Speaker 1: which supports attention, arousal, and alertness implicated a depression at ADHD. Yeah,
Speaker 1: but the brain, the brain's primary break system. It's dysfunction
Speaker 1: is high into anxiety. Glutamating is the main excitatory neurotransmitter
Speaker 1: involved in learning, memory, and neurotoxicity. Acetocholine, which shapes memory
Speaker 1: and attention. Also connected to Alzheimer's and movement neuropeptides, which
Speaker 1: is something you don't hear very often about. They modulate pain,
Speaker 1: but also deal with emotion and stress. That's why they're
Speaker 1: connected into our world. See when you see someone that
Speaker 1: goes into your office and they feel kind of off,
Speaker 1: something could be happening and in their brain maybe thought
Speaker 1: mood movement. They're not abstract, they're biological signals. So traveling
Speaker 1: across synapses at lightning speed, right, this is a neurotransmission.
Speaker 1: This is where neurotransmitters travel is through neurons. They communicate
Speaker 1: with each other, and these molecules are neurotransmitters. Knowing them
Speaker 1: isn't just about memorizing what they are. It's about how
Speaker 1: they understand, how they build behavior, and how they operate
Speaker 1: in the brain to build behavior. So we'll be looking
Speaker 1: at that also, how psychotropic ments can adjust them, modulates
Speaker 1: what they usually say, modulate the amount of this particular neurotransmitter.
Speaker 1: Remember this, neurotransmitters travel through neurons, hormones through the bloodstream
Speaker 1: much more specific. When it comes to neurotransmitters. Hormones are
Speaker 1: slower and not as specific. So the first one out
Speaker 1: of the get go is dopamine. It's the one that
Speaker 1: gets blamed for a lot of things, going too slow
Speaker 1: or too fast for instance, or too much really so,
Speaker 1: high levels of dopamine have been associated with psychosis and schizophrenia.
Speaker 1: It's really a strong theory, but it has not been
Speaker 1: proven to be always the case. But for now, also
Speaker 1: too low of levels for Parkinson's disease, this is caused.
Speaker 1: This has caused a lot of movement issues for people
Speaker 1: with Parkinson's. A side note, if you have somebody that
Speaker 1: has psychosis and you're trying to reduce the levels of dopamine,
Speaker 1: if you reduce the levels too low in certain areas
Speaker 1: of the brain, you can cause what they call Parkinsonian symptoms. Right,
Speaker 1: they start moving like a person with Parkinson's, they have
Speaker 1: shuffling gait, they could have pill rolling with their thumb
Speaker 1: and index finger. Because it's causing issues because now the
Speaker 1: dopamine levels are too low, and in the same case
Speaker 1: happens with people with Parkinson's if you raise their dopamine
Speaker 1: levels too high, guess what now? They have psychosts. Dopamine
Speaker 1: is located a lot of it in the substantia nigra
Speaker 1: and the ventral to mental area. This is where it's
Speaker 1: synthesized from the amino acid tyrosine, and then it travels
Speaker 1: from there to different areas. It's got four different pathways mesolympic.
Speaker 1: The mesolimbic is about reward and pleasure. This path lights
Speaker 1: up when someone wins money or uses drugs. Two metch
Speaker 1: activity here hallucinations and delusions. This is part of the
Speaker 1: dopamine hypothesis of schizophrenia. Remember, hypothesis is an educated guest.
Speaker 1: The theory is when you have a lot of studies
Speaker 1: that kind of supportive, but sometimes have mixed results, so
Speaker 1: it's not solid either. So in this case, this is
Speaker 1: where they're getting this theory from. So hallution, nations, and
Speaker 1: delusions is in the mesolimbic system. This is important to
Speaker 1: know for the E triple P. Mesocortical is tied to
Speaker 1: motivation and executive function. So low activity here is linked
Speaker 1: to negative symptoms like flat affect abolition. Member negative here
Speaker 1: means things that are taken away, so they don't have emotions,
Speaker 1: they don't have motivation, so that's the mesocortical mesolimbic. You're
Speaker 1: talking hallucinations and delusions. Those are the positive symptoms, and
Speaker 1: schizophrenia the negative. Located in the mesal corticle. The nigro
Speaker 1: striatal controls movement. Low dopamine Parkinson's disease. Antipsychotic meds that
Speaker 1: block dopamine can cause tremors and rigidity by interfering here
Speaker 1: tubero infantibulary area, that pathway is called. It regulates prolactin.
Speaker 1: And block this pathway and you get side effects like
Speaker 1: lactation or menstrual disruption. Yes, even men can lactate from
Speaker 1: their breasts with issues here in this part picular region
Speaker 1: of the brain. Once dopamine is released into the synapsid
Speaker 1: binds to what they call D one through D five receptors,
Speaker 1: each with different functions and locations way over the top
Speaker 1: for this particular licensing exam. After binding, it's either reabsorbed
Speaker 1: through reuptake via dopamine transporters are broken down by monamine
Speaker 1: oxidase MAO or c MT enzymes. Drugs like MAO and
Speaker 1: ebitors and antipsychotics manipulate these processes. And remember anything that
Speaker 1: ends with asee is an enzyme so monamine oxidase, which
Speaker 1: means they're broken down. Now we head to our next neurotransmitter,
Speaker 1: serotonin SO serotonin or at five HT as it's known
Speaker 1: though the receptors starts in the raphie nuclei in the
Speaker 1: brain stem and fans out across the brain. It is
Speaker 1: synthesized from the amino acid trip to fan. Remember that one.
Speaker 1: This has led to very popular stuff in society today.
Speaker 1: But again, like usual, anything you learn from societies usually
Speaker 1: over simplify, so be really careful with that. Make sure
Speaker 1: you always focus on research textbooks professors try to stay
Speaker 1: away from with social media or even the news articles
Speaker 1: tell you about something in world psychologies, a lot of
Speaker 1: times it's oversimplified and it's mostly done for clickbait. Back
Speaker 1: to this, so yes al tryptfan, which we know we
Speaker 1: get from turkey and dark chocolate boost serotonin. By the way,
Speaker 1: the levels of eltryp defan turkey are not the only
Speaker 1: thing that makes you tired later. A lot of it
Speaker 1: is actually coming from the high carbs that you're taking.
Speaker 1: The newer transmitter, serotonin modulates mood regulation, so low levels
Speaker 1: are associated with depression and this is part of the
Speaker 1: monamine hypothesis. There it is again hypothesis for this theory
Speaker 1: which suggests that deficits and serotonin are up anefferent and
Speaker 1: dopamine underlie depressive disorders. Hence, when you take an SSR,
Speaker 1: you're trying to increase the levels of serotonin. That's the
Speaker 1: rule of thought. They estimate about forty fifty of antidepressants
Speaker 1: will work sleeve cycles, especially the regulation of rem sleep
Speaker 1: is also involved with serotonin appetite and impulse control seen
Speaker 1: in eating disorders and impulse related behaviors. And believe it
Speaker 1: or not, there are a lot of serotonin receptors in
Speaker 1: your gut. Anxiety is dealt with SSRISE I like the
Speaker 1: serotonin reuptake inhibitors like fluoxetine which is prozac, or sertraline
Speaker 1: which is zoloft, and these are usually the first line
Speaker 1: treatments for both depression and anxiety disorders. Serotonin binds to
Speaker 1: a large family of receptors we mentioned earlier, five HT
Speaker 1: one all the way to five HT seven. After its release,
Speaker 1: it's mostly taken back up into the presynaptic neuron through
Speaker 1: reuptake transporters, the same ones targeted by SSRIs. When you
Speaker 1: block the reuptake, you leave more serotonin in the synapse,
Speaker 1: increasing its effects, and that's what you're hoping to help
Speaker 1: the individual with. The next neurotransmitter is neu upineffort, which
Speaker 1: is alertness, arousal, and depression oropenneferent also known as nora.
Speaker 1: Adrenaline is made in the locus curiolis in the ponds
Speaker 1: and plays a key role in your fight or fly response,
Speaker 1: but its everyday function is more subtle. It's fine tunes, attention, vigilance,
Speaker 1: and wakefulness. Psychologically, this means low epineffrin is associated with fatigue,
Speaker 1: core concentration, and low energy of major depressive disorder. I
Speaker 1: think you see where we're heading. High or openefferent agitation,
Speaker 1: hyper arousal and raising racing thoughts seen in mani our
Speaker 1: anxiety states. It's also targeted in ADHD treatments like atomoxetine stratera,
Speaker 1: a nor epinefern re uptake inhibitor to try to calm
Speaker 1: down those racing thoughts. Once released, nor epenefferent binds to
Speaker 1: alpha and beta a drenegic receptors that like dopamine and serotonin.
Speaker 1: It's taken back up were broken down by MAO TCAs
Speaker 1: tricyclic antipress, and it's not commonly used anymore, but they
Speaker 1: are used with treatment resistant clients like no. Tripolene work
Speaker 1: by blocking the reuptake of both serotonin and nora penefphrin,
Speaker 1: making them more available. Our next neuro transmitter is gabba.
Speaker 1: Gabba is kind of like stepping on the gas. I mean,
Speaker 1: glutamate steps on the gas and gabba pulls the brake.
Speaker 1: I'll repeat that again. So gabba is like pulling the
Speaker 1: putting on the brake. It's the brain's primary inhibitory neurotransmitter.
Speaker 1: It's a calming neuro neuron and preventing and prevents over stimulation.
Speaker 1: Gabba is synthesized, believe it or not, from the most
Speaker 1: excitatory neuron, glutamate. That's what I got mixed up earlier
Speaker 1: because glutamate steps on the gas pedal, while gabba puts
Speaker 1: steps on the brake. So low GABBA activities associated with
Speaker 1: what well generalized anxiety disorder, panic attacks and seizures when
Speaker 1: an inhibition is lost and neurons fire excessively. Because GABBA
Speaker 1: isn't controlling that. Benzodiazepines like lorazapam and dazepam remember pam
Speaker 1: and LAMB. They work by enhancing GABA a receptor activity.
Speaker 1: By the way, lorazepam also known as atavan and diazepam
Speaker 1: is value. They increase inhibition and producing sedation, muscle relaxation,
Speaker 1: and reduced anxiety, but tolerance and dependence are major concerns,
Speaker 1: so highly addictive. GABA does not get reabsorbed like de monomines.
Speaker 1: Instead is broken down by GABA transminaise. There's the a's again.
Speaker 1: Another target for seizure medications. Another neurotransmitter is glutamate. Glutamate
Speaker 1: is everywhere. Over ninety percent of excitatory synapses in the
Speaker 1: brain uses it. It powers learning, memory, and synaptic plasticity,
Speaker 1: especially in the hippocampus and cortex. Which makes sense right
Speaker 1: because we learn and remember things in our hippocampus as
Speaker 1: well as our cortex. Member a working memory or short
Speaker 1: term memories located in that frontal lobe, and it binds
Speaker 1: to multiple receptor sites, including NMDA, which is involved in
Speaker 1: long term potentiation. That's the mechanism behind learning something. You
Speaker 1: need that long term potentiation. AMPA receptors for fast synaptic
Speaker 1: transmission and kN eight receptors for modulating signals a MPa
Speaker 1: for fast synaptic transmission KNATE, which is kai NATE receptors
Speaker 1: from modulating signals too much Glutamate causes extotyxocity, excitotoxicity. I'm sorry,
Speaker 1: excito toxicity. These are neurons firing themselves to death. They
Speaker 1: can't stop. This happens in a stroke, a TBI and
Speaker 1: also Alzheimer's disease. Medications like Memantine block NMDA receptors and
Speaker 1: this reduces the data of this damage in dementia. So
Speaker 1: remember that Memantine dementia also blocking NMDA receptors. We're heading
Speaker 1: over to now to acetocholine. If you're a fitness person
Speaker 1: or a personal trainer in the past, you'll probably remember
Speaker 1: this neurotransmitter. It's central to learning and memory and as
Speaker 1: early decline as a whole of Alzheimer's disease. It's made
Speaker 1: from coline in a cetolchola and released widely in the
Speaker 1: cortex and hippocampus, as well as a neuromuscular junction for
Speaker 1: voluntary muscle movement. This is the one for the fitness people.
Speaker 1: In psychological terms, loss of colonegic neurons colononergic neurons is
Speaker 1: called equals memory deficits in dementia, right, because you're gonna
Speaker 1: need a seal colone as well for learning and memory
Speaker 1: medications like aerocept or donapizila. Sorry about that. My dog
Speaker 1: was going crazy there for a second. We're back at it.
Speaker 1: So we're in aerocept which is one of the medications
Speaker 1: that they'll use for dementia. Blocks. Acetyl colonist RaSE Acetyl
Speaker 1: colonis torase is what that's right, The enzyme that breaks
Speaker 1: down AH which increases availability. So again these asse always
Speaker 1: enzymes and the periphery AH plays a role in autonomic
Speaker 1: nervous system function also helps with salivation, digestive digestion, and
Speaker 1: heart rate. Member the autonomic nervous system are things that
Speaker 1: we're not controlling consciously. Are just happening, right. Our heart's beating.
Speaker 1: We don't have to worry about that part. Lastly is neuropeptides.
Speaker 1: This is what you don't hear much about, but they're
Speaker 1: associated with pain, stress, and attachment. Neuropeptides are slowly acting,
Speaker 1: longer lasting molecules will modulate rather than directly excite or inhibit.
Speaker 1: They control the amount. They often travel alongside traditional neurotransmitters
Speaker 1: and effect mood, pain, and interpersonal bonding. You've heard of
Speaker 1: some of these for sure. For instance, the first one
Speaker 1: is endorference, which is the body's natural form of opioids.
Speaker 1: It reduces pain and enhances pleasure, released a lot during trauma,
Speaker 1: intense exercise, or even laughter. Substance P involved in transmitting
Speaker 1: pain signals to the brain. By the way, substance P
Speaker 1: is one of the key neuropeptides involved in transmitting pain
Speaker 1: signals like I mentioned, and this is what pain medications
Speaker 1: and experimental therapies aim to block or modulate to reduce
Speaker 1: pain perception. So it's again a neurotransmitler also a neuromodulator.
Speaker 1: So if you're taking something and some pain strategies they'll
Speaker 1: target substance P, especially in chronic pain, neuropathic pain, and
Speaker 1: inflammatory conditions like capsacan creams. You remember probably use some
Speaker 1: of those capsacan creams like Cutenza. They'll actually deplete substance
Speaker 1: P from nerve endings over time. Used for a localized
Speaker 1: neuropathic pain like diabetic neuropathy, but certain antidepressants and anti
Speaker 1: convulsants like deloxitine, symbalta, or gaba pedtin. They don't directly
Speaker 1: block substance pe but they modulate the pain transmission at
Speaker 1: higher levels, indirectly affecting its pathways. It's a kind of
Speaker 1: interesting side note there for you, and you can see
Speaker 1: why those drugs can actually help relieve a little bit
Speaker 1: of pain if you have some from some kind of injury.
Speaker 1: So now we go back again. The last one is
Speaker 1: oxytocin vasopressing. You've probably all heard of oxytocin. It's known
Speaker 1: for its properties for attachment, trust, and social bonding, as
Speaker 1: well as vasopressin too. They're also studied in autism and trauma.
Speaker 1: These aren't first line targets of psychiatric medication though, these neuropeptides,
Speaker 1: but they do shape how people feel in deep embodied ways.
Speaker 1: So it is key to remember these when you're exploring
Speaker 1: trauma or chronic pain. Each neurotransmitter that we've talked about
Speaker 1: today acts like a lens on the world. Having too
Speaker 1: much or till little of these neurotransmitters can affect how
Speaker 1: we perceive the world. It can alter our energy levels
Speaker 1: and rewire our behavior. They won't the E triple P
Speaker 1: won't ask you to draw synapses from memory, but it
Speaker 1: will expect you to reason through a taste where an
Speaker 1: antidepressant isn't working or a new medication triggers tremors. So again,
Speaker 1: if you're taking a medication and it increases dopamine levels
Speaker 1: too high and causes psychosis, this is what it is. Right.
Speaker 1: It also hinges a lot on whether them stem from
Speaker 1: a gabba imbalance or serotonin drop. So you need to
Speaker 1: think like a system analyst and know the multiple transmitters
Speaker 1: and multiple levels. This is why when it comes to psychopharmacology,
Speaker 1: it's a very difficult process. It's not so easy targeting
Speaker 1: these neuro transmitters. Well, there you go, folks. This is
Speaker 1: the last fixed audio version. We'll continue through our journey.
Speaker 1: I believe we're heading into culture in our more recent
Speaker 1: updates soon