Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:07):
Today we're gonna be looking at the other four neurotransmitters.
We have a mic now, so hopefully this will sound
a little bit better in equality. For West. First we're
gona look at is nora perenephrin also known as nora adrenaline,
and is based in the locus corolius. That's locus is
l O c u S. Corolius is c o E
(00:29):
r u E. I'm sorry, c O E r u
l e u s in the ponds p o n
s and plays a key role in your fight or
flight response. So Nora penephrine fight or flight, but its
everyday function is more subtle. It fine tunes attention, vigilance
and wakefulness. So again it fine tunes attention, vigilance and wakefulness.
(00:53):
So if you think about it, lopepherne, what happens fatigue,
poor concentration, lower energy. Think of what psychiatric disorder that
could be associated with depression? High no apefferent is the
opposite agitation, hyper arousal. Think of mania. So maybe you
can see bipolar here. I don't know if nouropenefferent fluctuates
like that for bipolar, but we see in the mania
(01:14):
and anxiety but we also see them being targeted in ADHD. Right,
So you have things like atomoxetine stratera that will is
a norif nefrin reuptake inhibitor, allowing more nouropenefferne to stay
in the synapse to allow you to be more alert
and remember. Any kind of ADHD medication like atomoxetine, retolin
(01:39):
or aderall they help everybody to improve their attention. This
is why it's being abused a lot by college children
or college students. Once released, nora upeneffrin binds to alpha
and beta adronergic receptors, so these receptors are for adrenaline
or no effern similar to dopamine serotonin. It's taken back
(02:00):
up or broken down by NAO. The enzymes. Tricyclic antidepressants
TCAs like nor tripolen work by blocking the reuptake of
both serotonin and more ifnefferent so TCAs. The antidepressants are
much stronger than SSRIs and are not used very commonly
anymore unless the individual is not getting any success with
the SSRIs or SNRIs. We hit over an nowt of
(02:22):
gabba in gaba, We're going to wear it up with
glutamate you'll see why in a minute. Glutamate is the
most excitatory neurotransmitter. So you think about it, Glutamate is
the gas pedal, while gabba is the break, right, it's
the primary inhibitory neurotransmitter. That's what GABA is, the primary
(02:44):
inhibitory neurotransmitter, calming neuronal activity and preventing overstimulation. Oddly enough,
GABBA is actually synthesized from glutamate using the enzyme gad low. GABBA.
What is it associated with? Well, generalized anxiety disorder, panic attacks, seizures.
So you take things like diazepines for instance, like lurazepam
(03:07):
which is adavan or valume diazepam, and they work by
enhancing GABA a receptor activity, so increasing inhibition and producing sedation, right,
calming things down, muscle relaxation, reduced anxiety. But of course
with benzos we know tolerance and dependents are major concerns.
Highly addictive. GABA does not get reabsorbed like the melanomines. Instead,
(03:31):
it's broken down by a gabba transaminase, another target for
seizure medications. So the GABBA transaminase is in the enzyme.
Anytime you see ase at the end of a word.
That's an enzyme. So let's head over to glutamate, which
is everywhere. Honestly, it's everywhere in our system. It's over
(03:51):
ninety percent of our excitatory synapses in the brain. Use
it powers learning, memory and synaptic classicity, especially in the
hippocampus and cortex. And it makes sense. Think about it.
When you learn, when you add a new memory, when
you grew new neurons with synaptic plasticity, that requires energy
and work. So it doesn't surprise me that glutamate, the
(04:14):
excitatory one, is going to be there. It's got to
activate these things, and this is where you use up
a lot of energy. It binds that several different receptors
NMDA receptors which are involved in long term potentiation, which
is the mechanism behind learning. Right, long term potentiation, I
want to keep it in my long term memory in
the hippocampus. Short term memory is over in the pre
(04:35):
funnel cortex. Also the AMPA receptors for fast synaptic transmission
and knate kai NATE receptors for modulating signals. So AMPA
receptors for fast synaptic transmission and k and A receptors
for modulating signals. Too much glutamate causes what they call
(04:56):
exo excytosisicity excitote toxicity is a problem. It's when neurons
firing themselves to death, so over use in a sense, right,
too much excitement, and then they die off. This happens
unfortunately in stroke TBIs and even Alzheimer's. So sometimes what
they'll do they'll use medications to reduce the damage that
(05:19):
can be seen in dementia, like memantine mem A N
T I n E to block NMDA receptors. So again
they'll use medications like mamantine. Remember, Alzheimer's is a version
of dementia. The other version is vascular dementia. So too
much glutamate excitotoxicity. So we'll move on to the last
(05:41):
one of the neurotransmitters, and then we'll get to neuropeptides.
To wrap it up. Seedocholine. It's memory motor control in Alzheimer's.
Alzheimer's seedal colin is es central to learning and memory.
The acronym for or the abbreviation for acetocholine the ACH
and it's decline as a hallmark of Alzheimer's disease. It's
(06:03):
made from coline and acetyl CoA and release widely in
the cortex and hippocampus as well as neuromuscular junctions for
voluntary muscle movements. So let me explain this in a
different way. Loss of pol energic neurons, cholinergic neurons, and
neurons associated with coline equals a memory deficit in dementia.
(06:24):
You may take a medication which is commonly known like
aerocept also known as dnapezil. They work by blocking acetyl
colon esterase scetyl colon estates. Remember the ase at the end.
That means it's an enzyme, so it's blocking that enzyme
from breaking it down. That's what enzymes do. So this
increases the availability of the acetylcholine and the periphery. Acch
(06:47):
plays a role in atomic, nonomic, nervous system function, salivation, digestion,
heart rate. Unfortunately, there's nothing now that we can do
to stop or reverse dementia. All we can do is
mitigate it, and this is what they're trying to do
with the aeroceps. So don't be confused as it does
not cure Alzheimer's or dementia. It does not reverse it.
(07:09):
It just really slows it down in this issue with acetylcholine. Last,
but not least is neuropeptides, and they're slower acting, longer
lasting molecules, and modulate rather than directly excite or inhibit.
So they travel alongside traditional neurotransmitters and they affect mood, pain,
and interpersonal bonding. Endorphins bodies natural opioids are an example
(07:34):
of them. They reduce pain, enhance pleasure, and released during trauma,
intense exercise, or laughter. This is one of the reasons
we can relax or reduce the pain, enhance our pleasure.
Substance key is involved in transmitting pain signals to the
brain oxytocin and vacal press and crucial for attachment, trust,
(07:56):
and social bonding studied in autism and trauma. These aren't
the first line targets of psychiatric medication, but they do
shape how people feel in deep ways, especially embodied ways.
Something to remember when exploring trauma, chronic pain, or relational disorders.
We'll take a little deeper dive into this now and
(08:17):
look at it. So neuropeptides again small protein like molecules
that are produced by neurons, and they ride along with them,
I guess you can say. So let's look how they
affect the psychologically. Neuropeptides such as oxytocin, vasopressin, and endorphins
act as neuromodulators. We talked about that many of the
neuropeptides interact with the HPA, the hypothalmic p territory adenal axis,
(08:41):
regulating stress responses, which of course impact mood and anxiety levels.
Gene expression can influence long term changes in brain function
by affecting gene expressions. That's what neuropeptides can do as well.
They bind to what they call specific G protein coupled
receptors where they go trigger cascades that influence neuronal excitability,
(09:01):
emotional regulation, and so forth. So let's see how they
affect psychiatric conditions. So, depression will have low levels of
oxytocin or endorphins, which are associated with depressive symptoms. CRF
hyperactivities linked also to chronic stress and major depressive disorder,
and that's cortico trope and releasing factor. In addition to that,
(09:25):
elevated CRF and neuropeptide y NPY and balances are tied
to heightened anxiety and panic disorders. Npy in particularly has
a protective role and schizophrenia. Altered levels of CCK and
somatostatin are found in schizophrenia, particularly affecting dopamine regulation. Addiction,
(09:46):
you'll see edorphin, endorphins and dinorphins influence reward and withdrawal processes,
contributing to substance use disorders Autism spectrum disorder. Oxytocin dysregulation
is linked to social deficits in autism spectrum disorder, with
some studies exploring oxytocin administration as a potential therapeutic option PTSD. Again,
(10:11):
an MPY imbalance contributing to hyper arousal, so oxytocin therapy
is one thing they're looking at. Neuropyptide y enhancing the
NPY signal is being studied for its angeolytic and stress
resilience effects. Neuropeptides are complex, with effects varying by brain region,
(10:32):
receptor type, and even individual differences. The blood brain barrier,
penetration limits drug development. Overstimulation or inhibition of neuropeptide systems
can lead to unintended side effects as well, requiring precise targeting.
So again those are neuropeptides a little bit more complicated.
We saw the other neurotransmitters that will be covered them
(10:55):
again GABBA, lutamate and acelocholine and nora epinephern so nor
epineffern fight or flight, attention, vigilance, wakefulness associated with major
depressive disorder depression with low epinephrine, also associated with mania
and anxiety with high neuropinephrine. Use The lots being targeted
in ADHD with it's fritera, demoxetine, GABA inhibition and anxiety control, glutamate, memory, learning,
(11:22):
and exo excito toxicity. Remember with GABBA, it's associated with
generalized anxiety sort of panic attacks over here and glutamate
over excitement of it can lead to Alzheimer's disease traumatic
brain injury. Medications associated with it are memantine acetacholine. You're
(11:44):
looking at learning and memory. It's an early hallmark of
Alzheimer's disease for decline, a loss of calinergic neurons. That's
what's affecting the memory deficits and dementia. Medications associated or
aircept neuropeptides and dwarf friends substance p oxytocin and vas
oppressing and that's it. Next time when we meet, we're
(12:06):
going to go into the endocrine system and psychological functioning.
So hopefully you're enjoying this podcast, I'm really helping you
to study better for your E triple P
Today we're gonna be looking at the other four neurotransmitters.
We have a mic now, so hopefully this will sound
a little bit better in equality. For West. First we're
gona look at is nora perenephrin also known as nora adrenaline,
and is based in the locus corolius. That's locus is
l O c u S. Corolius is c o E
(00:29):
r u E. I'm sorry, c O E r u
l e u s in the ponds p o n
s and plays a key role in your fight or
flight response. So Nora penephrine fight or flight, but its
everyday function is more subtle. It fine tunes attention, vigilance
and wakefulness. So again it fine tunes attention, vigilance and wakefulness.
(00:53):
So if you think about it, lopepherne, what happens fatigue,
poor concentration, lower energy. Think of what psychiatric disorder that
could be associated with depression? High no apefferent is the
opposite agitation, hyper arousal. Think of mania. So maybe you
can see bipolar here. I don't know if nouropenefferent fluctuates
like that for bipolar, but we see in the mania
(01:14):
and anxiety but we also see them being targeted in ADHD. Right,
So you have things like atomoxetine stratera that will is
a norif nefrin reuptake inhibitor, allowing more nouropenefferne to stay
in the synapse to allow you to be more alert
and remember. Any kind of ADHD medication like atomoxetine, retolin
(01:39):
or aderall they help everybody to improve their attention. This
is why it's being abused a lot by college children
or college students. Once released, nora upeneffrin binds to alpha
and beta adronergic receptors, so these receptors are for adrenaline
or no effern similar to dopamine serotonin. It's taken back
(02:00):
up or broken down by NAO. The enzymes. Tricyclic antidepressants
TCAs like nor tripolen work by blocking the reuptake of
both serotonin and more ifnefferent so TCAs. The antidepressants are
much stronger than SSRIs and are not used very commonly
anymore unless the individual is not getting any success with
the SSRIs or SNRIs. We hit over an nowt of
(02:22):
gabba in gaba, We're going to wear it up with
glutamate you'll see why in a minute. Glutamate is the
most excitatory neurotransmitter. So you think about it, Glutamate is
the gas pedal, while gabba is the break, right, it's
the primary inhibitory neurotransmitter. That's what GABA is, the primary
(02:44):
inhibitory neurotransmitter, calming neuronal activity and preventing overstimulation. Oddly enough,
GABBA is actually synthesized from glutamate using the enzyme gad low. GABBA.
What is it associated with? Well, generalized anxiety disorder, panic attacks, seizures.
So you take things like diazepines for instance, like lurazepam
(03:07):
which is adavan or valume diazepam, and they work by
enhancing GABA a receptor activity, so increasing inhibition and producing sedation, right,
calming things down, muscle relaxation, reduced anxiety. But of course
with benzos we know tolerance and dependents are major concerns.
Highly addictive. GABA does not get reabsorbed like the melanomines. Instead,
(03:31):
it's broken down by a gabba transaminase, another target for
seizure medications. So the GABBA transaminase is in the enzyme.
Anytime you see ase at the end of a word.
That's an enzyme. So let's head over to glutamate, which
is everywhere. Honestly, it's everywhere in our system. It's over
(03:51):
ninety percent of our excitatory synapses in the brain. Use
it powers learning, memory and synaptic classicity, especially in the
hippocampus and cortex. And it makes sense. Think about it.
When you learn, when you add a new memory, when
you grew new neurons with synaptic plasticity, that requires energy
and work. So it doesn't surprise me that glutamate, the
(04:14):
excitatory one, is going to be there. It's got to
activate these things, and this is where you use up
a lot of energy. It binds that several different receptors
NMDA receptors which are involved in long term potentiation, which
is the mechanism behind learning. Right, long term potentiation, I
want to keep it in my long term memory in
the hippocampus. Short term memory is over in the pre
(04:35):
funnel cortex. Also the AMPA receptors for fast synaptic transmission
and knate kai NATE receptors for modulating signals. So AMPA
receptors for fast synaptic transmission and k and A receptors
for modulating signals. Too much glutamate causes what they call
(04:56):
exo excytosisicity excitote toxicity is a problem. It's when neurons
firing themselves to death, so over use in a sense, right,
too much excitement, and then they die off. This happens
unfortunately in stroke TBIs and even Alzheimer's. So sometimes what
they'll do they'll use medications to reduce the damage that
(05:19):
can be seen in dementia, like memantine mem A N
T I n E to block NMDA receptors. So again
they'll use medications like mamantine. Remember, Alzheimer's is a version
of dementia. The other version is vascular dementia. So too
much glutamate excitotoxicity. So we'll move on to the last
(05:41):
one of the neurotransmitters, and then we'll get to neuropeptides.
To wrap it up. Seedocholine. It's memory motor control in Alzheimer's.
Alzheimer's seedal colin is es central to learning and memory.
The acronym for or the abbreviation for acetocholine the ACH
and it's decline as a hallmark of Alzheimer's disease. It's
(06:03):
made from coline and acetyl CoA and release widely in
the cortex and hippocampus as well as neuromuscular junctions for
voluntary muscle movements. So let me explain this in a
different way. Loss of pol energic neurons, cholinergic neurons, and
neurons associated with coline equals a memory deficit in dementia.
(06:24):
You may take a medication which is commonly known like
aerocept also known as dnapezil. They work by blocking acetyl
colon esterase scetyl colon estates. Remember the ase at the end.
That means it's an enzyme, so it's blocking that enzyme
from breaking it down. That's what enzymes do. So this
increases the availability of the acetylcholine and the periphery. Acch
(06:47):
plays a role in atomic, nonomic, nervous system function, salivation, digestion,
heart rate. Unfortunately, there's nothing now that we can do
to stop or reverse dementia. All we can do is
mitigate it, and this is what they're trying to do
with the aeroceps. So don't be confused as it does
not cure Alzheimer's or dementia. It does not reverse it.
(07:09):
It just really slows it down in this issue with acetylcholine. Last,
but not least is neuropeptides, and they're slower acting, longer
lasting molecules, and modulate rather than directly excite or inhibit.
So they travel alongside traditional neurotransmitters and they affect mood, pain,
and interpersonal bonding. Endorphins bodies natural opioids are an example
(07:34):
of them. They reduce pain, enhance pleasure, and released during trauma,
intense exercise, or laughter. This is one of the reasons
we can relax or reduce the pain, enhance our pleasure.
Substance key is involved in transmitting pain signals to the
brain oxytocin and vacal press and crucial for attachment, trust,
(07:56):
and social bonding studied in autism and trauma. These aren't
the first line targets of psychiatric medication, but they do
shape how people feel in deep ways, especially embodied ways.
Something to remember when exploring trauma, chronic pain, or relational disorders.
We'll take a little deeper dive into this now and
(08:17):
look at it. So neuropeptides again small protein like molecules
that are produced by neurons, and they ride along with them,
I guess you can say. So let's look how they
affect the psychologically. Neuropeptides such as oxytocin, vasopressin, and endorphins
act as neuromodulators. We talked about that many of the
neuropeptides interact with the HPA, the hypothalmic p territory adenal axis,
(08:41):
regulating stress responses, which of course impact mood and anxiety levels.
Gene expression can influence long term changes in brain function
by affecting gene expressions. That's what neuropeptides can do as well.
They bind to what they call specific G protein coupled
receptors where they go trigger cascades that influence neuronal excitability,
(09:01):
emotional regulation, and so forth. So let's see how they
affect psychiatric conditions. So, depression will have low levels of
oxytocin or endorphins, which are associated with depressive symptoms. CRF
hyperactivities linked also to chronic stress and major depressive disorder,
and that's cortico trope and releasing factor. In addition to that,
(09:25):
elevated CRF and neuropeptide y NPY and balances are tied
to heightened anxiety and panic disorders. Npy in particularly has
a protective role and schizophrenia. Altered levels of CCK and
somatostatin are found in schizophrenia, particularly affecting dopamine regulation. Addiction,
(09:46):
you'll see edorphin, endorphins and dinorphins influence reward and withdrawal processes,
contributing to substance use disorders Autism spectrum disorder. Oxytocin dysregulation
is linked to social deficits in autism spectrum disorder, with
some studies exploring oxytocin administration as a potential therapeutic option PTSD. Again,
(10:11):
an MPY imbalance contributing to hyper arousal, so oxytocin therapy
is one thing they're looking at. Neuropyptide y enhancing the
NPY signal is being studied for its angeolytic and stress
resilience effects. Neuropeptides are complex, with effects varying by brain region,
(10:32):
receptor type, and even individual differences. The blood brain barrier,
penetration limits drug development. Overstimulation or inhibition of neuropeptide systems
can lead to unintended side effects as well, requiring precise targeting.
So again those are neuropeptides a little bit more complicated.
We saw the other neurotransmitters that will be covered them
(10:55):
again GABBA, lutamate and acelocholine and nora epinephern so nor
epineffern fight or flight, attention, vigilance, wakefulness associated with major
depressive disorder depression with low epinephrine, also associated with mania
and anxiety with high neuropinephrine. Use The lots being targeted
in ADHD with it's fritera, demoxetine, GABA inhibition and anxiety control, glutamate, memory, learning,
(11:22):
and exo excito toxicity. Remember with GABBA, it's associated with
generalized anxiety sort of panic attacks over here and glutamate
over excitement of it can lead to Alzheimer's disease traumatic
brain injury. Medications associated with it are memantine acetacholine. You're
(11:44):
looking at learning and memory. It's an early hallmark of
Alzheimer's disease for decline, a loss of calinergic neurons. That's
what's affecting the memory deficits and dementia. Medications associated or
aircept neuropeptides and dwarf friends substance p oxytocin and vas
oppressing and that's it. Next time when we meet, we're
(12:06):
going to go into the endocrine system and psychological functioning.
So hopefully you're enjoying this podcast, I'm really helping you
to study better for your E triple P
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