Neurotransmitters of the human body
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- čas přidán 12. 11. 2015
- This is a overview of some common neurotransmitters found in the human body.
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ADDITIONAL TAGS:
Neurotransmitters
An introduction to chemicals that transmit information across the body, their functions, and their receptors
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Amino acids
Monoamines
Catecholamines
Acetylcholine (ACh)
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found in:
Motor neurons
Brain: basal ganglia and nucleus basalis of Meynert
Autonomic nervous system (ANS)
Sympathetic (ganglion neurotransmitter)
Parasympathetic (both ganglion and final product)
Used in treatment of:
Alzheimer’s disease
Dementia
Receptors:
Ionotropic → nicotinic receptors, excitatory
Metabotropic → muscarinic receptors, excitatory or inhibitory
Serotonin (5-HT)
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found in:
Brain and brainstem
Pineal gland
Raphe nuclei in the pons
Limbic function (emotions/mood, hunger, sex, instincts, temperature) sleep
Used in treatment of:
Depression
Sleep regulation
Receptors:
Ionotropic → 5-HT3 receptor, excitatory
Metabotropic → 5-HT1-7 receptors, excitatory or inhibitory
Dopamine
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found in:
Brain and brainstem
Substantia nigra (reward, addiction, movement)
Hypothalamus (inhibits prolactin release)
Used in treatment of:
Schizophrenia, psychosis
Parkinson’s disease
Receptors:
Ionotropic → none
Metabotropic
D1 → excitatory (K+/Ca2+)
D2 → inhibitory (K+/Ca2+)
Norepinephrine
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found in:
Brain: Locus ceruleus, projecting to cortex, for arousal, attention, and anxiety
ANS: sympathetic neurons (final product, postganglionic neurons)
Used in treatment of:
ADHD
Anxiety
Cardiac failure
Receptors:
Ionotropic → none
Metabotropic
α1 and β1 are excitatory
α2 and β2 are inhibitory
Glutamate
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found everywhere in CNS:
Excites the cerebral cortex, spinal cord, brainstem, hippocampus, cerebellum
Used in treatment of:
Amyotrophic lateral sclerosis (ALS), Lou Gehrig's disease
Excites motor, sensory, and cognitive neurons
Receptors (all excitatory):
Ionotropic
NMDA receptor
AMPA receptor
Kainate receptor
Metabotropic
gamma-Aminobutyric acid
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found everywhere in CNS:
Inhibits the cerebral cortex, spinal cord, brainstem, hippocampus, cerebellum, basal ganglia
Predominately found in interneurons
Used in treatment of:
Anxiety and rehab for drug abuse
Inhibits motor, sensory, and cognitive neurons → sedation, muscular/cardiorespiratory relaxation, inhibits pain/reflexes
Receptors (all inhibitory):
Ionotropic
GABAA receptor → Cl- channel (ligand-gated)
Metabotropic
GABAB receptor → decrease cAMP and increase K channels
Glycine
Acetylcholine
Serotonin
Dopamine
Norepinephrine
Glutamate
GABA
Glycine
Found in the spinal cord:
Inhibits spinal cord interneurons
Used in treatment of:
Spasticity
Receptors (all inhibitory):
Ionotropic
Cl- channel
The lecture omits to inform how these NTs work in the NE cells of the Gut and its effect or relationship on the brain.This is an important factor.
Psychology test on the biological approach later today and this is exactly what I needed
Awesome video. Very informative and helpful. Thank you for making it easy to understand
FYI Cl is chlorine. If it was calcium, it would have been excitatory not inhibitory
If its Cl then it means its inhibitory and if its Ca it means its excitatory . Am i right??
@@jenny.8915 no those have different functions. Calcium is used to bind the synaptic vesicles to the pre synaptic neurons membrane. This releases neurotransmitters that could either be excitatory or inhibitory depending on the part of the brain it is released. Chlorines function is less clear but it does have an affect on the excitation of a neuron. Chlorine is most likely inhibitory alongside potassium. Calcium has less of a function on the action potential and more on the neurotransmission of signals across neurons. Sodium is excitatory.
He just misread his Cl- as Calcium in the last 2 slides. It's Chloride. Great summary!
Thanks for this informative sharing
beautiful video so informative and well paced
For the GABA and glycine you say Calcium channels, but use the abbreviation Cl-. Do you mean Chloride channels?
+chienn77 That would make sense, because Chloride would cause hyper-polarization and decrease the likelihood of an action-potential (resulting, I would assume, in less neural activity and, hence, sedation.) Calcium would do the opposite.
Yeah he meant Chloride. If GABA released Calcium we’d all seize up and die lmao
@@ProfShibe lol
What do you know about the impact of the neurotransmitters on an HSP ?
thank you
B2 is stimulatory (Gs)
You have a beautiful voice!
fascinating, thank you
Very important topics
Very good, thank you
Thank you
Very very good.
thanks
that is what ı was searching for
Nice video brother
Awesome video! However I heard Ca channel in the glycine receptor, but in the presentation, it was shown as Cl channel. what does it mean?
I guess is Cl channel, because is inhibitory
Glycine, did the sound just go out?
I learned a lot more reading the comments. HAHAHA
Same…
What about the peptides like vasopressin, somatostatin...
hormones not NTs
Norepinephrine worsens anxiety. One medication bupropion that works on NE and Dopamine for depression can worsen anxiety.
Kay true I think norepinephrine is actually the cause of anxiety
It dependent on the type of anxiety. Rarely social anxiety has a small benifet
Irregularities in norepinephrine levels or a quick raise will induce anxiety but not cause it. Anxiety is a stress response & norepinephrine alone, isn't responsible for it. As for bupropion/wellbutrin - that's an NMDA, which simply means that it not only affects dopamine, norepinephrine but acetylcholine & some other neurotransmitters based off regions being targeted. Lastly, irregularities in levels of one or more neurotransmitters will cause anxiety/depression symptoms as a response by brain trying to balance itself.
@@ShardulIyer I read your comments and i find your knowledge about brain chemistry amazing,when you say the brain trying to balance it self but the impact will be the individual to feel the side effects of homeostasis like depression and anxiety.I wondered if the brain try to rebalance it self why some many people cannot feel happy after quiting drugs,how many years need it for brain to work again as it should be.Could be other factors play role on mental illness like neurosteroids.I bring the neurosteroids on the spot cause in the past i had a terrible experience with a 5a reductase inhibitor that altered my production of neurosteroids like pregnenolone
@@MetatroN197924 it largely differs from person to person due to individual neurology thus hard to predict, especially over such comments. Again, i am not a medical professional but a research scientist so it will be reckless to suggest something that I am not familiar with. As much as I know, while the brain strives for homeostasis much like the body - the brain has regenerative limitations despite the fascinating nature of neuroplasticity which again is very much dependent upon site. Regarding the reaction you mentioned - it might have a link since compounds interacting with hormones can leave a lasting effect on production & thus cause variety of effects including desirable ones & side-effects as well. I can't say much & maybe an endocrinologist, neurology specialist might assist better.
That was chloride channel..
If calcium channel opens than it will show excitatory effect
It was really helpful
Hi if you're a medical student how can I contact you??I'm releasing USMLE question and answer books in amazon tomorrow for every part of medicine and I need some reviews and some help
Doesn't the D2 receptor causes Chloride ion channels to open to make the cell more negative, thus inhibitting it?
Can u elab?
Which is responsible for pain
Hey, im really scared that my neurons are damaged, can anxiety cause long term damaged neurons? Or they can recover?
czcams.com/users/johnglanvill
maybe this channel wil help
By supplemental dopamin you mean the amino acid L-dopa?
refering to treatment of Parkinsons
@@Byrial Yes.
10:36-10:45 absence seizure
lol?
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Wait wait so at 4:00 you are saying depression is treated with serotonin? I.e. you administer serotonin? I'm pretty the standard treatment is with SSRIs, which inhibit the reuptake of serotonin, not direct administration of the serotonin itself.
I think he meant that drugs that affect 5-HT are used to treat depression. Inhibiting the reuptake of 5-HT allows for more to be in the synaptic cleft at all times, meaning that in a way the depression is being treated with more serotonin.
thanks!
Tyler Schmidt these psych meds do jack shit and actually screw u up more. Notice what you’re saying, THEY INHIBIT THE REUPTAKE PROCESS. It’s hypothesis is this will make more serotonin roam in the brain which is false. It kills off neurotransmitters because it no longer has anything to transmit at the synapse. This is why they say there’s a need to increase the dosage. That’s because the body and brain no longer supplement it and the medicine is. What happens then? You poop out. You end up destroying neurotransmitters and reducing the amount you originally had. These meds are evil and they’re being taught from big pharma they’re not doing these functions which is outrageous.
Serotonin really makes my depression an anxiety worst don't believe the hype
How do you know its high serotonin that causes your depression?
What are Neuromodulator??????
Calcium is Ca why its written as Cl ??
Because Cl- is chlorine
How can Glutamate be reduced?
Taking l glutamine,zinc,tuarine and p5p together
thought serotonin receptors were recently found in the digestive tract?
Haley Andreotti Yes that correct
@arron frederick hey brother in how many months sero and dopa balance naturally
You forgot about the opioid receptors
1k likes reached
Norepinephrine is not used for adhd, dopamine reuptake inhibitors are tho
So are NRIs, like atomoxetine.
How can I give myself schizophrenia,,, and how can I inhibit norepinephrine,,,
Schizophrenia is hereditary. You can't get it unless your parents carry the genes.
Why would u want that for yourself like so curious 😂🤨
@@almaalvarado9606 to boost perception,,, can you see or talk to ghosts gods or demons in normal perception? no you can't,,,
Damnnn
My brain is lacking all of these
K= potassium?
No K = kalium
Kalium = pottasium
Yes,K is pottasium
I think you messed up right at the end of this video
not clear
stephen stahl
This guy don't know what his teaching norepinephrine don't help anxiety it actually causes anxiety
No, it doesn't. Norepinephrine may influence cortisol but there are plenty of other factors associated with norepinephrine-seratonin interactions or even dopamine-norepinephrine interactions, which is why atomoxetine fails as an NRI antidepressant but excels as adhd medication. However, it's so complex to simply state that whether norepinephrine, seratonin, dopamine, acetylcholine, gaba irregularities are causing anxiety which itself varies over a spectrum. Not to mention, norepinephrine helps in extreme cases where someone with chronic anxiety, will exhibit excess norepinephrine thus an overactive sympathic nervous system that is interestingly calmed down by low uptake of norepinephrine & regulation of it, instead of irregularities of levels which is what gives that feeling of anxiety and not the other way around.
@@ShardulIyer that is because of homeostasis, works in some case and in others makes anxiety worse. The excess norepinephrine inhibits further release of norepinephrine preventing an emotional cascade. Not all norepinephrine increasing drugs work the same way, some modulate how norepinephrine works in the brain, reducing symptoms.
@@xxaidanxxsniperz6404 isn't that why I mentioned to the original commenter that we can't simply assume that norepinephrine drugs work at same level & each patient also exhibit different results though atleast a baseline can be maintained for some, allowing for treatment options. Plus the modulating ones are the ones we call RUI/re-uptake inhibitiors as you correctly mentioned that not all create new norepinephrine but help regulate the compromised flow as with chronic conditions and homeostasis factors. Even partial agonist & complete agnoist behaviour have varying results leading me to state how you can't generically state that norepinephrine causes anxiety without knowing a person's history.
@@ShardulIyer you seem to know a lot about about neurochemistry, mind if I ask you how mirtazapine affects the metabolism of vyvanse? I have ADHD and barely used stimulants, in the past 20 mg of vyvanse would last 7-8 hours but with mirtazapine the effects only last 4 hours. My theory is that the rise in serum triglycerides adds to the metabolization of LDX, alongside its effects on some enzymes mechanics. It seems contradictory as mirtazapine increases norepinephrine and serotonin by binding to A2 receptors. I'm going to see if there is a difference if I take my mirtazapine after the effects of the vyvanse fully wear off instead of in the morning at 30 mg. 15 mg at night.
@@xxaidanxxsniperz6404 Hi, i am a research scientist by profession so will be reckless on my part to comment on your case. Having said that, I also strongly suggest not to share your dosage online - either on comments like these or even social media forums - this is bcoz you just dunno who you are talking to & any advice may result in personal damage. Now, without getting into complex interactions or neuro chemistry - i can however comment on how these two are cross-reacting with each-other. Vyvanse uses your metabolic rate which again depends upon your circardian rhythm, norepinephrine levels, etc. Now, once you do take mirtazapane - it starts to mess around these factors so while you still have Vyvanse compounds within you, they start to compete with mirtazapane compounds which each individually have respective affinity - the part where I mentioned agnoist behaviour. Due to this, mirtazapane might start slowing your metabolic rate, much like how melatonin at night - will potentially numb the impact of norepinephrine dependent medication & even substances like nicotine, caffeine. Therefore, I highly suggest to consult with your doctor about timing of these medication, to avoid such cross-reactions. Rest, i can't comment much as i am not qualified to medical diagnose/counslt as such. Hope this helped.
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Your shit keeps going black .