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.
@natnaelmerk84455 жыл бұрын
FYI Cl is chlorine. If it was calcium, it would have been excitatory not inhibitory
@xxaidanxxsniperz64044 жыл бұрын
@Qayyum Khan 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.
@joecaz Жыл бұрын
He just misread his Cl- as Calcium in the last 2 slides. It's Chloride. Great summary!
@chienn778 жыл бұрын
For the GABA and glycine you say Calcium channels, but use the abbreviation Cl-. Do you mean Chloride channels?
@twofingersmakes718 жыл бұрын
+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.
@ProfShibe Жыл бұрын
Yeah he meant Chloride. If GABA released Calcium we’d all seize up and die lmao
@aurora09baby Жыл бұрын
@@ProfShibe lol
@TinaWu3 жыл бұрын
Awesome video. Very informative and helpful. Thank you for making it easy to understand
@spidey52817 ай бұрын
beautiful video so informative and well paced
@tateandovidaАй бұрын
❤ Thank you so much for this video!!!!! You Are Appreciated!
@arvindm19452 ай бұрын
i want to know., the anesthesia., role in nerves., how it prevents the pain , by blocking the signals to the brain., or in which way. through animation if possible.
@essewaxegard94232 жыл бұрын
Psychology test on the biological approach later today and this is exactly what I needed
@Tvtcrvtvgcrvrvrv-ce5lx7 ай бұрын
Very important topics
@faithnduta8662 жыл бұрын
You have a beautiful voice!
@seyoumalemu3575 жыл бұрын
B2 is stimulatory (Gs)
@sparklelight5 жыл бұрын
Thanks for this informative sharing
@rishabhvaishnav51096 жыл бұрын
That was chloride channel.. If calcium channel opens than it will show excitatory effect
@blueshade268 жыл бұрын
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.
@OwenWithAHammer8 жыл бұрын
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.
@blueshade268 жыл бұрын
thanks!
@RebelRager887 жыл бұрын
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.
@KiloTray6 жыл бұрын
Serotonin really makes my depression an anxiety worst don't believe the hype
@Byrial6 жыл бұрын
How do you know its high serotonin that causes your depression?
@Voyager6023 жыл бұрын
that is what ı was searching for
@Mr.Sp0cK5 жыл бұрын
What do you know about the impact of the neurotransmitters on an HSP ?
@lanajovic62594 жыл бұрын
Hey, im really scared that my neurons are damaged, can anxiety cause long term damaged neurons? Or they can recover?
@elijahgesu11454 жыл бұрын
kzbin.info
@elijahgesu11454 жыл бұрын
maybe this channel wil help
@edmarlabor40873 жыл бұрын
I learned a lot more reading the comments. HAHAHA
@EvanRajala10 ай бұрын
Same…
@l98787 жыл бұрын
Norepinephrine worsens anxiety. One medication bupropion that works on NE and Dopamine for depression can worsen anxiety.
@KiloTray6 жыл бұрын
Kay true I think norepinephrine is actually the cause of anxiety
@daltonboehm95395 жыл бұрын
It dependent on the type of anxiety. Rarely social anxiety has a small benifet
@ShardulIyer5 жыл бұрын
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.
@MetatroN1979244 жыл бұрын
@@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
@ShardulIyer4 жыл бұрын
@@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.
@dalalm18216 жыл бұрын
10:36-10:45 absence seizure
@pginaeemidris20694 жыл бұрын
lol?
@francoisr40364 жыл бұрын
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@ethankrown3 жыл бұрын
You forgot about the opioid receptors
@HitmanR978 ай бұрын
Nice video brother
@johndoeble9 ай бұрын
My brain is lacking all of these
@Nickael77 жыл бұрын
What about the peptides like vasopressin, somatostatin...
@p1kto6 жыл бұрын
hormones not NTs
@Mjayy_onyekwere Жыл бұрын
Thank you
@pennwoman2 жыл бұрын
Very very good.
@王宇婕-o6t Жыл бұрын
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?
@arturomauriciobautistaroma5694 Жыл бұрын
I guess is Cl channel, because is inhibitory
@KiloTray6 жыл бұрын
This guy don't know what his teaching norepinephrine don't help anxiety it actually causes anxiety
@ShardulIyer5 жыл бұрын
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.
@xxaidanxxsniperz64044 жыл бұрын
@@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.
@ShardulIyer4 жыл бұрын
@@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.
@xxaidanxxsniperz64044 жыл бұрын
@@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.
@ShardulIyer4 жыл бұрын
@@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.
@Byrial6 жыл бұрын
By supplemental dopamin you mean the amino acid L-dopa?
@Byrial6 жыл бұрын
refering to treatment of Parkinsons
@nickjohn20515 жыл бұрын
@@Byrial Yes.
@lightbeingpontifex2 жыл бұрын
How can I give myself schizophrenia,,, and how can I inhibit norepinephrine,,,
@carmen_132 жыл бұрын
Schizophrenia is hereditary. You can't get it unless your parents carry the genes.
@almaalvarado96062 жыл бұрын
Why would u want that for yourself like so curious 😂🤨
@lightbeingpontifex2 жыл бұрын
@@almaalvarado9606 to boost perception,,, can you see or talk to ghosts gods or demons in normal perception? no you can't,,,
@melanieg.92834 жыл бұрын
How can Glutamate be reduced?
@texaspatriot91592 жыл бұрын
Taking l glutamine,zinc,tuarine and p5p together
@Bender20453 жыл бұрын
Glycine, did the sound just go out?
@manivannankannaiyan54203 жыл бұрын
Which is responsible for pain
@KeepPrayingCA8 жыл бұрын
thought serotonin receptors were recently found in the digestive tract?
@nickjohn20517 жыл бұрын
Haley Andreotti Yes that correct
@kaustubhsangale90273 жыл бұрын
@arron frederick hey brother in how many months sero and dopa balance naturally
@thegloryumoh3 жыл бұрын
It was really helpful
@medexams14633 жыл бұрын
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
@mercurious6699 Жыл бұрын
fascinating, thank you
@300Moritz7 жыл бұрын
thank you
@julesjgreig3 жыл бұрын
Very good, thank you
@santicruz40123 жыл бұрын
Doesn't the D2 receptor causes Chloride ion channels to open to make the cell more negative, thus inhibitting it?
@iQmliAwyrMRyPWfV7 ай бұрын
Can u elab?
@libertarianact76552 жыл бұрын
Norepinephrine is not used for adhd, dopamine reuptake inhibitors are tho
@kenhaze52302 жыл бұрын
So are NRIs, like atomoxetine.
@everythingissalad29694 ай бұрын
Snris
@muhammadsulaiman60235 жыл бұрын
What are Neuromodulator??????
@muskduh3 жыл бұрын
thanks
@bradanderson79782 жыл бұрын
I think you messed up right at the end of this video