Great video! I loved how you kept saying "and how does this happen?" and then you continued. It seems like in other educational videos, it's always cut prematurely for one reason or another.
one of the best videos to have explained this so seamlessly. I can say that cuz I have almost watched 7 or so videos on the same topic by now and urs was by far the best.
Great information 👍. If we think about physical properties and the physics of their potential a channel can be reinforced by continuing the flow of a molecule along the pathway. So the old saying ; "use it or loose it". Is very true to strengthening synapses and also on building pre-existing pathways within us.
Thank you so much. This was very informative and gave me information I've been trying to learn. I took a lot of Methylphenidate growing up and had crazy amounts of glutamate in my brain, life has been so different lately now that I'm 19 and this really does answer a lot. Ps. Don't give kids Ritalin/concerta/methylphenidate or Focalin/dexmethylphenidate, shit is bad for the brain, and permanently causes permanent changes and permeanant symptoms of ADHD through gene regulation, excitotoxic brain damage, and developmental changes. Everyone who takes this under 16, even just briefly, has permanently down regulated GABA and it's still fuckin FDA approved. ADHD is practically made up by the pharmacuetical companies and pediatricians should not be the ones prescribing it, they don't know about psycology or brain chemistry.
At 1:33, should it be metaBOtropic and ionoTROpic receptors, rather than metabolic and ionic? Are 'metabolic' receptors the same as 'metabotropic' receptors?
What causes the process of the post-synaptic firing 20 ms before pre-synaptic and the process of post-synaptic firing 20 ms after the pre-synaptic? Like what is the mechanism for the dendrite to go either way?
+Amit Ika im not exactly sure, but i think its about coincidence of... lets say signals. i remember an experiment with snails, wherethey made them connect a slight touch with a later painful touch (leading to an action potential in associated neurons) to investigate LTP. i guess for complex bevhaviour, we could think of one signal activated by former experiences associations and one from outside, or something alike.
In a nutshell, there is no mechanism. Individual neurons may have up to 10,000 inputs (aka pre-synaptic connections) each. This video is discussing the relationship between only two neurons. The mechanisms of LTP and LTD are basically nature's gain filter; if a pre-synaptic connection is consistently "synced up" with post-synaptic action potentials (i.e. pre fires ~20msec before post), that pre-synaptic neuron can be described as constructively interfering with the activity of the post-synaptic neuron. Over time, the concerted activation of the two yields LTP. However, if the post-synaptic neuron is firing *before* that same pre-synaptic neuron, then the signal from the pre-synaptic neuron is in essence irrelevant to the activation of the post-synaptic neuron. In other words, it's an unimportant connection. Because of the delay, the normal downstream effects of the release of GLU are diminished - fewer AMPA receptors will be inserted into the lipid bilayer at that synaptic cleft, making it more difficult for that specific synapse to trigger an excitatory response in the future (LTD). TL;DR: it's not that the post-synaptic cell fires before the pre-synaptic cell because of any one specific mechanism; the post-synaptic cell was simply excited beyond threshold by a different connection before the AP / NT from the pre-synaptic cell reached it. #betterlatethannever
That's a good question! The answer is its complicated...there are a number of different ways inhibitory synapses undergo plasticity. Some of these ways are similar to the hippocampal plasticity in the video. Calcium flowing through NMDA receptors activates calcium dependent kinases or phosphatases which cause the post synaptic cell to insert more GABA receptors or take in GABA receptors respectively. These secondary messengers can also phosphorylate GABA receptors making them more effective. But there are also other different ways; in some cases when an excitatory pre-synaptic neurone stimulates a post synaptic neurone, the post synaptic neurone will release messengers which diffuse back across the synaptic cleft and cause nearby inhibitory neurones to release more or less GABA in the future. Also neuronal activity has also been found to alter the number of chloride transporters in a neurone. Changes in the concentration of chloride within a neurone will change how quickly chloride ions flow into a cell when GABA channels are open, making the existing GABA channels more or less inhibitory. If you're interested in reading further, this is probably the best paper I've found! www.ncbi.nlm.nih.gov/pubmed/21334194
but why would an independent depolarisation/repolarisation in the postsynaptic cell automatically mean a reduction in NMDA receptors? i get how lower ca2+ flow causes less NMDA receptors, but doesnt there need to be a starting point?
Hey, thank you for sharing this knowledge. If you'd be so kind, i have a request; Do you know a paper approaching the topic of how exactly protein kinase is influncing the "recycling" of AMPA receptors? Thank you again, Severin Mittermayer
Excellent question! You might think so but the answer is no, with Hebbian plasticity the information is thought to be stored in the pattern of the relative strengths of all the synapses. Homeostatic plasticity changes the global, overall excitability of the neurone through either: Changing the threshold voltage of the neurone, making it more or less likely to fire, but not changing the strengths of the synapses Or through "synaptic scaling", where the strengths of all of the synapses are changed BY THE SAME FACTOR, eg the strengths of all the synapses are doubled or the strengths are all halved. That means that the pattern of synaptic strengths, relative to each other stays the same, and the information is not lost. This paper explains it very nicely: Homeostatic plasticity in the developing nervous system Gina G. Turrigiano & Sacha B. Nelson Nature Reviews Neuroscience 5, 97-107 (February 2004)
what determines which (pre/post synaptic neuron) fires first? And why do activities like studying cause the post synaptic neuron to fire within 20 milliseconds while some other activities don't?
the only thing that comes to mind is association or repetition. the more often something is done the more chances of an earlier action potential. since the cell has fired several times prior in that direction. and the more connections to a cell (association) the more action potentials reach a receptor along the axon, thus increasing the chances of an earlier pre-synaptic firing. . . this is just an assumption however.
Has anyone given much consideration to biological boundaries? That is to say, can learning to play ball with one’s dog, or interact with a spider, be creating such synaptic development in both species? As we learn each other’s behaviors, it must be acknowledged that mutual learning occurs. And perhaps consider the posdibility that we are not unique in our neuroplasticity.
Hey this really helped me understand HOW synaptic plasticity occurs but WHY does the fact that two neurons that fire together become more linked helps us learn? wouldn't it just make us repeat what we already do?
what do you mean the "if the presynatic neuron fires after", doesn't calling a neuron pre synaptic inherently mean it's fires "before" with respect to a post synaptic neuron
Dude your videos are great!!! really helped me with my neuro paper this semester. Would love to see some anatomy videos too. Thank you for doing this. Much appreciated. :)
What about synesthesia and art? For example, when I attempt to memorize a concept or an experience, I make pun out of the it and put it into 'memory palace.' Does that mean that, let's say, a neuron responsible for a smell, like an aroma of coffee, will try to connect(via dendrite or axon terminal) to visual responsible neuron when they are 'fired' together, i.e. smelling and seeing the coffee at the same time? Sorry for my bad English
Do you mind sharing your references you used for this video I'd really like to get into this topic by myself. I'm pretty new to this field and currently conducting research on this topic. Alternatively some key words (e.g Spike-Timing-Dependent Plasticity) besides neuronal plasticity would be very appreciated
please please this is so much scientific explain with another language for the ones like me who are not studying this stuff just curious abour memorie and how it work really i didn"t understand so much from the video i know u know what are you talking about but i get nothing from it.
Finally, an explanation on the biological process. Thanks for the upload! :-)
Hello, just wanted to say i'm in a neuroscience course during Covid-19 and this was a great explanation. thank you so much
Finally found an explanation for what strengthening a synapse means.
soooo good! 3 hours lecture in 7 min, and so clear !! Thanks a lot
Great video! I loved how you kept saying "and how does this happen?" and then you continued. It seems like in other educational videos, it's always cut prematurely for one reason or another.
You explain neuroscience more clearly than anyone else I’ve heard
This must be one of the best videos I've seen! Thank you!
Man, I needed this video to understand the whole spiking phenom. Thanks so much!
best explanation for this concept I have found, keep up the good work buddy!
one of the best videos to have explained this so seamlessly. I can say that cuz I have almost watched 7 or so videos on the same topic by now and urs was by far the best.
Great information 👍.
If we think about physical properties and the physics of their potential a channel can be reinforced by continuing the flow of a molecule along the pathway.
So the old saying ;
"use it or loose it". Is very true to strengthening synapses and also on building pre-existing pathways within us.
Hi, medstudent here and I gotta say this amazing!! Thank you so much!
Brilliant explanation! Thank you so much for making this video :)
This is the best neuroscience explanation
Saves much time! Love it.
videos good but just a tip your volume is in and out
This helped me significantly on one of my neuroscience exams, thank you 👌👌
Really cool! It was not only very informative but also a kind of entertaining and I truly enjoyed it. Thank you! ;)
Best teacher ever
Excellent! The best video ever. Thanks!
This is fantastic! so clear !
Fantastic job explaining a very complex subject simply!!!
That was class, Thank you!
This made it so much easier to understand ! Thanks
Thank you so much. This was very informative and gave me information I've been trying to learn. I took a lot of Methylphenidate growing up and had crazy amounts of glutamate in my brain, life has been so different lately now that I'm 19 and this really does answer a lot.
Ps.
Don't give kids Ritalin/concerta/methylphenidate or Focalin/dexmethylphenidate, shit is bad for the brain, and permanently causes permanent changes and permeanant symptoms of ADHD through gene regulation, excitotoxic brain damage, and developmental changes. Everyone who takes this under 16, even just briefly, has permanently down regulated GABA and it's still fuckin FDA approved. ADHD is practically made up by the pharmacuetical companies and pediatricians should not be the ones prescribing it, they don't know about psycology or brain chemistry.
apart from the volume problems at the beginning best video for understanding synaptic plasticity I could wish for
Thank you! That was SUPER helpful
Thank you so much for the video! Really.
Thank you very much, you wrapped this topic up quite nicely!
Great video. What would make the post synaptic receptor fire first?
I have this question too
Very goooood. Thanks for your help
Amazing video! Thanks lots :)
Great vid and amazingly well expalined! Thanks a lot .
At 1:33, should it be metaBOtropic and ionoTROpic receptors, rather than metabolic and ionic?
Are 'metabolic' receptors the same as 'metabotropic' receptors?
Beautifully explained!
his is a good video! hi from neuroscience enthusiast here!
Thank you so much ! Quick and clear
Beautiful video! Please do post more. Thank you very much.
Wow. Now I understand the role of Ca2+ in LTP and LTD better
Great video!
How does postsinaptic neuron despolirizes before the presinaptic does?
Superb! :)
Thank you ! That was a brilliant video 😀
What causes the process of the post-synaptic firing 20 ms before pre-synaptic and the process of post-synaptic firing 20 ms after the pre-synaptic? Like what is the mechanism for the dendrite to go either way?
+Amit Ika im not exactly sure, but i think its about coincidence of... lets say signals. i remember an experiment with snails, wherethey made them connect a slight touch with a later painful touch (leading to an action potential in associated neurons) to investigate LTP. i guess for complex bevhaviour, we could think of one signal activated by former experiences associations and one from outside, or something alike.
+Amit Ika i think this has to do with the neurons basically "wanting" to predict what happens next.
In a nutshell, there is no mechanism. Individual neurons may have up to 10,000 inputs (aka pre-synaptic connections) each. This video is discussing the relationship between only two neurons. The mechanisms of LTP and LTD are basically nature's gain filter; if a pre-synaptic connection is consistently "synced up" with post-synaptic action potentials (i.e. pre fires ~20msec before post), that pre-synaptic neuron can be described as constructively interfering with the activity of the post-synaptic neuron. Over time, the concerted activation of the two yields LTP. However, if the post-synaptic neuron is firing *before* that same pre-synaptic neuron, then the signal from the pre-synaptic neuron is in essence irrelevant to the activation of the post-synaptic neuron. In other words, it's an unimportant connection. Because of the delay, the normal downstream effects of the release of GLU are diminished - fewer AMPA receptors will be inserted into the lipid bilayer at that synaptic cleft, making it more difficult for that specific synapse to trigger an excitatory response in the future (LTD).
TL;DR: it's not that the post-synaptic cell fires before the pre-synaptic cell because of any one specific mechanism; the post-synaptic cell was simply excited beyond threshold by a different connection before the AP / NT from the pre-synaptic cell reached it.
#betterlatethannever
J. Dreessen thanks man...
great explanation, thank you!
Thanks for a great explanation!
Awesome, thank you!
your videos are very helpful
VERY HELPFUL!
THANKS!
How does synaptic plasticity work for "inhibitory connections"? Is it the same as for excitatory?
That's a good question! The answer is its complicated...there are a number of different ways inhibitory synapses undergo plasticity.
Some of these ways are similar to the hippocampal plasticity in the video. Calcium flowing through NMDA receptors activates calcium dependent kinases or phosphatases which cause the post synaptic cell to insert more GABA receptors or take in GABA receptors respectively. These secondary messengers can also phosphorylate GABA receptors making them more effective.
But there are also other different ways; in some cases when an excitatory pre-synaptic neurone stimulates a post synaptic neurone, the post synaptic neurone will release messengers which diffuse back across the synaptic cleft and cause nearby inhibitory neurones to release more or less GABA in the future.
Also neuronal activity has also been found to alter the number of chloride transporters in a neurone. Changes in the concentration of chloride within a neurone will change how quickly chloride ions flow into a cell when GABA channels are open, making the existing GABA channels more or less inhibitory.
If you're interested in reading further, this is probably the best paper I've found! www.ncbi.nlm.nih.gov/pubmed/21334194
Thank you for your response! I'll try to figure this out. Thanks.
Thanks! Just commenting to say that I like your speed
Thanks
That was extremely helpful
but why would an independent depolarisation/repolarisation in the postsynaptic cell automatically mean a reduction in NMDA receptors? i get how lower ca2+ flow causes less NMDA receptors, but doesnt there need to be a starting point?
Fucking GOLD right here mate, you're amazing!!
Great explanation.
This helped me so much, thank you :))))
Hey, thank you for sharing this knowledge. If you'd be so kind, i have a request; Do you know a paper approaching the topic of how exactly protein kinase is influncing the "recycling" of AMPA receptors? Thank you again, Severin Mittermayer
But wouldn't Homeostatic plasticity cancel out the effects of Spike-timing-dependent plasticity?
Excellent question! You might think so but the answer is no, with Hebbian plasticity the information is thought to be stored in the pattern of the relative strengths of all the synapses. Homeostatic plasticity changes the global, overall excitability of the neurone through either:
Changing the threshold voltage of the neurone, making it more or less likely to fire, but not changing the strengths of the synapses
Or through "synaptic scaling", where the strengths of all of the synapses are changed BY THE SAME FACTOR, eg the strengths of all the synapses are doubled or the strengths are all halved.
That means that the pattern of synaptic strengths, relative to each other stays the same, and the information is not lost.
This paper explains it very nicely:
Homeostatic plasticity in the developing nervous system
Gina G. Turrigiano & Sacha B. Nelson
Nature Reviews Neuroscience 5, 97-107 (February 2004)
Please make some more videos, these are great!!!!
Hi,
Could you mention some references for the content of the video?
what determines which (pre/post synaptic neuron) fires first? And why do activities like studying cause the post synaptic neuron to fire within 20 milliseconds while some other activities don't?
I'd like to know the answer to this as well
the only thing that comes to mind is association or repetition. the more often something is done the more chances of an earlier action potential. since the cell has fired several times prior in that direction. and the more connections to a cell (association) the more action potentials reach a receptor along the axon, thus increasing the chances of an earlier pre-synaptic firing. . .
this is just an assumption however.
Interesting..i took some notes mister👌
Thx for this in depth vid, I subbed.
How does inhibition work?
Are some synapses inhibitory? Why are they so?
Would they also go through LTP / LTD?
Has anyone given much consideration to biological boundaries? That is to say, can learning to play ball with one’s dog, or interact with a spider, be creating such synaptic development in both species? As we learn each other’s behaviors, it must be acknowledged that mutual learning occurs. And perhaps consider the posdibility that we are not unique in our neuroplasticity.
You don’t explain how Ldp works. You just say if the postsynaptic neuron fires first before presynaptics neuron.. how can this be possible??
Thanks a ton 😊
perfect video. Thank you
Great video man, good tempo, great job!
Hey this really helped me understand HOW synaptic plasticity occurs but WHY does the fact that two neurons that fire together become more linked helps us learn? wouldn't it just make us repeat what we already do?
you are the best dude thank you
Who fire the post synaptic neurons with in 20ms before the presynaptic neuron releases glutamate
Muchas gracias.
awesome! you deserve more subscribers, keep it up!
what do you mean the "if the presynatic neuron fires after", doesn't calling a neuron pre synaptic inherently mean it's fires "before" with respect to a post synaptic neuron
But how does this happen? Hehe. Loved it! :)
Thanks!
Brilliant!
Thanks a lot
Dude your videos are great!!! really helped me with my neuro paper this semester. Would love to see some anatomy videos too. Thank you for doing this. Much appreciated. :)
Thanks for this, really helpful
Can this be PROOF MRI by living subjects. Or TAKEN apart DEAD
great explanation. thanks :)
Perferct. thank you very much
What about synesthesia and art? For example, when I attempt to memorize a concept or an experience, I make pun out of the it and put it into 'memory palace.' Does that mean that, let's say, a neuron responsible for a smell, like an aroma of coffee, will try to connect(via dendrite or axon terminal) to visual responsible neuron when they are 'fired' together, i.e. smelling and seeing the coffee at the same time?
Sorry for my bad English
This is the idea behind the Pavlovian response! :)
Do you mind sharing your references you used for this video I'd really like to get into this topic by myself. I'm pretty new to this field and currently conducting research on this topic. Alternatively some key words (e.g Spike-Timing-Dependent Plasticity) besides neuronal plasticity would be very appreciated
What is up with the audio, huh?
wow nice
Good video
thanks, really useful
BEST.
THX!
thank you
Voice is not clear
U r a little bit fast sir .i am not able to follow u unless i play at o.75 speed
please please this is so much scientific explain with another language for the ones like me who are not studying this stuff just curious abour memorie and how it work really i didn"t understand so much from the video i know u know what are you talking about but i get nothing from it.
The video is literally called "Synaptic Plasticity", why did you expect there not to be complex language?
literally saved my lifeee
sort the sound out.
Love how I’m learning about synaptic plasticity but I’m not able to develop the plasticity to understand plasticity in time for my midterm 😂
Lo amo señor