Welcome to Science With Tal!
My name is Tal and I am a medical student with an honours degree in neuroscience. With this channel, my goal is to create somewhat animated videos that provide college-level lectures for college students. Hopefully these videos can help people study and get more intuition on what they are learning.
I base my content on topics that I've covered in my classes as well as on the respective readings that are shown in the conclusion section of each video.
I value my personal development as a content creator and artist a lot so do not hesitate to give me any feedback on the videos. It is an important goal of mine to get better throughout this journey and your input means a lot1!
For any business inquiries, consider sending me a mail at: [email protected]
Feel free to support the channel by subscribing and leaving feedback on the videos.
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Ok . Tvm
Ok . Tvm
Really underrated content, love the illustrations and the explanations!
Thank you very much for the feedback!
this is the best video about neurophysiology that i have been able to find! it is clear, precise and simple, thank you for this amazing work!
My pleasure, thank you for the comment!
great video!! Only a couple of things, why at minuti 1:20 at -50mV we have no current but at -20mV we have, what exactly happens between that two values? what is the factor that triggers the channels to open? and what happens at 0mV to have such a high inward current respect to -20mv and +20mv? Sorry, I'm bit confused. Thanks a bunch!!!
Hi, good question! This is something that I look into a bit deeper in this video about the Hodgkin-Huxley model (Hodgkin-Huxley Model of Voltage-Gated Channels Explained). At 11:39 to 13:34, what I try to illustrate with the sequential steps is that the current and conductance of sodium and potassium (which can be isolated from voltage clamp experiments) are drastically different. The reason why the sodium current happens first and closes quickly whereas the potassium current opens later and is sustained has everything to do with the kinetics of the voltage gated channels (which can be explained by the Hodgkin-Huxley Model). To answer your question more directly, the main factor that makes the current increase between -50, -20 and 0 mV for sodium is that since they are voltage-gated (VG) channels, the channels open a bigger pore with higher voltage and let more sodium ions enter, thus, leading to a higher current. For the +20 mV condition, recall that the equilibrium potential of sodium is about +60 mV so as the command voltage approaches that value, the sodium current diminishes since there is less net movement into the cell (let me know if you need clarifications on the equilibrium potential). On the other hand for potassium, its equilibrium potential is at about -80 mV so its current keeps rising. Let me know if this helps, thanks for the feedback!
@@sciencewithtal thanks a bunch!! all clear now, I will also give a look at the video you’ve mentioned
Vry brief and useful for saving the time and know the importance points Thanks a lot
Thank you!
Excellent video! It helped me so much. Very clear and concise.
Thank you!!
Can you help me I'm suffering from medication induced insomnia?
Hi, sorry to hear that you have to go through that. I may help you in understanding the mechanism behind the medication you take and your insomnia but I think the best solution would be to discuss this matter with a health professional so you can get the appropriate help.
Thank you!! Looking foreward to other videos on synaptic physiology such as dynamically primed synaptic vesicle states, tonic and phasic release, and loose and tight docked vesicles!:)
Thank you, I'll keep those topics in mind!
I am doing my master's thesis on action potential and to me, this is the perfect video to start with. I am really grateful to you for making this video. Thank you very much.
My pleasure, thank you!
great explanation! pretty much on par with quality of my lectures, but appreciated the alternative perspective
Thank you, glad it helped!
Really good video! Very clear and informative!
Thank you!
This is a great video, are the other sense pathways coming out soon? Really looking forward to them thank you.
Yes! Love your videos. Would love to see one on the visual system :)
@ishimathur1956 Thank you for the comment! To be transparent, as of yet I only have a bunch of drawings made for the other systems but not much beyond that :/ I am currently working on a pretty ambitious project that covers another aspect of human biology that will open doors to new topics. It is still in my plans to cover the other systems but it is hard to say right now when that will happen!
@MeowtheCat-jg7cx Thank you, I'll keep that in mind!
Your videos have been a real treat to enjoy.
Thank you!
Love this channel! Also, great timing with this one. Thank you so much for your work <3
My pleasure, thanks for the feedback!
You dedicated a lot of time and referred great scientific resources to make this WONDERFUL video. I can not thank you enough Tal 🙏
Im glad this video helped you, thanks for the comment!!
Thank you professir😄😄😄
My pleasure!
I can not describe how grateful I am for this video. Before watching, I spent hours learning the ltd and ltp which i did but COULD NOT grasp the stdp fpr the life of me but after this video I FİNALLY understood it all. Thank you thank you thnak you
Awesome! I'm glad the video could help you make sense of that !!
טל אתה ישראלי?
THANK YOUUUUUUUUUUUU
My pleasure, thanks!
keep going. you are doing a favour to those looking for better explanation and reliable source of studying 😍😍
Thank you very much!
Isn`t 2-AG broken down by MAGL (Monoacylglycerol lipase)? And is THC considered to have a retrograde effect or is this term solely used for the EC´s? ty
You are right, 2-AG does get broken down by MAGL but that is to produce arachidonic acid (AA). You still need DAGL (diacylglycerol lipase) to make 2-AG from DAG. In my opinion the terminology for retrograde implies that the postsynaptic cell communicates with the presynaptic one; hence, since THC is not sent by the postsynaptic cell but rather comes from blood circulation, it is not technically retrograde signalling as compared to ECs. Some people may still call THC retrograde because it binds to the same receptors as ECs but I do not find this to be retrograde personally; it seems this issue may be one of perspective. Hopefully that answers your questions, let me know if I can help further!
@@sciencewithtal Thank you very much and I think you are right it seems there needs to be a postsynaptic release of some kind for "retrograde"
I didn't fully understand why there is an inward current during hyperpolarization, such as when Vcommand is set to -70 mV. Because typically, inward current indicates depolarization. Could you explain this?"
Good question, that was something confusing for me as well! Basically, if I reword what I mention in the video: we have a cell at rest at -60 mV, and now we clamp it to -70 mV. To do so, the voltage clamp will send negative charges to push the membrane potential towards -70 mV. Given that the neuron wants to stay at -60 mV, the neuron will open leak channels (IL) that will send positive charges inside to get back to rest and this is what you see on the readout as the inward/depolarizing current. In other words, with voltage clamp you are measuring the current response of the neuron and since it gets hyperpolarized, its response will be to open channels and depolarize to come back to the resting potential. Hope that clarifies your question, let me know if I can help further!
Thank you very much! Crystal clear now.
Your channel is criminally underrated my friend. I hope you will continue to provide the students with this wonderful videos. God bless you
Thanks a lot, appreciate the love!
Can you explain more about the effects of magnesium on glutamate transmission? Or is there a video for that?
As far as this video explains, magnesium is involved with NMDA receptor transmission as it blocks the channel at rest. This property leads to the concept of coincidence detection described in the video. I do not know that magnesium has roles beyond this in glutamate transmission. Let me know if that clarifies your question!
Please do other special senses too, can we have them by the end of May?
I'll try my best! Do you have any in particular that you would like to see?
@@sciencewithtal Sight
I cannot stress how awesome this explanation is! Thanks for making this video!
My pleasure, thank you!!
Great information 👍
Thanks!
EXPLENDOROUS !!!
Could u please demystify this?! Somatic NS (involuntary) involves pain temperature sensors, if we touch a v hot object, we’d withdraw the subject involuntarily Here sensation is pain and temperature(somatic) but response aint voluntary its involuntary! Please explain, i never get the actual roles of ANS and somatic NS! THANK YOU
Good question! In the context where you would burn yourself, the sensation of pain is somatic because it is pain afferents that are picking that up. While traveling towards the brain, these afferents also synapse in the spinal cord to mediate different reflexes (for ex the withdrawal of your hurt limb). As such, the involuntary part comes from the reflex mediated by the spinal cord because they occur much faster than any cognitive processes and this is why they seem involuntary. As far as I know, the autonomic nervous system is not engaged in these reflexes. Hopefully that answers your question!!
Wonderful job!!!!!
Thank you!!
Anyone know where camkIV is involved? I know that that kinase is calmodulin Activates it, where it Phosphorylates CREB and MAPK causing Ubiqipuitin hydrolase synthesis/PKA R subunit degredation, and CREB to alter gene activation for synaptic growth. But my professor has said CAMKIV is active in associative pathways, where as calmodulin dependant adenylyl cyclase is activated in the Mossy Fiber Pathway, could you clarify?
What your professor is saying is that although LTP happens in both the CA3 to CA1 synapse (I am assuming this is the associative pathway your prof is referring to which is also called Schaffer collateral) & the mossy fiber pathway from MF to CA3 (see at 1:41 for reference for the pathways), the two pathways use different mechanisms to achieve potentiation. In the associative/Schaffer collateral pathway, LTP is achieved in the postsynaptic cell via CAMKIV (2:11 to 8:19); whereas, in the mossy fiber pathway, LTP is achieved presynaptically via de calmodulin dependant adenylyl cyclase (12:39 to 13:58). Hopefully that clarifies your question. Let me know if I can help further!
this is the best video ... I really understand what LTP, LTD and STDP is Thank you
My pleasure to help, thanks for the feedback!!
excellent explanation, thank you!
Glad you found it useful, thanks!!
gracias!! pensaba que nunca entendería el tema, me salvaste 💕💕
My pleasure to help, thanks!!
Thank you for this!
My pleasure!!
awesome
Thank you!!
Excellent work done💖
Thanks!! Glad I could help!
Super well made video! Thank you :)
My pleasure! Thanks for the feedback!
why myelin sheath does not covered the entire neuron ? Why there is gap Between Two myelin sheath ?
I talk about it at 5:27 but basically the gaps between the myelin sheaths (Nodes of Ranvier) contain the channels that regenerate the action potential signal otherwise it would decay and never transmit to the terminal. Hopefully that clarifies your confusion, let me know if not.
@@sciencewithtal Yes , that I know the significance of nodes of ranvier. I want to ask what factors determine that formation of myelin sheath by schwann cell does not start Just after the first myelin sheath ? Is there any type of protein causing such gap for transmission of nerve impulse ?
@@92-riyakumari52 Ah I see, sorry for the confusion. Good question, I am not too sure honestly I have never came across any literature that clarified that point. My best guess, as you point out, is that there is some type of protein interaction that signals which region of the axon should be myelinated or not. Let me know if you find anything about that topic!
@@sciencewithtal Thank you for your response . Sure, if I will find anything related to this , will ping you then ! Same to you if you find the answer of my question then let me know pls !!
Great video!! thank you for all the effort! But I couldn't find the videos about the autonomic nervous system nerves on your channel.
Thanks for the feedback! I didnt make an individual video about it yet but I talk about the autonomic nervous system of the spinal cord in this video (kzread.info/dash/bejne/ZYRr1KaRhb2thZM.html) from 32:29 to 37:00.
tysm!!!
My pleasure!
Very, Nice and comprehensive video!! I believe there is a small mistake in the final plots of m, n and h as the plot that you have made there are of m^3 and n^4 instead of simply m and n as they are marked there.
Hi, sorry for the confusion! The reason why I include m^3h and n^4 directly into the plots is to show that when we consider all the subunits together, it produces the same shape as the current recordings one can obtain from voltage clamp. The plots at first are indeed meant to represent m, n and h. Again, sorry if the axes got confusing because of that and also my fault for not responding earlier your comment must have slipped through my mentions!! Hopefully that clarifies my intentions!!
Beautifully illustrated, neatly organized and effectively explained in such a concise manner for a first year medical student to digest. Thank you so much for this video! <33 Keep up the good work! ✨
My pleasure! Thank you for the feedback!!
Thank you so much, this is so much easier to understand than trying to read papers to figure out what this pathway is and what it does. I really appreciate the work that went into this!
Thanks a lot! Glad you found the video useful!
What does the q in Gq protein stands for?? In Gi “i” is inhibiting and in Gs “s” is stimulating. I can’t find information anywhere…
To be honest, I don't know either. I guess it's one of those scientific conventions where you have to go with it and not think too deeply about it. Let me know if you ever figure out the meaning!
I could not understand until I saw your video. Thank you!
My pleasure!
MAN I LOVE YOU
!!
All your videos are superbly well-made and really thoroughly explained! Thank you so much :)
Thank you very much, it is my pleasure!
but how is the axial resistance (Ra) affected by myelin? does it increse, decrease or remain the same when there's myelin?
Myelin does not impact axial resistance because axial resistance is essentially defined by the radius of the axon lumen (inside). As such, adding myelin does not change it. If you consider the axon being like a pipe that conducts water, adding insulation layers around the pipe will not impact how the water flows inside (i.e. axial resistance). I hope that clarifies your question!