My name is Tal and I am a medical student with an honours degree in neuroscience. With this channel, my goal is to create an animated rendition of my lecture notes 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 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 lot!
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Hey, thank you for recording a video regarding this topic. This might be a stupid question, but I'm pretty new to the subject. How can "positive" current injected by an electrode lead to depolarisation of the cell when there're potassium cations leaving by means of the resistors. Shouldn't the voltage become more negative due to positive charge leaving the cell ? In addition to that, I was wondering how the capacitor normally behaves when there're depolarisations and hyperpolarisations (not imposed artificially). Thank you in advance😅.
Fantastic video. I am currently doing my minor in computational and theoretical neuroscience, and have no background in electrical engineering or calculus. Thanks to your videos I can be so much more confident in class, and actually feel like I am making progress. Thank you so much!
Good question, sorry if it was unclear. To put it simply, instead of activating adenylyl cyclase (like Gs does), the Gi G protein inactivates it which prevents the conversion of ATP to cAMP. Accordingly, it inactivates the pathways that Gs typically stimulates. Let me know if that helps.
Thank you so much! I watched the lecture that our professor sent us, and I didn’t understand any part of it. It only made sense to me after I watched this video. The animation made it really easy to follow as well. Again, thank you! <3
Hi! Great video by the way :) Not sure if you will respond but im still going to ask my question I tried the code myself, but instead of plotting it on a graph, i printed the values as an array of numbers My problem is that, the simulation i use displays sodium and potassium currents as picoamperes And im not sure on how to convert the results from the code to picoamperes Is it possible? Could you help out if possible?
Hi, I think the values of current are implied to be in nanoamperes. Nano is 10^-9 and pico is 10^-12 so you can multiply the currents by 1000 to get picoamperes. Let me know if that helps and if I understand your issue correctly!
Sure! Basically, action potentials are conventionally explained as propagating from the cell body to the axon terminal. While that is true and applies to most neurons, some neurons express voltage gated channels in their dendrites that allow the propagation of action potentials. The reason why neurons generate action potentials at their axon initial segments is because this is where voltage gated channels are most concentrated and thus the threshold is the lowest. However, when the action potential is initiated, it can propagate back to the dendrites provided that it expresses the necessary channels. This property is particularly important for plasticity in pyramidal cells (the major type of neuron in the cortex). Let me know if that helps!
There are a bunch of ligands that differ across the body. In the brain: epinephrine/norepinephrine, serotonin, histamine, and glutamate all activate Gq receptors. In the periphery (heart, lungs, kidneys, etc.), there are also Gq receptors. I know that the liver has Gq receptors for epinephrine. There are also Gq receptors on blood vessels that get activated by angiotensin. There are obviously more examples but these are some of the key examples that came to mind!
Thank you! But I am a little confused about glycine. The thing is that I feel awful when I take magnesiumglycinatet which contain around 2 grams of glycine. I read that glycine can active NMDA and glutamate. I watched your other video about NMDA and felt that that's why I didn't feel good when I take glycine. But in this video you said glycine is an inhibitory transmittor. Can you our someone explain to me how I make glycine inhibitory? Thanks!
Hi, sorry to hear that it makes you feel awful. I think you should bring up your issue to a doctor to get better guidance on how to manage it. In terms of the science, I want to mention that in addition of being an excitatory (NMDA in the brain) and inhibitory (brainstem & spinal cord) neurotransmitter, glycine is also a very important amino acid so it is pretty much ubiquitous in the body. As such, it is hard to pin point why your supplement makes you feel awful.
I saw another video on youtube about this and it might be because of to much chloride inside the cell instead of outside. When chloride rushes out of the cell after the binding of glycine it acts excitatory instead of calming.
@@christinefarneman4433 I guess this is a possible reason why but this is also something you cannot control (as far as I am aware). I still suggest you to get some medical advice!
Short term plasticity facilitation and depression ---- Broadly, short term plasticity can be classified as synaptic depression and facilitation. Depression refers to the progressive reduction of the postsynaptic response during repetitive presynaptic activity, while facilitation is an increase synaptic efficacy. The link between neuroplasticity and depression ---- The changes in neural plasticity induced by stress and other negative stimuli play a significant role in the onset and development of depression. Antidepressant treatments have also been found to exert their antidepressant effects through regulatory effects on neural plasticity. What is the difference between short term and long-term synaptic depression? Short-term depression and long-term plasticity together tune ... Synaptic efficacy is subjected to activity-dependent changes on short- and long time scales. While short-term changes decay over minutes, long-term modifications last from hours up to a lifetime and are thought to constitute the basis of learning and memory. What neurons are involved or causes in depression? Stress, which plays a role in depression, may be a key factor here, since experts believe stress can suppress the production of new neurons (nerve cells) in the hippocampus. Researchers are exploring possible links between sluggish production of new neurons in the hippocampus and low moods.
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!
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.
