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Uh Can you see that? Yeah, I can. Ok. Uh hi, everyone. My name is Arav and I'll be doing the first um few lectures of neuro. So, um this is the content. So we'll first go through all the memorization stuff and kind of like the basics and then we'll go through action potential generation, which should be a level stuff and then pharmacology and then synapses and then maths. I know lots of you. I mean, in my year, lots of people did not like this part. So it's like the nu inequation and stuff like that. So I decided to do like a whole kind of thing for that as well cos it's quite difficult. Um Yeah, and then this is how the slides will work. So they have all the content on the slides in short form and I'll, I'll try and explain it all anything which is extra. So you don't need to know that explicitly for exam will be in red and any cool revision tips which I found um will be in green. Unfortunately, I can't annotate the slides. Um Right now, hopefully I will be able to um while I'm doing it but for now, they're not gonna be annotated. So let's just get through it. Um So the nervous system main contains five main cells, neurons, which you should be familiar with. And then these four new ones. So, oligodendrocytes, astrocytes, microglia and ependyma, which we'll cover. So, astrocytes, um the three things you need to know about them is that they're the most abundant nervous cells. So most of the stuff in your brain and um will be made of astrocytes and they're involved in forming the blood, the brain barrier and they have loads and loads of different roles. I would recommend knowing at least a few of these because they can ask them potentially. So they can help in repairing cells forming synapses. So a synapse is made up of two neurons and um the astrocytes can kind of form around it. Um and that can be to reuptake and remove neurotransmitters and also to mature these neurons. Um Now we're gonna be talking about myelin production. So myelin is produced by different cells in the CNS and the PNS. That's quite a key point in the CNS, it's oligodendrocytes, but in the PNS, it's Schwann cells. So this diagram here, an oligodendrocyte can myelinate many different neurons. So one of these cells will kind of uh uh be surrounded by many neurons and it's able to kind of myelinate all of them. Whereas in the peripheral nervous system, each of these kind of myelination is one Schwann cell and um it's quite a key point. So uh here's a little cool way to remember it. Cops. So it's CO PSC NS is for oligodendrocytes. PNS is for Schwann cell. And another way to remember is Schwann cell. So, Schwann cells only myelinate one neuron and then the other cells, um Ependymin cells are basically just epithelium which line the ventricles of the adult brain. I don't have a diagram of the ventricles, but you should have learned it by now. Um They're basically where all your uh cerebrospinal fluid is kept and some of these cells can differentiate into choroid cells. So now they're quite specialized, they form the choroid plexus and these cells produce your cerebrospinal fluid. Um and microglia are essentially the macrophages which um are in your brain that they're neural origin. But macrophages which are in your blood um are not microglia. So only the ones in your uh neural cells um Here are different types of neurons. To be honest. It's just remember these, I guess. So, unipolar pseudo unipolar bipolar, they're drawn here. So unipolar has uh one nucleus and it er stretches out pseudounipolar. So pseudounipolar ha um seems like it has two axons. So you could potentially say it's bipolar, but it only has one connection. Whereas in bipolar, they have two connections to the nucleus. That's the key difference in those ones. And then multipolar. This is where your like huge neurons come in. And um the three ones they want you to know are pyramidal purkinje and Golgi. Um The pyramidal ones are mainly found in your cerebral cortex. And um as you can see here, they kind of form a pyramid. Your purkinje ones are found in the cerebellum and the Golgi ones are also found in the cerebellum, but in the granular layer and they're both, they both tend to be gaba neurons. So, Gaba is a specific type of neurotransmitter which you would have covered. Um Now a little bit more detail about the neuron, this is away level. So hopefully not too difficult. But if, if anyone does have questions in the chat, then just send them. Um but the axon branches from the nucleus and this point where it branches from is called the axon hillock. Uh dendrites also branch out from the nucleus, they're highly branched. And the SOMA also known as the cell body is just, you know, the same as other cells, nucleus ribosomes. Um And then there's also neurofilaments. This is the one thing which is quite different. They're involved in structure and transport of various things within the neuron. Um And synapses are gaps between neurons which we'll cover. Now, uh synapses also are a level. So this isn't too difficult. You just need to know about three different types of synapses. Um Axodendritic, axosomatic and axoaxonic. The names of these are self explanatory. So, Axo means the axon connects to the dendrite. So, axodendritic will connect to the dendrite, axosomatic will connect to the soma and axoaxonic will connect to an axon of the another neuron. And another key thing which is quite self explanatory is communication between nerve cells is always autocrine or paracrine. There is no endocrine or um there's no endocrine communication really between be between nerve cells. Um But one thing here is that you do learn an endo that nerves can release endocrine hormones. So the nerves in your posterior pituitary can release ADH and Oxytocin. But between nerve cells will always be autocrine and paracrine. Um Here's some definitions don't really have to go through this hopefully. Um But diffusion is just movement of particles from higher concentration to lower and flux is the number of molecules that cross a unit per area time, sorry, a unit area per unit time. Voltage is generated by ions. Current is the movement of ions and resistance is the barrier. So this diagram is quite good. So voltage basically pushes ions in and resistance will um try and prevent that movement. Uh And then these are ion channels. Um I they're quite self explanatory. They have usually two states open or closed and they can transmit ions uh through them. Some can transmit them both ways, some only one way and they will basically form the basis of all neurotransmission. Um So this is just a question. Um I don't know how I can access the chat but uh just read this question So strep pneumonia is a bacteria which has been shown to cause meningitis by passing through the blood brain barrier by hiding with within white cells. After being phagocytose name, a potential cell where simonia may, may hide within. So I'll give you a few minutes for that and then maybe I can check the chart for any potential answers. I can let you know what they say in the chart. You one person said microglia, OK. Uh Any other answers? No, just that. OK. I'll just um go through it. Unfortunately, the one person that did answer fell for the trap. So basically microglia r uh macrophages which are found in your brain. So if you kind of think about the blood brain barrier, the the barrier kind of connects the blood to the brain. So all of the kind of blood cell, the white blood cells in the blood are not actually neuronal macrophages. So your microglia, you'll basically find them inside like white matter and things like that. They'll kind of just be cleaning up in there. Whereas um bacteria which is found in the blood, they will hide within your typical white blood cells. So you for this, you could say uh just normal macrophages, you could say neutrophils, stuff like that. So it is quite a difficult question, but just to kind of highlight the difference between neuronal cells and blood cells, they are, they are different things. Um because of the blood brain barrier but yeah, at least you answered. That's good. So now we're gonna talk about some of the more concept stuff. So all the memory stuff is out of the way. Now, it's kind of how do action potentials to generate. So, resting membrane membrane potential was minus 70 millivolts. And what that means is that the inside is more negative than the outside. And there are four main physiological ions which contribute to this where it's mainly just potassium and sodium. Um But there is also calcium and chloride. Um Calcium is I uh quite important in producing um like synaptic transmission and things like that. And as you can see on this diagram, it basically shows where they're all found. You don't need to know the numbers of any of this. So just know on the outside, you've got way more N ACL and on the inside, you've got a lot of K plus and um yeah, and then a lot of sometimes a lot of people ask why is the inside? So um negative if, if the cl plus cl minus is on the outside is because many proteins in your cell will tend to be negatively charged, which causes the uh gradient. And there's also the sodium potassium pump which tries, which tries to maintain this negative gradient as well. And then in this green box, we have a few things which um help me kind of think about ions cos especially in the kidneys. It's quite difficult to. Um there's so many ions, things you have to worry about. So, in general, if you remember that sodium will follow chloride or chloride will follow sodium because it forms salt. It's quite self explanatory. Um Same with potassium and hydrogen. You'll see this a lot in the kidneys with acidosis and things. Um and also water follows N A plus. Um I think maybe you've done it in pom, but basically N A plus is the primary like osmolar ion. So water will tend to follow it and N A plus always tends to be opposite to K plus. This is just simply because of the sodium potassium pump. Um Yeah. Uh I talked about this already. So negative proteins and the pump create that er negative kind of gradient. And at resting membrane potential, all you need to know is that the membrane is more permeable to K plus. So you've got your high concentration of K plus in here. So K plus will slowly start to diffuse out and then you have your sodium potassium pump which will try and um take more of that K plus back in and get rid of the N A plus. So that's kind of how it's maintained. And then this is just one random thing which they want you to know on the slides um to measure membrane potential, use electrodes against a zero volt reference. So the reference could be saline or you know, electro nowadays, they're just programmed to have a reference so you can do that as well. So yeah, and um one thing which is not really relevant to neuro, but just in general, if there is something on a slide, they will ask you about it. It's just a thing. Um You'll see it in the mos like the most random stuff can come up. So remember all of these one line things on these slides and in your lectures. So now we're gonna talk about how the action potential actually generates. So these are all just different terms which you've all covered at a level. So, depolarization is when membrane potential becomes more positive. So that's your initial kind of jump up. Um Then after that, you've got overshoot, membrane potential becomes positive. So not more positive, it actually becomes past zero. That's what overshoot means. Repolarisation is just a general term for the membrane potential, decreasing towards resting. But then after resting, it's hyperpolarisation um where it decreases beyond your minus 70. So now we have graded potentials. I think this is the first thing which is slightly more in detail than a level, but it's still not that bad. So graded potentials are graded. So um if you have a weak stimulus, you have a slight increase and then a strong stimulus will increase a lot more. This is different action potentials which are just all or nothing. So if you have a stimulus reaching your threshold, this will fire whereas in graded potentials, uh the m the stronger the stimulus, the uh larger your um depolarization will be. And the way you can think about this is that if you just tap your arm, it's quite a normal like weak stimulus. But then if someone stabs you, it's a strong stimulus and they feel different. So that means there's gotta be something different in them. Um And a few other things you need to know is they cause the initial change in membrane potential, which can then cause your action potential and they kind of spread across the axon. So if you had your um site of depolarization here, uh your charge can leak from the axon and the size of the um kind of change decreases. This will come into use a little bit more when we talk about saltatory conduction. So now if your graded potential reaches the threshold potential, an action potential is fired. So a lot of potential is in there. But basically what it means is if the stimulus is strong enough, then you will get this all or nothing action potential firing. And they've drawn these lines here. So um the green one, let's say the graded potential reached there. So then the axon knew, OK, it's time to initiate the action potential. So now we're gonna talk about the action potential in a few phases. You don't need to know the names of these phases. But in cardio, there are nodal cell potentials and things like that, which you do need to know the names of like ob stroke and all of that stuff. But in this, you don't need to know anything which is good. Um So for each stage, you basically need to assess how permeability to sodium and potassium changes and which channels will open and close. So in up stroke, phase three, that's depolarization and you're covered at a level that's caused by sodium channels. So obviously, that means the permeability to sodium is increasing and that is signaled by your voltage gated sodium channels increa um er opening. So upstroke is due to N A plus influx and then you have repolarisation which is the decrease in membrane potential and that is mediated by potassium. So hopefully, that's all self explanatory. Um A few things here, potassium channels actually open slowly in obs stroke. So if you can see on this diagram, um while N A is um entering the cell, some potassium is also leaving. Um so potassium's channels are actually like the permeability for potassium does increase in phase three as well. So if they ask you a question like um when do potassium channels open? You have to say in depolarization rather than repolarisation, it is a thing which catches people out. However, because they're slow, this is just a point that you need to know potassium channels are slow. There are factors only felt. Um after all this N A has entered the cell. So their repolarisation occurs um after the obst and because they're slow as well, um hyperpolarization occurs because they'll close slowly, which means that your resting potential, sorry, your um membrane potential will fall below resting potential. So the whole reason of phase five is because of the slow closure of these channels and this forms re refractory periods. So the absolute refractory period is where action potentials cannot be triggered. So this is here in um like during repolarisation. And the reason for that is because sodium channels are actually closed, it's not possible for any sodium to enter your cells um to enter the axon. So that means you can't potentially even have an action potential. Um Whereas the relative refractory period, this is where some of the sodium channels are open. So this would be more of the um hyperpolarization kind of um point and some potassium uh sorry, some sodium channels are open and the membrane potential is quite negative. So you need a very strong stimulus to reach the threshold. So, um for example, um the the getting stabbed example is quite good because there's so much like going on. Uh the threshold is really, really high. You're gonna feel the pain really intensely because there are there is enough sodium to enter your uh axon to tell you oh you're being stabbed, there's lots of pain and stuff and to restore the resting membrane potential to um bring it back. Uh the sodium potassium pump is used as well as just uh normal open potassium channels. Ok. Now, let's talk a little bit about myelin. So we already know that where the myelin is produced by those various cells. So, oligodendrocytes and Schwann cells and its usage is for conduction of electrical impulses. Um It basically insulates your neuron and um saltatory conduction is what it's called, it's where action potentials jump between nodes of Ranvier. So nodes of Ranvier, if you can imagine this is like a big chunk of myelin, they're found in between these big chunks of myelin. And that's where the action potentials happen. And these nodes will have a high concentration of ion channels and they lack myelin. So I think I have do I have a diagram? No, maybe not. But if let's just use this one, if you see a s like if, if the stimulus acts here, this is where most of your ion ion channels will be concentrated. And then you know what I talked about before how the charge kind of spreads along the axon, it will spread until it reaches the other node of Ranvier. And then sodium will enter and then basically the nerve impulses jump. Um And if anyone wants me to like go through stuff again, please uh let them know in the chat. Um Cos I think covered that a bit fast, but we can now talk about conduction velocity. So nerve impulses can become faster through two main mechanisms. So, myelination as we talked about myelin is a conductor. So if a neuron is myelinated nerve impulses travel faster, if it's not, they will travel slower and a larger diameter will also increase the conduction of nerve impulses. And they don't mention this in the slides, but I'm pretty sure it's due to a larger diameter being able to hold more ion channels in one place. So if you think of an axon with, with a larger diameter, um it tends to have the largest, largest surface for ion channels to act upon. So you can potentially, you know, um uh cause foster debilitation. And um you can see this kind of manifesting a lot of diseases. So, MS is a disease of the C NS where you have demyelination and um MS has got loads and loads of symptoms, but a lot of them are due to impulses not traveling fast enough between your brain areas, which can lead to um like uh slowing movements and things like that. And there are lots and lots of conditions which involve um the destruction of myelin, which is why it's so important to understand what it actually does. So passive propagation, this is basically what I was talking about here. So the decremental spread across the axon um and it's basically small subthreshold depolarizations which decay across the length of the axon. And this is also influenced by your diameter and myelination. And the main reason for this is as it decays, um some sodium channels will start opening. And if it, if it reaches like a node of Ron via the sodium channels can potentially propagate an active potential which is active propagation. Um This diagram is quite good. So if all the sodium channels open up in this area, the depolarizations will start decaying and the nearby area will also start opening the sodium channels. And this creates your unidirectional propagation of your action potential. Cos if you imagine it starts here, only these ones are gonna open next to it. Um which then propagates it in only one direction rather than it going everywhere. OK. I did say that MS is not tested. Um But I'm being mean, so which myelin producing cell may be affected in MS and then I'll give you a few minutes as well to answer and it doesn't matter if you're wrong. Cos these questions are hard. So s someone said Schwann cells in the PNS and in oligodendrocytes in the brain. OK. Um Any other answers? That's it so far? OK. So um OK. Um uh kind of half right. So uh you did get which myelin cells there are in the body. So we talked about how there are two types of myelin cells, oligodendrocytes are found in the C NS only and Schwann cells are found in the PNS. So I mentioned before that MS um targets the C NS only. So uh for this one, uh it would be oligodendrocytes uh specifically, rather than Schwann cells. Um And potentially a way they could ask this is that they'll give you like a description of a disease. So they might say, oh MS affects the C NS um and then give this question. So, um good answer. Uh Now we're gonna talk about pharmacology. So this is kind of just a random thing which they added to neuro. Um But in second year, it will be very, very important. Um Most of second year actually revolves around pharmacology, but in first year, you'll be learning more about the systems. So um a lot of this is you just, they, they can technically ask you to find pharmacology, but I feel like it's a waste of a few months but in case, just learn it, it's the study of how drugs influence living systems. So for diabetes, for example, lowering sugar, lowering BP and things like that. Um and a drug is a chemical substance which interacts with a specific target in a biological system to produce an effect. And that's just a long definition, but it answers these three questions. Where is the drug effect produced? So when you take a drug, what's gonna happen? And where is this happening? What is the target of the drug? A lot of the times drugs don't just target like the pancreas or something. They target something very specific, which will come on to um like receptors, enzymes, transport um proteins or ion channels. Um And that is what their effect is for and what is the response produced after interaction with this target? That's essentially what does the drug do? And are there any side effects? So, um beta two agonists were my example for this one. Um uh I don't, I'm not sure if anyone knows what they are, but basically, it's a treatment for asthma and other um lung conditions. And essentially we're gonna over the course of these fusel, we're gonna try and answer these questions for beta two agonists. Um You don't need to know what they are, but I just thought it was quite a good example. So um drugs usually target four classes of proteins, especially in the nervous system. Uh receptors, enzymes transport proteins and ion channels. You will have come across pretty much all of these. Um by now, in various contexts and drugs can either enhance their activation or prevent their activation. So, uh when you enhance something, you are an agonist and when you prevent something from being done, you're an antagonist. So in this example, um a beta two agonist such as salbutamol is an agonist of the beta two adrenergic receptor. So what that basically means is that it binds to it and it activates uh the receptor and I'm not sure if anyone knows what that receptor does, but in the lungs, it causes um dilation, sorry, a re relaxation of your smooth muscle. So, that makes sense when someone has asthma, their muscles can start tightening up. Um And that will cause relaxation. So now we've answered the first question or the second one. the drug target is the beta two receptor. Um Now, let's talk about how well the drug works. So that's called drug selectivity. Um There are beta two receptors everywhere in the body. There are some in the heart like um there's some in blood vessels. So if you do take a beta two agonist through an inhaler, you can have effects in other parts of your body and a drug which has a high selectivity. They tend to be a lot more effective because they're localized and the low selectivity may introduce side effects and a side effect uh quite self explanatory, but something which is not intended and they increase as the dosage increases. Um on target side effects occur within the same target, off target, occur on a different target. So um for beta two agonists, um off target side effects could potentially be um due to beta two agonists binding onto like heart muscle. For example, I think you can get um tachycardia if you take too much of them and sorry, that's off target. Um And then on target side effects is you may cause too much relaxation of your smooth muscle um which can cause mucus build up and then yeah, I think we've pretty much answered everything. Um Where is the effect produced in the lungs and then what's the target? We've done that and the response produced as well. Um, ok, another quick question I think. Is it possible to have a break as well? Sure. We can, we can have a, what's the time we'll do an eight minute break until 540 then we can continue then? Ok. Yeah, I'll try and get the slides working, hopefully. Um, sure. So if everyone stays on metal but like take a eight minute break and then come back and we can resume. OK. Um I'll leave the question up as well and then we'll get started soon. I wasn't able to find a way to annotate. Yeah, but yeah, uh the question is during action potential generation, when do potassium voltage gated channels open? Is it repolarisation or depolarization? And what causes the relative refractory period and a severe S au so four or less, I think. Ok. Uh Have you got any answers? Not yet, but um the breaks just finished. So if you could read the question again, that might be useful. OK. Um So uh during action potential generation, when do potassium channels open? Uh and tho those are the two options and what causes the relative refractory period? Oh, I think I can see one. yeah, someone said repolarisation and um for the vs AQ some N A plus channels open is anything else? No, nothing else has come through? OK. I'll just wait a little. OK. I think someone said more positive membrane potential for the vs AQ. So for the first one, uh I mentioned before that potassium channels um oh OK. Someone said depolarization and membrane is hyperpolarized. OK. Um All good answers. So before I said do yeah, uh potassium channels are slow. So they open in depolarization. So they don't open in prepolarisation, they open quite early but their effectors felt in repolarisation. So um this question basically needs you to read um carefully. So um they open um quite early on, however, their effect is felt later on. So um the correct answer, there would be depolarization and then for the V SAQ, you can have a range of answers. So I think um I think pretty much everyone thought of a reason why. So the relative refractory period is basically basically the whole point of it is that you need a stronger than normal stimulus to reach your threshold. So why is that uh someone's membrane is hyperpolarized? That's correct. Um uh it's more negative. So you need a higher stimulus, so higher positive uh someone had more positive membrane potential um since it's a V SAQ, you need to be quite specific in what you're saying. So I think um I understand what you mean. So you need a more positive potential to reach a, a stimulus. However, um could be mis misinterpreted by some examiners. Um And then someone said some N A plus channels open that is also true. Some of them are open, which means you can potentially reach um a higher threshold. So how could I reword that? Um I think, I think to reword it, you need to kind of use these words. So you need to use words which kind of explain what you're thinking in a more concise way. So um potentially what you could say for your one would be greater threshold required or something. Or you could say um like someone else said, hyperpolarization has occurred or you could say um um potassium, so K plus channels, slow closing or something like that. OK. Uh There are a lot of answers. Um And in the actual exam you get, I mean, in my opinion, you get quite a lot of time for the multiple choice stuff. So um you can spend a little bit of time on that and then um walk away to that's excuse. OK. Now, synaptic transmission and also thank you everyone for responding. It's uh nice. Uh Because then you cos you can get more personalized feedback that way, I guess. So, now we're gonna talk about synaptic transmission. This is also all a level. So I'm gonna speed through it. Um So when your nerve impulses reaches your presynaptic neuron, it will cause depolarization. And this is where calcium comes in. Um this depolarization stimulates voltage gated calcium channels to open and a calcium influx over here. So, um what this does is it causes neurotransmitter, vesical exocytosis. And that's a lot of words. But basically, these little visa cors um with your neurotransmitters, they will fuse with the membrane and uh release the neurotransmitters into your synapse. And these neurotransmitters will then bind to postsynaptic receptors. So, um these are ion channels and then you see the little curvature like uh they will bind to that or something similar to that and they will then either cause another action potential to take place or we will see later uh in neuromuscular junctions, they can cause um contraction of muscle. They can cause um release of a hormone from a gland or something. And then neurotransmitter recycling is something I think um the other lecture after me will cover in epilepsy. Hence, or maybe that's the other neolecta, who knows, but it it it comes back. So um this neuromuscular junction is basically a, a specialized synapse which links to a muscle. So over here, you can have synapses, linking nerve to nerve and we talked about axoaxonic and axodendritic and stuff like that. But you can also have synapses linking to muscles. Um It's basically the same thing here, but the neurotransmitter is specific now, it's, it's called acetylcholine and the receptor um on the muscle is called a nicotinic acetyl cholinergic receptor. So that is stuff you need to know. Um and that will cause a change in end plate potential, which is just a fancy word for saying it depolarizes the membrane of the muscle um and the sarcolemma, all of this stuff will be covered in M SK. So um and cardio I think as well. So let's not do that. Um Now here are some disorders, disorders, always the most fun part I think cause it puts everything into a real life kind of situation. So, botulinum toxin, um Botox is um where that like where it's used in a good way, but there are also um bacteria like um which release this toxin. Um and it causes um paralysis and stuff like that. And the reason it does that is it inhibits the release of acetylcholine um because it's a protease which cleaves the snare protein. So I put this in red because um snare is not really mentioned anywhere in the syllabus, but this is what botulin toxin actually does. So I guess for the exams you can learn that it inhibits ac um acetylcholine release. But it cleaves a protein called snare which is found on vesicles. And it basically allows vesicles to bind to the membrane and release a um acetylcholine. So, if snare is not there, then um you cannot release acetylcholine and that means you cannot contract your muscle, which is where the paralysis comes in. OK? And now we have myasthenic stuff. Um There are two. So myasthenia gravis is an autoimmune condition. So, pom autoimmunity is when your own antibodies will attack stuff in your, in your bloodstream or in your tissues. So this is autoimmunity against your postsynaptic acetylcholine. So, you know, this long thing, nicotinic receptor, um and that does the same thing cause paralysis cause weakness and stuff like that. You don't need to know the symptoms at all. You don't need to know the symptoms of all of this stuff. But um just to know that it will generally cause issues with your muscle later on in um in your uh clinical years and stuff, you will need to know how all of these present. But as a first year, just kind of understand how it physiologically works. Um And then you have Lambert Eaton Myasthenic syndrome um or lens for sure. And that's the autoimmunity against your presynaptic calcium channel. So these ones here, you know, I think hopefully you can see my CSA. Um And yeah, they both do very similar things. So you'll get weakness. Um And those sorts of symptoms they clinically present differently, but you don't need to know about that. And a cool way to remember is L comes before M, these are both link to myasthenic syndromes. Uh And the reason L comes before M is because in Lamber Eaton, you have presynaptic autoimmunity. And in myasthenia gravis, you've got post synaptic and be C comes before M in the alphabet. So it's a good way to remember that. Um So we're at the last part now, the dreaded stuff. So in maths, um basically, um what you need to know for these equations. So you've got the Goldman Hodgkin KS one and then you've got the NS one is, you need to know when are you using each one? And how do you use each one? You don't need to remember the equation. They will give it to you in the question. Um You also get a, like a calculator uh in your mo I don't think you get a real one. You just have to use the one on your um ipad, but you do get an actual calculator in the exam. So that's good. Um So the N equation is used to calculate equilibrium potential, which is the potential at which electrochemical equilibrium has been reached. It's a weird definition. But if you basically imagine a membrane and it's got a certain ion on each side, let's just say potassium, it's got an intracellular store of potassium and an extracellular. So store the equilibrium potential is basically just what the membrane potentials should be to prevent movement of the ion between these two stores. So um I'm not sure what it is for potassium, but let's just say it's like minus 30 or something. So at minus 30 millivolts, no potassium diffusion will occur across the membrane. So um hopefully you understand that there in the lecture, there was maybe more of an explanation, but it's basically just you need to know, you need to use it to calculate equilibrium potential. So when, when you see a question which mentions that. Just think OK, announced equation. Um They can give it to you in two forms. If they're mean, they'll give you this one and if they're nice, they'll give you that one. So E equals minus RT over ZF which just ends up being a constant um uh where R is gas, constant T temperature, Z be careful for this one charge. So if you're calculating a positive charge, it will be like one for like maybe any plus plus two for calcium minus one, for chlorine, for example, something like that. Um F Farida is a number and then Ln is just log based. Uh don't, it doesn't matter if you have not done maths at a level. Um In the calculator, there will just be a button which says Ln and you can use it. And then X one and X two is what the actual use is like the useful stuff they need to type in. So they will tell you the intracellular iron concentration and the extracellular iron concentration you just have to put in your calculator. Um And then you'll get an equilibrium potential in millivolts. And then this equation, when you're gonna use this one, this is when they give you multiple ions. So if they just give you, I'll calculate the equilibrium potential for potassium, you'll go, you know, it's just one ion. So you're gonna have to use the NNS. This one's the more complicated one. And it's used to measure membrane potential for multiple ions. So the reason why this one is more useful than that one. I think they can potentially, I see that as well is because in biological systems, there's not only one ion like existing like I we saw before that there is uh sodium, potassium chlori, um chloride and um calcium. There are loads and loads of different ions at play, which is why this equation is more likely gonna be used. And it calculates it more accurately because it also takes into a account um permeability of ion channels. So here I've written it out, I mean, not really, I screenshot it from the slides but um how you calculate is minus 61 log um permeability to ion and then the ion concentration and then the subscript I means inside and o means outside. So if, if the channel is closed, then this P will be zero. And if the channel is open, this P will be one it's an open probability. So they can potentially even say oh the calcium channel is open half. So then you have to replace P with 0.5. So that's how you use all the equations. Um I'll put this up at the end again, but this is just a feedback QR code. So if, if you can scan it, that would be nice, I'll put it back up. Cos we're gonna be doing questions now on the equations um I was meant to um have like a way to label this, but I will just type it out. Um uh You, you guys can follow along, but I am just gonna work through it just so everyone can see how you're meant to do these kind of questions. So um if anyone gets an answer, you can put it in the chat as well before me. So the question is calculate an equilibrium potential of calcium ions across the membrane. Assuming the temperature is or feedback you are code is basically uh just feedback on how I've done as a med lecturer. I will, I will put it back up at the end after the questions. So um assuming the temperature is 37 degrees and intracellular values of calcium are 0.0001 and extracellular is two. So what you do here is use the N equation. That's the first thing. Um And then just so in values. So I think the main issue that people will have is either not knowing what's going on or using the wrong equation. So the reason we're using two here is because calcium is a two plus ion and then this is a bit annoying the formatting but multiplied by log and then X inside of the X outside. So X inside is 0.0001 and outside is two. So you put that in your log and I don't actually have a calculator So I'm not sure what this will be but whatever you get from that will be your answer. And then um another one, but this is um more to do with the uh G HK equation. So calculate the membrane potential. That's another way you can kind of tell actually if it says equilibrium potential, it's gonna be one ion and membrane potential is multiple ions. So um of this membrane and these channels are open. So potassium and chloride and the sodium channels are closed and they give you the concentrations for everything. So if you remember what I said before, if some, if an iron channel was closed, so the the uh sodium one, it will be zero before your number. So this part of the equation, we don't even have to measure because we're multiplying stuff by zero. So it's just gonna be um it's, it's just gonna be zero for that part of the question. So to do this one be minus 61 log permeability um of potassium is open. So that means one because it's fully permeable. So one multiplied by a concentration of potassium which is 0.1 internally, 00.1 internally. And then add the same thing for chlorine. We're skipping sodium as I said because the channel is closed. So same thing for chlorine, 0.02. And then we are dividing that by um the extracellular values. So just quickly do that 0.15 and then you put that in a cal clear and then you should get an answer. So, um that's it. I think for all of the neuro stuff, I'll put this feedback QR code up and I think we've got, I actually finished quite quickly. Um So if anyone has any questions or wants me to recap stuff from previous l then just message on the chat. Um I didn't catch why you're multiplying everything by one. So let me get the equation up. So the reason I'm multiplying stuff by one is basically because we're doing this calculation this one. Oh OK. We just blocked it out. Oh Well, um we're doing permeability to potassium multiplied by concentration of potassium. So over here, the permeability is one. And what that means um is the potassium channels are open because permeability is an open probability from 0 to 1. So if the channels open, you use one and if it's closed, you use zero. And if it's half open, you use 0.5 for example, or if it's three quarters open, you use 0.75. So that's where the one comes from. And then the 0.1 comes from concentration of potassium inside. So we set it over here somewhere. It's 0.1. And that's why we didn't bother doing the sodium calculation because probability is zero as any plus channels are closed. Yeah, we've, we've assumed it's one because it's open. Like if I if I changed this question and said sodium channels are half open, then we would have to redo it with um with 0.5 for the sodium instead if that makes sense. OK. Could you comment on end plate potential? That's fine. We've got, we've got time if you have any other questions, it's um it's always good to understand everything, especially if it's a simple topic as well because um they usually ask difficult questions if it's a simple topic because they're like, oh, everyone's done this already. Um Right. So end play potential is basically just the special way of saying depolarization in muscle. So I'm not sure how your lectures are going right now. But um maybe you've had the cardio one and maybe you've had the M SK one where they talk about the sarcolemma. And if I remember correctly, the way that all the calcium starts entering your um your s um sarcoplasm and stuff is due to depolarization of the membrane, which is due to a change in end endplate potential. So the acetylcholine binding to the membrane will cause depolarization, which um basically means the endplate potential has changed and then that's what causes all the potassium. Um Well, sorry, all the calcium being um sent to the sarcoplasm and then you know, actin myosin and stuff. OK. And yeah, if there's any other questions, uh let me know otherwise I think that's good. Right. Yeah, I think that should be fine Ok. And, oh yeah, my email is here as well in case you have a question after. Um, but yeah, great. I think we'll give it one more minute and then we can switch lecturers. Ok. Um This is one for anyone. Does anyone know any resources? Ok. So I think what I used, um, there's nothing in, uh there's nothing specifically for neuro, which I can think of but there is something called um Preclinic. It's a website, I think it was designed by Imperial students. Um I will send the name on the chart but it has a very rich um question bank which is designed specifically for first year. Um It includes PM and Bor. Um So a lot of people find that when they're revising, they can't find questions which are specific to Imperial because we don't use a spec as such. We just have the lecture slides. So pref is really good um because it has specific questions for Imperial only. And then apart from that, you should hopefully have a note bank which will have um not pause papers as such. But like I think there's med ed papers and other things on the um which should be helpful. But yeah. Well, um apart from that, um there's, there's not many questions which I found, which is really annoying, but there's loads of online resources. So you um it's always good to learn around the topic I found because in med like there's, there's so much to learn, you might as well just like you might as well read around because it's gonna come into use at some point. So osmosis is really good and um any like sort of youtube videos you can find which kind of delve into depth and some of these concepts is good, especially for Neo because um I mean, the ones I did were, were quite easy, but I found this, the C NS like coral spinal tracts and all of that really, really confusing. But yeah, I think that's it. Cool. Thank you. I think we'll switch over to the next lecture now. So when you're ready, you could just, so that means that you Yes. Should I just share my screen like um on 1/5? Yeah, that's fine. And if you could put your camera on to that would be useful. Yeah. Um clapping into the speaker, he doesn't have sex. I be very happy. Can you guys hear any background noise or is it fairly quiet? There's a bit of background noise. OK. Um Hopefully it shouldn't be too bad. OK. OK. Yeah. Can everyone see my screen? All right. Yeah, we can. OK. Um Warning I won't be able to see the chart or anything else while I'm presenting. I might switch, I will switch to mentee for a bit. So I will be able to check the chart at, at those points. But if anyone does raise any questions, just let me know. Um So today's lecture is on neurotransmitters and cranial nerves. Um This follows on nicely from the lecture that you just had, I'll avoid doing too much repetition in general. This should be a reasonably short lecture. There isn't too much that is challenging in terms of conceptual, although there are some specific bits that's because a lot of the conceptual stuff comes from a level knowledge. So I'll be focusing on the new editions that come on from a level allowing you to slot in the key facts and high yield knowledge within stuff that you should already know. Um And then focus a bit on how you can do a lot of the memorization that comes within this um specific techniques that you can use to help learn the key information. Um These are just the Tylers that I'll cover. Firstly, I'll quickly go over synapses and neurotransmitters in a general sense, the bulk of the time will be going over Gaba and glutamate, what their synapses look like how these two neurotransmitters um control neurological function. And then finally, I'll talk about cranial nerves, specifically the things that are unique to med to medicine as opposed to anatomy and unique to BRS. But there is some crossover with anatomy here in terms of the functions of cranial nerves. Firstly, the structure of a neuron, I think a lot of you guys should like in theory know the basic structures of neurons. It's just really getting down how to word the different functions in ways that could fit on A VS AQ or you could write down in a question. So first of all, you should know that signals come in through the dendrites. Something that many people forget is that dendrites have specific structures called spines. These are proteins found on the structure of the dendrites, almost like mini dendrites which help to further increase the surface area so that they can receive lots of neurotransmitters. Then the cell body where all of the dendrites connect together is called the SOMA. The way that you word the function of the SOMA is that it does signal integration. That is it takes all of the signals from all the different dendrites and combines them together in order to produce one single transmission through the axon and then the axon is where the transmission goes so that it can go on to the next neuron. Um You should already know the stages of synaptic transmission but because it helps me set up nicely. The stuff later in this lecture, I'll just summarize it again. Firstly, you make the neurotransmitter, then you release the neurotransmitter, then you activate the postsynaptic receptor and then you stop activating it by inactivating it. Um There are a few things to note about synapses which are basically characteristics that they want you to memorize. Um No, don't just memorize the terms but understand and be able to define what each one is rapid time scale just means that diffusion while it happens slower than electrical communication still happens very, very quickly. Diversity just means that there are different neurotransmitters and different synapses work in different ways. I will go over two specific examples, Gaba and glutamate to highlight some of this diversity. Plasticity shows that different neurons can connect with other neurons. Therefore changing which synapses you find within the brain and learning is after that neuroplasticity. Once you form a specific connection, it can become stronger and faster, the more you activate it. A lot of these are things that people know outside of medicine. But it's useful just to know how we define them in medicine and what terms specifically they want you to know for pom exams. OK. Um Again, I'm not gonna cover any of the a level or conceptual stuff purely the facts that I find that people often miss out fact. One is that when you produce the neurotransmitter, this is the active stage. This is where ATP is used. It is used when you take the neurotransmitter that you produce and you put it into a vesicle. Don't forget the neurotransmission is an active process. And hence, when you don't have ATP, this is where neurotransmission goes down. Next is that calcium ions will then um trigger the release of the neurotransmitter again for a level. But the third important fact is the exocytosis process, which is essentially now that you've packaged this neurotransmitter. And the calcium ions have forced it to move along. How is it released from the neuron? It happens through a process that is very complicated that they don't want you to know in detail but involves proteins on the vesical surface binding to proteins on the on the membrane of the neuron. This process is called docking and priming because it docks to the postsynaptic membrane and then it is primed to be released. Um then just the ex it's released called exocytosis. Um There are two key neurotoxins that they want you to know which activate at specific stages of this neurotransmission process. The fastest alpha latrotoxin stage two that I talked about before is the release of the neurotransmitter. When calcium ions come in, this is where alpha Latrotoxin activates because it causes these calcium ion channels to remain permanently open. This might sound like it, it increases neurotransmission, but it actually does the opposite because you only have a limited capacity to do all of that active process us of forming the neurotransmitter into the vesicles. So when you're constantly trying to do this, what happens is the neurotransmitter ends up being constantly released and very, very quickly, it will deplete and you'll have none left. Which means that the neur, which means that the neuron essentially becomes nonfunctional. The thing to remember about alpha latrotoxin is that the neurotransmitter it works at isn't one that causes muscle contraction or stimulation, but rather one that relaxes and stops your muscles from spontaneously spasming. We'll go over this one later. It's called Gaba. But just for now, recognize that it doesn't cause your muscles to relax, but rather it, it causes them to spasm because it prevents the relaxation. The second one is botulinum which works as a later stage. That is the release of the neurotransmitter. Once it's produced or the exocytosis, I saw this in the last lecture. Um Basically, it's that docking priming stage, which it works at, but specifically the neurotransmitter that prevents the release of is glutamate, which is the one that causes your muscles to contract. And so when you don't have this, your muscles remain permanently relaxed. It's important to remember that because they work at different neurotransmitters. One will cause muscle spasms the alpha latrotoxin. While botulinum will cause permanent relaxation, which is called flaccid paralysis where you essentially start to droop around. Um If you do forget this, you can try to think about the cosmetic use of Botox, which is often to relax muscles for cosmetic reasons after you've released the neurotransmitter, which is where all of the neurotoxins activate. The next thing is it moves across the synapse, it binds to postsynaptic receptors. There are two types of postsynaptic receptors. The fast is an ion linked receptor. What happens when the neurotransmitter bind is an ion channel will open, which will cause sodium or any other electrolyte to move across the membrane. This essentially has an electrical function where it changes the voltage across the membrane and causes electrical stimulation on the postsynaptic side. The other type is a G coupled protein which works very differently when the neurotransmitter binds the receptor has a protein which changes its shape and changes the structure. And then rather than electrical changes, what you get is a signaling cascade on the inside, whereby the change in protein structure causes a change in the chemicals on the inside of the cell, which then activates the continuation of transmission. Um This is something that they asked us to remember in my year, I couldn't see you guys needing to learn it um later on. But basically, the idea is is that in both of these receptors, you can have slightly different properties because they're made up of different subunits that combine together in complicated ways to result in different types of ion gated channels and G couple of protein. But it wasn't really that important when I did it. It shouldn't be that important for you guys. I've included this bit to just list out all of the different receptors that you come across in your course and just categorize them as ion linked or G coupled protein linked. Crucially, you should notice that the vast majority are ion linked. So if it comes up in an exam, you can just guess ion linked, I'm not gonna go over all of these because you'll probably see these in different lectures. But you can refer to this slide um later on or just take a picture. Um know that you do have to be able to memorize this and categorize them. Um Can you guys just give me one second as I attempt to make things quieter? Cool. I'm gonna apologize for that. I'm trying to, I just try to shoo people away to reduce background noise. Um It shouldn't be a problem again and I will just continue where I left off. OK. The next thing then is that often people misunderstand, what hyperpolarization and depolarization are in the context of postsynaptic receptors. Because at a level, you learn this grand idea that you always get depolarization fast and then hyperpolarization afterwards. The key thing to remember is that it's not just sodium ion channels that can be activated when you have a neurotransmitter, you have, this is the normal way that it happens. This is excitatory neurotransmission, excitatory synapses. But you also have what our inhibitory synapses where the ion channel that we talked about earlier, instead of allowing the normal sodium to come through is designed to allow chloride ions to come through. Which means that when you would normally have depolarization, you actually get a massive and early hyperpolarization and then it kind of ends and you get a different sort of refractory phase. So don't forget that this exists. The way that it then works is that you'll essentially have a single postsynaptic membrane and on it, you'll have different ion channels stimulated by different neurotransmitters. So what will happen is that when you want to cause an an action potential to fire, you'll stimulate the sodium ion channel. But if you want to inhibit it, you'll stimulate the chloride ion channel. And if both are stimulated, they essentially cancel each other out so that nothing ends up happening. Hence, it's useful to have those chloride ion channels so that it can be used to block the sodium ion channels. This is when depolarization and hyperpolarisation come in. And this is the explanation for how different neurotransmitters are able to be either excitatory through the sodium ion receptors or inhibitory through the chloride ion channels. Once you've attached to this post synaptic receptor, you then have to stop simulating the neuron because otherwise you would just have constant firing of neurons. There are two ways that we inactivate it and just, and get rid of the neurotransmitter from the synapse. The first is we use an enzyme to just destroy it and break it apart. Um Essentially just catalyzing hydrolysis and breaking it apart. The other is reuptake. That is when you're on transmitter binds to the postsynaptic receptor, it does so temporarily or reversibly, it will bind to the neurotransmitter for a few seconds and then, well, less than that. But just imagine like a few milliseconds and then it will detach, then a reuptake protein will suck it away back into the pre synaptic membrane. So that you remove all of the neurotransmitter from the synapse so that you stop stimulating it. Um The first question is here, I will present it now and hopefully it will give you the place to join. I have quite a number of, I have quite a number of many questions throughout. So it's useful if you guys join up now and then we'll just switch back to it as and when it happens, um there's no nice introduction slide. So I don't know how many people join or when, but I will give you guys like 20 seconds or so for a minute, right? Oh Can I hide ounces? Yeah. Yeah, fine. So this question is, how do we explain the mechanism of alpha latrotoxin? Um This is one of the neurotoxins that I listed. The other one being botulinum. And again, very important that you can distinguish between the two and explain it in V SA Q SBA S. Um any type of questions that they might ask you um as not to keep everyone delayed. I will just start with this first question and other people can hopefully join for the later questions. Yeah, da da. How do I see? Seven. Here we go. OK. Very responsive. I'm happy with that. And you're all correct, which is brilliant. So first of all, the inhibits calcium ion channels is something that I think a lot of people would say because you think that uh you want to stop neurotransmission So we stop the calcium ion channels, but actually, you're all correct, it stimulates it too much so that it ends up being depleted. The other thing that people tend to think is that because it's a toxin, it must cause flaccid paralysis like mass relaxation. In fact, it works at an inhibitory neurotransmitter with the chloride ions, which means that you get spontaneous like muscle contractions or spasms without them being prevented and then inhibits membrane proteins. That is literally just how botulinum works. Um The second question then is just open ended, which is what stage of neurotransmission can involve either enzyme degradation or reuptake. Um Responses are hidden. I will look at them in like the next oh I can see when people are responding. Cool think of this like A VSA Q. So try and word your answer in like one or two words, right? No problem. I perfect. OK. Yes. The word is inactivation. The reason why I put emphasis on the exact words on my slide is because a lot of the times because this content is so easy when they examine you on it, they often just examine you on key technical words like learning and plasticity and how exactly they define them, which is kind of just like a cheap trick because they're desperate to make this content harder. Um So just don't assume that it's too easy and just forget like what words mean what things? Um OK. This is the later. So I will go back to my powerpoint. OK. The next thing I'm gonna cover is the types of neurotransmitter. There are a number of different ways in which you can classify neurotransmitters. The fast is just the most basic on what does the neurotransmitter structure look like? This has literally no relevance to any of pom other than the fact that they can make you memorize it. So I've just listed it here. Um Some of them are literally amino acids. Like the things that you make proteins with some are structures called amines, which you guys come from a level chemistry, probably know what they mean. Fair enough. Um But it again, it doesn't have much clinical relevance. The last type is a type that you've basically never come across called neuropeptides. Hence why there's no examples. Uh The key thing to just remember is that um like which ones are, which type? So dopamine and noradrenaline are both amines while glutamate gaba and glycine or amino acids, the more important thing to remember is which of these neurotransmitters are excitatory versus inhibitory. Earlier when I was talking about postsynaptic receptors, I said that the receptors can either cause depolarization by being linked to sodium ions or hyperpolarization by being linked to chlorate by being linked to chloride ions. Here is the other element of it. Basically the sodium ion ones, the excitatory ones are triggered by specific neurotransmitters. Um while the inhibitory ones are triggered by different neurotransmitters. Firstly, glutamate, this is the most important neurotransmitter. Um and it is excitatory and it's found all across the brain if you only remember one very important. The next is Gabaa. This is the most important inhibitory neurotransmitter. That is while glutamate is the main one stimulating sodium ions across the brain. Gabaa is the main counter stimulating chloride ions across the brain. The other one that some people sometimes forget is glycine. Basically, this is like the Gabaa for your brain stem. It's inhibitory and it's found in the brainstem and spinal cord. Um It, it, there's also some found in the brain. None of that really comes up too much. Um So just remember it's mostly in the brainstem. Now, this is probably the hardest bit and they can genuinely, I think, ask you a full S AQ and just describe transmission across the glutamic synapse. So it's important that you remember all of these things and all of the key terms. Um But conceptually, it is the same as what we've already covered, which is why I tried to cover it first. So that you guys know the basic concept of how it works. Firstly, I said that you have to produce the neurotransmitter. The specific process to produce glutamate is to take one of the products that you should remember from the Krebs cycle that is alpha ketoglutarate and to convert it into glutamate. The process by which this happens is another reaction you should be familiar with transamination. Um You don't need to be able to say the reactants and the products just know that you get alpha ketoglutarate to glutamate through transamination. Yeah, then everything else that happens and if you ever have to explain it happens exactly how I said it before you synthesize it, you package it docking and priming, release it, it binds to and then it like it diffuses and then it binds to the postsynaptic receptor. And this is the other unique bit that is the, the synaptic receptor is an ion channel, which I've kind of hinted at before because it's linked to the sodium ions. But there are two different types which have two specific names that are NMDA or AMPA. I will go over the difference between these two. But if it's asked how glutamergic synapse works, you might just wanna name drop both of these. Then the inactivation stage. I said there were two ways enzymatic or reuptake. This one is reuptake, but specifically the reuptake channel that pulls the glutamate back into your neurons is called excitatory amino acid transporters or eaa T excitatory for glutamate amino acid. Just a a because that is the type of neurotransmitter that it is from the last slide and then just transport it. The only thing to remember is that because glutamate is so prevalent within the brain, all we have a lot of these channels on the glial cells which are cells that work around side the neurons to help remove excess glutamate into them. The final thing which we didn't cover at the start because it's quite unique to glutamate. And Gaba is that within the glial cells, you get the glutamate and you convert it into this almost like storage molecule molecule called glutamine. Um an easy stage to move out. So don't forget about it. Um I said this is like a little clip of that of the postsynaptic receptor for glutamate. I said there were two types AMPA and NMDA AMPA is very fast and very simple and very easy to remember. Basically, glutamate binds sodium ions moving through, moving through it quickly. The more complicated one is NMDA. Um just think it's more complicated and therefore it's slower, not only does it allow sodium ions to move through, but it allows calcium ions to move through. Um this bit gets a bit confusing, but I actually think it comes up a lot in medicine. So it's somewhat useful to know this is that the calcium ions act as second messengers and they don't necessarily interfere with the whole electron potential stuff that you learn at a level. The reason for this is that you have lots and lots of sodium and potassium and chloride. And so when they move around, they cause massive electrical changes, but you just have less calcium. So even if it moves around, it doesn't cause massive electrical changes. What it does do is it moves inside and it causes like more sort of chemical reactions by acting as these second messengers. You don't really need to know what these are just that it's not necessarily involved with the sodium as much. The final thing to remember about an MDA is that you need glycine. I have no idea why. This is conceptually makes sense because glycine is actually inhibitory, but you need both this inhibitory glycine alongside the glutamate to activate NMDA. And this is one of the other functions that glycine has. OK. Next thing Gaba synapse, this is the other synapse that they can ask you about and has lots and lots of details and probably just takes a while to memorize and understand just like you have to synthesize glutamate, you have to synthesize Gabaa. The funny thing is that you sympath synthesize Gabaa from the glutamate. And if you remember how to make glutamate, this is the first stage alpha ketoglutarate transamin to glutamate, which was on the last slide. The additional step is then to convert glutamate into Gaba. The process by which this happens is decarboxylation and therefore it makes sense that the enzyme would be glutamic acid decarboxylase. Um or at least the decarboxylase makes sense. This is commonly abbreviated G ad in an exam. Please do write it out in full. Then all of the other steps are the same, it packages together, it moves across, it's released into the synapse. It diffuses yada, yada, yada the unique part is step two when it binds to the receptor. Um the receptor is just an ion linked channel. There's only one type. So it's nice and simple. The key thing to remember is that because it's inhibitory, this is chloride ions, not sodium ions. This is a very important. The third thing is inactivation that is again, just like um glutamate. It's um reuptake rather than enzymatic and similar to glutamate. It also involves glial cells for the same sorts of reasons. The transporter on both the glial cells and the presynaptic membrane is called Gaba transporters, which is commonly abbreviated to GAT G at um again, brighter than four, generally similarly to glutamate. So a lot of similarities to glutamate here, which does make it easier but can make it confusing. You then have to store the gabaa within the glial cells almost. And what you do here is use Gabaa tea, which is Gaba transaminase not to be mistaken with the transamination. You do to make glutamate in the first place. And this for it forms a chemical called succinic semialdehyde, which is what gets kept in the glial cells essentially. Ok. Um I know that a lot of that is very difficult. It's also very important and probably the most important part that people tend to miss and get stuff wrong with. Um So don't neglect it and try and keep on top of how those things work. Epilepsy. The only bit I have here is very conceptual. Um The first thing is all of you guys should know that epilepsy is to do with electrical activity within the brain being abnormal. The thing that they want you to know, or at least I think they want you to know is that you can monitor electrical activity in the brain using a machine called an E EG um which stands for electroencephalography. Um And this makes sense for how we diagnose epilepsy. The more relevant bit of this lecture is the pathophysiology of epilepsy. That is I said that glutamate excites and increases the stimulation. While Gabaa inhibits and counteracts glutamate. In epilepsy, you have an imbalance between the two, either there's too much glutamate or there's not enough Gabaa. And this is what causes excessive excitation which causes things like seizures and all of the other good stuff. Then if that's what causes epilepsy, it makes sense that the pharmacology to this is drugs that do the opposite to the cause. That is if you have too much glutamate within epilepsy, you just have drugs that reduce the glutamate. And if you have too much Gaba, if you have not enough Gaba within epilepsy, you need to have less Gaba. Um you need to have increased Gabaa as a as a pharmacological drug for epilepsy. I believe that there is a spial just on epilepsy. I just included this five post here to link it to the whole glutamate Gaba concept. And hopefully they'll cover the specific drugs and their side effects and whatever else you need to know there. Um, I like the little transition. Um, hopefully anyone who wanted to join ment. Um, but didn't last time can join it now. Yeah. Cool. Which of the following is not a stage in neurotransmission at a glutaminergic synapse. I don't actually think they would ask you a multiple choice question like this. I think they would just get you to ride it out or have something a bit easier. Um I do think it's useful just to not get mixed up between the glutamate and the Gaba and everything else. Um Why I've included this, I appreciate the person who puts the thumbs up. It feels very nice to not be talking to a powerpoint. Thank you. OK. I will show responses. Yes. Brilliant. II almost looked at that and I was like, wait, that's not true. The question is not a stage in neurotransmission. OK. So reuptake is via EAA T. Um That's correct. Transamination is how you make glutamate and glutamate is an ion channel. This is the only one that is incorrect. Suiny aldehyde is formed from Gabaa, not glutamate, just don't mix up them in general. Um The next one is what post synaptic receptor relies on a Glycine coagonist be like specific with the letters here. There's basically two options. Cool. Great, two different options. Um The answer is NMDA. Um Amper I think of as being just ii somehow. Amper just sounds very faster because it's fast to say. And because it's fast, it's probably very simple. It's literally just like a sodium ion channel and that's it. And then I think an MDA is kind of long and slow to say. So it's probably got more things involved. It's got the calcium weird thing. It's got the glycine, that's just the more complicated, longer, slower one. That's why I remember the two and it still comes up like to this day. So these sorts of M pneumonics can be very useful because they can last for many years. Um And that will be for cranial nerves. So let's move on cool. Um In, in anatomy, you get given this table, um, a lot of the times different. Ok. This is not for, this is for anatomy, a lot of times for anatomy, you'll hear different things about the different functions. This table is just the standard reference that everybody uses. That doesn't mean that you need to know the nucleus table because all of this is pointless. Doesn't mean you need to know this table because all of this is useful. All of this is useless. And it also doesn't mean that they will ask you, ah, list all of the functions of the trigeminal nerve at once because it's a bit cruel to get you to list things. Instead they might just give you one of these functions here and ask you which one it is, it's not as hard as just memorizing the table. So don't try and do that instead try and make your own anky your own way to memorize anatomy. But I do want to focus on what is specific to BRS and also just give my opinion on anatomy. I was terrible at anatomy. I crammed it all before the exam. So any advice I give is basically advice on how to cheat and how to just memorize things easily. Um OK. And also I don't, I don't suggest the reason I point like study techniques out is because I think it's really, really hard to just go through the table one to like however many there are 1 to 12 and remember all of them and all of their functions. Hence, I'm trying to structure this in the way that I ended up actually being able to memorize it, which is far, far easier than if you were to like Ro memorize Anki for all of these. Um And then I'll just include the concepts within it the first way that you should probably learn it. And the easiest thing is to deal with all of the eye stuff. First, the ones involved in the eye are 234 and 62 is optic nerve, it gets sensory information, then you have movement, this involves the remaining nerves which are 34 and six, most of them are controlled by three. and then four and six, each innovate specific muscles. Um I'll get to what else three does in a second, but four controls the superior oblique muscle. Um Four is called the trochlear nerve. Um The superior oblique muscle, contrary to how all of the rest are named, moves the eye inferiorly and similarly, the inferior oblique muscle moves the eye superiorly. This is the opposite to superior rectus, inferior rectus and all of the others. So just don't get confused. Also, remember both like the superior oblique moves the eye down and out. But this is different to how you test it. This is anatomy. So I'm not gonna cover it, but just don't get confused there. Then the abusive nerves abducts the eye. Think about it, taking it away from the body, it moves it out. This is the lateral rectus. Um Yeah. But, and then the other thing I was gonna mention is that the only one of these that has another function is cranial nerve three. Not only does it innovate most of these muscles, but it also innovates muscles that don't control the movement of the eye. Specifically, the like muscles involved in pupillary constriction and the muscles of the eyelid. Um The muscles of these muscles are involved, not are involved in the motor in the parasympathetic sympathetic responses, specifically parasympathetic. Um So if you are asked specifically what the parasympathetic function is, which the difference between anatomy questions and BRS is that the BRS tend to focus on the concepts like parasympathetic. While anatomy tends to focus more on like just point at the structure, what innovates it. So it's useful to remember these sorts of details. Um So the parasynthetic innovation here is the, is the like sphincter pupil and the leva palpebrae superioris, which is the eyelid muscle. Then I like to group five and seven together and call them the branchy complicated ones which actually aren't as complicated, but they are just branchy. So the first one, cranial nerve five is the trigeminal nerve. It has three different branches. Um And the important thing to remember is that these all deal with a specific region of sensation or touch sensation to the face. So, um while you might just think, ah thalamic probably means around the eyes, the way that they always ask questions in anatomy is they'll point to like the tip of the nose, which is where you think ah is this maxillary or opt or ophthalmic? So, it's really important to remember the exact boundaries, like exactly the tip of the nose is always phthalamic. Um generally, if it's like around the ear, it's not maxillary, it's mandibular. Um So just remember those specific places, cos that's probably why they'll ask you in a spotter exam. The trigeminal nerve is mostly sensory, but it has one motor function that is chewing. Um or the muscles of mastication. These muscles are all innervated by the mandibular division, which is fairly intuitive because this is the one around the jaw area. The other branch you on is the facial nerve. The facial nerve is primarily motor as opposed to the primarily sensory nature of the trigeminal nerve. That is, it causes you to make all of your facial expressions because it has to control so many different like facial muscles. It has lots of different branches going through all of them, which can be remembered by the Pneumonic I've shown here. Um You don't need to remember this for BRS, but you do need to know it for for anatomy. Um However, it does have other functions which are listed here. Um The stuff that I have in red, I've covered separately on a like the end slide because they involve multiple cranial nerves. But remember that there is parasympathetic innervation from the facial nerve similar to cranial nerve three. But in this case, it does two things. One, it makes you cry. The facial nerve is the main nerve that makes you cry like through like la cremation. And the other thing it does is salivate. So produce saliva, this involves other nerves, which is why it's in red. Then taste is I'm not gonna cover it in this lecture, but it's the whole anterior one third, posterior two thirds. Um The facial nerve is the anterior one third. Um But again, it's red because it involves multiple nerves trying to separate the processes that involves multiple nerves helps you because this is normally how they an ask the questions. Normally, they'll say which nerves are involved in taste. For instance, rather than list like five functions of the facial nerve, they'll never ask at you like that. OK. These are my favorite cranial nerves because they are the easiest one and 81 is smell. It's a simple sense. Does nothing else. Eight, slightly more complicated because it does two sensory things that are very similar, hearing and balance. You can also link in cranial nerve two because this is just one sense that is your ability to see things. These are all my favorite cranial nerves to the easiest and I hate anatomy and I hate the complexities of anatomy. Um OK, nine and 12 personally my least favorite, but they're not actually that hard. They both have the word glossing. Nine is the glossopharyngeal 12 is the hypoglossal glossal is just like to do with the tongue. The reason why cranial nerve nine is my least favorite is because all three of its functions are done by other nerves and it doesn't really have its own unique standalone selling point. The first thing is parasympathetic to the salivary gland. You can remember that this is the same as the facial nerve, the parasympathetic functions of both of the of these nerves is involved with saliva. The other thing is it's involved in taste, which again links to the facial nerve. They have a lot of crossover of the facial nerve here and then swallowing is fairly intuitive because it's in, it's got like the PHN, it's got the word pharyngeal in it. So you can imagine that it involves the pharynx and that'll cover again these processes on the next slide, hypoglossal um is actually much simpler. It's just got one motor function that is, it moves the tongue in all of the positions. But if you think about it, moving the tongue in turn has a lot of other functions. Like it helps you produce speech, it helps you swallow. And sometimes it might kind of give you a throw off questions like which nerve like helps in swallowing. I I've never seen that but you know, just, just don't get caught off. Um What is this? Oh, I forgot there were more nerves. Yes. 10 and 11 are just the ones that do other things. So if you have the gloss, the sensory, all of the other categories, these are the ones that are left over. I do think learning it in this order kind of helps. Um So 10 is the vagus nerve. This is the main nerve that goes beyond like the face and the brain. It does mostly parasympathetic stuff that is parasympathetic heart regulation, slow down the heart, parasympathetic digestion, speed up digestion, but it crosses over with the glossopharyngeal nerve to do swallowing, then accessory nerve. This is one that people normally get right, it innervates two muscles. Normally it just points at these muscles and asks you, what is the nerve that innervates it? Ok. Um I think this is a key differentiator between VR S and anatomy because they can ask you about processes like taste and saliva and swallowing. Um and which nerves are involved. But in a spotter exam, when you're pointing at a structure, it's harder to do this. Um OK. The first thing is taste and tongue sensation. This is actually more anatomy than BRS. So I'm not covering it. Um Then you have saliva ss like salivation. I think that's the word. Um Basically, you have three different salivary glands, parotid submandibular sublingual. The sublingual gland is controlled by the facial nerve. And so is the submandibular gland and the parotid gland is controlled by the glossopharyngeal nerve. Somehow people always, always, always get this wrong because the facial nerve literally travels over the parotid gland. And people seem to think that that means that it innervates it. Please don't make this mistake. Um I say this because I made this mistake a lot. Um The next thing is swallowing, you should remember, this involves two nerves, the vagus nerve and the glossopharyngeal nerve. The first nerve that activates is the glossopharyngeal nerve, which then activates the stylopharyngeus muscle. I don't think you need to memorize the name of the specific muscles. But if you describe the stage of swallowing, the glossopharyngeal nerve activates fast, then the vagus nerve activates and that process of swallowing that you learn in gi and also in anatomy comes in here where you have like circular constrictor muscles that like move down the esophagus. And this, if you think about it happens after the pharynx and in the esophagus, which is where the vagus nerve goes through to activate all of the parasympathetic digestion. So I think if you think about it logically, the pharynx is the first bit and this is the glossopharyngeal and the vagus nerve is the second bit because this goes down to your stomach and does all the digestion stuff. So it also travels through the esophagus. Um And I don't think you have to remember all of the different things that the vagus nerve innovates, even though it's on that big blue table, I like it doesn't really matter like muscles of the soft palate except tensor Veli palatini. Just don't remember that. OK. This is the one thing that um OK, this is like the pretense to the next slide, which is very, very important. So basically, you'll probably hear that we have nuclei within our brain, within our brain stem. And you learn that nuclei are collections of nerve cell bodies. But then you learn nuclei in a different context, which is the concept of cranial nerves. And everybody just forgets what nuclei are and they get very confused by this little section of silvers. Basically, your cranial nerves are separate completely to your nuclei. Because if you think about a nuclei, it is a collection of cell bodies. But your cranial nerve is a collection of like axons. So if you think about it, think of your cranial nerves as like a little road that pass through the nuclei and pick up some of the stuff from the nuclei along the way. If you think about it like this, you can understand that a lot of the times these aren't corresponding to specific cranial nerves by the way, but a lot of the times these interactions can be very complicated. Like the one in orange seems simple. It's got some motor stuff, it's got some sensory stuff. This might be like um your trigeminal nerve, your sensory stuff being all the trigeminal sensory stuff and your motor stuff being your mastication. Um This one, it's also very simple. It's got one motor, one sensory, the black one. the green one though is an example of where it might get a bit more complicated. That is, it's got, it doesn't go through any motor nuclei, but it goes through two sensory nuclei. Um and it picks up sensory and then when you look at all of the cranial nerves together, you it's even more complicated because sometimes a single sensory nuclei or single motor nuclei can supply two different cranial nerves. Um In farer, none of this ends up mattering too much. Besides the next slide that I'll get onto. But in later years, the concepts of the different motor and sensory nuclear. I do come up, which is why I think it's important to be aware of how this works. Now, this is a really fun table that nobody really knows what it means. But they can still, it still is important. Basically, most of the time we describe nerve pathways as general. But there are a few that for some reason we describe as special, you don't need to know why they're special, But there are a few specific nerve pathways that are special. You should know the difference between afferent and efferent neurons. Afferent neurons are always sensory. Think about A as being before e in the alphabet and a being ascending. So this is the s the start of your like motor reflex. This is the first thing that happens, which is sensory because you sense first and then you respond to that sensory later, efferent is motor because it comes afterwards and it comes like down descending. Then what you have to remember is that there are a few specific functions that are done by the special system as opposed to the general system. And hopefully, you can then memorize whether it is special afferent or special efferent. There is one last word in here which is somatic and visceral. And this just comes down to raw memorization to remember basically the table that's here. So let me just explain it in a way that should flow nicely. The easiest one is the very bottom in this, in this table, which is the special visceral e efferent. They are efferent because they are motor. So they happen after the sensory, there is only one special efferent pathway which does all of the innovation of the stuff around the jaw, the face, the larynx, the pharynx, all the stuff that cranial nerves are involved with the other thing that could exist. Oh, yeah. Yeah. The other thing that could exist is special somatic efferent, which is other motor stuff. But instead of being visceral, it's somatic. This doesn't exist. So any time you see a muscle function that is special and done by cranial nerves, it must be special somatic efferent because there is no somatic efferent. Then the slightly heart of it is the sensory stuff. There are two groups of sensory stuff that are special. One is taste and one is hearing, imbalance. Taste is visceral, hearing imbalance, somatic. Why? I have no idea. But if you remember which way around visceral and somatic are the other words should make sense. If you think ah taste, I know that taste is sensory. So it must be afferent. But then you think, ok, was taste visceral or somatic? This has to be memorization. Um I will do the question on that specific thing so that hopefully you can think through that process by yourself. Yeah, I don't know why they make you learn and stuff like this, but it's just that OK. OK. This is the last question and then I will just summarize and that will be end. So, shouldn't have to hold out too much longer. So this is muscles, it is muscles controlling. So it's muscles. So it must be efferent. Yeah, I'll show the responses. Yes. OK. It's muscles which means it must be efferent because it can't be afferent because if it's afferent, it's sensory, then the word somatic versus visceral somatic doesn't exist. So any special muscle function has to be visceral. So it's special visceral efferent. Um Also, I'm aware that somatic and visceral do have meanings. Somatic normally means external. Visceral normally means internal. I tried to remember it like this but you have to remember that like the visceral efferent controls facial stuff that's not inside the body. So I don't think thinking about it in this way actually ends up helping also the fact that hearing and balance are somatic doesn't make sense to me because they still feel very internal to me. Um OK, describe the motor function of the glossopharyngeal nerve. Um I think this is a nice and hard question because it forces you to think slightly differently to anatomy. What is the answer? I do know? Yes. Yeah. OK. Cool. I'll accept two different answers here. Swallowing. Yeah, this is fine. So the main motor function in terms of like classically motor is that it um it triggers the start of swallowing. The other thing that is a motor function that is worth not forgetting is the fact that it does parasympathetic innervation to the parotid gland because even though this isn't like a muscle moving, this is still motor function because it's not sensory basically. So don't forget about that as well. Um But swallowing is perfectly right. That's the end of mental and just to summarize what we've been through, OK. The first thing that we looked at was synapse and neurotransmitters, we looked at the structure of neurons and specifically like how to define them in ways that are unique from a level and how to word their functions. We looked at the characteristics of synapse which again are very sim a very simple and often known by everyday people. But I looked at the key terms that they want you to know, then we recapped the stages of synaptic transmission. But we looked at of the things like neurotoxins which happen at the release stage and also the different forms of inactivation. Because this comes up later, we then classified neurotransmitters as either like by their molecular structure or either exci atrial or inhibitory. We covered the idea of exci atri and inhibitory, both in terms of the postsynaptic receptors being chloride or sodium ions. But also in terms of the neurotransmitters being anergic or like glycine or Gaba. We then looked at these specific neurotransmitters. We looked at how transmission works, glutamate, um synapses followed by Gabaa synapses. And then we combined the concepts behind this to look at things like epilepsy. Also remember that concepts like botulinum and alpha latrotoxin come back in here because they involve Gaba and glutamate. Finally, I looked at the functions each of the cranial nerves. We then looked at the functions where the cranial nerves converge. And I tried to do it in an order that I think is worth memorizing in. Then we looked at the cranial nerve nuclei and how this links to the special pathways that they want you to know. Hopefully all this was relatively simple. I don't think any of it is conceptually difficult. A lot of it is just can you memorize things and can you phrase it in exams? So Anki look at slides, say it to yourself, focus on being active rather than on the concept for this specific area of the course. With that I will pass over to um I don't know who's giving the next lecture, but this is the end for me any questions first. And if you have a feedback form, could you put the QR code up? Um I do not have a feedback form, but that's all right. I've done this same presentation before. That's fine. You have a question in the chart. Could you please go back to the slide of the other nerves of the other nerves? I assume this is this. Nope. Yes, yes. OK. I assume maybe you just wanna take a picture of this. Um Yeah, just, just think about it as eye sensory, swallow it like gloss, eye sensory, gloss, branchy, other um I classify cranial nerves in these four categories. And then I think ok, if asking about the facial nerve, which one is that? Oh, yes, it's branchy and then that kind of helps me a bit. Um But yeah, hopefully that was long enough. Cool, great. I think hang around for two more minutes to see if there's any more questions and if not, we will wrap up brilliant and we'll also put my email in the chart just in case anybody wants it. Um If you want to request slides or the slides will be available on metal. So um you guys can sit there and tomorrow we'll be doing the second half of neuros at the same time. So feel free to watch that if you find stay useful. But yeah, um I think that's it from us. If anyone has any questions, feel free to put in the chart and if not, that's the end of the session. So thank you for joining. The last thing I will say before people leave, I will do another lecture on muscle structure and contra on muscle structure and contraction, which is conceptually like one of the difficult bits because it involves all of the injury repairing and like how bones are formed in embryo and how they heal. So that'll be a lot longer and a lot more conceptually challenging. So do join that. Because I think it's something that people try and memorize but is when I say Anki doesn't help because it's very contextual. Um, unlike this area. Um, but yes, that's all for me. Cold. Am I all right to head off? Yeah, you can go. Yeah, I think we'll wrap up and end it there. Thank you everyone for joining and have a nice evening. Bye.