so this video will talk about action potential threshold in propagation of action potentials so it turns out that not all depolarization within a neuron produces action potentials you know for an axon to fire depolarization has to reach a threshold value for voltage now it turns out that that this threshold is basically the voltage at which voltage-gated sodium channels open so an ER membrane to depolarize by you know fifteen to twenty millivolts away from rest so what happens here the during depolarization is that maybe sodium permeability increases due to like a great potential and sodium influx might proceed potassium efflux which causes this depolarization wave that might get the voltage-gated sodium channels to open and if once those voltage-gated sodium channels open then essentially a positive feedback cycle will begin where even more sodium starts entering which means you get more depolarization which allows for even more voltage-gated sodium channels to open and we call this the all-or-none phenomenon basically what we say here is that an action potential either happens completely or does not happen at all because you needed a sufficient amount of voltage-gated sodium channels to open before the action potential takes off but once you start it you're not going to stop it so in fact this action potential is going to propagate down the axon of your neuron and it's gonna spread pretty quickly so propagation is basically the spread of the action potential where sodium influx through voltage gates causes these local currents that caused the opening of voltage-gated sodium channels nearby and because of this sort of you know positive feedback effect ultimately voltage-gated sodium channels start opening down the line of the axon kind of like a Domino rally where it leads to depolarization of that area which in turn causes depolarization of the next area so what's initiated the action potential South propagating you find that in non myelinated axons each successive segment depolarizes and the repolarizes propagation in myelinated axons differs because it's regenerated at little specific areas and since the sodium channels are closer the action potential origin are still inactivated you don't have a new action potential generated while the voltage-gated sodium channels are how their inactivation gates closed which means that action potentials can only move in a forward direction they don't move back they move in one way because they can't flow back because those inactivation gates are still closed so what we find here then is that let's say this is the action potential kind of like the front of it and if we're measuring voltage right here we say that in this local area of the axon there's currently no action potential present voltage is at a resting value and resting is due to the leakage channels so but nearby we can see the action potentials coming and what's happening here is that sodium is rushing in through voltage-gated channels causing a little local area of depolarization and that depolarization will stimulate the next segment of the axon to open up its voltage-gated sodium channels and then start to depolarize that segment so we find that is that if you're measuring right here we see that this is then it can be like the peak of the action potential where it's very depolarized because as voltage-gated sodium channels are opened you can see that back here where the action potential had been it's currently repolarized and probably even hyperpolarized and it's even starting to spread in this particular direction now measuring the same spot here we see that you know once the action potential has passed you know this place where we recording voltages it's hyper-polarization stage and so you can kind of think about this action potential is spreading kind of like a fuse where once you light that fuse the burning segments of fuse causes the next segment to ignite and that will actually continue down the line but the previous segments of the fuse are actually already burnt so it's not going to move back however what's really cool about action potentials is that the axons can reestablish their resting conditions that way another action potential could occur sometime later now action potentials are all like in they're independent of stimulus intensity in fact the way that your brain tells the difference between a weak and strong stimulus is not the size or the duration of action potentials rather it's the frequency and number of action potentials and received so higher frequencies of action potentials mean that there's a stronger stimulus a lower frequency means the weaker stimulus so if you look at this and think about okay stimulus intensity or voltage you might have a sub threshold stimulus kinda like what we saw back in muscle where it's not enough depolarization to lead to action potential generation now if our stimulus is above threshold then we'll get a certain number of action potentials that's generated but what's interesting here though is that increasing your stimulus well above threshold doesn't change the size of the action potential it just makes those action potentials more frequent so you can see you can fit more action potentials in the same amount of time here if your stimulus intensity is larger because you have a higher frequency of action potentials so this means that you know your brain can encode information by frequency of action potentials not the size of them and so the reason why action potentials don't overlap and therefore change size and they don't some eight like like our muscle twitches did rather there's a something called refractory period this is a period of time where the neuron cannot generate another action potential this is because the voltage-gated sodium channels are open so the neuron can't respond or than their stimulus there's two types of refractory we have absolute and relative refractory absolute refractory period is the time from the opening of those voltage-gated sodium channels until you get the resetting of the inactivation gate but this takes some time and you find that most of the action potential is in absolute refractory which prevents these things from overlapping so it ensures that each action potential is all or none it enforces a one-way transmission of nerve impulses relative refractory period occurs when the voltage gated sodium channels begin to reset so the inactivation gates are kind of resetting back into their open position so that way you can actually stimulate voltage gated sodium channels to open again and it's relatively in refractory because although the voltage gated sodium channels are resetting you're still a slightly hyperpolarized state and repolarization is occurring so threshold for action potential generations elevated it's going to take more stimulants to get some threshold that's why it's relatively more difficult to generate an action potential during the relative refractory period so just kind of checking this out here we see that okay here's resting voltage and if you get a stimulus we get our action potential while the voltage-gated sodium channels are open this is absolute refractory you can't stimulate the voltage-gated sodium channels to open more they're already open remember it's all or none in fact this this absolute refractory period ends right around the repolarization phase of the action potential where voltage-gated sodium channels start to close and their inactivation gates are closing rather now they also the inactivation gate start to reset as our voltage starts to repolarize back down towards rest in fact it's the hyperpolarization here that helps to reset those inactivation gates and opens them back up but the activation gates of your voltage-gated sodium channels are still closed here which is why you don't generate another action potential immediately now during this phase right here the darker blue this is called the relative refractory period because it's relatively more difficult to generate another action potential and the reason being for this is that if your hyperpolarized you're farther from action potential threshold which means it's going to take even more stimulus to get there you know if you compare hyper-polarization to rest at rest it takes a very little bit of stimulus to get to threshold during hyper-polarization it's even farther away which makes it more difficult to generate an action potential that's what's called relative refractory period but the significance of this is that it helps to keep action potential separate that way information stays as separate pieces of stimulus so there's different factors that can affect action potential velocity you know i've mentioned several times here that action potentials don't travel at the same speed some action potentials travel at like up to a foot a second some travel at 300 feet per second and what what changes the conduction velocity here is axon diameter and the degree of myelination you know turns out that larger diameter fibers or axons have less resistance so they have greater flow which me faster impulse conduction also if your action exons are more myelinated we find that it's going to change the type of conduction that can occur in continuous conduction is actually slower than what we call saltatory conduction so continuous conduction is a slower form of conduction that occurs in non myelinated fibers saltatory conduction Saltire means to jump so sulphate or conduction is where action potentials jump from myelin sheath gap to myelin sheath gap and because they can skip large segments of axons they can spread more quickly so each electrical signal appears to jump rapidly from gap to gap so this is showing an example of a graded potential remember in graded potentials once you get a stimulus as the great potential travels it decreases over time and distance and if it's too small to generate an action potential then you won't see one there'll be a sub-threshold stimulus now this differs from action potentials because in an unmonitored axon once you generate an action potential you know it's gonna spread pretty quickly however when when you don't have myelin it turns out that our action potentials kind of degrade more quickly and at this point where degrades right around threshold then you'll generate another action potential now if you get the generate action potentials more frequently it turns out that these action potentials are gonna travel more slowly you know think about these is taking more frequent smaller steps if you took more frequent but very small steps you're not gonna be walking very fast you're gonna kind of be shuffling your feet and moving kind of slowly and that's that's the kind of propagation we see in non myelinated axons where because of the lack of myelin you get lots of stimulus and current really quickly so that our action potentials degrade and in size quickly which means they need to be regenerated more often but regeneration the action potential takes time and so each of these four generations just takes extra time which means that on a whole this action potential spreads much less fast now that differs from saltatory conduction which occurs in myelinated axons now what's cool is that myelin functions it has an insulin and as an insulator then what you find is that current doesn't leak out of the cell as quickly so you can see that these action potentials degrade much more slowly which means they need to be generated much less frequently if you don't there generate action potentials as frequently that means are gonna travel faster because essentially the action potentials can skip from this node directly to the next and each node is the myelin sheath gap here and so at this myelin sheath gap that's the exact point where you're gonna need to generate another action potential before it can spread to the next node and you can think about this type of movement is like taking large leaps right if you can jump from spot to spot eventually you're gonna move a lot faster than if you to shuffle your feet as you'd find with you know not my own axons we take lots of frequent very small steps you know Saul story conduction is we're jumping from node to node and as a result the action potential can zoom down the axon much more rapidly now we can kind of classify action potential propagation by the fiber type and so nerve fibers fall into three major categories we have Group A fibers B and C fibers Group A fibers are the largest in diameter they're heavily myelinated and you find that this is the type of fibers that transmit motor fibres - you know skeletal muscle as well as sensory information from joints and these can transmit action potentials at like a hundred fifty meters per second which is about four hundred feet per second or 300 miles per hours it's really fast you know about instantaneously as far as our bodies are concerned Group B fibers are intermediate diameter and they're because they're lightly myelinated as well they only transmit action potentials at fifteen meters per second which is still like forty five feet per second and about thirty miles per hour which is still pretty fast you're gonna find these you know pretty commonly throughout the body and Group C fibers the smallest diameter and they're unmyelinated which means they can only transmit action potentials that like one meter per second which is about three feet per second or two miles per hour so B and C fibers include autonomic visceral motor and sensory fibers remember the autonomic nervous system is part of your unconscious sensory division and and motor division and these actually can transmit action potentials more slowly than like your somatic motor system which is much more rapidly