Neurons and Action Potentials

hi. In this lesson, we'll be talking about the cells that compose the nervous system, or neuron. Now the nervous system is a network of nerve cells, or neurons that transmit signals throughout the body. The neuron is the major cell of the nervous system, and it will both send and receive electrical and chemical signals, and we'll get into more about that in a little bit. But neurons aren't the only important cells of the nervous system. We also have these cells called glia or glial cells, and these are going to serve to both support and protect neurons. But truth be told, their role is not very well understood. Yet it's clear that they do certain things, but it's also clear that they're doing a lot of behind the scenes stuff that we haven't quite grasped yet. So here you can see a neuron and we'll talk about its anatomy in just a little bit. And this is a Lyle cell. Technically, this is actually known as an Astra site, and that actually comes from it's almost star like appearance, with all these appendages going out in every which way. Now the nervous system, it can actually be broken down into two components the central nervous system and the peripheral nervous system. The central nervous system is going to be, uh, the brain and the spine. And the peripheral nervous system is basically everything else. So here you can see we have our central nervous system, and I'm gonna just kind of outline it in blue. Here is our spine, the brain, and that is our central nervous system. Now, all of these other nerves you see projecting from the spine, that's all part of the peripheral nervous system. And with that, let's actually go ahead and flip the page.

neurons are the signaling cells of the nervous system, and they'll actually transmit electrical signals, which they'll then translate into chemical signals to release to other neurons. Now, when neurons receive chemical signals, they'll actually translate these into electrical signals. So neuron zehr going to use a combination of electrical and chemical signaling now neurons actually do have decent variety of morphology is that is to say, they don't all look the same. However, there are certain features that they'll share, and we'll go over those now. So my point is, not every neuron is going toe look like this one right here, however, neurons will have a cell body, and that cell body is going to contain the nucleus, which you can see right here. Projecting from the cell body is what's known as the ax on, and the axon will be connected to the cell body by a region called the Axon Hillock. Basically, this right here, this little area that's gonna connect the cell body and the ax on now the acts on acts as the wire. So it's going to transmit the electrical signal to its tip known as the terminal. Now the terminal of an ax on is going to connect to the dendrites of another neuron. And those dendrites are these basically branch projections almost like branches on a tree. And they're going to receive signals not just from one neuron, but from a bunch of other neurons. And when two neurons connect, like at the terminal of the ax on and the dendrites, what we have is known as a synapse, and this is a connection between the acts on terminal and the dendrites. And that is where theological signal is going to be converted into a chemical signal that chemical signal being nure Otranto emitters and those will be released across the synapse to bind to receptors on the dendrites of another neuron. We'll get into the specifics of this in just a little bits. Don't worry. So you're going to see networks of neurons connected to each other like you see here. Except here. We only see two cells. In actuality, there's going to be many, many cells, all connecting to each other and projecting too far away parts of the body quite frequently. So with that, let's actually go ahead and turn the page

neurons and glia are what are going to make up with central nervous system and the peripheral nervous system. Now the responsibility of the central nervous system is to receive information from the body and integrate it to coordinate various responses. For example, if you see a ball flying at your face, probably want to duck or jump out of the way. Right. So that is going to be sensory information taken in that your brain processes and then coordinates a response and shoots it out to your peripheral nervous system to actually act out that movement. So the brain is really like the, you know, the control center for all of this, and the spinal cord is basically just a bundle of neurons and Goliath that will extend down from the brain. And, uh, you know, essentially branch out into all of these different nerves of the peripheral nervous system. Now the peripheral nervous system sends signals to and from the brain and spinal cord, and it is going to contain thes little clusters of cell bodies that you'll see in the central nervous system is well, but they have a different name, so we call them ganglion or ganglia. Ganglion is the singular ganglia. Would be, um you know, plural, multiple, gangly ins. Uh, and this is just a cluster of neuron cell bodies. And basically, what we'll see is the nerves will be, uh, you know, made up of bundles of Exxon's, and often the neuron cell bodies will all be kind of clustered together in one place. Now, thes bundles of axons will actually be broken down into sort of two categories. We can have sensory neurons, and these were gonna be nerves that transmit sensory information. Uh, you know, ultimately to the brain and the spinal cord. So they're gonna bring in information from our sensory systems and bring it to the brain. Motor neurons are going to project from the spine out to effect organs like muscles and glands. So these air gonna be the guys that actually sends signals to do things like duck. When you see that ball coming towards your face Now, you'll also see what are called inter neurons. And these air, basically just neurons that transmit information between other neurons so they'll connect, sometimes connect sensory and motor neurons. However, sometimes sensory and motor neurons will directly connected to each other, and we'll see an example of that. What's important to note, though, is the Interneuron Zehr actually going to be the main type of neuron in the brain. Now, with that, let's go ahead and flip the page.

in this video, we're going to introduce some terms. That will be very helpful for you as we move forward and talk about neuronal signaling or the signaling between neurons. And so the first term we're going to introduce here is electric current. And so electric current can be defined as the flow of electric charge. Now, when you think of an electric current, you may think of an image that looks something like this, where you have some kind of battery and we know that electrons, which can be symbolized with the symbol right here, will flow through a wire here and it will be used to power some kind of device such as this light bulb here. However, electric currents do not necessarily require the flow of electrons and in fact the electric current that's utilized by neuronal signaling is not going to be electrons. Instead it's going to be ions and the flow of ions will generate this electric current. Now the term electric potential refers to the electric potential energy per unit of charge and it is measured in units of volts, which can be abbreviated with a V. And the term voltage refers to the difference in electric potential between two points and results from differences in charge. And so if we look at our image on the left hand side over here, notice towards the top, we have these positive charges and towards the bottom we have these negative charges. And so because there is a difference uh in electric potential between these two points, we have a positive charge here towards the top and again a negative charge here towards the bottom. What that means is that there exists a voltage here in this image. And if we were to take, say, a positively charged particle and place it here, what we would see is that this positively charged particle would repel all of the positive charges towards the top, and it would be attracted towards the negative charges towards the bottle. And so this positively charged particle would make its way and move towards the negative charges. Now when it comes to neuronal signaling, the electric potential can be created using an electrochemical gradient. And so an electrochemical gradient is really just the combination of a chemical concentration gradient and an electric potential gradient across the membrane. And so if we take a look at this image down below, which will notice is that it represents a biological membrane here in the middle and which will notice is we have a bunch of ions on the left hand side which represents our extra cellular space. And we also have a bunch of ions on the right hand side which represents the intracellular space inside the cell. And what you'll notice is that when we look at the ion concentration gradients of these three ions, sodium ion, potassium ion, and chloride ion, they have gradients that um exist as this image shows. So in the extra cellular space there tends to be a large concentration of sodium ion and as you cross the membrane towards the inside of the cell, there's a low concentration of sodium ions. So we can put low here and high here. And what you'll notice is that the potassium ion concentration is opposite of the sodium ion concentration. So there's a high concentration of potassium inside in the intracellular space and there's a low concentration of potassium on the outside of the cell. And then the chloride ion concentration resembles that of the sodium ion, where there's high concentration of chloride and ion on the outside of the cell and low concentration of chloride and i on on the inside of the cell. And so the cell is able to create these concentration gradients through utilizing these ion channels or this membrane protein here that can transport ions. And so we'll get to talk more about this transport ion in a different course. But ultimately, what you'll see is that uh there are going to be uh sodium ions pump towards the outside of the cell. So that's what creates the high sodium on the outside of the cell. And then there are going to be potassium ions pumped towards the inside of the cell and there will be more uh sodium pumped out than there is potassium pumped in. And so over time, what ends up happening is there is a build up of positive charge on the outside of the cell. And so that's something that's important to keep in mind that on the outside of the cell, there is going to be in a net positive charge. And on the inside of the cell there's going to be a net negative charge across the membrane. And so what that means is that there exists a voltage across the membrane. And we refer to this electric potential. Uh we refer to this as the membrane potential. And so the membrane potential, of course, is going to involve the biological membrane. Uh and so it's the difference in electric potential between the interior and exterior of a cell which will be separated by the membrane and which will notice is that when the cell is in a resting state, basically when the cell is in a normal resting state and it's not really doing anything, it will have a resting membrane potential. And that is really just the baseline membrane potential of the cell. And that resting membrane potential is going to be negative, meaning that the inside of the cell will be more negative with respect to the outside of the cell, which will be more positive. However, the membrane potential can change. And this will be critical when we start to look at these neuronal signaling. Uh And so hyper polarization is a term that refers to the membrane potential becoming more negative. And deep polarization is a term that refers to the membrane potential becoming more positive. And so we'll get to utilize these terms uh more as we move forward in our course and discussed uh neuronal signaling. And so that here concludes this video, I'll see you all in our next one.

in order for ions to get from one side of the membrane to the other, they're gonna need ion channels, these air just protein channels that essentially form a poor through the membrane and allow for the passage of a specific ion. And that's pretty key to note here that thes ion channels, they're going to be selective for specific ions. Now, these iron channels are both critical in establishing membrane potentials and in the transmission of electric signals and neurons, which we're gonna learn about in just a second, which are called action potentials. Now, there are these, uh, special type of ion channels that I want to briefly mentioned called leak channels. They're called leak channels because they actually basically let potassium ions leak out of the inside of the cell, which, hopefully remember, is where they're very highly concentrated. And this is in order to help maintain the negative resting potential or the negative potential of the membrane when it's at rest of neurons. So basically, thes leak channels are going to be like a special case of ion channel that allow these potassium ions to leak out of the interior of the cell. And it's just to help maintain the negative, the negative potential in there. Now, the rial stars of the show are the gated ion channels. These are the guys who are going to be critical Thio neurons sending electric signals and these air ion channels that open or closed in response to stimuli. So their gated by some signal that they have to receive. And we're going to see two major types ligand gated ion channels which open in response to ligand binding. So, like a ligand binds to a receptor and that causes an ion channel to open or voltage gated. This is, um, you know, kind of crazy stuff here, but basically these iron channels will open in response to specific membrane potentials. And these air gonna be the particular types of gated ion channels that air crucial to sending electric signals through. Uh, but the Exxon will through neurons in general. So we're really gonna be focusing on two types here sodium channels, which you can see here in blue, and you just write it and read to be crystal clear. We have potassium channels over here. Now, what's the difference? Well, sodium channels will actually have an extra sort of state of being that we won't see in these potassium channels. Basically, with the potassium channels, they're either open or they're closed. And if they're open, the ions can move through them. If they're closed like you see here, passage is blocked. The ions will just bounce off of them. Know ions, air getting through the membrane. So so sodium channels just like that. They haven't a closed state and an open state, but they also have this special state we call inactivated. And usually it's, uh, this is thought of, as they call it, the ball and chain model. Basically, you have this chain with a ball on the end that is attached to the the ion Channel and given a certain, uh, a certain condition, let's say that ball will actually plug up the ion channel like you see here, and that's going to cause it. Thio not allow any ions through. So three states closed open inactivated ions. Onley will flow through in the open state, and the significance of the inactivated state will become clear in just a moment when we actually talk about steps of the action potential. So the other uhh ion mover shall we say that is critical for maintaining and establishing membrane potentials. These sodium potassium pumps or an ACA at P aces. I like to call it now. These are pumps that, uh hopefully this isn't the first time you're seeing these. We've talked about them before. They will use ATP to actively pump. That's why so, actively, their meaning, ATP is consumed and they're gonna pump three sodium ions out of the cell, and they're gonna bring to potassium ions into the cell. And this is with each cycle. You can't get rid of the sodium ions and not bringing potassium ions. ITT's like three go out to come in one cycle. Repeat so you can see a model of that happening here. I don't actually care that you know the specific steps of what's going on. I just want you to know that ATP gets consumed. We have three sodium ions that leave the cell. This is out. This is in, and we have gonna jump out of the way here. These two potassium ions that come into the cell. Okay, so there is a special type of potential which we call equilibrium potential. This is going to get back to those leak channels. Basically, it's the membrane potential, at which point there's no net movement oven ion in or out of the cell. So basically, while you know some ions are still moving in and out of the cell, the concentrations in and out of the cell are static there. There's no change. There's no net movement here now. Why is this important? Well, remember that there's both concentration Grady INTs and these electric potential Grady INTs, that air acting on the ions right now. Those leak channels we mentioned before they are going to allow potassium toe leak out of the cell along its concentration radiant. But at some point it will reach equilibrium potential because it will have sort of competing forces. So there's going to be a concentration radiant that causes sodium. I'm sorry potassium to want to move out of the cell, but remember that the interior of the cell is negative exterior positive. So at some point, the potassium is going to stop moving out of those leak channels because it's going to reach its equilibrium potential, which we would write Oops, we would rate as E with little K under there it's going to reach its equilibrium potential, where basically the force driving it to move along, its concentration radiant, will be balanced with the force trying. Thio drive it inward with against its concentration ingredient but with its electrical radiant. So those leak channels actually will get potassium Thio hit a point of equilibrium potential when the cell is at rest. All right with that, let's go ahead and flip the page.

There's a very special Siris of events that will happen when a cells membrane potential hits a certain specific point and leads to what's called an action potential. Some cells, however, will have shifts in their membrane potential that vary in magnitude and actually aren't going to generate this action potential. We call those potential fluctuations graded potentials and basically graded potentials actually code their information based on the signal amplitude. So essentially, the magnitude of these membrane potential shifts are going to result in different signal amplitude. And it's the differences in those magnitudes that air going to code information action potential is all or nothing. It is a binary signal. It's either on or off. It is zero or one, and it is a transient shift in membrane potential. So it's a, uh changing membrane potential that does not last very long, and it sends this all or none signal. So if an action potential ascent, that's a one. If there is no action potential, that's a zero and the intensity of a signal like, for example, if you want Thio, send a signal basically telling your muscle to contract just a little bit versus sending a signal to like, really, you know, super contracted the difference in those signals. They're all you know. They're all being sent his action potentials. But the difference in those intensities is coded by the frequency of the action potentials. Because action potentials again are a binary signal, all or nothing, there is no difference. An amplitude. There's no magnitude to be calculated or to be factored in. It's just one thing. So what is the action potential? Well, it's basically a Siris of events that are going to occur across the membrane of a neuron, and it's going to result in electric signal being sent down the ax on. So essentially you're going to start off in a resting state. This is just the cell at resting potential. Nothing's happening. It's just chilling out. And at that state, these voltage gated sodium and potassium channels that are going to be all over the ax on membrane those they're gonna be closed now, in what's termed the rising phase, the membrane potential is going to be deep polarized, and remember, that means it's going to get mawr positive or less negative. However, you want to think about it, and this is this deep polarization is going to cause some of these voltage gated sodium channels around the membrane toe actually open. Now there is a special membrane potential, which we call the threshold, and this is essentially a point a point in membrane potential that, if crossed its action potential time it is on. If you don't reach it. No action potential. So you have to cross this threshold in order to actually have an action potential. Now, if the threshold potential is reached, all those voltage gated sodium channels are gonna be thrown open. And because of the way the membrane potential has been established, right where sodium ions want to move into the cell both because of their concentration radiant. That's one trying to symbolize here. Concentration, radiant and because of the negative charge inside the cell. So when threshold is reached and those voltage gated that voltage gated sodium channels, open sodium is just gonna rush into the cell full steam ahead. Now, remember that the inside of the cell is negative, but we have a huge influx of cat ions. This is going to dip, polarize the membrane potential. So here, if we look at our chart, we started off with resting phase right, We have our voltage. This is our essential er membrane potential Here it's resting at this negative value, but due to deep polarization zones, it will cross the threshold. And then we have the rising phase right where the membrane potential shoots up because of all of those sodium ions entering the cell Now at the ah, essentially, when the sodium channels reach this super deep polarized point, they're going to become inactivated. And the potassium channels which are also voltage gated but gated toe open at thes, you know, deep polar deep polarized potentials. So here in the falling phase, we're gonna have our potassium ions flowing out of the cell. They're gonna rush out of the cell because the voltage gated potassium channels open. Now, remember, at rest, those potassium ions are more or less gonna be at their equilibrium potential right there. Their concentration radiant causes them toe, want to leave the cell, and the electrical radiant causes them to want to enter the cell. And they're going to hit that equilibrium potential thanks to our leak channels. So here we're now deep polarized, like we're about plus 40 million volts so essentially the inside of ourselves has become positive at this point. So now potassium is gonna have the double whammy that sodium had before. Right now, potassium is gonna want to move, so sodium is gonna go in the cells. Potassium is gonna wanna go out of the cell because of the concentration, radiant. And because now the cell interior has become positive. So perhaps I should express it as wanting to go out away from the positive charge and towards the negative charge. Okay, so now with these potassium ions rushing out of the cell, this F flux of cat lines, all these leaving cat lines cause re polarization of the membrane potential. So our membrane potential is going to go back down. Here's the thing. It actually is going to undershoot resting membrane potential. And that's because of, uh, this refractory period, which is essentially the time during which another action potential cannot be generated because our potassium channels air inactivated and no potassium is getting through some sodium channels air still open. Right? So that's actually going to cause this hyper polarization. That's what we refer to this as. It's a hyper polarization, because we're actually going to go past resting membrane potential. Right? Resting membrane potential is up here in our graph, we're gonna undershoot that and the cell will actually have toe work to get back to resting memory and potential. And this time between Thea undershoot and actually getting back to the resting state. That is our refractory period. And it's important because it ensures that there won't be another action potential until the Selcan stabilize itself get back to its baseline. And it ensures that by inactivating those sodium channels, right, they're not just closed. Even if the cell were to experience a membrane potential that will allow those sodium channels toe open, no sodium still gonna get through because they've been inactivated because that ball and chain has plugged up the channel. So even if the voltage will allow them to open, no sodium is getting through. And that means no action potential until we hit this resting phase again. Okay, that is those of the phases of the action potential. Let's actually flip the page

neurons generate their electric currents by moving ions across the membrane and down along the ax on to propagate their action potentials. Now the diameter of an ax on will actually influence the speed of propagation of an action potential. Basically, the larger diameter is the lower the resistance, meaning faster action potentials, so larger diameter, faster action potential. But diameter is not the on leeway to speed up in action potential. In fact, our axons are almost all covered in Milan now. This is a fatty substance that insulate the ax on and actually speeds up the action potential. And this is very similar to how wires, for example, are wrapped in plastic or rubber to insulate their electric currents and cause them thio. Move with lower resistance. Move faster. No, the myelin sheath, as it's called, this fatty covering over axons, is generated by glial cells, but not by a single goal. I'll sell, and it's also not continuous. It has thes gaps that we call nodes of Rhonda, named after the guy who discovered them, and it actually takes multiple glial cells to cover the ax on of a neuron. So here you can see the glial cell of the central nervous system responsible for Milo Nation. That's Ah, just another way of saying a knacks on being covered in Milan. Write it down for you, Milo Nation. These are a Liga dangerous sites and you can see one right here. This isn't a leg, a dangerous site. It will actually multi mile innate multiple axons. And you can see that it is currently myelin aiding in this image. 123 different acts ons. And this stands in contrast to Schwann cells, which are glial cells of the peripheral nervous system responsible for Milo Nation. However, they Meilin ate a single acts on and I'm just gonna jump out of the way here. You can see that we have Schwann cells along or acts on right, and it actually takes multiple Schwann cells. 2,000,008, the ax on of this neuron. And you can also see the gap there. That is a note of Ron via. We also have nodes of Rhonda here. It's another node of Ron V a. So this mylan helps speed up action potentials. But hopefully you're thinking and you're saying Wait, if we're covering the ax on, how do we have ion channels there that can exchange ions with the extra cellular fluid. The answer is those ion channels air packed in the nodes of Rhonda. And this basically leads us to the crux of how an action potential moves along the ax on. Now it's termed salt hitori conduction. And basically, this is just a fancy way of saying that the action potential more or less jumps between thes nodes of Ron va along the ax on, and it essentially moves from one note of Ron via to the next. And what this sort of looks like is here. So here we have our open open ion channels, Right? Are action potential is currently here, and it's moving this way now because of these open ion channels, which are, if you concede here at a node, right, this is a node right here this opening in the Mylan. So here we have the action potential, right? Uh, the interior of the cell has become positive, the exteriors negative. That is our action potential. And it's moving along so literally, these sodium ions are going to defuse down the membrane to carry this action potential. Those ions air moving right electric current is flow of electric charges ions air moving. And when they get to the next note of Ron, Va. They're gonna cause deep polarization that will open the ion channels there and allow those sodium ions to rush in so that the action potential can keep moving along the axon. Now what's really cool that gets back to that whole concept of inactivation of the sodium channels is if you think about this, there's nothing preventing the action potential from moving backward, right? Nothing except inactivated sodium channels. You see where the action potential has just been. There are going to be inactivated sodium channels where the action potential is headed. Those sodium channels are Onley closed. They're not inactivated, meaning that even though as these sodium ions Russian at the location where the action potential currently is in the ax on and because there's nothing preventing them from diffusing in either direction. Even though we want the action potential moving this way, there's nothing preventing them from diffusing in either direction in the ax on. However, even if they get over here, these channels are inactivated, meaning, uh, these sodium ions causing deep polarization, aren't going thio do anything. The action potential. Can Onley move this way? Because Onley closed sodium channels will open when stimulated by a deep polarization by those sodium ions moving along the ax on. So again, this results in salt hitori conduction, which is basically just the propagation of the action potential along Meilin ated axons, where it hops from one road of note of Rhonda to the next. So with that, let's go ahead and flip the page.

what happens when the action potential reaches the end of its journey, When it makes its way to the ax on terminal and is ready to be converted into a chemical signal? Well, the ax on terminal will have formed a junction with another sell. This junction is called a synapse. It's that connection between neurons that allows them to pass signals along signals are almost always going to be traveling from the pre synaptic sell to the post synaptic cell. That is the cell that had the action potential moving through it to the cell on the other side of the synapse. Now, I say almost always, because there are some very notable exceptions, including the Endo Cannabinoid system, which throws these rules out the window. Also, the gas nitric oxide, which can act as a neurotransmitter, basically diffuses in any direction it pleases. It is not bound by these restrictions, however. We're not gonna be bothering really with those exceptions. So you can basically safely assume that synaptic transmission will, you know, basically always go from the pre synaptic sell to the post synaptic cell. It's not until you get into like, more advanced neuroscience stuff where you have to actually worry about those exceptions. So signals, as we've said, can be chemical neural transmitters. Right? The neuron will release neurotransmitters into the synapse. However, not all synapses are chemical synapses, some are electrical and we've actually seen these in other places. These air gap junctions, right? Those protein channels that connect cells together actually will allow the action potential to pass directly from one cell into another cell. Those are electrical synapses. However, we're going to be looking at chemical synapses, and these chemical synapses will contain voltage Gated calcium channels, Thes voltage. Gated calcium channels are critical to neurotransmitter release. So how does this actually all go down? Well, of course you're gonna begin with the action potential, finally making it to the acts on terminal of the pre synaptic cell. That is so here we have our sodium and potassium channels that allow the action potential to move its way along the ax on until it finally reaches the terminal. Here it's going to cause deep polarization and that deep polarization opens thes voltage. Gated calcium channels, thes voltage gated calcium channels will allow calcium ions into the cell. Thes calcium ions act as a signal to synaptic vesicles. Now, in the acts on terminal, you will have lots of these synaptic vesicles, and they are basically going to just be hanging around storing neural transmitters nt. So what? I mean, they're neural transmitters. When they get the calcium signal, they actually bind to the membrane of the acts on terminal and fuse with it. And in this process, they release. They're nure Otranto emitters into what's called the synaptic cleft, this space between the acts on terminal of the pre synaptic cell and the membrane of the post synaptic cell. So these neuro transmitters will diffuse across that gap that synaptic, cleft and bind to receptors on the post synaptic membrane. And in binding, these receptors will actually see the signal be transducer it to the other cell. Now there are going to basically be two kinds of receptors will see on that post synaptic membrane, their eye on a tropic receptors and Motaba tropic receptors, and you don't really need to worry about knowing these terms. I'm throwing them out because it just makes it easier to describe two different categories of post synaptic membrane receptors. So these I on a tropic receptors basically are just membrane receptors that act by opening an ion channel. Pretty simple. So by that, by virtue of that, essentially they are going to be ligand gated ion channels which we talked about before they open in response toe ligand binding like narrow transmitters. Narrow transmitters are a ligand. So here we have a neurotransmitter called acetylcholine. It will bind to this I on a tropic receptor which will open it and allow these ions to move in and out of the cell. Now, on the flip side, you have Motaba tropic receptors. These act through second messengers and they're often going to be G protein coupled receptors. So the neuro transmitter will bind, and then a bunch of stuff is gonna happen in the cell, and they can have a wide variety of effects. For example, they can lead Thio Uh, you know, increasing numbers of receptors on the membrane or they can actually also lead thio ions moving in and out of the cell. They're much more varied, whereas the eye on a tropic receptors are very cut and dry. Like in Bynes ions. Either come in or out of the cell with that, let's go ahead and flip the page

the binding of neurotransmitters will either increase the likelihood of an action potential or decrease the likelihood of an action potential occurring in the post synaptic cell. Now this is as a result of changes in the membrane potential of the post synaptic cell, and the's are going to be due to what are called excited Torrey Post synaptic potentials and inhibitory post synaptic potentials. So if there is a deep polarization of the post synaptic membrane, what we have is an excited Torrey Post synaptic potential or an E p S P. Because, boy, is that a mouthful. And this is a deep polarization of the membrane, which increases the chance of an action potential occurring now inhibitory post synaptic potentials or i ps ps will hyper polarized the membrane and decrease the chance of an action potential. Now remember, this could be happening through I on a Tropic or Motaba tropic receptors, but because it's probably a little easier to think about this in terms of I on a tropic receptors. If a nyongo tropic receptor allows positively charged ions in, we're going to have deep polarization, so it's going to be causing E P s ps if a ni on a tropic receptor allows negatively charged giants are an ions in It's going to cause a hyper polarization or a night PSP. Now e P s ps can actually be summed together. They can add to each other and d polarize the membrane potential up to the threshold of an action potential. So you can add E P s PS together to cross the threshold and cause an action potential. Right again, it's the E P s PS. Aren't going thio generate the action potential, They're going to get the celled across the threshold and then it will generate the action potential on its own. Now the sodium channels that will actually trigger the official action potential are located in the acts on hillock. So these excited Torrey post synaptic potentials have to carry their deep polarization from the Dent, writes to the axon hillock in orderto actually cause the action potential. Now there are two ways that you can combine thes post synaptic potentials. We think of them as temporal summations or spatial summations. Now, temporal summations are essentially when a bunch of these post synaptic potentials occur in quick succession and add together to become a larger deep polarization. So here we have. This is our pre synaptic cell, right? Here's are synapse right here. That's the synapse. And here is our post synaptic cell. So what's happening? Basically, if a high frequency of action potentials come in so that's like one. And then right after that, another and then right after that, another and so on and so forth that's going to lead to a lot of neurotransmitter release. And that's going to cause, ah, bunch of little deep polarization zones. Right? So let's say that's action potential number one And then this one was a result of action potential number two, and so on and so forth. Eventually these action potentials will some together and cross the threshold potential. And when they cross the threshold potential, it's action potential time, right? Boom were happening. Go through the whole process. So essentially with temporal summation, you have a quick succession of action potentials that lead to a quick succession of deep polarization that add together to cross the threshold. Now, spatial summation is basically when things happen at the same time, but in close proximity. So we have simultaneous action potentials, right, coming in together to the same post synaptic sell. They're gonna release their neurons. We're gonna get an E p s p over here and an E p s p over here too excited, Torrey Post synaptic potentials. And those will some together, as you can see here, here's number one Here's number two, and that will get them to cross the threshold or get the membrane potential to cross the threshold leading to an action potential. So these air two ways that post synaptic deep polarization can add together to actually lead the post synaptic sell to generate an action potential of its own. But remember that post synaptic potentials can also be inhibitory and can decrease the likelihood of an action potential. With that, let's go ahead and flip the page.

neurotransmitters are the signaling molecules of neurons but on their own they don't really do much. They need receptors in order to exert their effects and they're going to exert their effects when they bind to receptors. Now a single neurotransmitter will have many different types of receptors that it combined and it is the type of receptor it binds to that determines the effect of the neurotransmitter. So I'm making this distinction because I don't want you to think, oh this neurotransmitter has X effect. No this neurotransmitter binding to this particular receptor will have X effect. Now neurotransmitters have to be removed from the synapse after they've been released in order to have action potentials come in as discrete signals. You don't want to just pile up neurotransmitter in the synapse and leave it there because then you're not gonna be able to tell the difference between one signal and another. So Euro transmitters are removed by either re absorbing them and this is going to be a main job of glial cells. They're going to often be responsible for re absorbing neurotransmitters. So essentially sucking them up into those cells and removing them from the synapse or neurotransmitters can be degraded. They'll just be broken down in the synapse so that they can't bind to the receptors anymore. Now the first neuro transmitter I want to talk about is acetylcholine. Not because it's the most important but because it was the first one to be discovered by Otto Louie who actually believe it or not woke up in the middle of the night from a dream and in his dream, he had figured out how he was going to run an experiment on a frog heart to determine whether or not neurotransmitters existed more or less and guess what rest is history? His dream came true, so to speak. Now. Acetylcholine is a neurotransmitter used by the peripheral nervous system as well as the central nervous system and it does or it binding to its various receptors has a variety of different effects. So I'm not even going to try to generalize there, There is no generalizing here. In fact, to illustrate that point even better, let me tell you about the difference acetylcholine has if the neuro muscular junction versus heart. So the neuro muscular junction is the connection between motor neurons and muscles. It's basically a synapse, but technically because it's not between two neurons, it's considered a junction instead of a synapse. This is getting into nitty gritty jargon stuff that you don't need to worry about for your purposes. Please feel free to think of this as a synapse Now it is that connection between motor neurons and muscles and the receptors. There are going to be ion a tropic receptors, you don't need to worry about memorizing this name, just know that these are ion tropic receptors that will allow in ions. Acetylcholine actually has an excitatory effect at the neuro muscular junction and causes muscle contraction conversely in heart muscle as opposed to skeletal muscle. Acetylcholine has an inhibitory effect. So you see, really can't generalize with neurotransmitters, it excites one type of muscle inhibits contraction in in a different type of muscle. Now, acetylcholine will also have an inhibitory effect in some parts of the parasympathetic nervous system, which is a division of the peripheral nervous system. Now acetylcholine is removed from the synapse by degrading it with the enzyme settle colonist race. Another class of neurotransmitters is rather are the amino acids. These are amino acids which include glutamine, glycerine and Gabba. Gabba is what everyone calls it because its name is gamma amino butyric acid and no one wants to say that or write that. So Gabba it is please don't even worry about memorizing that name. Just know Gabba. So glutamate is going to be the major x excitatory neurotransmitter of the central nervous system that is, its binding to receptors often leads to excitation of the post synaptic cell. Whereas Gabba is the major inhibitory neurotransmitter of the central nervous system. So it's binding to its receptors will generally lead to hyper polarization of the post synaptic membrane. No Xanax is a very common drug prescribed for anxiety. It is part of a class known as benzodiazepines, Don't worry about that, saying it if you're curious and it will actually act on Gaba receptors technically it will act on a receptor called gaba a Now, you know what else acts on this receptor ethanol. Now, the reason I bring this up is because lots of people like to mix ethanol and Xanax and that's a really bad idea and I'm going to explain why biochemically now ethanol stimulates these Gaba receptors. It almost acts like Gaba. So when ethanol comes in contact with these Gaba receptors, they respond as if Gaba had been bound. Right? So ethanol stimulates those receptors. Xanax has an interesting effect on them. See these Gaba a receptors their ion channels right there, chloride or this is a chloride ion channel. What Xanax is actually going to do is keep the channel open longer so it modulates the effect of this channel. It causes it to become more effective at its job basically. So the reason you really don't want to combine ethanol and Xanax is because ethanol stimulates the receptor and Xanax causes it to stay open longer. This is an inhibitory neuro transmitter. It will depress various systems of the body and can actually lead to death. So please, next time you see someone do this, tell them not to because it's a very bad combination. Mono means are another class of neurotransmitter and they contain an amine and an aromatic ring and that's because they're derived from the aromatic amino acids or the amino acids that contain aromatic rings. There are three major types of Monami sorry, there are three uh types of mono means that I want you guys to know those are serotonin dopamine and norepinephrine serotonin is a well, it's the major transmitter of the enteric nervous system which is the nervous system around your gut. So very important there in the central nervous system though it's involved in feelings of happiness and I don't really want to try to make any more specific statements about serotonin. However, I will leave you with this. The drug known as ecstasy chemical name M. D. M. A. Acts on serotonin pathways and serotonin receptors and I just bring it up because it's street name is ecstasy, you know, and this neurotransmitter is involved in feelings of happiness. Hopefully you can put the connection together. Dopamine is actually a technically a cata cola mean, which is a subcategory of mono means dopamine is involved in reward pathways of the brain and actually dopamine is going to be the neurotransmitter that people focus on when talking about addiction. And a lot of illicit drugs will actually uh stimulate these dopamine reward pathways which reinforces that addiction now nor epinephrine is also a cat akala, mean and it acts as both a hormone and a neurotransmitter and it's used as a neurotransmitter in the sympathetic nervous system. So acetylcholine is the neurotransmitter of the parasympathetic nervous system. Norepinephrine is the neurotransmitter of the sympathetic nervous system and we'll talk more about those uh different divisions of the peripheral nervous system in a different lesson. Now neuro peptides are peptide neurotransmitters and they include things like substance P neuro peptide y ghrelin and endorphins. Now I only really want you to be aware of endorphins though ghrelin actually comes up in our lesson on uh the endocrine system because it is a hormone as well as a neuro peptide that is involved in appetite. Now endorphins, these the ones I want you to really know about these are endogenous opioids meaning there opioids produced by the body, that's what endogenous means. Now generally speaking, they're going to be involved in suppressing pain signals and inducing a sense of euphoria. Now the term opioid here hopefully jumps out at you because there's a whole class of drugs called opioids that stimulate these same receptors that endorphins do and that's why opioids are a major class of painkiller drugs right now I mentioned earlier nitric oxide, that's a gas that can act as a neurotransmitter and it doesn't obey those pre to post synaptic transmission rules. It diffuses widely and kind of just goes whichever way it wants. Now the last thing I want to talk about here are neurotoxins. We've talked about neurotransmitters but neurotransmitters aren't the only things that bind to these receptors. Right. In fact we've mentioned that this drug ecstasy interacts with serotonin receptors. So there are also poisons that can interact with these receptors. And neurotoxins are poisons that are destructive to nerve tissue. Now here I have a picture of a very angry looking puffer fish. Right? And puffer fish considered a delicacy in sushi restaurants is very dangerous to eat because it contains tetrodotoxin. This is a neurotoxin that prevents action potentials This neurotoxin blocks those sodium channels. So tetrodotoxin prevents action potentials from being fired and can very easily lead to death. That's why it takes a very skilled chef to prepare puffer fish. They have to make sure they, you know, don't cut into the areas that contain tetrodotoxin and remove the portions of the meat uh and you know, get them away from all those toxins. So with that, let's call it a day, See you guys next time.