Neurons and Action Potentials - Video Tutorials & Practice Problems
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1
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Nervous System
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Hi. In this lesson, we'll be talking about the cells that compose the nervous system or neurons. 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, 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 under stood 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 glial cell. Technically, this is actually known as an And that actually comes from its almost star like appearance with all these appendages going out in every which way. Now, the nervous system can actually be, broken down into 2 components, the central nervous system and the peripheral nervous system. The central nervous system is going to be, 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 kinda 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.
2
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Neurons
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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 neurons are going to use a combination of electrical and chemical signaling. Now neurons actually do have a decent variety of morphologies, 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 to 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 axon, 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 axon. Now the axon 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 axon 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 gonna receive signals, not just from 1 neuron, but from a bunch of other neurons. And when two neurons connect, like at the terminal of the axon and the dendrites, what we have is known as a synapse. And this is a connection, between the axon terminal and the dendrites, and that is where, the electrical signal is going to be converted into a chemical signal. That chemical signal being neurotransmitters, 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 bit, 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 2 cells. In actuality there's going to be many many cells all connecting to each other and projecting, to faraway parts of the body quite frequently. So with that let's actually go ahead and turn the page.
3
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Central and Peripheral Nervous System
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Neurons and glia are what are going to make up 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, you 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 gala that will extend down from the brain and, 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 these little clusters of cell bodies that you'll see in the central nervous system as well, but they have a different name. So we call them ganglion or ganglia. A ganglion is the singular. Ganglia would be, you know, plural, multiple ganglions. And this is just a cluster of neuron cell bodies, and basically, what we'll see is the nerves will be, you know, made up of bundles of axons and often the neuron cell bodies will all be kind of clustered together in one place. Now these bundles of axons will actually be broken down into sort of 2 categories. We can have sensory neurons, and these are gonna be nerves that transmit sensory information, 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 effector organs like muscles and glands. So these are going to be the guys that actually send signals to do things like duck when you see that ball coming towards your face. Now, you'll also see what are called interneurons, and these are 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 connect to each other, and we'll see an example of that. What's important to note though is that interneurons are actually gonna be the main type of neuron in the brain. Now, with that, let's go ahead and flip the page.
4
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Membrane Potential
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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 this 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, 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 bottom. 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 a membrane. And so, if we take a look at this image down below, what you'll notice is that it represents a biological membrane here in the middle and what you'll notice is we have a bunch of ions on the left hand side which represents our extracellular 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 gradient exist as this image shows. So, in the extracellular 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 Ion. 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 anion on the outside of the cell and low concentration of chloride anion 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 there are going to be sodium ions pumped 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 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 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, we refer to this as the membrane potential. And so the membrane potential of course is going to involve the biological membrane. 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, what you'll 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. And so hyperpolarization is a term that refers to the membrane potential becoming more negative and depolarization is a term that refers to the membrane potential becoming more positive. And so we'll get to utilize these terms, more as we move forward in our course and discuss, neuronal signaling. And so, that here concludes this video, I'll see you all in our next one.
5
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Ion Channels and Pumps
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In order for ions to get from one side of the membrane to the other, they're gonna need ion channels. These are just protein channels that essentially form a pore through the membrane and allow for the passage of a specific ion. And that's pretty key to note here that these ion channels are going to be selective for specific ions. Now, these ion 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, special type of ion channels that I want to briefly mention 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 you 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, these 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 real stars of the show are the gated ion channels. These are the guys who are gonna be critical to, neurons sending electric signals. And these are ion channels that, open or close in response to stimuli, so they're gated by some signal that they have to receive. And we're going to see, 2 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, you know, kind of crazy stuff here, but basically these ion channels will open in response to specific membrane potentials. And these are gonna be the particular types of gated ion channels that are crucial to sending electric signals through, the axon, or through neurons in general. So we're really gonna be focusing on 2 types here. Sodium channels, which you can see here in blue, and let me just write it in red 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. No ions are getting through the membrane. So, sodium channels just like that, they have an a closed state and an open state, but they also have this special state we call inactivated. And usually it's, 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, 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 to not allow any ions through. So 3 states, closed, open, inactivated. Ions only will flow through in the in in the open state, and the significance of the inactivated state will become clear in just a moment when we actually talk about the steps of the action potential. So the other, ion mover, shall we say, that is critical for maintaining and establishing membrane potentials, these sodium potassium pumps or nakat piases, I like to call it. Now these are pumps that, you know, 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 I say actively there meaning ATP is consumed, and they're gonna pump 3 sodium ions out of the cell and they're gonna bring 2, potassium ions into the cell. And this is with each cycle. You can't get rid of the sodium ions and not bring in potassium ions. It's it's like 3 go out, 2 come in, 1 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 3 sodium ions that leave the cell, this is out, this is in, and we have, I'm gonna jump out of the way here, these 2 potassium ions that come into the cell. Okay. So there is a special type of potential which we call equilibrium potential, and this is gonna get back to those leak channels. Basically, it's the membrane potential at which point there's no net movement of an ion 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. They're there's no change, there's no net movement here. Now why is this important? Well remember that there's both concentration gradients and these electric potential gradients that are acting on the ions. Right? Now, those leak channels we mentioned before, they are going to allow potassium to leak out of the cell along its concentration gradient. 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 gradient that causes sodium, or 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 write as, e with little k under there, it's gonna reach its equilibrium potential, where basically the force driving it to move along its concentration gradient will be balanced with the force trying to drive it inward with against its concentration gradient, but with its electrical gradient. So those leak channels actually will get potassium to, hit a point of equilibrium potential when the cell is at rest. Alright. With that let's go ahead and flip the page.
6
concept
Action Potential
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There's a very special series of events that will happen when a cell's 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 amplitudes, and it's the differences in those magnitudes that are going to code the information. Now action potential is all or nothing. It is a binary signal. It's either on or off. It is 0 or 1. And it is a transient shift in membrane potential, so it's a change in membrane potential that does not last very long, and it sends this all or none signal. So if an action potential is sent, that's a 1. If there is no action potential, that's a 0. And the intensity of a signal, like, for example, if you want to, send a signal basically telling your muscle to contract just a little bit, versus sending a signal to like really hard, you know, super contract it. The difference in those signals, they're all, you know, they're all being, sent as 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. It's all or nothing. There is no difference in 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 series of events that are going to occur, across the membrane of a neuron, and it's going to result in an electric signal being sent down the axon. So essentially, you're gonna 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 axon membrane, those are gonna be closed. Now in what's termed the rising phase, the, membrane potential is going to be depolarized. And remember that means it's going to get more positive or less negative, however you want to think about it. And this is, this depolarization is going to cause some of these voltage gated sodium channels, around the membrane to actually open. Now, there is a special membrane potential which we call the threshold, And this is essentially, a point, a a point in membrane potential that if crossed, it's 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 gradient, that's what I'm trying to symbolize here, concentration gradient, and because of the negative charge inside the cell. So when the threshold is reached and those voltage gated, that voltage gated sodium channels open, sodium is just going to rush into the cell full steam ahead. Now, remember that the inside of the cell is negative, but we have a huge influx of cations. This is going to depolarize the membrane potential. So here, if we look at our chart, we started off with resting phase. Right? We have our our voltage, this is our mem essentially our membrane potential here. It's resting at this negative value, but due to depolarizations 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, essentially, when the sodium channels reach this super depolarized point, they are going to become inactivated. And the potassium channels, which are also voltage gated, but gated to open, at these, you know, depolarized potentials. So here, in the following 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 channel is open. Now remember, at rest, those potassium ions are more or less gonna be at their equilibrium potential. Right? Their, their concentration gradient causes them to want to leave the cell, and the electrical gradient 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 are now depolarized, right? We're at about plus 40 millivolts. So essentially, the inside of our cell 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 cell. So potassium is gonna want to go out of the cell because of the concentration gradient, 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 efflux of cations, all these leaving cations, cause repolarization of the membrane potential. So our membrane potential is gonna go back down. Here's the thing, it actually is going to undershoot resting membrane potential. And that's because of this refractory period, which is essentially the time during which another action potential cannot be generated because our potassium channels are inactivated. And no potassium is getting through, some sodium channels are still open, right, so that's actually going to cause this hyperpolarization, that's what we refer to this as. It's a hyperpolarization because we're actually gonna 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 to work to get back to resting membrane potential. And this time between, the 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 cell can 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 to open, no sodium is still going to 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 are the phases of the action potential. Let's actually flip the page.
7
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Myelin and Saltatory Conduction
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7m
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Neurons generate their electric currents by moving ions across the membrane and down along the axon to propagate their action potentials. Now, the diameter of an axon will actually influence the speed of propagation of an action potential. Basically, the larger a diameter is the lower the resistance, meaning faster action potentials. So, larger diameter, faster action potential. But diameter is not the only way to speed up an action potential. In fact, our axons are almost all covered in myelin. Now, this is a fatty substance that insulates the axon 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 to, move with lower resistance, move faster. Now, the myelin sheath, as it's called, this fatty covering over axons, is generated by glial cells, but not by a single glial cell, and it's also not continuous. It has these gaps that we call nodes of Ranvier, named after the guy who discovered them, and it actually takes multiple glial cells to cover the axon of a neuron. So here you can see the glial cell of the central nervous system responsible for myelination. That's just another way of saying an axon being covered in myelin. Write it down for you. Myelination. These are oligodendrocytes and you can see one right here. This is an oligodendrocyte. It will actually myelinate multiple axons, and you can see that it is currently myelinating in this image, 1, 2, 3 different axons. And this stands in contrast to Schwann cells, which are glial cells of the peripheral nervous system responsible for myelination. However, they myelinate a single axon. And I'm just gonna jump out of the way here. You can see that we have Schwann cells along our axon. Right? And it actually takes multiple Schwann cells to myelinate the axon of this neuron. And you can also see the gap there, that is a node of Ranvier. We also have nodes of Ranvier here. This is another node of Ranvier. So this myelin helps speed up action potentials. But hopefully you're thinking and you're saying, wait, if we're covering the axon how do we have ion channels there that can exchange ions with the extracellular fluid? The answer is those ion channels are packed in at the nodes of Ranvier. And this basically leads us to the crux of how an action potential moves along the axon. Now, it's termed saltatory conduction, and basically this is just a fancy way of saying that the action potential more or less jumps between these nodes of Ranvier along the axon, and it essentially moves from one node of Ran BA to the next, and what this sort of looks like is here. So here we have our open ion, open ion channels, right. Our action potential is currently here and it's moving this way. Now because of these open ion channels, which are if you can see here, at a node. Right? This is a node right here. This opening in the myelin. So here we have the action potential. Right? The interior of the cell has become positive, the exterior is negative. That is our action potential and it's moving along. So literally, these sodium ions are going to diffuse down the membrane to carry this action potential. Those ions are moving. Right? Electric current is flow of electric charges. Those ions are moving. And when they get to the next node of Ranvier, they're gonna cause depolarization 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 only closed, They're not inactivated. Meaning that even though as these sodium ions rush in at the location where the action potential currently is in the axon, 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 axon. However, even if they get over here, these channels are inactivated, meaning, these sodium ions causing depolarization aren't going to do anything. The action potential can only move this way because only closed sodium channels will open when stimulated by a depolarization by those sodium ions moving along the axon. So again, this results in saltatory conduction, which is basically just the propagation of the action potential along myelinated axons where it hops from one node of Ranvier to the next. So with that, let's go ahead and flip the page.
8
concept
The Synapse
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What happens when the action potential reaches the end of its journey when it makes its way to the axon terminal and is ready to be converted into a chemical signal. Well, the axon terminal will have formed a junction with another cell. 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 presynaptic cell to the postsynaptic 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 endocannabinoid 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 going to be bothering really with those exceptions, so you can basically safely assume that synaptic transmission will, you know, basically always go from the presynaptic cell to the postsynaptic 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 neurotransmitters. Right? The neuron will release neurotransmitters into the synapse. However, not all synapses are chemical synapses, some are electrical and we'd actually seen these in other places. These are 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. So those are electrical synapses. However, we're gonna be looking at chemical synapses and these chemical synapses will contain voltage gated calcium channels. These voltage gated calcium channels are critical to neurotransmitter release. So how does this actually all go down? Well, of course, you're going to begin with the action potential finally making it to the axon terminal of the presynaptic cell that is. So, here, we have our sodium and potassium channels that allow the action potential to move its way along the axon until it finally reaches the terminal, here, it's going to cause depolarization and that depolarization opens these voltage gated calcium channels. These voltage gated calcium channels will allow calcium ions into the cell. These calcium ions act as a signal to vesicles. Now, in the axon terminal, you will have lots of these synaptic vesicles and they are basically going to just be hanging around storing neurotransmitters. NT. That's what I mean there. Neurotransmitters. When they get the calcium signal, they actually bind to the membrane of the axon terminal and fuse with it and in this process, they release their neurotransmitters into what's called the synaptic cleft. This space between the axon terminal of the presynaptic cell and the membrane of the postsynaptic cell. So, these neurotransmitters will diffuse across that gap, that synaptic cleft and bind to receptors on the postsynaptic membrane And in binding these receptors, we'll actually, see the signal be trans induced to the other cell. Now there are going to basically be 2 kinds of receptors we'll see on that postsynaptic membrane, they're ionotropic receptors and metabotropic 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 2 different categories of postsynaptic membrane receptors. So, these ionotropic 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 to ligand binding like neurotransmitters. Neurotransmitters are a ligand. So, here we have a neurotransmitter called acetylcholine. It will bind to this ionotropic receptor which will open it and allow these ions to move in and out of the cell. Now, on the flip side, you have metabotropic receptors. These act through second messengers and they're often going to be g protein coupled receptors. So the neurotransmitter will bind and then a bunch of stuff's going to happen in the cell and they can have a wide variety of effects. For example, they can lead to, you know, increasing numbers of receptors on the membrane or they can actually also lead to ions moving in and out of the cell. They're much more varied whereas the ionotropic receptors are very cut and dry. Ligand binds, ions either come in or out of the cell. With that, let's go ahead and flip the page.
9
concept
Postsynaptic Potentials and Summation
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The binding of neurotransmitters will either increase the likelihood of an action potential, or decrease likelihood of an action potential occurring in the postsynaptic cell. Now this is as a result of changes in the membrane potential of the postsynaptic cell, and these are going to be due to what are called, excitatory postsynaptic potentials and inhibitory postsynaptic potentials. So if there is a depolarization of the postsynaptic membrane, what we have is an excitatory postsynaptic potential, or an EPSP because, boy, is that a mouthful. And this is a depolarization of the membrane, which increases the chance of an action potential occurring. Now inhibitory postsynaptic potentials, or IPSBs, will hyperpolarize the membrane and decrease the chance of an action potential. Now remember, this can be happening through ionotropic or metabotropic receptors. But because it's probably a little easier to think about this in terms of ionotropic receptors, if an ionotropic receptor allows positively charged ions in, we're going to have depolarization, so it's going to be causing EPS fees. If an ionotropic receptor allows negatively charged ions, or anions in, it's going to cause a hyperpolarization or an IPSP. Now, EPSPs can actually be summed together. They can add to each other and depolarize the membrane potential up to the threshold of an action potential. So you can add EPSPs together to cross EPSPs aren't going to generate the action potential, they're going to get the cell to cross the threshold and then it'll generate the action potential on its own. Now the sodium channels that will actually trigger the official action potential are located in the axon hillock. So these excitatory postsynaptic potentials have to carry their depolarization from the dendrites to the axon hillock, in order to actually cause the action potential. Now, there are 2 ways that you can combine, these postsynaptic potentials. We think of them as temporal summations or spatial summations. Now temporal summations are essentially when a bunch of these postsynaptic potentials, occur in quick succession and add together to become a larger depolarization. So here we have, this is our pre synaptic cell. Right? Here's our synapse right here, that's the synapse, and here is our postsynaptic cell. So, what's happening? Basically, if a high frequency of action potentials come in, so that's like 1, and then right after that another, and then right after that another, and so on and so forth, it's gonna lead to a lot of neurotransmitter release. And that's going to cause a bunch of little depolarizations. Right? So let's say that's action potential number 1, and then this one was a result of action potential number 2, and so on and so forth, eventually, these action potentials will sum together and cross the threshold potential. And when they cross the threshold potential, it's action potential time. Right? Boom. We're 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 depolarizations 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 postsynaptic cell, they're gonna release their neurons, we're gonna get an EPSP over here and an EPSP over here, 2 excitatory postsynaptic potentials, and those will sum together, as you can see here. Here's number 1, here's number 2, 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 are two ways that postsynaptic depolarizations can add together to actually lead the postsynaptic cell to generate an action potential of its own. But remember that postsynaptic potentials can also be inhibitory and can decrease the likelihood of an action potential. With that, let's go ahead and flip the page.
10
concept
Neurotransmitters
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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 gonna exert their effects when they bind to receptors. Now a single neurotransmitter will have many different types of receptors that it can bind, 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 wanna just pile up neurotransmitter in the synapse and leave it there because then you're not going to be able to tell the difference between one signal and another. So neurotransmitters are removed by either reabsorbing them, and this is going to be a main job of Lyle cells, they're going to, often be responsible for reabsorbing 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 neurotransmitter I wanna talk about is acetylcholine. Not because it's the most important, but because it was the first one to be discovered by Otto Lawy, who actually, believe it or not, woke up in the middle of the night from a dream, and in his dream, he 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. This 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 gonna 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 at the neuromuscular junction versus heart. So the neuromuscular junction is the connection between motor neurons and muscles. It's basically a synapse, but technically, because it's not between 2 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 a synapse. Now, it is that connection between motor neurons and muscles, and the receptors there are gonna be ionotropic receptors. You don't need to worry about memorizing this name, just know that these are ionotropic receptors that will allow in ions. Acetylcholine actually has an excitatory effect at the neuromuscular 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 a 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. Synapse by degrading it with the enzyme acetylcholinesterase. Another class of neurotransmitters is, or rather, are the amino acids. These are, amino acids which include glutamine, glycine, and GABA. Now, GABA is what everyone calls it because its name is gamma Aminobutyric acid, and no one wants to say that or write that. So, GABA it is. Please don't even worry about memorizing that name, just know GABA. So glutamate is going to be the major excitatory neurotransmitter of the central nervous system. That is, its binding to receptors often leads to excitation of the postsynaptic cell, whereas GABA is the major inhibitory neurotransmitter of the central nervous system. So its binding to its receptors will generally lead to hyperpolarization of the postsynaptic membrane. Now, Xanax is a very common drug prescribed for, anxiety. It is part of a class known as Benzodiazepines, don't worry about that, just 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, they're ion channels. Right? They're chloride, or this is a chloride ion channel. What Xanax is actually gonna 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 neurotransmitter, 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. Now, monoamines 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 amino acids that contain aromatic rings. There are 3 major types of monomy sorry, there are 3 types of monoamines 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 MDMA, acts on serotonin pathways and serotonin receptors. And I just bring it up because its street name is ecstasy, you know, in, this neurotransmitter is involved in feelings of happiness, hopefully you can put the connection together. Dopamine is actually a, technically a catecholamine, which is a subcategory of monoamines, And 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, stimulate these dopamine reward pathways, which reinforces that addiction. Now, Norepinephrine is also a catecholamine, 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, different divisions of the peripheral nervous system, in a different lesson. Now, neuropeptides are peptide neurotransmitters, and they include things like substance p, neuropeptide y, ghrelin, and endorphins. Now, I only really want you to be aware of endorphins. Though, ghrelin actually comes up in our lesson on, the endocrine system because it is a hormone, as well as a neuropeptide, that is involved in appetite. Now, endorphins, these are the ones I I want you to really know about, these are endogenous opioids, meaning they are 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 pain killer 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 postsynaptic transmission rules. It it diffuses widely and kinda just goes whichever way it wants. Now the last thing I wanna talk about here are neurotoxins. We've talked about neurotransmitters, drug, ecstasy, interacts with serotonin receptors. 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. 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, and, you know, get them away from all those toxins. So with that, let's call it a day. See you guys next time.