Neurons and Action Potentials: Videos & Practice Problems

The nervous system consists of neurons and glial cells, with neurons transmitting electrical and chemical signals. Neurons have a cell body, axon, and dendrites, forming synapses for communication. Action potentials are all-or-nothing signals generated when the membrane potential reaches a threshold, influenced by ion channels and the sodium-potassium pump. Myelination by oligodendrocytes and Schwann cells enhances signal speed through saltatory conduction. Neurotransmitters, such as acetylcholine and GABA, bind to receptors, leading to excitatory or inhibitory postsynaptic potentials, ultimately determining action potential generation in the postsynaptic cell.

Nervous System

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. However, 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 glial cell. Technically, this is actually known as an astrocyte, 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 two components: the central nervous system and the peripheral nervous system. The central nervous system is 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 going to 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

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. Neurons 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. 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 going to 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 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 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.

Central and Peripheral Nervous System

Neurons and glia make up the central nervous system and the peripheral nervous system. 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? This is the sensory information that your brain processes, and then it coordinates a response and sends it out to your peripheral nervous system to actually act out that movement. The brain is really like the control center for all of this, and the spinal cord is essentially just a bundle of neurons and glia that extend down from the brain, branching out into all the different nerves of the peripheral nervous system.

The peripheral nervous system sends signals to and from the brain and spinal cord and contains little clusters of cell bodies that are also seen in the central nervous system, but they have a different name. We call them ganglia; 'ganglion' is the singular, and 'ganglia' would be the plural. This is just a cluster of neuron cell bodies. The nerves are made up of bundles of axons, and often the neuron cell bodies are all clustered together in one place. These bundles of axons are broken down into two categories: sensory and motor neurons. Sensory neurons transmit sensory information ultimately to the brain and spinal cord, bringing in information from our sensory systems. Motor neurons project from the spine out to effector organs like muscles and glands, sending signals to act, such as ducking when you see a ball coming towards your face.

You will also see what are called interneurons, which are neurons that transmit information between other neurons. They connect, sometimes, sensory and motor neurons, although sometimes sensory and motor neurons will directly connect to each other. What's important to note, however, is that interneurons are the main type of neuron in the brain. Now, with that, let's go ahead and flip the page.

Membrane Potential

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. The first term we're going to introduce here is electric current. Electric current can be defined as the flow of electric charge. When you think of an electric current, you may think of an image with a battery, and electrons will flow through a wire and be used to power a device such as a light bulb. However, electric currents do not necessarily require the flow of electrons; in fact, the electric current utilized by neuronal signaling will be ions, and the flow of ions will generate this electric current. The term electric potential refers to the electric potential energy per unit of charge and is measured in units of volts, abbreviated as V. The term voltage refers to the difference in electric potential between two points and results from differences in charge. If we look at our image, towards the top, we have positive charges, and towards the bottom, we have negative charges. Because there is a difference in electric potential between these two points, there exists a voltage here in this image. If we were to place a positively charged particle here, it would repel all the positive charges towards the top and be attracted towards the negative charges towards the bottom. This particle would make its way and move towards the negative charges.

When it comes to neuronal signaling, the electric potential can be created using an electrochemical gradient. This gradient is the combination of a chemical concentration gradient and an electric potential gradient across a membrane. Looking at the image below, it represents a biological membrane in the middle, with a bunch of ions on the left hand side representing our extracellular space, and a bunch of ions on the right hand side representing the intracellular space inside the cell. In the extracellular space, there tends to be a high concentration of sodium ions, labeled as high, and as you cross the membrane towards the inside of the cell, there's a low concentration of sodium ions. The potassium ion concentration is opposite of the sodium ion concentration, with a high concentration of potassium inside the intracellular space and a low concentration on the outside of the cell. The chloride ion concentration resembles that of the sodium ion, with high concentration of chloride ions on the outside of the cell and a low concentration on the inside.

The cell creates these concentration gradients through utilizing ion channels or membrane proteins that can transport ions. Sodium ions are actively pumped towards the outside of the cell, creating a high concentration on the exterior and potassium ions are pumped towards the inside. More sodium is pumped out than potassium is pumped in, resulting in a build up of positive charge on the outside of the cell. This is critical to remember as on the outside of the cell, there is a net positive charge and on the inside, there's a net negative charge across the membrane. This results in a voltage across the membrane, referred to as the membrane potential. The membrane potential is the difference in electric potential between the interior and exterior of a cell, separated by the membrane. When the cell is in a resting state, it will have a resting membrane potential which is negative, indicating that the inside of the cell is more negative with respect to the outside which is more positive. However, the membrane potential can change, which will be critical when we start to look at neuronal signaling. Hyperpolarization refers to the membrane potential becoming more negative, and depolarization refers to it becoming more positive.

We will utilize these terms more as we move forward in our course and discuss neuronal signaling. That concludes this video; I'll see you all in our next one.

Ion Channels and Pumps

In order for ions to get from one side of the membrane to the other, they're going to 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 in neurons, which we're going to learn about in just a second, which are called action potentials. Now, there are these special types 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 potential in there. Now the real stars of the show are the gated ion channels. These are the guys who are going to be critical to neurons sending electrical 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 going to be the particular types of gated ion channels that are crucial to sending electrical signals through the axon, or through neurons in general. So we're really going to 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 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 ion channel, and given 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 to not allow any ions through. So 3 states, closed, open, inactivated. Ions will only 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 the steps of the action potential. So the other ion mover, shall we say, that is critical for maintaining and establishing membrane potentials, are these sodium-potassium pumps or Na⁺ K⁺-ATPases, as I like to call it. Now these 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 going to pump 3 sodium ions out of the cell and they're going to bring 2 potassium ions into the cell. And

Action Potential

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 is 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 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 contract it really hard, the difference in those signals, they're all 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 occur across the membrane of a neuron and results in an electric signal being sent down the axon. 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 axon membrane, those are going to 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 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 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 going to be thrown open. And because of the way the membrane potential has been established, where sodium ions want to move into the cell, both because of their concentration gradient and because of the negative charge inside the cell. So when the threshold is reached and those 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 the resting phase. Right? We have our voltage, this is 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, 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 depolarized potentials. So here, in the following phase, we're going to have our potassium ions flowing out of the cell. They're going to rush out of the cell because the voltage-gated potassium channels are open. Now remember, at rest, those potassium ions are more or less going to be at their equilibrium potential. Right? 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; we're at about plus 40 millivolts. So essentially, the inside of our cell has become positive at this point. So now, potassium is going to have the double whammy that sodium had before. Right? Now potassium is going to want to move, so sodium is going to go in the cell. So potassium is going to 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 going to 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 going to go past the resting membrane potential. Right? Resting membrane potential is up here in our graph; we're going to undershoot that. And the cell will actually have to work to get back to resting membrane potential. And this time between the undershoot and getting back to the resting state 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 would allow those sodium channels to open, no sodium is still going to get through because they've been inactivated because that ball and chain have plugged up the channel. So even if the voltage would allow them to open, no sodium is getting through, and that means no action potential until we hit this resting phase again. Okay. That's the phases of the action potential. Let's actually flip the page.

Myelin and Saltatory Conduction

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 Ranvier to the next, and what this sort of looks like is here. So here we have our 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 a 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.

The Synapse

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've 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 going to 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 its way to the axon terminal of the presynaptic cell. 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 transduced 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 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.

Postsynaptic Potentials and Summation

The binding of neurotransmitters will either increase the likelihood of an action potential or decrease the likelihood of an action potential occurring in the postsynaptic cell. This is a result of changes in the membrane potential of the postsynaptic cell, and these changes are 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. This is a depolarization of the membrane, which increases the chance of an action potential occurring. Now, inhibitory postsynaptic potentials, or IPSPs, will hyperpolarize the membrane and decrease the chance of an action potential. Remember, this can happen 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 EPSPs. If an ionotropic receptor allows negatively charged ions, or anions in, it's going to cause hyperpolarization or an IPSP.

Now, EPSPs can 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 the threshold. 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. 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 to actually cause the action potential.

There are two ways that you can combine these postsynaptic potentials: temporal summations or spatial summations. Temporal summations are when a bunch of these postsynaptic potentials occur in quick succession and add together to become a larger depolarization. So, here we have this scenario: this is our presynaptic cell, here's our synapse, and here is our postsynaptic cell. Basically, if a high frequency of action potentials comes in, like one, and then right after that another, and so on, it’s going to lead to a lot of neurotransmitter release. That's going to cause a bunch of small depolarizations, eventually summing together and crossing the threshold potential. When they cross the threshold potential, it's action potential time. 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.

Spatial summation is when things happen at the same time but in close proximity. So, we have simultaneous action potentials coming together to the same postsynaptic cell, which will release neurotransmitters, generating an EPSP over here and an EPSP over there, two excitatory postsynaptic potentials that will sum together. Here’s number 1, here’s number 2, and that will allow them to cross the threshold, leading to an action potential. These are two ways that postsynaptic depolarizations can add together to lead the postsynaptic cell to generate an action potential of its own. However, 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.

Neurotransmitters

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 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 want to 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 glial cells, they're going to often be responsible for reabsorbing neurotransmitters, 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 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 Loewi, 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? The 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 its binding to its various receptors has a variety of different effects. So I'm not even going to try to generalize; 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 the 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 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 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, you really can't generalize with neurotransmitters. It excites one type of muscle, inhibits contraction 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 glutamate, 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 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 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 three types of monoamines that I want you guys to know. Those are serotonin, dopamine, and norepinephrine. Serotonin is, 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 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 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 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, drugs, 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. They have to make sure they don’t cut into the areas that contain tetrodotoxin and remove the portions of the meat, and get them away from all those toxins. So with that, let's call it a day. See you guys next time.

Here’s what students ask on this topic:

What is the role of myelin in action potential propagation?

Myelin is a fatty substance that insulates axons, significantly enhancing the speed of action potential propagation. It acts similarly to insulation on electrical wires, reducing resistance and allowing faster signal transmission. Myelin is produced by glial cells, specifically oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. The myelin sheath is not continuous; it has gaps known as nodes of Ranvier. These nodes are crucial because they contain ion channels that facilitate the rapid jumping of action potentials from one node to the next, a process called saltatory conduction. This jumping mechanism allows action potentials to travel much faster along myelinated axons compared to unmyelinated ones, ensuring efficient communication within the nervous system.

How do neurons transmit signals using action potentials?

Neurons transmit signals through action potentials, which are rapid changes in membrane potential. This process begins with depolarization, where voltage-gated sodium channels open, allowing Na⁺ ions to enter the neuron, making the inside more positive. If the depolarization reaches a threshold, an action potential is triggered. The action potential propagates along the axon as the depolarization causes adjacent sodium channels to open. Following this, repolarization occurs as voltage-gated potassium channels open, allowing K⁺ ions to exit, restoring the negative membrane potential. The action potential travels down the axon to the axon terminal, where it triggers the release of neurotransmitters into the synapse, facilitating communication with the next neuron. This all-or-nothing process ensures precise and rapid signal transmission.

What are the differences between excitatory and inhibitory postsynaptic potentials?

Excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) are changes in the membrane potential of a postsynaptic neuron. EPSPs occur when neurotransmitters bind to receptors, causing depolarization by allowing positively charged ions, like Na⁺, to enter the cell. This increases the likelihood of reaching the threshold for an action potential. In contrast, IPSPs result from neurotransmitter binding that causes hyperpolarization, often by allowing negatively charged ions, like Cl^-, to enter the cell. This makes the membrane potential more negative, decreasing the likelihood of an action potential. The balance between EPSPs and IPSPs determines whether a neuron will fire an action potential, thus playing a crucial role in neural communication and processing.

How do neurotransmitters influence neuronal communication?

Neurotransmitters are chemical messengers that facilitate communication between neurons at synapses. When an action potential reaches the axon terminal, it triggers the release of neurotransmitters into the synaptic cleft. These molecules bind to specific receptors on the postsynaptic neuron, influencing its membrane potential. Depending on the type of receptor and neurotransmitter, this can result in excitatory or inhibitory postsynaptic potentials. Excitatory neurotransmitters, like glutamate, increase the likelihood of an action potential, while inhibitory neurotransmitters, like GABA, decrease it. The precise effect of a neurotransmitter depends on the receptor it binds to, highlighting the complexity and specificity of neuronal communication. This process is essential for various physiological functions, including muscle contraction, mood regulation, and sensory perception.

What is the significance of the sodium-potassium pump in neurons?

The sodium-potassium pump is crucial for maintaining the resting membrane potential of neurons. It actively transports three Na⁺ ions out of the cell and two K⁺ ions into the cell using ATP. This creates a concentration gradient, with a higher concentration of Na⁺ outside and K⁺ inside the neuron. This gradient is essential for the generation and propagation of action potentials. By maintaining a negative resting membrane potential, the pump ensures that neurons are ready to respond to stimuli. Additionally, the pump helps restore the ion balance after an action potential, allowing the neuron to return to its resting state and be ready for subsequent signals. This active transport mechanism is vital for neuronal excitability and function.