In this video I discuss some ways that drugs can influence the functioning of neurotransmitters by binding to receptors on postsynaptic neurons. I explain the difference between agonist drugs which increase effects of a neurotransmitter and antagonist drugs which reduce the effects of the neurotransmitter. I explain how nicotine acts as an agonist for the neurotransmitter acetylcholine and how neuroadaptation relates to addiction. Next I explain how caffeine acts an an antagonist for the neurotransmitter adenosine and how this relates to the familiar “crash” that people experience after using caffeine.

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Video Transcript:

Hi, I’m Michael Corayer and this is Psych Exam Review. In previous videos, we’ve seen how neurotransmitters can bind to receptor sites and influence the firing of postsynaptic neurons. In this video we’ll see how drugs can play a role in this process and influence a neurotransmitter’s functioning.

Now we can broadly divide the effects of drugs into being either agonists or antagonists. This refers to how the drug influences the neurotransmitter’s functioning at the receptor sites on a postsynaptic neuron. So an agonist drug is going to be a drug that increases the effects of the neurotransmitter on the postsynaptic neuron.

An agonist increases neurotransmitter effects while an antagonist drug decreases the effects of the neurotransmitter on the postsynaptic neuron.

So now let’s look at two common drugs to determine whether they would be considered agonists or antagonists for the neurotransmitters that they influence. It’s important to remember that these are simplifications so drugs can have multiple effects on different areas of the brain or different neurotransmitters and so we’re going to be focusing only on a single neurotransmitter and this is going to be a simplification. So remember that these aren’t the only possible effects of the drugs that I talk about in this video. So let’s start with a drug that’s fairly common, and this is nicotine.

So the neurotransmitter that’s influenced by nicotine is acetylcholine or ACh. So let’s imagine that we have some acetylcholine here and we’ll say that this is our nicotine over here and now let’s look at a postsynaptic neuron and we’ll give it some receptor sites for acetylcholine.

Ok, so what normally happens in this synapse is that acetylcholine would be released by presynaptic neurons and acetylcholine would travel across the synapse, bind to these receptor sites, and when it binds to these receptor sites what this does is it causes ion channels to open and this makes it easier for positive ions to flow into this neuron. This means it’s going to be more likely that this neuron fires an action potential. So acetylcholine normally opens the ion channels and increases the likelihood of this neuron firing. So what does nicotine do? How does nicotine get involved in this process?

Let’s again imagine we have some neuron here with receptors for acetylcholine and nicotine is gonna get into the bloodstream by inhaling smoke from a cigarette and that’s gonna carry it through the lungs into the bloodstream and then into the brain and what the nicotine does is if the nicotine gets into the synapse, it’s going to be able to bind to these same acetylcholine receptors.

The nicotine doesn’t just bind to these receptors, it actually causes those same ion channels to open. So the nicotine essentially plays the same role as the acetylcholine. This means that when we introduce nicotine into these neurons here we’re going to essentially boost the effect of acetylcholine. It’s going to be as if we have more acetylcholine in these synapses.

This means that nicotine is going to be an agonist for acetylcholine, it’s going to increase the effect of acetylcholine because it’s going to bind to the same receptors and cause the same ion channels to open. So you might be wondering, if you remember from a previous video, I said that acetylcholine plays a role in some brain areas associated with learning, memory, and attention. So you might be wondering, wouldn’t this be a great thing if we could just put in a bunch of nicotine, wouldn’t that boost these areas, wouldn’t we get some sort of benefit from using nicotine?

Unfortunately, it doesn’t really work like that because what happens is the brain responds to drugs. The brain tries to change itself to maintain normal functioning and what’s going to happen is if we keep flooding these synapses with nicotine, the brain’s going to think there’s too much acetylcholine here. Because the brain thinks that this is acetylcholine, it’s binding to those same receptors. So what’s going to happen is the brain is going to change, we have a process called neuroadaptation, where the brain changes itself and what it’s going to do, or one of the things it’s going to do, is it’s going to start adding receptors here. It’s going to reduce the sensitivity of this neuron.

It’s going to say, “ok, if you keep firing all the time, I’m going to make it harder for you to fire.” What this means is now, when we release acetylcholine, we might not have enough to actually cause this neuron to fire. We might not be able to do it on our own. So now we’re going to need the nicotine to be there to help out. And over time we’re going to need more and more of that nicotine because we’re going to keep making these neurons less and less sensitive to it.

So what happens is people who are addicted to cigarettes, they’re addicted to nicotine, this means that they can’t function normally without nicotine. They can’t produce enough acetylcholine to keep up with these desensitized cells. They need more and more nicotine over time to get the same level of functioning. When nicotine isn’t present, they try to quit, what they find is they have problems concentrating, they have difficulty, and this is going to continue until the brain starts adapting in the other direction. Until it says ok, now that there’s not so much going on here, we’re gonna make it easier for these neurons to fire. That process is going to take time, that’s why it’s hard for people to quit using nicotine immediately. It often takes time for them to adjust and for these cravings to reduce.

In a future video we’ll talk about other aspects, withdrawal and dependence and psychological addiction. But for now, that’s a general introduction to why nicotine is addictive. And that’s because of its agonist effects on these acetylcholine receptors.

Let’s look at another example of a drug and other common drug, and this is one that you probably use and this is because it’s the most commonly used psychoactive drugs in the world and this is caffeine. So caffeine has a relationship with a neurotransmitter called adenosine. This is a neurotransmitter that I didn’t talk about in the previous video but what adenosine does is it helps signal that we’re tired. It helps induce feelings of drowsiness.

So let’s imagine that we have some adenosine molecule here. And now let’s imagine that we have some caffeine molecule here. And let’s look at a neuron some part of a neuron here with some receptor sites for adenosine. Ok so normally what happens is adenosine is floating around in here. It gets released to signal feelings of drowsiness and tiredness and it binds to receptors and what the adenosine does when it binds to these receptors is that it signals for this neuron to inhibit function, it slows the neuron down. That’s why we feel drowsy or tired.

So what happens when we take in caffeine? Same receptors here on some neuron. Now we’re going to add some caffeine in here. Caffeine gets into the bloodstream, into the brain, and starts binding to these receptors. But in this case, the caffeine binds to the receptor but it doesn’t do anything. It doesn’t have that same inhibiting effect that the adenosine would have.

It doesn’t slow the neuron down. In fact, the neuron is going to speed up because it used to be getting adenosine signals but now the caffeine is blocking those signals. What happens is, over time, of course the adenosine keeps on building up because it can’t get to its receptors.

The caffeine is making us temporarily feel more alert and awake, as long as it’s blocking these receptors but the adenosine is still being produced and the adenosine is still floating around here. This means you can probably guess what’s coming. What happens is the caffeine doesn’t stay in your body permanently. We all know that you drink some caffeine it doesn’t have a permanent effect on you. It has a temporary effect and then it gets broken down by the body. So eventually this caffeine is going to get broken down.

Now you can see what happens when the caffeine gets broken down, is that we’ve accumulated lots of adenosine in the meantime. For a couple hours we were wide awake but the whole time we were producing more and more adenosine and this adenosine is suddenly going to rush to all of these receptor sites on all these neurons and this is why we’re going to experience this crash. We were blocking the effect of adenosine, caffeine is an antagonist for adenosine at these receptors sites, but when the caffeine is finally broken down, we have this sudden rush of adenosine. Or it feels like a sudden rush, it actually accumulated over time, and this is why we experience this caffeine crash a few hours later. You’ve probably experienced this yourself.

Ok, so those are some examples of an agonist drug and an antagonist drug at the receptor sites on postsynaptic neurons. I hope you found this helpful. If so, please like the video and subscribe to the channel for more.

Thanks for watching!