[MUSIC] Okay, so what we just talked about was release. And that is release of neurotransmitter that is packaged into synaptic vesicles from the synaptic terminal. Well, the synaptic terminal, the point of that is to get a message across to a second cell. That's the post-synaptic cell. This meeting is the synapse. And these two neurons [COUGH], the cell with the synaptic terminal, which is the pre-synaptic cell, and the post-synaptic cell, they are separated by a short distance called the synaptic cleft. And the molecules of nerve transmitter are going to make their way over to here where they're going to be received. We'll talk about that in the final segment. But what we're going to talk about right now is the fact that, as you send this message out, as the synaptic terminal sends this message out, it has to have an endpoint. A message that doesn't have an endpoint is like a lecture that never ends, that's interminable. Not so good. So in order to make a punchy point, we have to have a beginning. We've got a great beginning because we know that release is triggered by an action potential, by calcium influx, an action potential. But now we need an end point and we use three different mechanisms to terminate the message of a neurotransmitter. One just happens naturally, which is diffusion. These molecules are going to diffuse out. And this post-synaptic cell has ears, but those ears are only concentrated right here. So if the molecule is over here, the cell isn't hearing about it. It doesn't matter. So diffusion is a very effective way to terminate, to end, contribute to the termination of a message. The second way is through something called re-uptake. And re-uptake [COUGH] is typically in the pre-synaptic terminal, there are channels or transporters. They're actually not channels, they're called transporters. And these transporters take this neurotransmitter back up. And you'll be happy to know that neurons totally believe in recycling. They're not going to let that neurotransmitter go to waste. They'll re-package it, they'll put it right back into a new vesicle, which is actually recycled as well, and so then this cycles back. So the neurotransmitter is taken up by these re-uptake transporters. So re-uptake is a really, really important way to terminate messages. And this is really important for drugs like serotonin and dopamine. And there are drugs that act on the serotonin and dopamine re-uptake transporters that can be used both therapeutically, for instance, to treat depression. And also that unfortunately engage circuits that lead to abuse of drugs. And so, for instance, cocaine acts on a dopamine transporter. The third way that we terminate a message is through degradation. And in the case of degradation, what we have is enzymes that sit out here in the synaptic cleft that are just chewing up this neurotransmitter. [SOUND] It's like Pac-Man. [SOUND] So they're just going to eat up this neurotransmitter and the molecule that the neurotransmitter where this is really, really important is acetylcholine. So in acetylcholine, there is a enzyme that sits in between the pre-synaptic and the post-synaptic cell, that eats up that acetylcholine. It eats it up a lot, so very little of it actually makes it all the way across the synaptic cleft. If you block that enzyme, and that enzyme is called acetylcholinesterase, which is abbreviated like that, if you block that, you'll have a lot of acetylcholine. Remember that acetylcholine is the neurotransmitter that is used by motor neurons. And so in fact, this blocking acetylcholinesterase can be used for therapeutics, in the case of people that are not releasing enough acetylcholine, or don't have enough receptors for the acetylcholine. We can boost the amount of acetylcholine in the cleft by inhibiting the acetylcholinesterase. And that's useful for people with diseases such as myasthenia gravis. People also use acetylcholinesterase inhibitors for nefarious purposes, and a lot of pesticides. Drugs such as ceron are based on blocking this, and the effect of that is that the acetylcholine, there's so much acetylcholine that floods this post-synaptic cell, which in the case of motor neuron is a muscle. So the motor neuron is talking to a muscle. And now the motor neuron is not ever shutting up. That means that the muscle is contracted, and it stays contracted. Well, it's okay to contract, but it's not okay to stay contracted. So imagine if your diaphragm stayed contracted, no more breathing. And so that's that's the problem with these acetylcholinesterase inhibitors. Okay, and in the final segment, we're going to look at receptors. How do we hear the message? How does the post-synaptic cell hear the message? [MUSIC]
