[MUSIC] Okay, so we've almost come full circle. Now, we've released a message from the presynaptic terminal and the issue here, the next hurdle is to make sure that the postsynaptic cell receives that message. And receives it through a type of protein, these are actually multi protein complexes called receptors. And receptors are going to populate this postsynaptic membrane, so that as your transmitter makes its way across the synaptic cleft, some portion of it that which is not either diffused away, taken back up through reuptake or degrade it through enzymatic degradation. So the survivors will actually make it over to these receptors. Now lets just take a look at what the receptors look like. Here's the cell membrane and these are transmembrane protein complexes and they form an actual pore and through this pore, the ions can travel. So the potassium ions can go out, the sodium ions can come in, chloride ions can come in, things like that. So, normally these receptors are closed, dions can't come in. But when a neurotransmitter binds to the receptor or a couple of neurotransmitter molecules bind to the receptor, the receptors now going to open and pore becomes available for, as a highway for the ions to travel along. And which way they travel? Depends on the type of receptor and so as it turns out, we have two basic classes of receptors, there are receptors that have an excitatory effect. And so once again if we return to our cell, which is sitting [COUGH] at -65 millivolts, any receptor that takes the membrane potential closer to 0 and closer to this magical place that is the threshold for an action potential if you go closer to that, that's an excitatory receptor. On the other hand, if there is a receptor that actually takes the membrane potential away from zero makes even more negative, then, this taking us away from the threshold for the action potential, and so that is an inhibitory [COUGH] receptor. So they come in two flavors, and the most ubiquitous excitatory receptor is a a glutamate receptor. And the most ubiquitous inhibitory receptor is a GABA receptor. The neurotransmitter involved is the same thing. So, the neurotransmitter involved that binds to the inhibitory GABA receptor is a GABA molecule. And the neurotransmitter that binds to the excitatory glutamate receptor is glutamyl. Okay, so that's how these receptors receive the message and they integrate all this incoming information to either make it more likely for them to fire an action potential or less likely to fire an action potential. If they're more likely, if this cell has an action potential, and it results in this cell also firing an action potential, then we've got a game of telephone tag. And that's how the nervous system, that's how communication between neurons happens throughout the nervous system. Now let's think about what impact these receptors have on disease and therapeutics. So, one impact is there are diseases where we lose these receptors and one such disease is called Myasthenia Gravis. We mentioned this in the last segment. So in Myasthenia Gravis, let's walk over here to this lovely image [COUGH]. This is an image from a human. Here is a motorneuron synaptic terminal. And you can see these little synaptic vesicles, okay. And so all those synaptic vesicles contain acetylcholine, which we will abbreviate as ACh. And over here is the muscle. The muscle is a very, it has this convoluted appearance where it has this folds. And that doesn't particularly matter, but what you see in black, all this black, these are acetylcholine receptors. And the acetylcholine has to make it across this cleft to get to the acetylcholine receptors. In Myasthenia Gravis, there are antibodies that the body makes, unfortunately by mistake against these acetylcholine receptors. And so the antibodies destroy acetylcholine receptors, the muscle doesn't, either has fewer or they're just not concentrated. And therefore, this signal is sent from the motoneuron terminal, but it's not received by the muscle. And so again, as we talked about in the last segment, what do we do about that? Well, we rely on the fact that there are a few acetylcholine receptors that have escaped being killed by the antibodies. And so we just try and boost this signal. We know that the motor neuron terminal can release acetylcholine and now were going to stop degradation. We're going to give acetylcholine asterisk inhibitor to try and keep the acetylcholine a round longer so that it can find it's way to the few remaining acetylcholine receptors. And that's a pretty effective therapeutic. The other therapeutic obviously that people with Myasthenia Gravis get is let's dampen down that immune system, so that you're not making all those antibodies, so that the acetylcholine receptors won't be degraded. And so, there is Immunosuppressants that are given to these patients as well. [MUSIC]
