January 20, 2011

020 Facilitation

In this video, Leslie explains all about facilitation and illustrates how it causes a stronger and longer signal in the post-synaptic cell.


Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, I’m talking about the process of facilitation, and we’re going to look at how this leads to a longer and stronger response in the post-synaptic cell.

Here, I’m looking at a neuron, and let’s say there’s an action potential that comes along this axon and enters into the axon terminal. I’ve drawn this terminal a little bigger than the previous ones because there’s a lot of stuff that I wanted you to see in here. As we’ve mentioned before, when the action potential reaches the axon terminal, it causes voltage-gated calcium channels to open, calcium ions rush in and that causes the vesicles to fuse with the membrane, releasing neurotransmitters, causing a signal in the post-synaptic cell. Now, this calcium that rushes in also causes depolarization because this has a positive charge. Usually, what happens after that is voltage-gated potassium channels open and potassium rushes out of the cell, repolarizing the membrane, ending the signal, ending calcium coming in, ending the neurotransmitter release.

In the process of facilitation, we have this facilitatory neuron, or you can call this a pre-synaptic synapse, and this neuron releases the neurotransmitter serotonin. When it releases that neurotransmitter serotonin, that binds to the receptor, and this is a metabotropic receptor, and this one specifically activates a G protein. That G protein activates adenylate cyclase. Adenylate cyclase converts ATP to cyclic AMP, which then activates a protein kinase, specifically protein kinase C, so I’ll put a C right here. That protein kinase phosphorylates the voltage-gated potassium channels, and what that does is it shuts those channels so potassium cannot leave as easily as it would have in a regular situation.

So the net result here is, we have an action potential that comes down, we have depolarization, but instead of repolarization happening quickly, repolarization takes longer to happen. It causes the action potential, the signal here, to last longer. And, of course, what that’s going to do is it’s going to cause more vesicles to fuse with the membrane, and you’re going to end up with more neurotransmitters being released. That, of course, is going to result in a greater signal in the post-synaptic cell.

So once again, action potential comes along, voltage-gated calcium channels open, calcium ions rush in. But we have this secondary neuron, a secondary synapse that releases serotonin, binds to the receptor, activates a G protein, which activates adenylate cyclase, converts ATP to cyclic AMP. That activates a protein kinase C, which phosphorylates the voltage-gated potassium channels, causing them to close, allowing the signal to last longer and for more neurotransmitters to be released, resulting in a stronger signal, a longer signal in the post-synaptic cell.

That’s really it for this video. If you have any questions, go ahead and leave them in the comments, and I’ll be happy to answer them. That’s it for this video, and I’ll see you in the next one.

You may also like

The Blood Supply to the Kidneys

The Blood Supply to the Kidneys

Page [tcb_pagination_current_page] of [tcb_pagination_total_pages]