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9.6 Synapitic plasticity VI

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Advanced Neurobiology I

Peking University

3.9 (272 ratings) | 29K Students Enrolled

Hello everyone! Welcome to advanced neurobiology! Neuroscience is a wonderful branch of science on how our brain perceives the external world, how our brain thinks, how our brain responds to the outside of the world, and how during disease or aging the neuronal connections deteriorate. We’re trying to understand the molecular, cellular nature and the circuitry arrangement of how nervous system works. Through this course, you'll have a comprehensive understanding of basic neuroanatomy, electral signal transduction, movement and several diseases in the nervous system. This advanced neurobiology course is composed of 2 parts (Advanced neurobiology I and Advanced neurobiology II, and the latter will be online later). They are related to each other on the content but separate on scoring and certification, so you can choose either or both. It’s recommended that you take them sequentially and it’s great if you’ve already acquired a basic understanding of biology. Thank you for joining us!

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SH

Dec 19, 2018

An informative site which provides bunch of information.

SB

Jul 27, 2018

This was a true challenge and magically eye opening!

From the lesson

Synaptic transmission & Synapitic plasticity

Let's continue with synaptic transmission and synapitic plasticity.

9.1 Synapitic plasticity I13:03

9.2 Synapitic plasticity II8:45

9.3 Synapitic plasticity III12:17

9.4 Synapitic plasticity IV15:03

9.5 Synapitic plasticity V10:00

9.6 Synapitic plasticity VI7:32

Taught By

Yan Zhang
Professor
Yulong Li
Research Fellow

Transcript

We are recording the transmitter because we are seeing

the postsynaptic receptor gated by the transmitter.

They are open.

Once they are open, they will allowed ions, positive ions get into a cell.

And that's the reason we see this increase in the membrane potential,

because there's more positive ions getting into a cell

while you record is the membrane potential increase.

But as I just mentioned this, you cannot distinguish

what is a transmitter increase, postsynaptic sensitivity increase.

And what he described, what the student described answering my question is

while you can measure in the transmitter release, then the question is how?

How are you going to measure transmitter release?

You can no longer use this postsynaptic cell as a reference, right?

Because then you are going to be different, then they are going to

be difficult to measure it, to distinguish the possibility.

Okay, so one way, design an independent sensor that

is different than the postsynaptic receptors but

can be sensitive to the amount of transmitter released, right?

So there are a number of ways.

How do you do it where you can sense the glutamate release, right?

If you are using optical methods,

then you can design some sensor that can sense glutamate.

How do you do it?

You can use some glutamate binding domains and then they're coupled with some

fluorescent protein, and hoping that this sensor will be sensitive to glutamate.

Well, indeed, people have already developed that and

displayed it on surface and they can sense glutamate.

So that will be one way.

The other way to sense a transmitter release is you can

have a way to directly measure the exocytosis in a presynaptic cell.

For example, if the presynaptic cell, they have the release of transmitters,

then they will have increase of the membrane area because of

the vesicle will fuse with the plasma membrane, right?

So if you have a neat way to measure how much the membrane area increase,

for example, by measuring the capacitance.

Then we say in this case it would detect indeed there is

a much larger membrane area increase, comparing with our LTP, okay?

You have your control, right?

So he says, at least this correlate if we assume

the transmitter is correlated with the vesicle membrane and

that will be the increase of the transmitter release.

And there's other ways, for example, you can also,

Put some artificial transmitter, for example,

isofluorescence, if you think, into the vesicles.

And if we get release, you'll see that isofluorescence will decrease.

Again, then you can compare before the plasticity and

after the plasticity, if there's change or not.

And we can also try that, because of the presynaptic terminal have this vesicle,

and this vesicle is acidic, has a lot of proton inside.

And then you can put some fluorescent protein that is pH sensitive.

And if the vesicle gets released, then these proton

acidic environment is going to be changed into neutral environment.

And if you put the pH-sensitive indicators there, then the pH will be different.

So you indirectly measure the pH sensor.

But because you strategically put a pH sensor only inside the lumen side,

so you can use that as an indirect way to measure exocytosis and

transmitter release.

So at least the way to do that is to have an independent

way to measure the transmitter release.

You can also measure from another source.

For example, in this case you can now measure the postsynaptic receptors

because you want to directly study whether this effect is here or here.

You want to distinguish whether it's pre or post.

But what you can do is, and people have done that,

if there's another adjacent cell, for example, a glial cell.

It turns out that some of the glial cell

will sense the release of glutamate,

to open up the special transporter on the glial cells,

to sort of regenerate more glutamate in the future.

So then you can record this glial cell.

You are not recording this postsynaptic neuron.

You are recording this glial cell.

And you say, you can do the control experiment.

The glial cell can sense different amount

of glutamate release leaking out from the synaptic cleft.

And then you are using the plasticity protocol to induce it and

then recall a glial cell as your independent way to measure

the amount of transmitter released.

Okay, all of those things can demonstrate a transmitter release is auto or not.

Then here's another question is very excited to answer.

How do you do the experiment to probe whether

the postsynaptic sensitivity is auto or not?

Previously you are just measuring independent weight,

the transmitter release is changing or not.

But how do you design an experiment

to directly test that postsynaptic sensitivity is changing or not?

And a difficulty to really add a glutamate.

But see we have a ways to use uncaging, right?

We can use the cage glutamate.

We can just use in the sense, UV light.

Because if we directly inject glutamate,

it will trigger a lot of side effects, the desensitization, diffusion.

But you can use an uncaging glutamate, and

there you can directly measure the sensitivity changing or not.

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