Receptors

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Del curso dictado por The University of Chicago

Understanding the Brain: The Neurobiology of Everyday Life

671 calificaciones

The University of Chicago

Understanding the Brain: The Neurobiology of Everyday Life

671 calificaciones

Learn how the nervous system produces behavior, how we use our brain every day, and how neuroscience can explain the common problems afflicting people today. We will study functional human neuroanatomy and neuronal communication, and then use this information to understand how we perceive the outside world, move our bodies voluntarily, stay alive, and play well with others.

De la lección

Neural Communication + Embodied Emotion

Neurons are the cells of the nervous system responsible for communicating, relaying, and integrating information. Neurons "talk" to other neurons through a special type of language that involves electrical signaling within individual neurons, and the use of chemical compounds known as neurotransmitters to communicate between neurons. In this module, you will learn more about how a neuron functions at rest, how information is relayed within a neuron, and how neurons relay information to other neurons or target tissues. In the second half of this module, you will be learning about how the body and emotions work together to produce our everyday emotional experiences. We will look at the enteric nervous system and learn how to discern whether the sympathetic or parasympathetic system is impacting our current emotional state.

Neurotransmitter Synthesis5:21

Neurotransmitter Release5:46

Clostridial Toxins: Botox6:09

Signal Termination7:02

Metabotropic Receptors7:08

Wrap-Up: Neurocommunication2:11

Conoce a los instructores

Peggy Mason
Professor
Neurobiology

[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]

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