© Distribution of this video is restricted by its owner
Transcript ×
Auto highlight
Font-size
00:00 Sorry about that, although I'm sure just happy to start a minute late

00:06 opposed to anything. All right. when we were meeting on Thursday,

00:13 were we talking about? Thank active transport. Um What we're trying

00:24 do with this is we were trying uh compare primary secondary active transport.

00:31 had talked about passive transport. passive transport doesn't require any sort of

00:36 . It's dependent solely upon gradients, . All right. So active transport

00:45 the other hand, has a dependency energy being used in some way,

00:49 or form two different types, active secondary, right or sorry, primary

00:53 secondary, primary active transport. We uses energy directly, secondary active transport

00:58 says use indirectly. Then we got by time passing and then the weekend

01:04 . Was it a good weekend? . Ok. Hm. Ok.

01:09 we need to work on that a bit. Ok. So our first

01:13 we want to look at here is want to look at primary,

01:16 So the sodium potassium A TP A is a good example of a pump

01:20 . It's a good example of primary transport. We have endo activity.

01:26 why it's not beeping and doing All right. So this is

01:29 our pump. It has enzymatic It's an A TP A, it

01:33 the A TP release energy that causes confirmational change so that you move uh

01:39 out of the cell and move potassium the cell exchanges three sodiums to two

01:44 . This next slide shows you like the steps along the way. You

01:48 do them. At the same time you're open to the outside, you

01:51 an affinity towards potassium. When you're towards the inside, you have an

01:55 for sodium. When sodium binds, sits there and goes, I'm ready

01:59 go out and nothing happens unless the TP is available. That's when you

02:04 it inside out. And now it's I can't bind here anymore. So

02:07 gets kicked out, potassium binds up then once the two potassiums binds,

02:12 causes a confirmational change for the A uh ace to turn itself around

02:17 back out and it releases the potassium the cell. So at the expense

02:21 one A TP, we're pumping three out two potassiums in. OK.

02:26 , what we're doing in the process by moving that sodium out, we're

02:30 more and more sodium, we're creating and greater gradient. Does that make

02:34 ? If you have a closet? you're putting ping pong balls in the

02:37 , the more ping pong balls you in the more the ping pong balls

02:41 to come out, right? Same of principle. So this is what's

02:45 on. We're putting sodium outside, wants to come back in. We're

02:48 potassium on the inside, it wants come out and it's going to try

02:52 use leak channels to do so and will. But for the most

02:55 you're trying to create an environment that , hey, um potential energy here

02:59 want to use it and this is secondary active transport comes in. So

03:03 is an example of secondary active It's a sodium. This particular example

03:08 a sodium glucose cot transporter. All , sodium wants to come in desperately

03:15 gradients right, potential energy glucose wants come in but you don't want to

03:20 the energy to pump glucose in That would be absolutely terrible because that

03:26 a poor use of energy, You worked hard for your glucose.

03:31 you agree with that? Like you in line at Taco Bell had to

03:35 people around you. That's a lot energy, right? So you don't

03:40 to expend that energy that you're earning eating that Taco Bell. I guess

03:45 energy there. So you want to energy that you've already stored up and

03:50 and this is what we've done. got this large gradient for sodium.

03:53 sodium binds and when sodium binds, makes the glucose binding site available when

03:59 binds the co transporter changes shape so it opens up, sodium can leave

04:04 glucose can leave. And this is we move glucose against its own

04:09 So glucose, there's lots of glucose cells. Glucose outside cells is

04:14 Would you agree with me on Yeah, because glucose is being used

04:18 the cells for all sorts of So keeping glucose outside the cell is

04:21 useless, but I don't want to the energy. This is how I

04:24 it inside. This is just an , right? Does the example make

04:31 ? So there are tons and tons tons and tons of co transporters.

04:36 you think you need to memorize them ? No, if you understand cot

04:40 , you think you're good. So this is just the examples you

04:44 see up here there's our sodium glucose , we have amino acid transporters,

04:48 have a phosphate transporter. Got all these are just different examples. Notice

04:54 we see in each of these pictures , right? In each of these

04:58 , we're using the potential energy for one ion say potassium or sodium.

05:04 there's others for example, proton right? Or not protons pump but

05:10 cot transporters that are there to move object against its gradient. This is

05:16 a cot transporter does. This is active transport. All right, you

05:21 see this over and over and over where you'll see a specific example,

05:25 might see this actually, I know going to see this in about three

05:28 . I'm never going to ask you the sodium potassium or it's NKCC transporter

05:34 . But it tells you in the name sodium potassium two chlorine. And

05:38 it uses the sodium gradient to pump potassium in plus two chlorine. In

05:44 inside the cell no changes electrically because moving two negatives and two positives kind

05:49 cool. All right, this is example of the cot transporter an exchanger

05:55 the same sorts of energy, In other words, they're moving things

06:00 they're moving things in opposite directions. you might see textbooks refer to it

06:04 an anti port system, right? might see the co transporters referred to

06:08 a SIM port system sim for same for against or opposite directions, but

06:14 the same sort of thing. It's exchanger, you're exchanging one down its

06:18 or down its gradient to move something its gradient. And that's what these

06:21 just examples of. Again, don't , please do not memorize the

06:26 right? That's not what we're We're trying to understand conceptually what's happening

06:32 . This slide just shows you how these things show up and how many

06:36 types of things there are. So can see kind of in this image

06:39 got a pump, we got right? We have leak channels,

06:43 have co transporters, we have voltage channels, we have different types of

06:48 . Here's an exchanger, here's some different types of things and they're just

06:52 pop up over and over and over . And so the key thing,

06:55 important thing for you to take with is do I understand conceptually what an

07:01 is? What a cot transporter What secondary active transport is versus primary

07:05 transport versus the different forms of passive . If you understand that, I

07:10 throw random names at you and you'd like, yeah, OK, I

07:13 it. I understand what that right. That's the idea. So

07:19 we good with this? And I have said that probably in two minutes

07:23 three minutes on Thursday, but it a weekend and I figured we needed

07:27 go home. All right. Any ? Yes, ma'am. Uh

07:40 Yes. So, so the exchangers doing that as well, but they're

07:45 the, the ion for ion. , that's kind of the way that

07:48 can think about it. It's, substance for substance and usually it's ion

07:51 ion, hence the term exchanger, ? But this isn't the only way

07:57 get things across that membrane, Some things are too big. We

08:01 about, for example, the anionic proteins, you know, and how

08:04 play an important role in terms of inside of the cell being negatively

08:08 I think we mentioned that if we mention that we're going to mention

08:12 All right. These things are just big, but your cells are going

08:16 be playing an important role of moving things that's part of its job.

08:21 so it doesn't use transporters or, uh carriers to do this.

08:27 it uses a mechanism of secretion using . Right now. Again, a

08:33 of the stuff is going to be to you. You've probably seen this

08:36 . So, what we're talking about is making a protein that it should

08:40 either secreted so released from the cell into the environment, extracellular fluid,

08:45 maybe you're making a protein that needs go into the surface of the cell

08:49 serve as a receptor or some sort interaction with the external environment. And

08:55 way you're doing this, what you're do is you're going to use the

08:58 sort of production cycle to do this this is something you've already learned way

09:04 when. All right, basically, you're gonna do is you take that

09:08 into plasma curriculum, you make your in the rough er, right.

09:12 it's a secretary molecule, it stays the uh the of the uh of

09:19 uh rough er, and then what happen is portions will be pinched off

09:24 then that little vesicle will move from to the Golgi, from the

09:28 You'll be sorted and tagged and bagged then you'll be sent to where you

09:32 to go. And that's what this trying to show you. So if

09:36 being secreted, that vesicle will contain soluble proteins that will then just be

09:41 outward. And if you're going to on your membrane, they're going to

09:44 inserted along the way, but still through the same process. And now

09:48 that vesicle comes to the surface and with the surface that uh uh transmembrane

09:54 is now sticking outward, facing the environment to interact with it.

10:00 when this happens, you regulate this one of two ways. All

10:04 most things in the body are gonna regulated in a non constituent way,

10:09 you're always just kind of producing it then when you need to actually release

10:14 or put it into the surface, going to regulate the presence of that

10:17 the movement of that vesicle up to surface to be released or whatnot.

10:22 other way you regulate it is by uh the old production at the far

10:28 end. In other words, at , at the RN A level,

10:31 ? So the transcription level, all . So when you're constituently making

10:35 what we're saying is we are just constantly be producing this, constantly making

10:40 . And then we're not really kind controlling when we're producing or when we're

10:45 or stuff like that. So this kind of like a, a cell

10:48 activity, but the regulated stuff as mentioned, this can be done at

10:52 level of release or it could be very much earlier. Um, but

10:56 when you're, um, when you're about release, it's gonna be done

10:59 right there at the release level. ? That's what we're saying. When

11:02 regulated, it's like, ok, gonna have vesicles and they're just gonna

11:06 sitting aside waiting for you to tell when to release that material.

11:12 Anyway, here have um like like an allergic response to bees or

11:17 like that, like a, like an anaphylactic response, right? No

11:22 , no one has anaphylax. that's good. You do.

11:25 So I'm not asking what it You could be allergic to just

11:29 It doesn't matter what it is. the reason you have that kind of

11:32 is because the cells are already primed ready to go. They didn't have

11:35 be, oh, we just got by A B um, what do

11:39 do now? It's like, we got stung, release the chemicals

11:43 it's already there. That's the regulation , right? So, vesicular transport

11:51 this process. All right. It's we're dealing with large things.

11:55 primarily proteins, right? They're too to be using uh some sort of

12:01 or some sort of um uh like , you're gonna require energy because you're

12:07 with big old bubbles, right? these, these vesicles are made up

12:10 plasma membrane So they are part of end the membrane system. And there

12:16 a couple of different processes. when I was in your seat,

12:20 had three processes. Now there's like . All right. It's just because

12:26 we learn more, it's like, , well, we can divide this

12:28 out. All right. So the primary processes, we go endocytosis and

12:35 . And that's pretty simple. Endo in exo means out, right?

12:39 basically, I can take things in I can push things out of the

12:43 . Notice I have phagocytosis sitting over . Phagocytosis is a specific type of

12:49 . It actually is kept separate from because this is an active form of

12:54 in materials uh that you're actively hunting . All right. And it's typically

13:00 by cells of the immune system like and monocytes and neutrophils. Their job

13:06 phagocytosis, hunt for things that shouldn't in the body and then bring them

13:10 and destroy them. But regardless if doing endocytosis or exocytosis, what you're

13:17 with is you're dealing with a very flat plasma or uh plasma membrane.

13:22 right. So think of the earth your flat to you to you.

13:29 it feel flat? It does, it? I mean the horizon goes

13:33 a pretty long distance, right? can't really see the curvature of the

13:38 from your perspective, right? So our purposes, the earth is

13:44 but we know better it's not If you wanted to bend the

13:48 it'd be pretty hard to do from perspective. Right? And that's the

13:52 thing that's true for a cell, plasma membrane, for those little tiny

13:57 , the plasma membrane is pretty large pretty flatt. And this is what

14:01 trying to show. You. Look how long and flat that thing

14:03 All right. This is, this the and you can imagine it's going

14:05 be the same thing for a plasma . All right, if I want

14:08 bend that, I need help to so. And so we have proteins

14:12 do that. One of these proteins heard of? All right, you've

14:16 of clain, right? Do you hearing about Clari clain coated pits?

14:21 right. Well, what's Clari it's class of molecule whose job is to

14:27 a membrane that appears flat and bend against its will so that it bends

14:32 a little tiny bubble, right? what this is trying to show

14:37 There are other types of proteins that discovered since. And so the class

14:42 collectively referred to as the, all . And they basically coat the plasma

14:48 and bend it to its will. right. So, Clarin isn't the

14:52 one and part of the the the of naming these different types of processes

14:57 endocytosis and exocytosis is kind of dependent the presence of which proteins are

15:03 All right. We're not, don't about that so much. All

15:05 But the idea here is that these are there to create the vesicles to

15:13 them to bend so that you can the membrane to turn into that

15:19 All right. Not so bad. how I get my vesicle, that

15:22 that go someplace where does it And why does it go? Do

15:28 just kind of float around the inside the cell randomly when I went to

15:33 ? They did, right. They went where they kind of went.

15:39 the thing is is that everything in cell has a direction, has a

15:44 and is doing something. It's not it in a non random fashion.

15:48 right, there are molecules called the and the snaps. All right,

15:54 snares are molecules that are associated with vesicle and the molecules that are associated

16:01 the membrane that serve as a way the two to recognize each other.

16:06 other words, it's a way to molecules to or vesicles to the

16:11 So the vesicles nowhere to go. ? So if I'm trying to secrete

16:16 the lumen of the digestive tract that vesicle isn't just wandering around the

16:21 going, I don't know where to . Maybe I'll go down here to

16:23 basal side and release myself out into actual body, which would be a

16:28 thing. Instead, what it's doing it's being directed to the apical surface

16:33 there is a dock for it to and wait to be told. Remember

16:36 I said the regulatory portion, the is like, OK, I want

16:40 to go hang out here until we you to release your stuff. And

16:43 what this is not a great picture you. It's gonna be here in

16:46 a second. I'll show you. right. The purpose of the other

16:50 is the, the snap is to everything has been released, I want

16:54 recycle everything. So basically, it a dissociation of these snare molecules.

17:00 , there are V snaps and T . Just think V for vesical T

17:04 target, that's the easy way to it. And all this stuff costs

17:08 . So moving things in cells cost . Uh I thought I had a

17:14 showing the snares and snaps. I it's when we do the synapse that

17:18 show this a little bit more All right, because one of the

17:23 that it does is that the they don't just come and hang out

17:27 the membrane like this, they actually emerge with it. So they're not

17:32 , they're not closed there, half half. And so that's what they're

17:36 for is that signal, we'll get that again, eventually we'll get to

17:40 . So if are you with Yeah. Mhm And the membrane has

17:49 , right? So the ones that snares are there. They have the

17:53 for the V snares and V snares the T snares. And again,

17:57 purpose here is just like a dock a boat, right? The boat

18:00 find the dock. But if you tie it off, it's just gonna

18:04 around. And so that's kind of idea here is that they basically come

18:07 and they lock in place. So that vesicle can't move anywhere, I

18:12 I, again, I may have , let me just see.

18:15 I thought I had a picture maybe or three. We're gonna look at

18:19 when we talk about the synapse in couple of lectures, we're gonna look

18:21 the neuromuscular junction as an image and neuromuscular junction is a perfect example of

18:27 because between the neuron and your there are thousands upon thousands of bests

18:34 pre lined up ready to go so you can do this, right?

18:38 don't have to, oh, we to make up the vesicles with full

18:41 the neurotransmitter. Tell the muscle what do. It's they're ready to

18:45 right? So let's just kind of this down, endocytosis, exocytosis

18:52 and um pinocytosis, I think we're , yeah, here we go.

18:56 , the different forms of endocytosis is first thing. So how we're bringing

19:00 in notice on this list here, is kept aside. All right.

19:04 we're gonna look at endocytosis and phagocytosis I think we have exocytosis or maybe

19:08 was what I was already referring to is just how we release the materials

19:14 the cell. Now, it's all scary. All right. First pinocytosis

19:25 back in the day. So I'm of giving you why we name things

19:29 . You know, they saw macrophages things that, you know, that

19:31 around. So they call that, literally means cell eating. All

19:35 that's the next slide, right? then what they noticed is that cells

19:39 actually have this imagination and the cell would come along and they would just

19:44 of enclose around a portion of of the extracellular fluid that was kind

19:48 around the cell was, you just like a little pinch off,

19:52 ? And they would say, what is causing it? Well,

19:54 is nothing there causing it's what basically it is doing, it's picking up

19:57 water and whatever happens to be in environment in that water at that

20:01 So if we have eating, we have drinking. So pinocytosis is basically

20:08 drinking and it's very nonspecific. So not actively going. Oh, this

20:14 the stuff that I want. It's this area. So I'm bringing it

20:17 , it's basically just bringing in a of the materials and the extracellular fluid

20:21 a vesicle and then whatever the cell out of that, it will uh

20:25 and destroy whatever it doesn't need, will then secrete out later.

20:29 So that's basic. Typically, when think, we think that the

20:35 as I said, doesn't do things . It's actually actively seeking to grab

20:41 . And so here what you're gonna is you're gonna have receptors on the

20:44 of the cell. Things are gonna binding to those receptors that when you

20:48 that receptor, it's gonna trans locate a region of clain or some

20:53 And basically say, hey, I up what we're looking for and once

20:56 get enough of the things bound up that, that's gonna activate the clan

20:59 cause it, that imagination to fold . And then now you've created that

21:03 for endocytosis. All right. So call that receptor mediated because a receptor

21:08 involved and it's specific for the thing you're hunting for that makes sense versus

21:15 , which is like, well, we grab or grab. All

21:19 So for example, I see the, the furrow brow and it's

21:22 . If you have a fur I can usually read that in the

21:24 . But if everyone's staring at me this, it's really concerning. All

21:28 . So for example, there is specific molecule x that the cell is

21:33 to bring in for the purposes of from the environment or maybe they're using

21:37 as a way to transport across to other side. So like for

21:42 between the bloodstream and the brain, example. So what it would do

21:47 like, OK, I'm binding things and once I get enough things bound

21:50 , I'm gonna create my vesicle, I move the vesicle over and then

21:54 do exocytosis on the other side. right. That would be an

21:58 All right. Then we have caviar endocytosis, which is called potocytosis.

22:04 is where they started noticing the different of cot um this was noticed uh

22:10 in the vasculature. So in the I just gave right, it would

22:14 like, oh I'm pinching off and , I'm creating a vesicle. The

22:19 is I'm not using Clarin, I'm a different type of Coomer and this

22:22 why it was distinguished as something unique different. All right. And

22:27 trying to move things across uh the because you're too big to leak through

22:33 be an example. So the vasculature very, very thin and you basically

22:37 transporting things quickly across. All So do those three kind of make

22:43 or do you need a better? , ma'am. So, potocytosis would

22:51 be the the first one that we , we we would say is

22:56 The others are primarily using Clan. again, probably when you're standing up

23:01 or working on somebody digging your fingers somebody, we may have found out

23:06 there's actually more to it than All right, if you go on

23:13 , you get to watch fun videos phagocytosis. All right. So the

23:16 here with phagocytosis and endocytosis. endocytosis, remember you have a flat

23:22 that is invaginated, right? it's going downward and then closing

23:28 Phagocytosis is targeted towards the thing that trying to destroy. But notice what

23:33 cell is doing is it invaginated its and it's reaching out, isn't

23:39 And these are really like I they are cool videos on youtube that

23:42 can watch, just look up neutrophil bacteria. That would be an easy

23:46 . And you'll get to watch it the neutrophil is actually chasing the bacteria

23:50 . And then finally, you see , it actually reaches out, extends

23:54 cytoplasm creates these proto extensions, They're not really arms, it's just

23:59 reorganization of the act in it reaches and then encloses the thing that it's

24:05 to consume. And so it encloses in a vesicle and then you can

24:09 that vesicle and then merge it with lysosome and just, you know,

24:13 those enzymes to break down whatever it that you've engulfed. So that's

24:18 So it literally is, looks like grabbing something and, and eating it

24:22 . All right. Again, all these require a TP. Um This

24:31 an example to show you this process uh using a Lyo. It's not

24:39 great example, but it's showing you you can recycle using this Clarin.

24:45 so here you can see we got over here. Here's an Endo,

24:51 endo is simply the fancy word for vesicle that you've brought into the

24:56 right? So Endo is the same as a, what would it be

24:59 faga zone? What do you It's an endo that I just created

25:07 cytosis? So, an endos is the vesical that I brought in.

25:12 so I'm gonna digest things here. how am I gonna digest? I

25:16 to merge with the Lycos. You remember what lysosomes do, right?

25:19 all took our bio one. We our cell, right? It's a

25:23 of enzymes. Merge Lyo with an those enzymes now destroy whatever is

25:28 But you know what um there are for some of the molecules and I

25:33 to recycle those so I can use classroom to form and then I've used

25:38 cla in to pinch off and use classroom to reform and I can just

25:41 back and forth over and over creating lysosomes over and over again.

25:47 kind of cool. It kind of sense. So this process is specific

25:52 it's recyclable. Is that a good ? Good work, bad work.

26:00 . How do we feel about vesicular , endocytosis? Thumb up. I

26:06 that more of those and then we're ready for this one. Everyone know

26:14 osmosis is. If I gave you test question about what is osmosis?

26:18 now, could you all answer it your entire human phys grade dependent upon

26:22 definition of osmosis and your explanation of ? Are you confident that you could

26:26 an a and go on and practice ? Some people are going.

26:32 of course. So I should just ahead and skip it then.

26:35 no. All right. The reason say that is because over the course

26:40 your academic career, you've probably been multiple definitions, right? Every year

26:43 have to learn it and you sit and memorize it for the test.

26:46 vomit the answer out right. Here's and then you promptly go. I'm

26:51 really sure. I understand this. sound about right. OK. My

26:57 today is to make osmosis simple. right. So you're ready for the

27:02 answer. If you have this you'll never go wrong. Don't let

27:06 chemists confuse you. What do chemists care about? Do they care about

27:10 ? No. What do they care the stuff in the water?

27:13 The solutes, right? So whenever give you a definition, they're talking

27:16 solute concentrations, right? And what's to the water with all these solute

27:22 ? And it's confusing, especially on test when you're like under pressure and

27:26 got 38 seconds to answer this All right. So throw all that

27:30 away. Let's keep it simple water osmosis is the diffusion of water down

27:34 gradient that's all it is. If have high water concentration, low water

27:38 , which way is water gonna it's gonna go down its gradient.

27:41 at the end we can move on knowing that it's not that simple,

27:47 ? That we're not just looking at , we're looking at water plus other

27:51 , we need to consider the solute well. So if I have 100%

27:54 , how much solute do I 0%? If I have 50%

27:59 how much solute do I have? see if you keep it with that

28:04 mind, like I'm always dealing with is my water percentage? You don't

28:09 to worry about anything else, So they can throw all sorts of

28:13 at you to make you feel confused like, you know, you have

28:17 much sodium and this stuff all you do is ask the question is all

28:20 , what is my water percentage? I know I have more water over

28:22 and less water over there, water gonna move in that direction as long

28:26 there is no barrier that prevents the of water. OK. So,

28:31 far you're good with me, So when a membrane is permeable to

28:35 , it allows water to move if impermeable to a solute, solute doesn't

28:38 . So water is gonna continue to down its gradient until it reaches its

28:43 pressure. That's why I throw everybody . Osmotic pressure. You remember osmotic

28:50 ? What is the definition of osmotic ? You wanna know? Mhm.

28:58 , that's technical. And I'm not it could be. Right. I

29:02 know. I, I, but , it's hard. Right. All

29:05 . So every fluid has its own . Hold up your water bottle real

29:11 . Is the water escaping? See, water, water is the

29:13 escaping from those things? No. ? Because the water pressure on the

29:19 , you can put them down. water pressure on the inside cannot overcome

29:23 internal pressure of the plastic holding it the moment that the internal pressure overcomes

29:29 outward pressure, water flows out. ? So that pressure that that fluid

29:33 , whether it be the big the small jug or my tea sitting

29:36 here, there is a hydrostatic right? Hydrostatic, the water

29:42 All right. Now, if I a container that's 100% fluid and 50

29:50 100% water and 50% water, each those do they have hydrostatic pressures to

29:55 ? Yes. And so as water from the 100% to the 50% what's

30:00 to the pressure over here? Hydrostatic is going up, what's happening to

30:04 pressure over here? It's going There's gonna be a point where the

30:08 become equal so that water molecule that's to move over when both those pressures

30:14 equal, it's gonna come over and gonna be uh uh there's too much

30:17 over here. You got to go or you have to kick another one

30:19 out. And so you now have that point where those two pressures are

30:25 is called the osmotic pressure. All , let me give you a

30:31 Do you guys know what a smart is? Yes. You guys know

30:37 smart car over here. OK. many people can you fit in a

30:40 car? I heard 43. All . You guys are going clubbing tonight

30:49 you have eight friends. I didn't , can you fit eight people

30:55 I asked the question, how many can you fit in a smart

30:58 Right? You could probably get about , right? But let's say you

31:01 that ninth person and you shove them there. What's gonna happen on the

31:04 side? Someone's gonna pop out, reach the pressure point that is like

31:10 osmotic pressure for the car. It's osmotic pressure because it's not water.

31:13 that's the kind of the same principle . Water will continue to move down

31:18 concentration gradient until the pressure to where going opposes its movement. That's the

31:25 . That's osmotic pressure. Isn't that ? Isn't that so much easier than

31:31 sort of strange explanation with solute concentrations stuff like that? Yeah.

31:37 So when the chemists try to confuse just go no water concentration,

31:42 osmotic pressure. Ah No, no simple it's the opposing pressure that

31:48 the movement of water. That's all is. So, osmolarity is what

31:54 concern ourselves with in biology or really physiology. You know, you get

31:59 learn all about molar and stuff, we never talk about osmolarity or do

32:02 guys ever talk about that in like ? No, no. OK.

32:07 this is a new term. So osmo, it's dealing with solute.

32:11 for example, what it does, , I shouldn't give you the

32:14 The definition simply it describes the number particles in a solution. It doesn't

32:19 what the particles are. It just the question, how many are

32:24 So if I have like 100% sodium , right? And so I'm like

32:28 one mole of sodium chloride. And I drop that into a fluid,

32:31 still have a mole of sodium don't I? Right? But I

32:37 have sodium and chlorine that are dissociating their respective ions. So I don't

32:43 one molecule, I have two particles each sodium chloride. So my osmolarity

32:50 two osmoles if that makes sense. if your molar, so you

32:56 one mole in a liter is one , right? When you're dealing with

33:02 something like sodium chloride that dissociates, would become two particles. So that's

33:07 os moles per liter. All That makes sense. So it's counting

33:13 number of particles. It does not what the particles actually are and that's

33:17 your body is watching, right? when you become thirsty, the reason

33:23 thirsty is that your osmolarity has right? And your body wants to

33:28 it back up to the proper solute balance or concentrations. All

33:35 So our concern is then what does and solute do in the body when

33:43 change waters, solute concentrations? All . And again, the other example

33:50 have up here is glucose, glucose dissociate. It just goes in the

33:53 and it sits there. So one of glucose would still be one

33:57 All right. I'm not gonna make do math just so you know,

34:00 you ask the question, if you a math equation, I know I

34:02 said it once just reinforcing, there's gonna be math on the test.

34:08 right. No equation balancing figure. chemist taught you all that stuff.

34:14 I want to show you here is first, just a couple of,

34:17 , of scenarios when we're dealing with and salt. All right. So

34:21 the left here, what you're looking is you're looking at a picture of

34:24 normal cell under normal conditions and we're a whole bunch of stuff. We're

34:27 looking at the sodium potassium pump, looking at sodium leak channels and we're

34:31 at chlorine and the anion accelerate. not even showing the anti Oh

34:36 it is. There. It All right. And this is what

34:38 see in a normal cell under normal . So the concentration of potassium is

34:43 high on the outside. Sodium is . Lots of an cellular proteins.

34:47 is is fairly low on the And you can see we've got pumps

34:50 are active that are moving sodium and to create that imbalance of of

34:56 right. Chlorine is moving in the of of where there is positive

35:02 It's just following along. And then cell, your proteins are stuck on

35:06 inside and to keep everything nice and water is moving in and out so

35:09 you have your normal happy cell. . That's a normal circumstance. All

35:15 . If we treat this normal happy with this chemical called, do you

35:19 it's horrible smelling up there. When I first learned about it,

35:22 thought it started with a W-2. right. So Waban kills the sodium

35:28 pump. All right. So you're longer able to pump. And so

35:31 that happens, ions are gonna move their concentration gradients to reach equilibrium.

35:36 that's what this uh right side image trying to show you is that we're

35:39 to reach an equilibrium. All And when that happens, what's uh

35:44 amount of ion on the inside, as a function of those, the

35:49 of the proteins is gonna draw water the cell. And when you draw

35:53 into the cell, what you're doing you're dropping the osmolarity inside the

35:58 right? In other words, there's water, the cell swells up and

36:02 you've created an environment that's not conducive the chemical reactions that would normally take

36:07 in the cell. So when cells , that's bad. Ok. So

36:14 does this body deal with this right , in this condition? What we're

36:17 is we're giving it a poison. what is, it's literally creating a

36:22 . All right. So it's killing cell and that it's done,

36:27 But under normal circumstances, the body how to maintain based on how it

36:33 the inside of the cell relative to outside of the cell. So there's

36:36 , this a whole bunch of mechanisms your body that we're going to explore

36:41 during the renal system stuff that is for ensuring that you have the right

36:45 of water and the right amount of in your body so that your cells

36:49 normally. But let me just kind show you what's going on here.

36:52 your normal osmolarity throughout your entire except for one place which we'll ignore

36:56 right now is roughly 300 million All right, no matter where you

37:01 , just one place is different and gonna ignore that. Now,

37:04 it's 290 but 290 is a horrible to work with. So 300 is

37:08 we're gonna stick with. Ok. you can see in this top

37:11 look, we got everything in everything is in balance. And then

37:14 we're gonna do is we're going to a whole bunch of solute here on

37:18 outside, right? So the osmolarity . So when that happens, when

37:25 added solute on the outside, in , we have diluted the outside,

37:31 we? Right. If I was solute now I've turned into 70%

37:35 I've gone from 50% water to like water, right? So that's the

37:41 thing that the chemist confuse us about they talk about solutes and they ignore

37:45 . So here, what I've done I've increased the amount of solute or

37:49 the amount of water on the So what does water do? It

37:53 outside? And when that water leaves cell, it causes the cell to

37:56 . Now, the inside of the has a greater osmolarity. And when

38:01 change the osmolarity inside the cell, cell becomes nonfunctional. It doesn't,

38:05 not creating the environment to allow the to work inside the cell. The

38:10 is failing. So what does it ? It introduces these co transporters,

38:17 exchangers to the cell surface so that can then move ions around so that

38:24 is brought back into the cell so we can create an equilibrium when you

38:31 that equilibrium. Now, the cell able to function water salt balance

38:38 Similarly, we can do the same . If we decrease the os outside

38:42 comes in cell swells up. We pumps and channels in places to pull

38:47 out of the cell. So water . I think this is the place

38:52 may be wrong where I give you better example of this. You're

38:57 what do you mean? Well, I've been doing this for so long

38:59 keep you the same examples over and again. Do you guys remember high

39:04 ? Did high school suck or? it awesome? It sucks.

39:08 When people answer that question, it me which group you're in,

39:13 I mean, you know, the I'm talking about, right? Every

39:16 school has the groups, right? you have the popular group? Like

39:20 prom queen? You know, you have that. Um, people are

39:23 in their head like, you you have the, the one girl

39:29 everyone wants to date or wants to , you have the guy that's dating

39:34 girl, right? You have the that's the best friend of the

39:43 You know, he's kind of trying , you know, be, he's

39:45 that friend zone, right? He's to, you know, when he

39:48 away, I'm right there to, pick everything up. I'll be the

39:52 , you know, this one and they have their group of friends that

39:55 of hang out with them, watch things for a little bit. You

39:58 see them there. I don't But every school has that and if

40:03 going, no, it doesn't trust . It did. You were probably

40:07 girl. All right. Now, , why bring this up? Your

40:13 are high school politics. All Sodium is the girl. The popular

40:22 . Sodium loves to hang out with . Water loves to hang out with

40:26 . Wherever sodium goes, water Sodium and water. Take the same

40:31 when one goes to the restroom, other one follows but there's an impermeable

40:36 there. So water has to wait . Water is the guy in the

40:40 , right? He's the cool quarterback or whatever they are the couple in

40:45 . So a sodium goes water All right. Chlorine is the one

40:51 trying to weasel in on water's He's just waiting for water and sodium

40:56 break up. And so when sodium and hangs out, chlorine goes,

41:02 sodium goes. Yeah, water is . But you know, I'm on

41:06 fringes and then wherever sodium and water , all their friends go worse.

41:10 wherever water goes because he's the cool . Potassium follows wherever sodium goes,

41:16 goes, wherever water goes, all the other ions follow because they follow

41:23 and then remember waterfall of sodium. you remember that if you ever get

41:28 , just go. Oh yeah. school politics. All right. And

41:35 what you're seeing here is basically I'm these ions. Why? Because water

41:42 gonna go and hang out wherever sodium . That's what's really going on

41:47 Now, we have some weird friends that group. You know, the

41:52 Jock guy always has that one friend not particularly bright. A little

41:57 Right. But eventually we'll get things . That's right. Is our slow

42:04 . So wherever water goes, urea , but it takes a sweet time

42:09 get there. All right. And what this is trying to demonstrate.

42:13 Urea uh is like, oh, water, water goes, Urea and

42:16 Urea goes, oh, wait a . I need to go back the

42:18 direction to balance things out. And it does. And it's actually one

42:22 the things that the kidney has to up with is that it's constantly moving

42:26 e and then kind of goes. . Well, you know, I'm

42:28 go back this direction and it, only get rid of about half the

42:31 , your body is trying to get of at any given time because of

42:34 it slowly moves down its gradients. water salt movement is going to be

42:45 upon that balance, that osmolality or osmolarity of the body. So far

42:50 me, you're like, I'm not anyone here. Not sure.

42:57 Now, let's see how this actually to your lives, right? So

43:04 is something that if you're planning on health profession is something that you need

43:07 understand. All right, and it with this question of osmolarity because what

43:12 dealing with is uh solutions for the part, right? So if you

43:17 a hypertonic solution, it's also referred as being hyper osm. Um And

43:22 that would basically say hyper iso you already know that prefix what it

43:26 . It's the suffix, the tonic referring to the solute and this is

43:31 we get kicked in the pants again those crazy chemists because they don't care

43:36 the water and most of the stuff put in our body, we're not

43:39 about the water we're carrying what we're in, right? So you guys

43:43 here ever used Visine because you have eyes, right? One person is

43:48 their head. Two OK. Three . The rest of you need to

43:52 out outside for a little bit longer stare at your screens for a while

43:56 eyes will start feeling and what do do you put via in Ive is

43:59 isotonic solution, right? Iso meaning solute concentration as your tears. So

44:09 just adding fluid but it's not affecting tenacity of the tears themselves.

44:18 when we're talking about our bodies, the most part, we're talking about

44:22 in osmolarity or osmolality, right? most common causes I mentioned the sodium

44:27 sodium goes, water follows and glucose play a role as well. So

44:32 when you eat food basically, it's water to wherever the glucose is.

44:36 then when glucose starts moving around the , that's when you're drawing water into

44:41 blood to kind of dilute out the . But once you move into the

44:43 , water goes to where the cells . I'm gonna show you the effects

44:49 these things. And I want you see if you can predict why.

44:52 here what we're doing is we're you can see this is ECF and

44:56 F. All right. So, what we're gonna do is we are

45:00 or injecting into our person here, liters of uh basically same osmo.

45:08 it's isotonic saline. All right. you can see here, I started

45:11 , you can see osmolarity is 2 90. So you can see if

45:16 inject 1.5 liters of fluid into the fluid, I get swelling in the

45:21 fluid, but I don't see any in the uh intracellular fluid. Why

45:25 that be? Why do you think would be not that it's impermeable because

45:32 has water. That would be a guess. OK. It's impermeable but

45:36 know it's not because plas membranes are to water. So why do you

45:42 same osmolality? Right? Because it's I've injected in and there's no change

45:48 the osmolality. So there's nothing drawing in or out, right? That's

45:53 key thing that you need to Is water being drawn in a particular

45:57 . When I see osmoles, I to be doing that. Ok.

46:00 let's see what happens when we add water to a system. Here we

46:04 up at the top. There's your . You can see same osmolality.

46:07 . I added 1.5 liters of pure onto the ECF and you can see

46:12 I get initial swelling because whenever I anything in anything, it's initially going

46:16 swell up. But look what happens time. Does it balance out?

46:25 , it starts moving over into the fluid so that you get not equivalent

46:29 but you get balance in terms of that fluid is gonna go. All

46:36 , now, why should this be , really important to you? All

46:40 , you have a friend who's right? And you being an entrepreneur

46:46 not entrepreneuring, but you know, anxious young pre health student, you're

46:50 , oh, I've been learning how inject people with ivs. Let me

46:53 you an IV of pure water. know what's gonna happen? That's what

47:00 is right here, right? I'm water into the extracellular fluid. Where

47:04 it going into the cells? And you add too much water into the

47:11 , they, and now you have person who has no red blood cells

47:18 carry oxygen, drowns in their own . So when you're dehydrated, if

47:26 here and here working in the usually get one or two, you

47:29 one. So what do you give sailing? But sailing makes me

47:36 Yeah. But it keeps the cells exploding, but I'm giving them water

47:39 the same time and it will eventually itself out. Ok. Lactated

47:46 D five LR. All right. an impossible situation. You get a

47:53 of pure sodium chloride. No jam it into their extracellular fluid.

47:59 doesn't sound like a lot of Does it? What do you expect

48:02 happen? All right. There's no in the fluid because remember there's no

48:08 , right? But what did I do as I changed the osmolarity?

48:11 see it went from 290 to 3 . So where is the water gonna

48:17 ? It's gonna go down its concentration until it reaches equilibrium, right?

48:23 so we get swelling on both sides the membrane, right? That's the

48:30 . So the the principle to carry from this is that water is gonna

48:35 down its concentration gradient. It's gonna where there's extra solute, which is

48:42 the chemists talk about and your body trying to balance out and trying to

48:47 you as close to 300 mil osmoles it can. Despite the fact that

48:52 live in Houston and you're sweating all water out of your body,

48:56 Despite that, we're not putting a of solute and water into our

49:00 It's always doing that. And so we consider any thing, when it

49:05 to electrical, when it comes to this stuff, we have to ask

49:08 question of water, salt and that's our body spent a lot of time

49:14 this stuff. Does this kind of sense? Iiii I think I explained

49:22 well enough. I don't know, I didn't. They're all staring at

49:27 like you have no idea what I . OK, because you're doing this

49:33 , but I think you're cold. . Questions. All right. So

49:45 way that we move things through a . So like when you go

49:49 go to Taco Bell or whatever, you're trying to do is you're trying

49:52 get materials from outside your body into body, even though you don't think

49:56 the digestive system being outside the It is, it's just a tube

50:00 happens to travel through your body like whole throat doughnut, right? That's

50:04 the external surface. And so what trying to do is you're trying to

50:07 things from the external circle to the parts of the body. So that

50:10 it has to has to cross over . So what we refer to as

50:15 movement is what is called epithelial And there are two different types,

50:21 ? I can move through a All right. That would be trans

50:26 self uh transport or I can be the cells which is not that

50:33 you're gonna see that less often, that would be paracellular transport. That'd

50:37 leaking through the leaky junctions or the tight junctions, the leaky tight

50:42 , you guys learned about tight right? Ok. All right.

50:46 , if I'm moving from the, hollow portion of an organ, all

50:52 , what I'm doing is I'm absorbing the body. And if I'm moving

50:57 the body across the cell into that , that's secretion. And what I

51:02 have up here is a definition of I'm leaving the body altogether, that's

51:06 , right? So when you're making , that is secretion and then when

51:10 pee urine out that's excretion, You sweat, that's excretion.

51:17 Now, one of the key things when you're dealing with epithelial transport is

51:23 have two plasma membranes that you have cross and we have different concentrations of

51:29 ions on either sides of those So either you're going to have to

51:34 uphill to get into the cell and you're inside the cell, then you

51:38 have a high concentration. So then gonna go downhill, right? So

51:42 an uphill on a downhill or you're into the cell which would be downhill

51:46 then you have to be pumped out other side if that makes sense.

51:50 there's always going to be an uphill there's always gonna be a downhill,

51:52 never going fully downhill across both membranes fully uphill both membranes. All

51:57 And so this is what this is of showing you here. But we

52:00 a couple of examples so that you kind of see here. So in

52:03 the first example, you can see talking about sodium sodium, remember we

52:06 lots of sodium outside the cell, little sodium inside the cell. So

52:10 from the loin into the cell is to be a passive event. It

52:14 require energy. Sodium comes in and I don't want the sodium inside the

52:18 . So what do I have to ? Pump it out? So I

52:21 a pump to do so. All , I've got lots of potassium inside

52:26 cell. Why? Because I'm pumping in. So what it's gonna do

52:28 it's going to leak out the But if I'm trying to secrete

52:32 I just introduce those types of channels here on the lumen. So even

52:36 I'm pumping potassium in out, it ok. So it can go in

52:41 direction but it's going out of the . What about glucose? Well,

52:45 remember what we said about glucose, , there's lots of glucose inside

52:49 So in order for me to get the cell, what do I need

52:51 get inside the cell cot transporter? ? So here's our sodium glucose co

52:58 transporter. Glucose goes in the It gets pumped out of the

53:02 Sodium does what about glucose itself? , now I'm going downhill because I

53:05 have glucose freely running around my That's a waste of glucose.

53:10 what do I have is I have transporter so it just binds it up

53:14 sends it out into the blood or into the intertrial fluid gets picked up

53:17 the blood and then moved off to it needs to go. This would

53:20 an example. What's the last one ? oh yeah, chlorine secretion.

53:25 , I'm using that NKCC to move into the cell. I'm using the

53:31 as the driver of that, that energy and then I have a

53:36 So I'm moving chlorine up against its and I'm secreting chlorine out down its

53:41 . So you see half is half is down which one comes first

53:46 upon which thing you're looking at. right. So what this does is

53:56 us to transition away from moving things the membrane to talking about how cells

54:02 to each other, right? Self communication. Now, I hate that

54:12 book says this and I'm just gonna it this way, almost 100% of

54:16 communication between cells is through chemical There's some rare exception that it's

54:22 but even when we talk about we think of neurons being electrical,

54:27 really chemical, right? They use aspects of signaling, but they're not

54:32 doing electrical signaling. When you're talking electrical signaling, what you're doing is

54:35 changing the cell membrane um and you're a discharge. In other words,

54:40 are moving in and out and you're a signal along the surface through the

54:44 of these ions. When you're dealing chemical messages, what you're dealing with

54:48 some sort of molecule that's being released the cell and then another cell binding

54:52 that molecule. So there are four methods. We can do gap junctions

54:57 would be a form of electrical then contact dependent local signaling and long

55:02 or hormone signaling. And I just to kind of walk through these.

55:05 I'm gonna show you some very specific that you can use to help you

55:09 , conceptually what we're dealing with. this is the gap junctions. This

55:13 another term for this would be Jurin you're if you're juxtaposed to somebody,

55:19 are you right next to? So juicy signaling is a term that

55:25 to two cells touching each other or in contact with each other talking to

55:30 other. So this upper picture right through the gap junction is an example

55:34 of electrical signaling, the ions are between the cells. So the cell

55:40 communicating through some sort of chemical what it's doing is it's having an

55:44 exchange. And so a current is from cell to cell to cell.

55:50 , what is a gap junction? , it's a bunch of proteins that

55:54 the an open pore, these proteins called connections. There's multiple ones and

55:59 very, very small, they allow the movement of small molecules. Contact

56:06 signaling is a little interesting. All , it's another type and this is

56:10 chemical form of signaling. And this when two cells come into contact with

56:13 other. One has a cell surface that is a receptor. The other

56:18 has a cell surface protein that is lien. And when they come into

56:22 with each other, then the one the lien is telling the one with

56:26 receptor what to do. We usually to these types of molecules as cams

56:30 cell adhesion molecules. So like the system uses this form of communication.

56:36 have one immune cell, another immune that come into contact with each

56:39 they touch each other and they use leg and receptor binding to tell the

56:44 with the receptor how to respond to sort of immuno, basically immuno

56:50 All right. But this isn't the type of cell to cell recognition.

56:53 are other cells that do this as . All right. This type of

57:00 is what you're more familiar with. right. So we have a dorine

57:04 . This is a cell talking to . Do you ever talk to

57:08 Do you write yourself notes, reminders , what to do? That's in

57:12 , what it's doing is that it out a signal that then comes bind

57:16 and binds to a receptor on the to actually regulate what's going on inside

57:19 cell. Right. Kind of like reminding yourself, you know, I

57:24 to do this and you just create to do list. It's kind of

57:26 same sort of thing. So it's talking. All right, paracrine,

57:31 the other hand, is nearby, next to but nearby signaling. All

57:37 . So if I'm re releasing a , it's that signal is a chemical

57:43 traveling out and cells that are nearby can pick up and respond to

57:46 As long as you have the right . If you don't have the right

57:49 , you're never going to respond. we just ignore those. OK?

57:53 here, it's not touching. If touching, that's still x.

57:59 So that's the kind of the key . There has to be a direct

58:02 , a direct interaction. All Um So the material is traveling some

58:09 of distance. So even though these cells are like near each other,

58:13 not touching each other, that's why not Jurin. So like a synapse

58:18 be a form of paracrine signaling, Jurin because they're not touching the cells

58:23 are not interacting. All right. other thing I would say is that

58:27 this uh this signaling molecule leaves, has a finite distance, it can

58:32 because of enzymes in the body and mechanisms that remove the signal itself.

58:37 these are not particularly long distance autocrine, obviously, you're self

58:43 but with paracrine, you're not, not like you're reaching out to the

58:46 side of the room or the other of the body. It's like just

58:49 area right here. Think about being by a bee, right? You

58:52 local eye swelling, you don't get everywhere. This last is long distance

58:59 . There's no book or no picture any book that does a good picture

59:03 this. But the idea is that is a blood vessel traveling some distance

59:07 the body. So here are the that are releasing their chemical, that

59:11 goes into the bloodstream, it travels distance away to the cells that have

59:15 right receptors and you get a right? This is what hormones

59:20 All right, this is the endocrine . So long distance signaling falls into

59:24 category. All right, we refer this when uh the signal goes into

59:29 bloodstream, we refer to it as hormone hormones have varying sizes and uh

59:34 which will cover it, I think the next lecture. But the idea

59:38 is I'm using one part of my to tell another part of my body

59:42 probably more than just one what to . Does that make sense?

59:48 So for example, your uh your anterior pituitary releases chemicals that control

59:56 gonads that control your adrenal glands that digestion, they control all sorts of

60:01 at some distance away. It's not signaling, it's using a chemical message

60:05 do. So. Now when that goes, it's going to find a

60:11 and there are lots of different types receptors, we have them classed out

60:15 . You can see ligand gated G protein couple receptors, catalytic intracellular

60:20 activated. I want to cover these two here right down. Then we'll

60:24 the other three in the next All right. But these are just

60:29 of like different structures, how they differently. That's really what it boils

60:34 to. And there's some very generic that every receptor does. And so

60:39 you learn the generic thing, then doesn't matter what the receptor is,

60:43 can pretty much figure out how the system is gonna work. And far

60:47 often I see students trying to memorize individual type of receptor and what it's

60:53 , right. So let's kind of the big picture stuff. So this

60:57 here is the picture from your And you can see what do I

61:00 is I have a receptor ligand It has these molecules and enzymes that

61:06 some second messenger that results in the of a downstream protein. Here it's

61:10 kind, right? But in what we have is we have recognition

61:15 then we have a changing of an signal to an inside signal, that's

61:21 , right. I'm changing it from form to the next. And then

61:24 inside signal goes and activates some sort effector. An effector is a molecule

61:29 causes an effect. Right. So modulate, we change what's going on

61:36 , or we're transmitting that signal and the modulation is, what activity are

61:40 doing? Are we turning something on are we turning something off? All

61:45 . And then, so that turning or off results in a response in

61:48 cell and then you have to turn off because your cells are like your

61:53 and don't waste energy and I'm paying bills and yada, yada yada.

61:57 . So anything you turn on, have to turn off your dad tell

62:01 to turn off the the lights when leave the room. OK? Just

62:05 sure because I say that all the . I thought no, no,

62:08 never gonna say that I'm like constantly off the lights, turn off the

62:12 , turn off the lights. Let's if you guys can see what I've

62:17 described up here in very generic Gotta pull out my pin. All

62:27 . So when we're talking about receptor , what we need first is we

62:30 a plasma membrane. So I'm going draw a plasma membrane. Look at

62:33 a fantastic artist. I am. you. All right. So what

62:37 we need for dealing with receptor What do we need receptor. All

62:42 . I'm gonna draw a receptor. receptor is going to be this

62:46 OK. So our acceptor is the giant R, I apologize because I

62:50 to do this without support. So our r it's a receptor. What

62:54 to the receptor? A lien, ? Or a ligand? All

62:58 So we're gonna make the diamond a . Now again, I apologize for

63:02 artwork. All right. So the step is the receptor needs to be

63:07 to recognize the ligand. If you a ligand, that doesn't recognize the

63:10 , nothing's gonna work. That's the step, right? But notice this

63:14 an outside signal. So this is ECF right over here is the IC

63:19 and so that outside signal has to an inside signal. So we need

63:24 to convert that outside signal into the signal. And so when the ligo

63:28 to the receptor, it changes the of the receptor and the change of

63:32 shape of that receptor changes what that is associated with. All right.

63:36 that receptor is associated with a OK. So I'm going to make

63:42 box for the transducer. So we a transducer and then that transducer does

63:51 , right? It's going to activate in that system inside. So it's

63:58 that external signal into that, that , the external into an internal

64:02 Now, not all systems have this step, but I'm going to draw

64:06 in here so that you can see . All right. And usually,

64:10 not always what we have is we some sort of enzyme that's associated.

64:18 put it easy for enzyme, some of enzyme associated with the internal side

64:22 the membrane so that the transducer can along and change its activity.

64:27 what we're doing is we're using the to turn on the enzyme,

64:33 And usually what we're going to create a result of that if that exists

64:37 some sort of second messenger. All . So that's our second messenger.

64:41 need a new shape in there. think I'll do a triangle. All

64:45 . Now, the second messenger's job to activate the effector. All

64:52 And again, what is the effect we're not concerned about? Um,

64:55 need a new shape here. Uh gonna try to do something weird.

65:02 do. That was tough. What we have here is the

65:12 And so this activates the effector and the effector goes on and does something

65:18 change in the cell, right? change in the cell could be something

65:26 turn on something that I turn I can turn on gene expression,

65:30 can change the activation of other right? It's, it could be

65:36 variety of different things. But if see this right, it doesn't matter

65:41 the system is. OK. All the systems signaling systems that we're going

65:47 look at, have something like The one exception being that maybe we

65:52 a system that is missing that internal at which point that transducer is just

65:57 the effector. That kind of makes . I can leap over that.

66:01 when you look at a, at , at a system and you see

66:05 pattern, all you gotta do is oh OK. This is something I

66:07 know. Now, I just maybe have to memorize now the different

66:11 OK? So what I wanna do I want to show you a couple

66:14 these systems and then we'll be done you can go home and you can

66:19 all this information and say, look at all the things I learned

66:23 or didn't. Yeah, I could hear you. Sorry. It is

66:35 activating some sort of factor. Let's that one first. OK? What

66:44 looking at here is we're looking at system like a synapse. OK?

66:52 here we are at the synapse here our message, right? That's our

66:57 . The signal is binding to the . There's not even a transducer in

67:01 system because what that message is doing binding up to a channel and that

67:06 is now opening, this is a gated channel. So when I open

67:10 channel ions flow in or they flow , right, we always draw with

67:15 flowing in stuff, but it could the flowing out and which is going

67:19 cause the cell to either hyperpolarize or depending on which direction the ions are

67:25 , which causes a membrane potential Which means I'm either activating the cell

67:30 deactivating the cell. So far, basic. Everything downstream is more or

67:36 ignored, right? The receptor in case is acting as an effector.

67:42 . That's the easiest my favorite, G protein coupled receptor. Why is

67:48 my favorite? Well, because I in a field that was primarily focused

67:53 this. Plus, there's only 5000 these. So you know, you

67:57 one, you learn them all. . G protein couple receptor, seven

68:01 membrane region. As we mentioned last , it is called G protein couple

68:05 because it is coupled with a G . A G protein is a hetero

68:09 protein, hetero, meaning different kinds meaning three parts. So it's a

68:14 part, different part protein has an , a beta and a gamma

68:19 Now, is that really important? all know it's just something that you

68:23 pick up and you hold on All right, when a ligand binds

68:30 a G protein couple shapes receptor, changes the shape which is interacting here

68:35 the G protein region, right. that causes a change in the G

68:39 the alpha subunit. Basically the alpha job is to bind up to a

68:47 and then has a TPX activity that the cleavage of a TP release

68:53 All right. So what it it says, oh, I'm going

68:56 , and then it holds on to GDP until it's to let go.

68:59 when I bind up to that, when I change the shape of that

69:03 protein, it kicks out the GDP says, bring on the A TPATP

69:08 it and when A TP binds, causes the chimeric protein to separate into

69:11 parts, an alpha subunit bound to and then a beta gamma subunit that

69:16 off and does its own thing and kind of ignores but it has its

69:19 activity, right? We really have now, two transducers, an alpha

69:24 a beta gamma. All right. then the alpha goes off and does

69:27 thing. It, it cleaves that TP. So basically, it's GTP

69:32 . Um our, it's, it's TP activity, basically cleaves, it

69:37 the energy and it comes back and , I'm ready to hang out with

69:39 again, right? And then you can repeat that process over and over

69:43 over again as long as the channel opened up. So this is kind

69:47 what it looks like. All Now, see if you see the

69:51 . All right. So here what have, we have our G protein

69:55 , coupled to the G protein couple . Here's our ligand, it binds

69:58 that. See, we're bound up the GDP, right. We activate

70:02 . See, I'm activating. So kicking out the old GDP. Go

70:06 . I don't like you anymore. in the GTP. All right.

70:09 I'm gonna do is I'm gonna separate and I'm gonna go downstream and I'm

70:12 go, start looking for things that can activate. What am I

70:15 I'm activating some sort of enzyme. enzyme doesn't matter right now. I

70:20 activate this 10, wait, maybe can go activate something else.

70:23 look, that's what beta gamma is . It's activating two different things,

70:27 . And so now I'm kicking off signaling cascade. All right. That's

70:33 particularly helpful because it's pretty generic, it? First one, you guys

70:36 to know signaling through Adal cycles. is the most common type of G

70:43 coupled receptor signaling that exists primarily because nose has all these G protein coupled

70:49 and this is the system that it . All right, we're going to

70:53 more specific. Now, here's our , here's our G protein, here's

70:58 ligand, it binds to it here's the alpha subunit. In this

71:02 case, it's an S subunit. , that doesn't matter. It's activating

71:06 enzyme in the membrane, that enzyme the membrane is called a cycle,

71:11 ? Biologists name things for what they like or for what they do.

71:15 is an enzyme it says so in name, it's a cycle. So

71:17 is it doing? It's taking a cleaving off two of the proteins and

71:24 that last little uh uh phosphate and binding it around and rebinding it to

71:29 ribo sugar to create a molecule called A MP. That cyclic A and

71:35 . So I bent it right back . Really? That's the bent

71:40 All right. And that cyclic A P is now a second messenger.

71:44 can do things. All right. this is the, the second messenger

71:49 moving on. Typically, what admiral does it binds to and activates another

71:56 , an factor called protein KSE This is the most common protein kind

72:04 . You can see in this thing a couple of sub units, get

72:06 cyclic K MP. It, the , when you activate the system,

72:10 happens is, is that it can and activate other things downstream, not

72:15 one thing, many things. So can activate this and it can activate

72:20 and it can activate this over And so you're turning on multiple things

72:23 turning off multiple things in the You can turn on gene transcription or

72:29 off gene transcription through this mechanism. so you can turn a single molecule

72:35 into a massive response inside the cell of the cascade event and how it's

72:40 out to all sorts of different Protein cyclic and P A no

72:49 they all go together. So it's hand in hand. Second, most

72:56 type signaling through phospho dias PDES for . Right here. Once again,

73:05 is light. Look at this. this is how your eyes work.

73:08 going to go in a lot of here a little bit later. But

73:10 essence, same thing. We got G protein. You activate the G

73:13 . What is it doing is an phospho, what do you think phospho

73:18 do? They're looking for Dior to , aren't they phosphor? So that's

73:25 it's doing. It's looking for a bond, cleave it. All

73:28 So that's what it does. It that cyclic GMP which is like cyclic

73:33 MP, right? So it has little cycle cycle and it's gonna

73:38 sorry, that bond right there. it's gonna turn cyclic GMP into

73:43 All right. Now, there's a why it does that. We're not

73:46 to go into it, but it, it, it changes the

73:50 of the cell. So that channels closed because you get rid of the

73:53 that's opening the channels and off it . Does that look any different?

73:59 though there's a lot of different molecules receptor transducer enzyme, second messenger.

74:10 would this be defector? Here's another , phospholipase, man. Another

74:20 Yes, another one. All But notice they're all the same receptor

74:25 transducer enzyme, second messenger, second messenger, Ector. All

74:36 Now, what's going on here? we talked about phospho and no PP

74:42 . I said we're gonna come back it. Well, here we're coming

74:45 to it. And there it this phospholipase looks for PP two and

74:50 cleaves it. So here's pip You can see that right there.

74:53 that head and what it does, cleaves that off and it gives you

74:58 glycerol and it gives you IP three nool trios. IP three is a

75:04 easier, isn't it? And each those molecules are now second messengers.

75:09 , diacylglycerol is second messenger to activate K AC. If I have a

75:14 kine A and a protein kine do I have a protein kine

75:17 Yeah, I do. Ok. right. If I have a fossil

75:21 , what do you think? A , IP three goes and acts as

75:28 second messenger to activate and open So, basically what you can do

75:35 you can flood the cell with All right. Now, why is

75:40 important? Well, calcium also serves a second messenger. It binds to

75:44 molecule called calmodulin. See how clever name is. I'm a modulating

75:50 calcium modulated protein. Ridiculous. How some of these names are. And

75:58 it does is when this gets it acts a lot like protein kine

76:01 does, it turns things on and things off. And so what I'm

76:06 by releasing the calcium is I'm, spreading the wealth. I'm spreading the

76:10 to activate other things and you're sitting looking at me, I can see

76:15 looks on some of your face. have to memorize all this stuff.

76:18 I say you had to memorize No, I said you had to

76:21 the pattern and I'm giving you three of really strong common pathways. All

76:29 got to remember is calmos an It's activated by calcium. I open

76:33 through an effector. What's that It's a channel. How did I

76:37 that? Oh, through a second . It's basically putting all the pieces

76:42 , right? Is my last slide . Yay Raonic acid pathways.

76:53 nothing to memorize on this slide. is just an example. So you

76:56 heard of a Raonic acid when you of a Raonic acid, what do

76:59 think of spiders? Yeah, I too. It has nothing to do

77:03 spiders. All right. But it everything to do with um uh pain

77:08 modulation. It has to do with contractions, all sorts of stuff.

77:14 interferes with the production of these these molecules downstream. They affect this

77:21 right here. Where is it So there's cox and cox too.

77:25 , aspirin gets in the way of things irreversibly blinds it. So the

77:29 doesn't go forward. But why I'm this thing up here is not to

77:33 how and what Aon acid does. want to show you. What are

77:36 doing here? What's that? What's ? Right. What's this transducer?

77:48 this enzyme? So, what does become down here? Well, I

77:53 , really here. What's this right ? That's our second messenger,

77:58 Here's another enzyme, right? What's ? Oh, sorry, there's the

78:01 enzyme, right. What's this acting second messenger? What's that receptor right

78:08 ? An factor. What's calcium doing messenger? Do you see? You

78:15 , you don't have to memorize and every step, you can look at

78:19 like this and you'll see it up over and over. Granted. Right

78:23 , we're looking at G protein couple . When we come back on

78:27 we got three other classes of receptors we're gonna be looking at and I

78:31 you to look at them through that lens. What's the receptor? Is

78:36 a second messenger? Is there a and all this stuff? And you're

78:39 sit there and go. Holy This is so easy. Why do

78:41 make molecular biology hard? You guys a great day. I will see

78:46

-
+