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00:01 alright, I think we're going There we are. Alright, so

00:12 we are, one more day, many days till the end of

00:17 No one is keeping track three more . See these are the important things

00:24 I was a long time ago I high school um forward grad school and

00:30 were counting down and I taught math down by prime numbers, so you

00:36 every day would come in the vice that we're looking at us funny because

00:39 wear like a different tie or something what's going on today, Oh

00:43 nothing just counting down the days. what we're gonna do is we're going

00:48 look at the parts of the I we're going to kind of dive down

00:52 little bit deeper, so we're gonna with the rods and the cones,

00:55 gonna see some complexity stuff that may may not be important. I'll point

00:59 like this is important, this is important, you know, that sort

01:02 thing. And then what we're gonna is we're gonna look at the mechanisms

01:06 allow us to actually turn light energy an action potential, which is called

01:12 transaction. Um and it's it's basically a g protein coupled receptor pathway.

01:18 was the first one discovered. So kind of interesting in that sense but

01:22 literally going to be doing some some which are kind of I think are

01:27 of interesting, so hopefully we'll get all that and then what we'll do

01:30 we'll jump into the ear and look the structures of the year and how

01:33 ear hears? And I think we that when we're talking about the

01:37 ear does two things. It plays role in hearing, also plays a

01:40 in equilibrium or balance right. And we're gonna get hopefully get through the

01:45 part. And so our starting point is where we left off, we

01:48 talking about the rods and the And so remember we said the retina

01:52 multiple layers of cells. And so we're just gonna do is we're gonna

01:55 of look through a couple of these and we kind of tend to focus

01:59 on the rods and cones because these the photo receptors use the ones that

02:03 receive that light energy and convert that energy into a graded potential that then

02:09 transmitted through the bipolar cells and ultimately the ganglion cells to be submitted up

02:14 the visual cortex so that you're perceiving light energy. And so we have

02:19 two different types of cells Roger because they look like rods cones,

02:22 name because they look like cones. what they do is they respond to

02:27 wavelengths of light and allow us to within that particular spectrum. Now you

02:35 see here, we got kind of compare contrast thing. And so you

02:38 , we have Rogers only one type rod cones and humans, there are

02:42 types of other species that may have , like chickens have four. You

02:47 , So it's just different. And , what do they do?

02:50 the rod is primarily responsible for night . Alright. It's the one that

02:54 you to see kind of in the notice, kind of in the dark

02:58 you can't really see in the Whereas the cones, they play a

03:02 in color vision. So it's really of daytime vision in terms of where

03:07 located. Well, the outer you can see outer segment is simply

03:11 series of folds that then turns into kind of elongated structure. And within

03:17 are these kind of membrane bound They look like pancakes stacked on top

03:21 each other. And so where we're to be looking in terms of the

03:25 transaction pathways occurring within those pancakes, in the cones, this is actually

03:30 membrane folded on itself over and over over again. So structurally they're

03:35 Um Which is why they come up their unique appearances. Um In terms

03:41 where they're located, if we take retina, remember we said we have

03:45 round structure if we flatten that out think of it as kind of a

03:48 eye that kind of expands outward towards edges, we're gonna see the rods

03:54 located on the edges on the whereas the cones are gonna be located

03:58 what is called the central uh phobia , which is basically the center of

04:02 bull's eye. And you can see terms of numbers, the number of

04:07 heavily outnumber the number of cones by significant margin. But that doesn't

04:12 It's just that you're covering a greater and we're going to see kind of

04:15 picture in that of that in just moment. So as I said,

04:19 rods are primarily night vision, so where there's dim light. What that

04:23 is is that the reason that you're to see in dim light is because

04:28 has a high degree of sensitivity towards . And so you can send a

04:34 at a single rod cell and stimulate rod cell to fire. All

04:38 And so you perceive even minimal but because they are so sensitive,

04:45 you overstimulate them, they stop All right. And so in

04:50 the cone cells, they're very they very low sensitivity. It takes more

04:55 energy to stimulate them. And so you get a lot of photons that's

05:01 they turn on. And so all a sudden now you kind of see

05:03 , when it's dim my roger kind working and then what happens, it

05:07 too bright. And then the rods working and the cones kind of take

05:11 . Alright, so that's kind of that works. And so the other

05:15 of that is the acuity All And this is going to have to

05:18 with the degrees of concentration. All . And so what we're going to

05:22 is because they're so highly concentrated, cones, we have a high degree

05:27 acuity. Whereas the rod to kind spread out, they cover larger visual

05:33 that you get kind of a blurrier . Alright. In other words they're

05:37 quite as acute now they'll use the I tend to use and we're going

05:41 see a little bit later and if not tech savvy, I apologize but

05:46 the easiest one you can think about . You know? So back when

05:50 was growing up, you had basically standard definition like 480 p.

05:57 I see people looking at me like ? And then high def came out

06:00 couple of years back about 20 years when I was 7 20 p or

06:04 80 P. All right. And now you're starting to see the four

06:08 TVs and what those represent are the of pixels over a certain area.

06:13 right. So if I have a that is oh I don't know,

06:16 inches tall. It's saying there's 480 from top to bottom. Whereas with

06:21 7 20 it's 720 pixels. If 10 80 that's 1000 and 80.

06:26 four K is 4000 and so and forth. So what you're doing is

06:30 getting smaller and smaller and smaller So that gives you greater acuity,

06:36 put it this way, which would rather do watch a movie on an

06:39 television or would you like to watch movie on a brand new spanking four

06:42 tv? The four K. It's realistic, right? You can tell

06:49 that's on an old tv. It's yeah, that looks kind of like

06:53 . Alright, so that's that acuity that's what we were kind of talking

06:57 on Tuesday when I told you kind look at that piece of paper or

07:01 that that thing that your you know your laptop or whatever and look right

07:06 forward, you can see it's very clear, but if you don't

07:08 your vision you can see it's kind blurry out here. Alright, that's

07:12 example of acuity, it's like you tell there's stuff there but it's not

07:16 clear. So what do you do you turn your eyes to kind of

07:19 and see what's going on. The thing that I want to point out

07:24 again, has to deal with the portion is the convergence. Alright,

07:30 convergence recall is the number of cells are attached to the next level of

07:36 . Alright, so I have given example previously, it's like you can

07:41 and I'm gonna use this number for , there might be 100 rods and

07:45 the 100 rods, there might be bipolar cells and for 10 bipolar

07:50 there might be one ganglion cell not making up numbers but it's it's

07:54 of an easy thing to do. you go A factor of 10

07:58 So that would be an example of degree of convergence. Going from lots

08:01 cells to like one cell with Part of the region of high acuity

08:06 because you have low degrees of So you might have one cone to

08:12 bipolar to one ganglion cell. So means your field. If a ganglion

08:18 represents your visual receptive field, you what your brain perceives light coming

08:24 Then for a cone, the light field is very very small. Whereas

08:29 the rods it's actually rather large because ganglion are receiving information from so many

08:34 cells. That's again that security. we're gonna see this hopefully in just

08:38 minute. But this is kind of overview so you can do this.

08:41 simple compare and contrast. What does one do? What does that one

08:46 ? And so here is looking at retina. Alright, this is what

08:50 optometrist does when he shines or her shines that light in your eyes.

08:55 is what they see in the back your eye. Alright. We said

08:58 goes in but it doesn't come out it's getting absorbed by that uh that

09:02 or not really, that pigmented layer epithelium. And so you can see

09:07 this uh is you know, there's down here is kind of representing where

09:11 are. So the blue dots represent , the green dots represent cones.

09:16 if you use this graph, you see out on the periphery, it's

09:19 rods and then all of a sudden , it drops right down and in

09:23 very center of the eye, there's and lots of cones and then moving

09:27 out through the retina. You see and lots of rods again. So

09:30 like lots of rods and then nothing lots of rods. Again, if

09:34 go cones, very few cones and of a sudden lots of cones and

09:37 no cones or very few cones. that frame of reference though, is

09:43 the back of this. I And you can see the back region if

09:46 shining light directly in the back of eye, what you're doing is you

09:49 that large bullseye, you guys play . I mean if I'm saying bull's

09:53 , you know what that is, . You know, with the bulls

09:56 , there's a single bulls eye. then there's another smaller dot. That

10:00 dot is called the trying to see plays darts here because you're at the

10:07 where you need to be learning how play darts. All right. I

10:11 , that's that's what college is all , right? Going to the

10:14 go into the pubs, learning how play darts. We don't drink at

10:16 pubs. We just played darts. single bullseye double bull's eye. There's

10:22 big circle, smaller circle. More for the smaller circle. Okay,

10:27 . See we know you're just not along with my game this morning.

10:31 right. So the bigger circle is the Macula Lutetia. Alright, So

10:36 basically where light goes and hits. , so that's where your light's

10:42 But the center of the macula Lucia the phobia centrales. That is where

10:47 highest concentration of cones are located. when you think of the focal point

10:52 the eye, that's the phobia centralist this region called the macula Lutetia.

10:58 , you can also see if you in the back, you'll see this

11:01 where blood vessels and all the nerve are entering into the eye. And

11:06 this is all the axons of the cells, there's no need to put

11:12 uh photo receptor cells or bipolar, not room for it. This is

11:17 optic disc. And because there's no photo receptor cells, it's also your

11:23 spot. And so it's a little spot in your eye where no light

11:27 actually hitting. And so what your does, it actually fills in the

11:31 for you. It's a really, small thing. I don't know if

11:34 when I was in third grade, taught us this optical illusion where it

11:37 like you draw a dot. And an X. On a piece of

11:41 and you stare at the X. then you move the people, you

11:43 the paper back and forth and you watch the dot disappear as it passes

11:48 where the optic nerve is located. optic disc. All right now notice

11:53 is gonna be on the medial side the eye. And then so again

11:57 pointed out here with the periphery that's here on the edges. This is

12:00 you're gonna see. Mostly rods. mean there aren't any cones, but

12:04 are mostly rods there. So I this, we're going to come back

12:12 in terms of how the rods and cones work. We refer to con

12:16 vision as faux topic we refer to as uh rod dependent vision as sco

12:24 . Alright, so faux topic. easy way I remember this photo

12:27 photographs color. All right. And you're an R. T. Purchase

12:32 black and white, I'm sorry. just messed everything up. But really

12:36 this basically says is look my vision dependent upon how much light is

12:40 Alright, when it is dark and is very little light, my roger

12:44 be stimulated because very little light is to stimulate that. And so that's

12:48 be the first level, that's the stuff that gets turned on. So

12:51 now depending on scope topic. Vision about when you wake up in the

12:54 of the night. You don't turn the light, you're just going to

12:56 bathroom or whatever and you're moving around room and you can see objects in

13:00 room, right? You can see pile of laundry in the corner.

13:05 think it's a pile of laundry because , you remember that's where you put

13:07 laundry, It might be a you're not quite sure, but you're

13:11 going to turn on the lights to out because we know that's the

13:13 you don't turn on the lights to out, right? But you can

13:17 of see the general shape, you see the dresser, there's enough light

13:21 through from outside that you can probably around the room, but you can't

13:26 the details of what's in that So that's an example of sco topic

13:31 , you turn on the lights now have enough photons that your your rods

13:36 oversaturated. So they basically stopped working now your vision is now dependent upon

13:42 or skills beyond cones. Now you discern colors, you can discern shape

13:48 right in the dark. It's really to discern color. It's kind of

13:52 dark or it's not dark, So that's the idea. Now,

13:58 adapt very, very quickly. think about when you go outside after

14:03 to a matinee. Have you ever to a matinee? You know what

14:08 is, that's a show during the in texas. If you go to

14:12 matinee, it's dark in the you open the door, What

14:16 You're blinded, right? And everything bright, It's like white and you're

14:21 , okay, I can't see Right, But you still managed to

14:26 to your car because you do All right. Maybe you cover up

14:30 little bit here. The reason you're to see quite a bit quicker after

14:35 blinded by the light is because those are re stimulated because it got

14:41 just like your rods do. But reset all the mechanisms inside very,

14:47 quickly. It takes about 2-3 minutes reset a cone rods on the other

14:53 , Adapt very slowly. If you them too much light, it takes

14:55 about 10 minutes to adapt. Think going from a bright space to a

14:59 space and how long it takes for eyes to adjust to the dark

15:03 Yeah, you can see the shapes stuff, but it's your now you're

15:06 kind of working on those cones and cones are going, I can't see

15:10 . And it takes about 10, minutes for you to kind of really

15:13 able to see well. And the is it takes about 30 minutes before

15:17 rods are actually ready. There was great show on. Mr what is

15:22 ? Mystery buster? Mystery mythbusters. they asked the question, this is

15:28 a fun one. Why did pirates patches? Alright. You think

15:33 because it looks cool, right? guys aren't interested in pirates, are

15:39 ? Mhm. Alright, why do wear patches? Well, maybe they

15:43 their eyes knocked out? No, the, the theory behind this,

15:46 from the artistic and how it looks is that the pirates had to be

15:51 on deck where it was sunny and when they had to go and fight

15:57 , right, it would be dark it's very hard to see. So

16:00 you're fighting someone who's already dark adapted your light adapted, you're going to

16:04 the loser. So what they did they put a patch over there,

16:08 gotta do it like this so that are light adapted in one eye,

16:11 adapted in the other. And so they went downstairs you just lift up

16:15 patch and now you can see just myth buster said, is this

16:23 They tried it and guess what? , so maybe I think it had

16:30 to do with that, It looks . Alright, bipolar cells are weird

16:37 hard and we're gonna use one example a bipolar cells. These are there

16:41 multiple types of bipolar cells. But in essence what a bipolar cell

16:47 , is a cell that's downstream of photo receptor cell and its job is

16:53 turn on or turn off the ganglion downstream. So notice it's either going

16:58 be an on cell or an off . Alright, so what they do

17:02 usually you'll have a photo receptor cell you'll have to bipolar cells associated with

17:06 one that's gonna be the only one gonna be off. I'll give you

17:09 example. You don't need to know , but there's like the blue versus

17:12 . So some cones will be sell some will be yellow cells.

17:17 so they're basically turning, if blue hits it, it's gonna it's gonna

17:21 one photo one bipolar cell. If hits that particular cone, then it's

17:26 be the the other bipolar cell. really what this does is that it

17:31 for your brain to understand contrast much than it would than if the information

17:37 up here and it started processing. what we're doing here is we're really

17:40 of processing information and stimulating pathways That information never even leaves the

17:49 All right. And so they kind served as a point. So this

17:52 what this is trying to show you . Here's our cone and says one

17:55 here is off center, one is center. So when light hits this

18:00 , this receptive field and light hits receptive field in the center. So

18:05 this cone happens to be in the then it's going to turn it

18:08 But if the light is not hitting , then that's going to turn

18:11 And so you get a different So basically what you're doing is you're

18:15 here, I got out side by , one is in the center,

18:18 is not. If this one gets , this one definitely um sends a

18:24 . This one definitely does not and creates this greater contrast between dark and

18:31 . Again, I'm pointing this stuff over here, light out here,

18:35 over there. The reason your eyes perceive the difference is because right now

18:40 getting their bipolar cells going, oh more light out here than there is

18:45 here. So if I'm looking at receptive field in the center of that

18:49 field is saying it's more dark. I'm turning the off centers on and

18:55 turning off centers or the on centers . It's kind of how it

19:00 But when you think bipolar cell, is what you need to think downstream

19:04 the photo receptor upstream of the ganglion modifying signal. Okay, we're going

19:11 see at least this example a couple times to help you understand, we

19:17 about receptive fields, receptive fields simply remember when we talked about touches the

19:21 in which a neuron is receiving input a from a receptor. Alright,

19:27 we have receptive fields in the we said that cones have very,

19:32 small receptive fields, we have rods have very large receptive fields and this

19:36 trying to show you what that looks . So the ganglion cell.

19:41 so remember we have the photo We have the bipolar and then we

19:44 the ganglion cells. The ganglion cell the receptive field. Because what we're

19:51 about is the number of cells that converging on that ganglion cell. And

19:56 in the Phobia Centrales where we have , we have very few or we

20:03 very or very little convergence. So kind of a 1-1 to 1 is

20:08 example that's being shown. Alright. if you look on the periphery you

20:12 have a gangling sale, but there'll lots of cells affiliated with that.

20:16 right. And so it's basically telling the area in which I'm going to

20:21 light. So if light stimulates over , I still stimulate the gangling

20:25 Light stimulates over there. I can stimulate that one ganglion cell and I

20:30 have a lot of acuity when that . I don't know where the light

20:33 . It's some place within this But if I have only a

20:37 then when light hits that one, stimulating. So I know exactly where

20:41 light is coming from. I have high degree of acuity and that's why

20:45 use that, why we use an like this. Your eyes are not

20:51 . All right, But you kind get the sense this would be an

20:56 where you have high convergence. You see the stuff in that picture,

21:02 ? I mean, you can perceive that is back there. What is

21:06 come out right? Does it look a mountain? I mean No,

21:12 it's kind of fuzzy. You can it's very blocky, right? But

21:16 brain looks at that and says okay that kind of that blocky image type

21:21 over there. Yeah, that's kind a mountain. It's kind of like

21:24 you look at your peripheral vision, you focus forward and kind of look

21:27 here you can see there's stuff out , it's kind of fuzzy, I

21:31 what that is that looks like a over there. It has kind of

21:34 the the shape of what I expect be a person to be and how

21:38 I know I can go and look Oh yeah, that's definitely a

21:41 Alright, so your brain is taking shapes and stuff and saying this is

21:45 I think it should look like. on the periphery that's just fine.

21:52 is at 4K. Look at the , the number of pixels just say

21:57 there to there is A significantly it's about 10-fold greater than pixels from

22:03 to there and you get much much sharpness. So in areas of high

22:10 right, you're going to have greater . Alright, sorry, hi convergence

22:15 lots of things you're gonna have lower . So this is an example over

22:19 of high convergence over here. This lo convergence. So you're going to

22:24 much much, much greater degrees of . All right. And again,

22:31 just correlating directly to the receptive Small receptive fields, great yield high

22:39 , large receptive fields leave yield low . And typically those fields are out

22:47 on the periphery. Here we are , looking at the bipolar cells.

22:56 right. And what we're doing here we're kind of looking at that center

23:00 surround. So, what this So, down here, this is

23:04 ganglion cell right here. These are cells. And so these three cells

23:10 the receptive field of this ganglion Now, we have two ganglion cells

23:14 here and they both have the state field. Okay, that's kind of

23:20 . Right? They have the same field. Well, why does that

23:23 ? Well, they're receptive fields One is an on center, one

23:26 an off center. So what it is that when this ganglion ganglion cell

23:32 stimulated, that means light is hitting portion of the receptive field when it's

23:37 center, this cell is going to stimulated. And what it's saying is

23:41 is hitting on the outside of that field. And so this is that

23:45 thing that I was talking about. when light hits the center, it

23:49 you a sense that there's more light the center of the receptive field.

23:52 it makes it brighter if it's not the center is hitting the outside,

23:57 the outside should be brighter. The is darker. Now, I want

24:01 to think about a three dimensional object light height hitting it? Think of

24:04 apple. Right? You get the . You have that little bit of

24:07 shine. Actually, there's a great right here. If you look at

24:10 , the shiny bottle, I mean see how the light hits that and

24:14 kind of comes out at you and can kind of see the three dimensional

24:17 as a result of the light hitting bottle. Does the metal bottle?

24:22 . Alright, That's because more light hitting the center of the object for

24:27 receptive field. And so it gives a sense that this is popping out

24:31 you. Whereas if it was concave would be absorbing in the middle,

24:35 of like what we see over All right. And so it gives

24:39 a sense of the center is darker that's why you get that dark

24:43 You get that contrast. And this just a way for the brain to

24:46 the contrast better before it ever gets . All right. So, we

24:52 these fields that are basically working against other ones. A positive field.

24:56 is a negative field. And this is just saying on off as

24:59 , you know, is it light the center or is it not?

25:02 I told you there's many different And this is just one of

25:07 Okay, but what do we have photo receptor cells? What does photo

25:13 cells do receives light converts it into to a greater potential. That goes

25:21 a bipolar cell, which modifies a . And then that is going to

25:26 a ganglion cell. It sends a up to the brain. All

25:31 That's what you guys need to know now. All right. But it's

25:34 complex. What's going on along the . That's less of what you need

25:38 know. Just know. It's So, what I want to do

25:43 is I want to transition I want move down into the molecules what's actually

25:48 on in these rods. And these , we're gonna use the rod as

25:51 example. The same thing is happening the cone. It's just differently

25:56 Remember we said in the rod, have these little tiny pancake structures.

26:00 , these uh little tiny um uh is what they're referred to as.

26:07 , membrane bound disks now embedded in disks in the rod embedded in the

26:14 of the cone. Is our structure the photo pigment photo pigment is what

26:21 the light energy and converts the light ultimately into a signal. So,

26:26 just basically is there to absorb life different types. And so, really

26:30 we have here is we have two to it. We have a g

26:33 coupled receptor. That's what the green is. It's called option. And

26:37 upon where you are, you have types of options. So like in

26:40 rod you have rod options. See it is right there, rob Dobson

26:44 the cones. It's called Photo ops . So just option is good enough

26:49 us. Alright, so that's the that's a g protein coupled receptor now

26:55 learned and hopefully you haven't flushed from brains what G protein coupled receptors do

27:01 there are part of a signal transaction . A molecule comes along binds to

27:06 receptor activates a receptor and then something downstream. Do you guys remember

27:11 Okay, so what that tells us if this is the G protein coupled

27:15 it needs to have some sort of and it does the ligand is this

27:22 kill right here is retinol. if you go and look at a

27:25 of vitamin A, you'll see it's long chain with these little tiny rings

27:29 the ends. And if you clip right now, if you get a

27:31 and a retinol so that's with the retinol. Alright, now retinol is

27:38 pre bound to our G protein coupled . All right, so this is

27:44 weird case where I have a receptor already has its ligand attached to

27:51 So if I'm bound to my my leg is bound to the receptor

27:54 would usually tell you what's what are doing with the receptors that on or

27:59 . It's on. Okay, so kind of the first thing that's kind

28:03 weird. Now, the other thing want to point out, do not

28:06 these numbers. All right. I want you to see, do you

28:09 that there there's overlap? You guys the overlap. Do you see that

28:13 different? They have different peaks. . And what this represents is the

28:20 in which light energy can be traveling stimulate those different types of receptors.

28:25 you've learned at some point in your that you have these three cones and

28:28 have names. There's the red the blue cone and the green

28:31 All right. Those are terrible The reason they're called that is because

28:36 this peak value right here. All . Those peak values tell you kind

28:41 what wavelength of light you're kind of at visible light, but that's not

28:45 these actually work. All right, overlap here is the other thing I

28:50 to really kind of highlight here. at the rod. The rod overlaps

28:54 everything. So this is the light by. I'm just gonna make up

28:57 word gray light. I mean if is a No, there's no such

29:01 as gray light. Right? So stimulated by the save wavelengths of light

29:06 your cones are stimulated by the difference is that it doesn't give you the

29:12 of color. Alright. It's basically what we said. Very little bit

29:16 energy activates the rod. Too much basically over stimulates it so it can't

29:21 anything. So what this is basically is that at low levels of light

29:27 stimulating the same way you stimulate these so you're able to see but you

29:32 really perceive color. I think I to this. Yeah. So this

29:37 what color perception really is. You learned your Roy G biv?

29:42 okay. How many colors are Really? If you had to guess

29:47 do not say eight. We're That's Roy Jeep at seven.

29:52 How many thousands? She? You wouldn't want to go higher or

29:58 . Higher. How many? How ? I heard a number infinite.

30:05 probably way too many. Well, gonna do this. You're probably

30:10 There's probably an infinite number of All right, but I'm going to

30:15 the harder question. How many colors the human eye perceive a small portion

30:24 infinite? Yeah, you're correct, correct. How many? It's in

30:34 millions. That's absolutely correct. It's the millions. All right.

30:39 how many colors can you name The are like seven Roy G biv,

30:45 ? You you can probably go to 40. You don't think so.

30:49 think higher or lower? Well, right, ladies, I want you

30:53 name five colors of blue. Go . Navy. See another one.

31:03 blue. I heard another one, , turquoise and teal. All

31:10 Some of the guys are standing on are blue. How do you guys

31:14 cornflower? Some some layers are like , I do. Yeah. You

31:19 . So here here's the fun Alright, I'm gonna ask the guys

31:24 what color is this red ladies, color is that? Scarlett?

31:35 my point is is that we can lots of colors. I want to

31:38 you. All right. Everything You see your Roy G biv up

31:41 What color is her shirt is Is it up there? What about

31:48 sweatshirt for hoodie? What color is ? It's pink. Alright, we're

31:53 go with the guy answer pink. we see pink up in the color

31:59 . Huh? All right. What is showing you is the wavelengths that

32:06 can break out the colors as But can saturate colors with white and other

32:11 and with black and other combinations to different degrees of these different colors.

32:17 you've ever played with Photoshop or any of thing where you can manipulate

32:21 you'll know that you can hit about million colors. Right? And the

32:26 because of the way these cones actually . Notice what I said, we

32:30 them red, green and blue, their real names are the STM and

32:33 L cone And it refers to the of light that they're being stimulated

32:37 And what it shows you is if look at this, if this is

32:39 percentage of stimulation. All right, you can stimulate something 0%. Up

32:45 100%. Can't overstimulated above 100. under stimulate below zero. Right?

32:50 that's a nice simple range 0 to . I can have say, for

32:55 , I'm gonna use the green the green cone, Which is named

32:59 here's the range of green stimulates Look at that. I am not

33:03 maximally stimulated. I'm stimulated somewhere around . So when you think of a

33:10 , what it is is not the of a single cone, but a

33:15 of all three cones in the So again, let's go here and

33:19 can see I'm barely stimulating the I am sort of stimulating around 50%

33:26 the red cone and I'm stimulating the cone about 75%. So my brain

33:31 perceiving that color right there. so green, the perception of green

33:37 a result of the degree of stimulation each of these cones and simultaneous stimulation

33:45 all three of those cones, This why we're able to see millions of

33:50 , right? Because it's whatever that happens to be alright now,

33:56 if you've gone and played with Photoshop you're like adjusting your C.

33:59 M. K, which is really colors. Or if you're adjusting your

34:03 and you're like, you know, goes up a dot that goes down

34:06 dot what you're doing is the same that this is doing right, that

34:11 eyes are doing when, when light it at a particular wavelength. It's

34:14 at this wavelength I'm gonna stimulate the by this much, I'm gonna stimulate

34:17 green by this much. Or I'm gonna stimulate the green cone,

34:21 red cone and the and the blue . Or the SML cones at these

34:25 different percentages. And so now you're orange, if that makes sense?

34:31 , I always ask this color or color. Always ask this question to

34:36 . So, it's just something you want to put a star by is

34:39 is color perception? Is it perception a single cone? Or the perception

34:43 stimulation of all the cones? Something those lines. So make sure you

34:48 that? All right. The scary . Not scary at all.

34:55 this again. Uh This is a machine. Right, basically asked the

35:00 of All right, if I stimulate , how do I get the whole

35:04 to create an action potential. And we said, this is photo trans

35:09 . Alright, so, we're gonna photo pigment and you can see this

35:12 the picture from your textbook. And I've color coded it to match

35:16 you see over here. So, pigment is the green thing. Uh

35:20 have translucent, which is a G . Alright, so this is translucent

35:25 . Alright, we have a photo race PDE is how it usually

35:30 So as PDE right there, we a channel which is a unique

35:35 It's stimulated to open when it's bound the cyclic GMP. So it's called

35:40 cyclic nucleotide gated channel. So the happens to be GMP. So it's

35:46 GMP. Alright, so these are things Oh and then we also have

35:50 late cyclist up here. Guan. cyclist is what makes cyclic GMP.

35:55 . So in essence what we're just at. And when you're looking at

35:59 picture, you're going to be asking question, what do all of these

36:01 do when there is light energy or there is not light energy. All

36:06 . And so I'm gonna use this because I started when I started teaching

36:10 class. This is the picture I . I've color coded it to

36:14 To match that. I'm sorry. the wrong direction. Come on.

36:18 thing. Yeah. To match this that you can kind of go

36:22 But it's it's basically the same I even put the same color.

36:25 is just remind you what we're just at. Alright, so what I

36:29 to do first is I want to at this with regard to the

36:34 All right, so imagine no Alright. No. Like what's going

36:38 ? Well, we have one late over here, One late cyclist takes

36:43 nucleotide GTP. Alright. And what gonna do is it's gonna cleave off

36:48 two last phosphates. And it makes cyclical molecule. And we said this

36:52 GMP is what binds to this channel causes it to open up. And

36:58 that channel opens up sodium comes into cell and when sodium rushes into the

37:02 , what do we call that? polarization? So in the dark your

37:09 are d polarized and typically when we d polarized, what that means is

37:13 cell is activated. Okay. So we have here is we have a

37:18 that is being turned on in the . Now can you see in the

37:25 you don't perceive light in the dark very definition. But what we have

37:30 is a cell that's already turned on active. All right. And so

37:35 it's doing is that when you de , that's gonna spread throughout the whole

37:40 and it's going to cause the release neurotransmitter, the neurotransmitter happens to be

37:46 . And so what is doing is it's not being stimulated, it's telling

37:50 bipolar cell downstream is I'm not being . Do not send a signal up

37:54 the brain. And so you perceive how very backwards. That's not how

38:03 would design it was No, of I wasn't in charge of creating the

38:11 . Now if you have sodium coming the cell eventually you're going to fill

38:15 the cell of sodium and it's gonna working. So you need to have

38:18 way to remove sodium and so we something that's called the dark current.

38:22 the dark current is basically taking an sodium potassium pump. And as sodium

38:27 in you pump it back out. so what you do is you create

38:29 natural flo of course potassium is going . You want to also create a

38:34 for potassium to leave and so potassium . So to ensure that the system

38:39 working, you have a dark circuit a dark current. Alright, so

38:45 the dark there's mechanisms in place to sure that the current keeps happening if

38:51 is coming in, you want to it out so that sodium can keep

38:55 in. So now we have light comes along and stimulates the photo

39:09 Now we said the photo pigment has parts to it, it has the

39:12 protein coupled receptor part, that's the molecule, it has the uh the

39:17 that's already there, that's called retinol exists in two states. The state

39:22 you find it in in the dark it stimulated is the cis transformation.

39:29 you can see the little picture right . You can see the little tail

39:31 it. So if my hand portion kind of the ring of the retinal

39:36 , my finger represents the tail. would be the cis confirmation,

39:41 And what's gonna happen is light comes and plays with that little joint and

39:47 that sis turn into trance. so what I'm doing here is I'm

39:54 the shape of the molecule and you at the very beginning of the semester

39:57 I change the shape of molecules, happens. Okay, now this molecule

40:03 to be inside that particular option, is a specific size. If I

40:11 inside there like this and I change shape, what am I going to

40:14 to the shape of option do you ? What do you think you're gonna

40:23 shape? And when you change the of molecules, something happens.

40:30 So changing the shape of red and change the shape of options, change

40:33 shape of option option does something In other words, I've activated the

40:38 protein coupled receptors now. Really? you very much. Here we

40:50 Double check. Alright, so this just trying to show you here's the

40:54 confirmation. You can see there there's 11, that's the 11 carbon.

40:58 happens is you change the shape of the trans shape? So the tail

41:01 big. What happens is when the gets big, it no longer likes

41:04 shape, it changes the shape of option molecule. So now what you've

41:08 is you've activated opposite opposite is now of turning on the pathway that's downstream

41:16 protein coupled coupled receptors are called G coupled receptor because they're coupled to it's

41:22 a trick question. What is G proteins thank you very much.

41:27 all there in the name. So gonna happen is you've now activated That

41:33 retinol is no use anymore. So want to get rid of it and

41:36 reorganize it. So you're gonna send on its way. It's gonna go

41:39 to the pigmented epithelium and that pigmented that absorbs light is gonna say I'm

41:44 twist you back into the right shape I'm gonna send you back in a

41:46 of minutes. All right. But other thing because the opposition has changed

41:52 . What that does is it changes relationship to the G protein when you

41:58 a G protein coupled receptor. Remember there to turn on or activate the

42:02 protein. The G protein is normally by GDP. And what that does

42:07 that confirmation all change here causes a in the shape there. That says

42:11 don't need you anymore. Go G. D. P. I

42:13 something new. I want GTP so kicked the GDP out of the place

42:18 comes in GTP has energy and it I want to be activated. And

42:22 that's what you're doing is you're activating . That's the name of this particular

42:27 protein it's called transducer because when they discovered it they're like oh look we're

42:32 light energy from light into this signal then they discovered 40,000 others good on

42:41 . So we just call them G now. So transducers becomes activated.

42:47 right now notice we haven't done any yet. We're just doing step by

42:50 . We go to the next go to the next step.

42:56 The G protein remember has two parts it is the alpha subunit, beta

43:00 subunits. We're focusing on the alpha here because it's bound up to

43:04 T. P. It has energy it's saying I've got to go turn

43:07 on and when the thing that it's to turn on is this molecule called

43:11 dia strays Now there's lots of different diess traces in the body. They

43:15 do kind of slightly different things. it says it's a phosphor restoration of

43:18 it's doing is it breaks phosphate Right? Fossa di ester bonds that's

43:26 its name. So what you do when the G protein comes along and

43:29 foster diaspora. Foster diaspora says I'm for these diaspora bonds. Where can

43:33 find one? It says oh look have them right here on cyclic

43:37 So it's targeted cyclic GMP. The of cyclic GMP we said is to

43:42 keep this channel open and I've got thing over here constantly making cyclic

43:46 And so it's able to bind this . But if I start chewing up

43:50 GMP, I no longer have the to open the gate. If I

43:55 have the key to open the what's going to happen to the

43:58 It's going to close. So phosphor hates his job is to chew up

44:03 GMP basically cleaved that bond. So you just have regular GMP. That

44:09 doesn't recognize that channel. So you cyclic GMP when you lose cyclic

44:15 the next step is of course, the channel closes when the channel

44:19 sodium can't come in. If sodium come in, you are no longer

44:24 polarizing the cell. If you're no de polarizing the cell, then that

44:30 polarization becomes hyper polarization. This is weird use of that term. The

44:35 polarized cell now has less sodium. no no deep polarization or there's hyper

44:42 . Five hyper polarization have no signal cause release of inhibitory neurotransmitter. If

44:49 not releasing inhibitory neurotransmitter, I am longer inhibiting the bipolar cell. If

44:55 no longer inhibiting the bipolar cell by cell begins to fire and that signal

45:03 received by the ganglion cell and the cells send it off to the brain

45:08 says guess what? At this point where light hit. So I stimulate

45:18 photo receptor cell which causes the loss inhibition for my brain to perceive life

45:27 than what I would expect it to . But I'm not in charge of

45:31 these things. All right. So is kind of a way that you

45:36 put it up. So I walked all those steps and you're sitting there

45:38 , man, that's a lot of . No, it's really just step

45:40 goes to step B step B goes step, see it's just a Goldberg

45:44 machine. Just start at the beginning work your way through. But you

45:47 kind of say okay, what's going in the dark versus what's going on

45:50 light And you can just say all , in the dark. I had

45:53 retinal. The channels were open. membranes d polarized. That means I'm

45:57 neurotransmitter. It happens to be its inhibitory. I put green because

46:02 stimulating this cell. And when I'm the cell and really I'm stimulating it

46:07 to fire basically, you're not allowed fire. So, the bipolar cell

46:12 not doing anything. All right. over here, in the light,

46:16 light causes that retinol to change shape it changes shape, that cascade of

46:21 that we just describe from transducer and of PDE to the destruction of cyclic

46:27 causes the sodium channels to close. means this membrane hyper polarizes. Which

46:33 I'm no longer releasing neurotransmitters. If don't release the neurotransmitter, there's nothing

46:39 the cell. So the bipolar cell active and starts sending a signal and

46:44 why your brain perceives light. That's a nutshell, everything we just

46:51 it's right here. So, we've talked about this. So, I

47:03 I decided to repeat it. So adaptation is simply adapting to the amount

47:09 light in the dark. The rods going to be activated first and then

47:14 light levels rise, they become oversaturated over activated. So they stop

47:19 In essence. They're basically they can't anything other than bright at that

47:24 And so they get downplayed. And now the cones take over and that's

47:28 you start dealing with the faux topic . All right, that's that light

47:38 . This is one of those slides again you're gonna be tempted to go

47:42 and try to see this. This is a representation of a much more

47:48 process and I don't even want you learn what all these things are.

47:53 is what I want you to know this. All right. In the

47:56 cycle we said the cis retinal turns trans retinal. Trans rational is kicked

48:00 and sent away to go get rico . This is the recon jiggering.

48:06 , so what it basically says is light comes along, I'm going to

48:10 the shape of the retinol. Once that trans retinol, what I do

48:15 I kick it out to the pigmented , a whole bunch of stuff happens

48:19 that it gets back to its original and now once it's back to the

48:22 cyst shape, I'm going to escort very carefully and insert it back into

48:26 option molecule so that it can perceive receive light energy again and go through

48:31 whole process all over again. All . I mentioned it takes longer for

48:37 to adapt it. About 10 minutes a rod to adapt. Whereas for

48:42 it takes about three minutes now. is that? Well the cones aren't

48:48 dependent upon these pigmented epithelial cells. also have the same sort of system

48:56 them so they can reset themselves. right. But the idea is

49:03 All right. You don't need to all this stuff. The simple thing

49:06 is you have to record jigger the in order for you to see it

49:11 . Alright. Use it. It to be fixed so light hits the

49:27 . It stimulates the photo receptor Photo receptor cells are going to act

49:31 the bipolar cells, bipolar cells act the ganglion cells. The ganglion cells

49:37 the signals or produce that action potential then travels up to the visual

49:43 But there's a process. So the nerve is simply the uh all the

49:51 of all those ganglion cells leaving the . Alright, so that nerve represents

49:58 the receptive fields going forward. They crisscross and so fibers are going

50:03 go to both the left and the hemisphere. Alright. First place they're

50:08 to go. Is there going to thalamus? Remember we said in the

50:12 we have the lateral genic Hewlett That's the first place information goes from

50:17 And then from there it's then sent to the primary visual Cortex which we

50:22 v. one. This slow down slide. I don't want you to

50:29 again. All right. What I you to see here is that when

50:32 look at those layers you can see six layers. Remember we talked about

50:37 the cortex always has six layers. is an example of that. And

50:41 I want you to see here is you have different groups of cells in

50:46 locations. So for example you have magnets, cellular cellular cells.

50:50 They play a role in high Alright. Try and even see if

50:54 even show here. So it's the , they're showing you down here.

50:59 , parvo cellular cells deal with spatial and colors. I love the names

51:04 the areas where you're processing. Conor blobs. I thought there was a

51:11 that it was organized. When I started looking at this stuff, I

51:14 looking at stuff and I was like I don't get it. You don't

51:17 to get it either. It's all . All right. But the idea

51:20 that information is broken apart spatial Understanding the distance between objects is broken

51:29 from color which is broken apart from which is broken apart from movement and

51:35 these different things are being processed at levels within the cortex and then they're

51:41 to other areas. Remember what I . Visual Processing takes place in a

51:46 of different parts of the brain. focus on b. one not a

51:51 that you need to know. I want to show you the complexity.

51:55 you have V. One, here's . Two, there's V.

51:58 V three A. Here's V. over there. Down along the

52:02 there's V five and you can see basically information is being sent to a

52:07 bunch of different areas. You can just as an example. V three

52:10 processing motion, right? So when perceive motion, think about motion.

52:16 see if somebody moving that's easy. think about a video game. Why

52:21 it look like on a video The person is moving correctly.

52:26 Is because they can mimic But you in terms of the number of sprites

52:32 they use in some cases what movement like in your brain fills in the

52:37 and says oh that's what the movement like. All right, so the

52:43 cortex is vast because we are visual , we are dependent on vision to

52:52 our environments. All right, we're . Our eyes are on the front

52:57 our heads and on the sides looking danger. Right? We hunt by

53:03 and whether that means going to taco and hunting where they're going out into

53:07 bush and hunting you're hunting. I that's all we have. Yes.

53:14 , so I'm gonna stop there for second. I know we talked about

53:17 confusing things. So this is your to say wait a second. I

53:20 understand this and I know that no is going to raise your hand because

53:23 all a bunch of do it, it. Uh huh. Yeah.

53:31 . Yeah. Yeah. Yes. to. All right. So,

53:35 questions of visual cascade. Alright, just gonna focus in on their

53:43 Okay, But you can walk through think of each of those slides as

53:47 the next step. All right. I want to do this because I

53:50 this is easy to remember in the . The cell is already active,

53:55 ? Because what you have is your cyclic GMP. That's what Guadalupe cyclist

54:00 . It produces cyclic GMP, cyclic . What it wants to do is

54:04 wants to bind to that receptor that that receptor. It opens the channel

54:09 channel then allows sodium to come So you have lots and lots of

54:13 inside the cell causes deep polarization. polarization results in release the neurotransmitter release

54:18 neurotransmitter causes the bipolar cell not to stimulated. Alright, it's an inhibitory

54:26 . It's like pressing on the All right. So when the light

54:31 along, what it's gonna do is going to stimulate the change in the

54:35 of that retinal molecule. Alright, photo pigment is opposite and retinol.

54:39 , if I change the shape of retinol, that means I change the

54:42 of the option if I change the of the option the G. Protein

54:46 which the G protein coupled receptor is changes shape and when it changes shape

54:52 it does, it kicks out a energy particle GDP and replaces it with

54:58 unused one. So now has energy so it can go do stuff.

55:03 . So that's what this is And saying, look I'm kicking out

55:06 old and replacing it with the unused now I'm gonna take that. I'm

55:10 use that unused portion or really that plus this active portion. And what

55:17 gonna do is I'm gonna stimulate the molecule down the road. And that's

55:21 called phosphor dia stories. All And again, the chemistry background would

55:27 you to go phosphate ester bonds. what the case. It's It's an

55:30 that breaks that. Alright. But not there. It's okay.

55:35 What it does it takes cyclic Right? We're making lots of

55:39 And what we're gonna do is we're break that little bond. That's a

55:43 bond like this. We're gonna break . So, there's only one

55:47 So basically what I've done is I the shape of this molecule into that

55:51 . So once I change the shape now has a different function. It's

55:55 capable of binding this. So if can't bind this this can't open if

56:01 can't open. sodium can't come If sodium can't come in I can't

56:06 polarize if I can't be polarized, can't block the stimulation of bipolar

56:11 So simply by removing the cyclic Right? Breaking that bond. That's

56:17 that does. What it does is creates this cascade of events that ultimately

56:21 in no neurotransmitter being released, no being released. The bipolar cell will

56:28 de polarize on its own and then sends a signal to the Was that

56:35 ? I know I was talking over but was that helpful in understanding.

56:44 , and that's what all these little are. Yes, sir. Is

56:50 no independent? So, you can when you have intense intense light.

56:57 , the intensity of light represents primarily number of photons that are being

57:03 Right? So the brighter it is what that means is there's more

57:07 That's not always true because we remember we said, there's amplitude as well

57:10 that's going into something entirely different. right. But if you have lots

57:14 light receptors, that means you have recycle these faster. So just think

57:19 bright light. The first thing that is if I have too much

57:22 my my pupils are going to constrict let less light in so I can

57:28 or regulate. But let's say I keep shining in bright light. Then

57:31 happens is is I start over using uh photo pigment. So it's you

57:39 the photo pigment has to go through whole recycling thing. And like in

57:42 cone it takes about three minutes to a single molecule. So if you

57:48 using too many of those up what you start perceiving is white

57:53 Right? So if if basically if have overstimulated my eyes, everything just

57:58 bright and white, that's kind of it looks like. Well, that's

58:02 brain perceives. So that kind of the question. Yeah. Anyone

58:08 Yes, sir. Where? so rods and cones. This is

58:16 rod in the cone. Alright, that's kind of the shape right

58:19 See there's and there's the uh the bound disk, that's what that's supposed

58:23 represent. Alright, So, I my art's terrible, but that's that's

58:27 this is. Is So when you of the rod and cone, they're

58:30 ones that are doing this pathway. the rod in the corner of the

58:34 that are upstream. Let me I had a better. Yeah,

58:45 guess that's going to work. All . So, what this is showing

58:49 this is your rod. Now, could be a cone. I could

58:52 this and say let's do the exact thing in a cone. Alright,

58:55 here's your bipolar cell. So, you're talking about photo transaction, you're

59:00 this is what occurs in a rod a comb. All right. And

59:05 because of that stimulation of the right the cone that you're able to then

59:09 the cells downstream. Okay. Another . Yeah. Yes. I wouldn't

59:33 , so remember what we're saying here when I when I convert cyclic GMP

59:37 GMP, I'm no longer able to the channel so it's not GMP closing

59:43 channel. It's the loss of the to keep the door open. Imagine

59:48 a door jamb, cyclic GMP is door jamb. If I kicked the

59:51 jam out of the way, the slams shut, I have to put

59:54 cyclic GMP back into place. And really the bounce between visual visual

60:00 The idea of light versus dark is is the photo pigment hitting here.

60:05 the photo pigments hitting here or sorry light's hitting the photons hitting the photo

60:10 then I'm chewing up cycling GNP faster I can make it. If photons

60:15 not hitting then I'm making cycle GMP than I'm chewing it up. So

60:19 kind of the balance that you're playing is how much cycling GMP I have

60:24 correlates with how much sodium is able come in more cyclic GMP more sodium

60:30 cyclic GMP. Less sodium. That of makes sense. Yeah, I

60:36 it's first time going through it. see this every day then it's like

60:41 . All right. But that's that's of the idea here is you're you're

60:46 a system and trying to keep balance the two. I think I'll quickly

60:51 eyes are responding to I mean you your move your you know, your

60:55 of vision across the room and think quickly you can discern color and shape

61:00 stuff like that. So it's being to change and respond to all that

61:06 that's coming in very, very That makes sense. Was there another

61:13 over here? Want to learn about here is a little bit easier.

61:20 right. Don't know why that point there. All right. So remember

61:28 said the ear it was a problem hearing equilibrium when we think of the

61:31 . We think of this portion out . There's actually three parts of the

61:35 . We have the external ear. ear is basically your oracle or peanuts

61:41 it's called as well as the ear , which is called the external acoustic

61:45 auditory medias Medias is just a word means tube or tunnel. Alright then

61:50 have the middle ear. Middle ear the space between the tim panic membrane

61:57 what is called the round window and oval window basically this is where the

62:01 are that allow for light or the . Excuse me. Sound waves to

62:06 transmitted between the outside of your body the actual sound detecting devices which is

62:13 in the inner ear. Now the ear has two parts to it.

62:17 are is the cochlear and vestibular Alright. So this is a fluid

62:22 structure. You're gonna see it over over again. Right here. It's

62:26 this this all this stuff right So the cochlea is the thing that

62:31 like a snail shell snail shell. . It's the one that actually converts

62:36 waves into nerve impulses or the structures it. Do. And then the

62:40 apparatus is all this weird looking stuff there, basically, it's responsible for

62:45 our position of our head space. basically it's responsible for equilibrium. All

62:51 , So just going through the structures quick, the oracle, that's your

62:56 you would call your ear. So it's the skin flap in the

62:59 underneath. It has this really weird and that weird shape is what allows

63:03 to direct sound to the next which is the external acoustic mediastore

63:09 Meet us. You might call it canal. And so basically sound waves

63:12 going to travel down to that to tim panic membrane, which will vibrate

63:16 the same frequency and intensity as the waves traveling to it. And so

63:22 the acoustic auditory um and the acoustic us, you have fine hair.

63:26 have sarah Municipal guns. So that's earwax, that's what they produce.

63:30 there to protect the meet us. so basically collects airborne particles,

63:35 all sorts of horrible nasty things. the media's itself is there to direct

63:40 to that tIM panic membrane when you into the middle ear. All

63:47 What you're gonna see is a couple first. I'm just gonna point out

63:49 station or auditory tube. This is opens up to the nasopharynx. Nasopharynx

63:54 nasal cavity pharynx, his throat. it's the point where those two things

63:59 . And so when you need to your ears, what you're really doing

64:01 you're trying to collaborate the pressure in middle ear to the external environment.

64:05 the easy thing. All we gotta though, right? And basically what

64:09 doing, you're opening up that tube of spreading it and allowing air to

64:13 back and forth freely through that. right now, the reason we want

64:18 do that is if you've ever noticed the pressure gets high and then things

64:22 of sound a little muffled. It's same way if anyone here play drums

64:27 . So when you bang on the and you put your hand on the

64:29 side, it makes a less vibrant . It's kind of a thud.

64:34 ? That's what happens when that tim membrane can't vibrate if you put pressure

64:38 it greater than the pressure on the side. It doesn't vibrate quite as

64:42 . And so that's when sounds kind muffled. So that's what we

64:46 Right, You've been on an you go up to altitude was

64:50 yeah, I can tell I can the pressure things are sounding a little

64:54 more muffled on saturday. Do that well. Oh and advice if you

65:01 frequently and there are usually kids on right? Always carry dumdums,

65:09 dums, those little tiny lollipops. cheap and you can give them to

65:14 kid and their parents will be grateful they will suck on that. And

65:18 sucking action also pops ears which is makes kids cry on airplanes. Well

65:24 whole bunch of other stuff anyway in tim panic cavity um we have the

65:30 in the round window which we'll get in a little bit here we have

65:34 tim panic membrane which is where you're be receiving sound waves. The tim

65:38 membrane is associated with three bones. malice, the Incas and the stay

65:42 . These are called the obstacles malice the hammer. The Incas is the

65:46 the anvil, the staples is the . Those are what the names

65:50 And they're based on their shapes Alright. And what they do is

65:55 serve as amplifiers and they're going to amplifying the vibrations that are received at

66:01 tim panic membrane. To to the membrane which is the oval window.

66:07 . Round windows over here and we're get to that in just a

66:10 So sound wave travels through causes Tim panic membrane. Tim panic membrane

66:15 it vibrates, causes the movement of malice in the Incas then stay peas

66:19 moves back and forth at the same or same as the tim panic

66:24 But you've amplified the the size of wave. Alright, So wavelength is

66:31 , we're going to see on the slide I think. All right.

66:34 , have you ever been to a ? They've all been a concert,

66:37 . Music is really, really loud when they first start playing the

66:40 you're like ah it's too loud. after a couple of seconds you're

66:43 not so bad, Right? And reason for that is because we have

66:48 within these structures, the tensor tympani this temper the tensor stampede ius.

66:54 what they do is they wrap around bones. And so if you create

66:57 much vibration, those bones, they and they reduce the amount of amplification

67:03 that allows our ears to adjust so we don't damage the inner ear.

67:09 not perfect, but they're helpful. right, going to the inner

67:19 Alright, We have bony structure with nous structure. Alright? So what

67:25 you have if you take a look this thing is you're gonna see there's

67:28 parts and there's member nous parts and gonna go and see a picture in

67:32 here, I gotta make sure what we got going on. All

67:36 Um Well, we'll see these. the bony has three basic structures and

67:41 is what you're seeing out here. have the cochlear we have this region

67:45 that's called the vestibule. The not the vestibular, the vestibule.

67:49 then you have these rings, those called the semicircular canals. When you

67:54 through them. What you're gonna see you're gonna see these memory nous regions

67:59 the actual structures are that are able have the receptors that detect movement of

68:06 within the membrane, this labyrinth. the bone kind of sits on the

68:10 . They're still fluid there. But they have these little other regions inside

68:14 have membrane that have fluid inside And what you're looking at is you're

68:18 at the movement of the fluid inside membrane, this labyrinth and you're gonna

68:21 texting that movement. So what the do where the visual course, sorry

68:29 the eyes are responsible for taking light and turning it into action potentials.

68:34 ears while you're dealing with sound energy sound energy is a form of

68:39 You're really looking at movement. So are mechanical receptors that we're looking

68:45 Alright. And so within the bonus and the cochlear we have the cochlear

68:51 . We're gonna be looking at the organ. The vestibule contains these two

68:55 of you trichomoniasis actual which play a in balance. The semicircular canals have

68:59 semicircular ducts which also play a role this balance or equilibrium. Come on

69:08 , we are. Alright when we at light, we said it was

69:12 radiation. It had this really weird wavelength sounds a little bit easier to

69:17 . It's kind of like a rope have these periods within the wavelength where

69:22 you're doing is when sound travels, you're doing is you're pushing molecules,

69:26 molecules are compressing and bouncing off each and then spreading apart. So we

69:31 is compression and rare faction and that's by that wave. So you can

69:37 here here's the compression. Here's the rare faction over and over and over

69:41 . Just repeated. So again you a wavelength. That's your pitch.

69:47 ? When you see wavelength think frequency in hertz pitch high notes versus low

69:53 . Alright, high notes are when wavelengths are close together. Low notes

69:56 when the wavelengths are far apart. right, intensity again deals with desk

70:02 , its amplitude. That's loudness. , when I yell high decibels,

70:11 ? That's the amplitude. Alright, I can pay imagine I could hit

70:15 high C. I can't hit a seat. But imagine if I could

70:19 could do a soft high C. I could do a loud high

70:24 All right. Same pitch different All right. So what I wanna

70:34 is I want to focus here on cochlear. All right, So here's

70:38 coakley. It looks like a snail shell. So hard to say

70:43 Alright. So we're just looking at thing and what we've done is we've

70:46 through that and so what you're looking is you're looking at one of those

70:50 and you can see there's 123 different regions in here. So you can

70:54 the bony part. And why you three regions is because you have a

70:58 part as well. So here's bony it's kind of lined by this or

71:03 have in it this membrane. And this right here is that cochlear duct

71:07 you're going to have the structure that detects sound. Alright now, down

71:13 in this picture, what we've done we've taken that Coakley and we've unwound

71:17 . All right. And so what can see is that we really have

71:21 right there represents that. And it's tube that goes up and around.

71:25 goes all the way to the top then it turns on itself and then

71:28 all the way back down. So is going up. This is coming

71:31 down, right? And in between two tubes. That is that cochlear

71:37 . That's what this is. All . And so if you look here's

71:40 stay peas, there's your oval window there. There's the round window.

71:46 ? And so this part of the going up is called the scallop to

71:51 or the vestibular duct. All when it turns on itself, that's

71:55 helical trauma. And then when it back down the other direction, it's

71:59 the scallop timpani or the tim ducked. So vestibular duct, tim

72:04 , ducked. And sitting in between the cochlear duct or the scallop

72:10 Alright, so the membrane that separates out. This is called the vestibular

72:19 . This is called the basil er . So the frame of reference because

72:23 have this structure right here where we're be texting sound. The basil er

72:28 represents the floor of the cochlear And you can see within that structure

72:33 is where we have what is called organ of corti. The organ of

72:36 is the sound detecting device. again, same pictures are now focusing

72:47 on the organ of corti. It's called the spiral organ. Alright,

72:51 here we are. You can see have nerve fibers. Those nerve fibers

72:56 associated with receptor cells. These receptor are called hair cells. They're called

73:01 cells. Because when you look at , they got these little tiny cilia

73:04 up on top of them like this looks like a little tiny hairs.

73:07 right overlying the hair cells is another . It's a really stiff membrane kind

73:16 gelatinous in nature. And so what have is you have three rows of

73:21 cells and those are actually in The little hairs are actually embedded in

73:27 territorial membrane. And then you have solo hair cell called the inner hair

73:32 cell sitting over here to the side it's not embedded. All right.

73:37 then you have other cells that we're going to bother with. And so

73:40 neurons that are associated those receptor cells and they converge and they form what

73:47 called the spiral ganglion. And then spiral ganglion basically is going to afford

73:51 cochlear nerve. And then you have from the vestibular apparatus, the spiral

73:57 , the semi circular canals that's going form the vestibular nerve of the

74:03 Cochlear nerve got that one. Remember from last unit vestibular cochlear. So

74:13 it is, looking a little bit at the hair cells. There's your

74:16 outer hair cells. You're one inner cell. Your inner ear is not

74:20 with yellow. That was probably somebody LSU coloring that. And so if

74:25 have this is the row of cells actually detect sound. These three over

74:32 . Are there to modulate sound to how you're perceiving sound? So again

74:39 or modulating information before it ever gets the brain. So what is actually

74:46 on when you hear a sound that looking structure. Look at I

74:58 look at the ear, it's like . See how weird looking it

75:02 If you look at an ear long , you're just gonna be like

75:04 that is the weirdest looking. It like a dried apricot. All

75:09 But that shape direct sound in a particular way towards the oracle. So

75:17 wavelength and the intensity is what And it's going to bounce off the

75:22 portions of your little little dried it's going to bounce in and go

75:28 that oracle and it's going to hit tim panic membrane and it's going to

75:32 a tim panic membrane to vibrate. what all this stuff says up

75:36 Alright, that tim panic begins to . It's going to cause the malice

75:40 move, it's going to cause the to move the state piece to

75:43 But in the process what you're doing you're amplifying the movement right? Remember

75:49 the amplitude, that's the loudness. the reason you're doing that is because

75:53 you're moving on the other side of stay peas is a membrane called the

75:57 window, right? That oval window , just like the other one does

76:02 frequency. It does so more And the reason it needs to be

76:05 vigorous is because on the other side that window is what is fluid not

76:09 ? I was about to say It's fluid. Alright. Is it

76:13 to move air fluid? What do think? Yeah. Right. Because

76:21 are further apart so I'm amplifying so I can move that fluid and what

76:27 doing is you're moving that fluid at specific frequency. Alright. So when

76:32 hearing sound and I know we hear frequencies very very quickly. But you

76:37 imagine just a single frequency, what doing is if it's at C note

76:42 the 10 panic memory, that C is being transferred to the oval window

76:47 the frequency of that C note is move that water at the same

76:52 None of the pictures that do this this justice. But remember we're talking

76:56 is a wavelength. If you are short wavelength, what's going to happen

76:59 that that wave is going to travel and then down and going to stimulate

77:04 along the vestibular membrane near the oval . If it's a deep note,

77:10 that wave is going to be much longer and it's going to travel further

77:15 before it stimulates the vestibular membrane, not going to sit there and

77:18 I'm going to travel until boom, gonna hit some point. It's basically

77:22 wavelength determining how far it's going to . Right? So the longer the

77:27 , the further it travels, the the wavelength, the shorter it travels

77:31 the vestibular membrane. Now remember the membranes, the roof of the cochlear

77:37 inside the cochlear duct because it is fluid filled chamber, there's fluid

77:41 And if I push on a fluid chamber, I'm moving fluid and what's

77:44 going to do, that fluid has go someplace. And so what it's

77:49 to do is it's going to displace basal layer membrane at the same

77:54 So, for example, if I , let's see what do they

77:58 They don't show it here. So say I am stimulating the vestibular membrane

78:02 . The fluid underneath is going to pressed on and it's gonna displace the

78:09 membrane just underneath it. All So, if I have a short

78:14 , it's going to go here and and it's going to push down.

78:18 , eventually that sound, that wave a form of energy and so,

78:22 needs to be dissipated in one we're not getting to the sound.

78:25 just want to get rid of the . And so that wave will then

78:28 through and then eventually go to that window in the round window just kind

78:31 bulges out, absorbs the energy and it goes away. You ever seen

78:35 stress dolls where you like squeeze them their eyes, Right? That's kind

78:39 what it's doing. It's like I'm a force and so the energy is

78:43 at the round window. But what want to do is what happened with

78:47 energy as it passes through the cochlear . All right, Well, when

78:52 passes through the cochlear duct, what doing is you're moving that fluid here's

79:01 vestibular membrane. Here's the base layer in between. Is that sectorial

79:06 And that that hard won the one doesn't move. And if I'm moving

79:10 this, the fluid is rolling through that particular location and it's gonna roll

79:20 and move and vibrate those hair The fluid is going to cause the

79:26 cells to vibrate back and forth? so those hair cells are detecting the

79:32 of the fluid inside the cochlear duct that particular location. When I'm detecting

79:38 sound, what I'm really detecting is and so basically what you're doing,

79:43 just saying at this point I expect frequency. So if I stimulate this

79:48 , this is the frequency I'm And so your brain goes, I've

79:51 been I've been told that I have this frequency. So this is kind

79:58 showing you how that movement occurs, ? So the tech tutorial membrane basically

80:02 more or less stays straight. And when the fluid comes down, that

80:08 remembering is going to go up and . And so basically what you're doing

80:10 you're bending hair cells back and forth the fluid flows right over it.

80:16 is referring to that pressure wave that all the way around. So that

80:20 center signal as a result of the in the shape here because those hair

80:24 are waving back and forth. That's I detect sound. So this is

80:30 closer look at what's kinda going So, here's your hair cell,

80:34 can see the stereo cilia, the one is called the Tennessee liam.

80:38 so what you're asking the question is I've been towards the Tennessee liam,

80:41 happens when I've been away from the liam, what happens? So the

80:45 is if the Tennessee liam is being or if you're bending the hair cells

80:49 the the cilia towards the penicillium that's lead to deep polarization, so activation

80:56 then if I move away that's going reduce the number of you know,

81:00 potassium moving in. So what happens you basically are sending no signal,

81:04 hyper polarizing. So what you're doing you're trying to bend the hair cells

81:10 a particular frequency to detect it. frequency where am I stimulating along that

81:17 membrane? All right amplitude is how movement do I see? Nice.

81:29 a loud noise causes lots of Right? So the more vigorous shake

81:35 left perceived the sound that's more action at that particular location. How we

81:42 ? I see you guys getting I'm really I've got two slides

81:45 You want to finish them now. want me to wait until tomorrow

81:49 Its I mean this gets it out the way. Alright, so again

81:52 with regard to the auditory pathway the comes in, it's what you're gonna

81:57 is you're trying to get up to uh to the temporal lobe and so

82:03 first spot is gonna be the cochlear found in the medulla, you basically

82:07 , you have the superior and the Oliveria nuclei they play a role in

82:12 you respond to loud sounds as reflexes directional sound and then you go to

82:18 medial nucleus of the thalamus which basically send that information up to the temporal

82:24 . And remember the temporal lobe is in the same way as the length

82:28 that base layer membrane. So high are going to be one side of

82:31 temporal lobe, low notes are on other side. So those nerves know

82:34 where they're going and that's why your perceives the right sound. The last

82:39 I damn. I didn't have Alright, I'm done, I'll just

82:43 too I think nope, I had there. Alright, so this is

82:47 trying to show you how the the is shaped. So you can see

82:52 different sounds are gonna ricochet in different . And so it kind of gives

82:55 a perception of where the sound is from because of that specific uh way

83:01 it enters into the ear. There go. And then lastly in terms

83:05 how does your brain know where it's from, It's because the information is

83:08 to both years and they arrive at times and the way that it rides

83:14 at your brain tells you from the it goes. So you can know

83:19 it's coming in terms of height because the shape of the ears and you

83:23 know which side it's coming from because when it arrives on one side or

83:27 other and there's actually because of the low notes and high notes are treated

83:34 differently. But basically the easy thing remember right is direction is based on

83:41 timing that arrives at each year. , we're done. We can we've

83:46 up, equilibrium is easy. Easy . You're late. And I got

83:54 recorded,

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