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00:02 this is lecture 16 part two and have to discontinue the recording. We're

00:09 it up here with technical reasons. we talked about this red, green

00:16 blue. So you have blue green cones and red cones. So

00:21 you're seeing blue color which comes on 444 130 nanometer range, you're just

00:31 blue cones, 100% of blue And depending on the hue of that

00:38 color, right, lighter versus darker different tinge to you will be activating

00:46 different number of these blue photo So closer to 400 you'll be activating

00:53 of blue cone photo receptors and for 30 will be activating close to 100%

01:00 blue cone photoreceptors and to perceive blue , that's all you need is activation

01:06 blue cones to perceive green color. , green color is a combination of

01:15 , blue and red. So when perceiving green color, you have 31%

01:21 of red cones, 67% activation of cones And 36% activation of these blue

01:31 . About the same amount. 36% of blue cones. Now, what

01:38 if you had a palette color palette you wanted to get color yellow,

01:46 would mix green and red. And will give you yellow. So if

01:52 activate 83% of red cones, 83% green cones. And there's about 550

02:00 wavelength range. It will activate green red cones to give you yellow

02:07 So it's like color mixing and color . You can think about it as

02:14 perception. What if somebody is missing blue cones? They don't express the

02:22 cones then their perception is going to limited. From where the green cones

02:29 about 450. They would lose about nanometers of light that they're perceiving in

02:36 world. The color world that the person would be seeing would be

02:42 What about if you lost the red would lose on this uh end

02:49 If you lost green, you'd actually in pretty good shape, you'd lose

02:54 lot of green like star green But you would still be able to

02:59 some of that shade with mixing red blue. So now just look a

03:06 bit more yellow than green. So world would be a little bit more

03:12 . And some artists that have color or different perceptions in color, they

03:19 the world in a way that they it. And it's really interesting to

03:22 the world that other people see And I also talked yesterday in class

03:27 how many times you're arguing with your or a spouse or or or

03:34 Remember about? No this is This is black. No this is

03:39 is dark dark blue. It's like this is not. This is no

03:43 is not fusion. This is You know why why is that?

03:47 obviously it's not necessarily color blindness. what about differential expression levels of these

03:54 receptors? Their distribution in the retina very slightly among us as individuals.

04:01 so our interpretation of color, you you always have to express certain number

04:07 plus minus of these photoreceptors. What you're an outlier region of minus certain

04:12 of photo receptors by expression? Now green hues are not going to be

04:17 strong, your blue hues are not to be a stronger, your red

04:20 are not going to be a strong your color perception is going to be

04:23 little bit different. Can be interpreted . Oh no, I'm just kind

04:30 like mind blown because you said that if they like painted their perception that

04:35 be seeing but at the same time like are you really saying because you

04:38 the activated cones that they don't Yeah, yeah. Yeah. That's

04:44 , that's right, that's right. it's interesting to think about it

04:50 And this is what you know what have, you know these different wavelengths

04:55 we talked about and we have the mixing with these three step types of

05:00 cones. We red, blue and , you have yellow, you have

05:06 , you have different shades of blue red and indigo and violet and teals

05:13 stuff like that when you mix green and blue. So it's like a

05:17 palette, you have these three colors how many different ratios of these colors

05:22 can mix in order to produce a hue. Yeah, red, blue

05:28 yellow. What the primary colors blue and yellow. The three things

05:35 we base everything off? Uh That's good question. Um I also would

05:41 why can't we have chromatic vision and photoreceptors, you know, So we

05:47 actually distinguish color at night, You ? So it's just the way the

05:52 is built. There are certain So the theme of even today will

05:57 is that the retina sees certain things it has certain things. That's a

06:02 question. Why? Uh Maybe there some deeper reason. I'm not thinking

06:09 about like evolutionarily avoid the sunlight which yellow to preserve your vision. So

06:15 don't kill off the yellow cones as . Maybe because the oceans are blue

06:22 the forests are green and the blood red. I you know, I

06:27 flesh, the flesh is red, know, I don't I don't

06:31 You know, it's uh maybe maybe it's over the evolution. Maybe it's

06:37 to know if there was one master photoreceptors that diverged into three colors.

06:44 don't know enough about that. You , Maybe there was an attrition from

06:49 or seven and our world was a more colorful until we saw that,

06:52 know, like we lose that color quickly because of certain stimulus in certain

06:57 length. So All right, so question. Let's let's let's maybe try

07:04 find an answer for it someday. , so now we're gonna talk about

07:10 transaction that happens in photoreceptors and then gonna move more into the actual circuit

07:17 the retina and the communication. So we have to convert the signal of

07:21 into an electrochemical signal. And we talked about metro tropic signaling. When

07:27 talked about ligand gated G protein coupled that can activate downstream secondary messengers enzymes

07:35 channels. They can score little science open those ion channels and hear what

07:41 in the photoreceptors is light that activates protein and the molecules that are found

07:50 the photo pigment that can disable in case G protein complex and can reduce

07:56 on the secondary messenger and can close ion channel. So, we saw

08:02 different scenarios in the chemical neuro But now we're seeing that we don't

08:07 a chemical we need light. And way it happens is that you have

08:12 in the option and it's in the configuration. When light hits it becomes

08:17 cis configuration that change the conformational change the light hits this, it actually

08:25 this G protein coupled uh complex and the production of cyclic GMP threw phosphor

08:33 stories. So it converts cyclic GMP GMP. Now in the dark the

08:41 neurons the photo receptors are d polarized the dark and there's influx of sodium

08:50 cyclic GMP gated sodium channels. So are cyclic GMP gated sodium channels.

08:56 in the dark the sodium coming in these motor receptors are D polarized.

09:03 because there's no lights, the jew , which is translucent, is an

09:09 . And in the light now you activation of retinol and activation of the

09:16 protein trans Doosan and conversion of cyclic into GMP. Again through the fossil

09:22 stories and in the absence of cyclic , this sodium channel is closed.

09:30 in the light the photo receptors will polarize. This is a member of

09:37 . So this is in the the member of potential photo receptors is

09:41 polarized and in the light it hyper . It's counterintuitive to what we talked

09:46 in the past when you have a membrane potential and you have a stimulus

09:51 that stimulus positive stimulus. In this light would be D polarizing. But

09:56 light is hyper polarizing and that's because the intricacies of the retinal circuit that

10:01 pretty complex. And we're going to a glimpse of that when we talk

10:06 retinol circuit and a few slides. this is this is different from what

10:11 discussed, cones require more energy to bleach. They require more energy to

10:18 perceive light more light broads get saturated bright light. And so then you

10:24 have activation of cones. Now today going to start talking about the receptive

10:31 properties. Uh these photo receptor bipolar , retinal ganglion sauce and lateral nuclear

10:41 . And so when it when you a spot of light, we were

10:45 about the moon. We said that moon is going to activate a certain

10:49 in the retina. So if the is there and you're looking at the

10:53 that's on the side a little then it's going to be this nasal

10:57 . Looking at the moon there and micro meter patch of that retina is

11:02 to be looking at the moon. does that entail in the receptive

11:08 That spot that is looking at that , That spot in the retina 140

11:14 spot on the retina that's looking at spot in the space at that bribe

11:20 . So it would activate many many receptors. And as it turns out

11:29 one of the best technologies that I uh use for what is receptive field

11:37 of course in the retina, its of the retina that when stimulated with

11:44 changes the cells membrane potential. So a there's a spot that spot is

11:53 everywhere in the retina. If there's bright spot then that's the moon,

11:58 rest of the sky is dark or . And you're only seeing the moon

12:05 it's only those cells underneath that 140 that are going to get activated by

12:14 life, there's going to be a in the member and potential of those

12:18 . And these are collections of photo . And so the retina, which

12:29 I'm gonna draw here. one of artists renditions has collections of the photoreceptors

12:48 is illustrated in the diagram on the . Those collections seem to have a

12:55 zone and the surrounding zone and they're to as center surround or concentric.

13:07 that means that there is a certain of the other staffers that is gonna

13:12 served in the center zone here. center of the receptive field versus the

13:21 receptive field. This is in the . The analogy, the best way

13:26 understand it is that somebody taps on shoulder, You know, somebody tapped

13:31 the shoulder. How do you know somebody tapped on the shoulder and not

13:34 your knee? They're gonna be spinal that contact the skin area, the

13:41 and muscles on your shoulder that's gonna to one of the spinal nerve

13:47 We talked about like thoracic, one to right. And this is gonna

13:53 your brain. And if somebody taps on the elbow, you're not going

13:57 say that's my shoulder again. So another receptive field, there's other nerve

14:03 in the elbow that will tell either the same nerve or adjacent nerve,

14:10 it's the elbow that got tapped, taps on the back left. You

14:17 , it tells your brain there's an here. The process is so this

14:21 the receptive field. The nerve endings the show the receptive field for the

14:26 the uh elbow receptive field for the and so on. So he's receptive

14:34 here that's looking at the moon. just receptive field, this area of

14:38 micrometers. And beneath that 140 micrometers are collections of the photo receptors.

14:45 this is another reason why is that that? Because the nature build it

14:49 this. So retina, what retina is that certain photo receptors, the

14:55 that the life will hyper polarize And some of the bipolar cells actually

15:01 get deep polarized. Okay, it's direct catholic. And then lighten the

15:09 field in the surround and actually hyper the surrounding photo receptors And through horizontal

15:19 . So it talks about horizontal cells are actually an inventory can now cause

15:25 hyper polarization of these bipolar cells. this is an indirect pathway.

15:31 it's getting a little bit complicated but worry and stick with it. There

15:35 certain things that I will want you know for the exam from these

15:40 But so underneath the center surround regions the center will have collections of the

15:46 receptors and that 140 micro meter let's say is going to be this

15:54 . And in that 140 micro meter there's gonna be several center surround receptive

16:04 that are going to be processing the about that moon, on this piece

16:10 the retina here. Okay. And if if there there on center ganglion

16:21 . And why is that all of sudden? Wait a second. You're

16:23 about receptive field properties, retina and . G. M bipolar cell receptive

16:29 properties. So you can shine something the photo receptors and you really can

16:36 synaptic potentials from bipolar cells and you record action potentials only from retinal ganglion

16:46 . Ultimately, then when you're looking the stimulus which is light stimulus here

16:51 this yellow bar, you're looking at sticks here, these are action

16:58 So that's why now we're talking about ganglion or on center off center ganglion

17:06 . Ultimately this input from clumps of photo receptors in the center of the

17:11 gets communicated through the circuit the director direct circuit. There is another level

17:17 complexity at the level of the bipolar which diverges into the tropic dramaturgical bipolar

17:24 and metabolic tropical dramaturgical bipolar cells. we can already start picking up activity

17:30 activity in bipolar cells. So we what receptive field properties they have and

17:36 can start picking up action potentials that connected to these bipolar cells at the

17:41 ganglion cell level. And so if shine the center, let's say this

17:47 the bright spot in the moon. center gets activated. And that's connected

17:53 the retina all the way down to retinal ganglion cell, then this would

17:59 an on center cell and on center will produce the most action potentials in

18:06 retinal ganglion cell when you shine the in the very center of that collection

18:11 the photoreceptors. But if you were change a little bit of an

18:16 looking at that moon and now the light of whatever variation in the moon

18:22 looking is going to be on the part of this concentric uh receptive field

18:32 gonna with the light here exposing the ring. Now you get the least

18:39 potentials. So this retinal ganglion cell most reactive to the center light and

18:47 least reactive to the surround light objects bright and light. The perfect example

18:53 an eye, you know, dark , dark, darker or whatever,

18:57 know, lighter. Uh The interesting is if you haven't even illumination,

19:05 this this gets evenly illuminated throughout your looking at one bright spot of

19:13 The retinal ganglion cells that are receiving from evenly illuminated receptive fields. They

19:22 have a uniform pattern of action potentials it's almost unchanged from the dark to

19:29 light condition. So there's no change the dark. There's no change if

19:33 all dark and if it's all there's not much change in the firing

19:38 of these retinal ganglion cells. The cells will do the opposite retinal ganglion

19:45 that are connected to these collections of receptors when the outer ring of those

19:52 of the photo receptors is activated. when the retinal ganglion cells will produce

19:56 most action potentials. But when they're or the whole of the donut is

20:02 stimulated with light will produce the least potentials in those retinal ganglion cells.

20:09 the same goes is that it's even across the receptive field. Then you

20:15 have even pattern changed pattern of action . So essentially if you were to

20:26 up the retina and also this is thing is sometimes you can have for

20:31 center ganglion cells you can have a spot. So you don't have to

20:35 an illumination and the surround. But just much darker spot in the

20:40 And rather than surround and you'll still the least number of actions potentials from

20:46 on central ganglion cells. But you'll a lot of action potentials from off

20:51 gang themselves because the area around the spot is going to be lighter so

20:55 you're seeing what you're seeing here is and luminous. So if you take

21:04 and you say, okay what what you see? And you connected to

21:09 computer that can process the information from optic nerve. And you ask what

21:17 of receptive field properties do you What what are you processing at the

21:22 of the retina there's a lot of coming in color motion, depth,

21:29 of this. But is retina perceiving or is retina perceiving structuring images within

21:39 uh anatomical delineations that it has within retinol circuits and then communicating that information

21:48 higher centers and to other areas of brain. Super charismatic nucleus, superior

21:54 asse lateral nucleus. So retina is poor for example at depth perception.

22:03 some of these uh hierarchically more complex features of visual information. It's a

22:12 of the new cortical processing. What realize is that as I walk you

22:19 the retina. So from the eye the L. G. M.

22:27 into the primary visual cortex. Area . One or area 17 in primary

22:33 cortex in the primary visual area we what we call the primal sketch of

22:44 outside world. So it would be to construct that sketch and have motion

22:52 depth and color. All done by circuit of those three major players cells

22:59 two intermediary inhibitory cells that control the . So a lot of information of

23:06 all of the visual information comes in . But the retina in the end

23:11 you connected to the computer and say you're really processing is retina, These

23:16 and lighter spots of contrast and luminescence these patterns across the retina that are

23:23 off centers around like patterns there are of the photo receptors that are looking

23:31 different angles of the visual light or stimulus and that's because that's the way

23:38 is, that's the way our threaten have built. Uh and now if

23:45 look at the downstream circuit there's actually a bit of information in this diagram

23:53 uh and it looks a little bit but I want to remind you of

23:59 things and I also want to tell that if you don't exactly understand how

24:03 this deep polarization hyper polarization happens and does this inhibition have to do with

24:11 . So just important thing to know that the dark and light potentials.

24:19 the dark photo receptors are d polarized the light are hyper polarized. That's

24:24 important key piece of information to get false questions with multiple choice question then

24:32 are the types of neurotransmitters that these major subtypes right now? In the

24:38 we're discussing. And also the horizontal that are found here, what are

24:42 neurotransmitters that glutamate receptors released? Glutamate cells release glutamate and retinal ganglion cells

24:53 glutamate. Okay so it's excitatory pre signaling and all of them.

25:02 In this circuit that processes information now cells are actually gaba cells so their

25:12 cells but in this circuit the flow information from photoreceptors, bipolar cells retinal

25:21 cells, it's glued in eight release you would say oh then it's all

25:25 to accept for. Remember we talked how the response of the cell depends

25:31 the post synaptic receptor rather than that the neurotransmitter molecule we used an example

25:41 nicotine acetylcholine receptor in the C. . S. Which is D.

25:46 the most versatile Colin receptor which is tropic. And it was opening potassium

25:52 and was causing hyper polarization. There opposing actions. So I am a

25:58 in literal tropic and have opposing physiological and biophysical effects or opposing physiological downstream

26:06 effect. And so it happens that of the bipolar cells express on a

26:12 and bikini interceptors and other bipolar cells minimal tropical Eden interceptions. M.

26:19 stands for medical topic intimate receptor six for subtypes six. So glutamate,

26:28 it's excited to hear that glutamate is released it's going to excite and is

26:34 to de polarize themselves. So deep here means deep polarization here. And

26:39 plus here doesn't mean and excited to out means assigned conservative synapse decolonization,

26:46 , hyper polarization capitalization. Alright so polarization there's glutinous media and that means

26:54 there's gonna be deep polarization of the self and that means that this is

26:58 sign of conserving because the retinal ganglion only have the tropic ample kinda in

27:05 N. B. A. It's going to be d polarizing. And

27:10 conservatives on the other hand if you glutamate here and that glutamate binds to

27:19 medical tropic glutamate suffers this glutamate which have with deep polarization will release glutamate

27:28 to medical. Tropical automated suffers is to inhibit the cell so it's gonna

27:35 an opposite effect. So it's signed burning tonight. Now this is placed

27:44 the context of life. The first wanted to explain to the scientists survey

27:49 is glutamate is released and the that means deep polarization, polarization,

27:54 and radicalization leading the tropic glutamate is . That means it's hyper polarization.

28:01 there's no glitter mate, that means just deep what happens in the

28:09 The member is hyper polarized. There no glutamate believes so this is D

28:17 . So this shows you an example a code here in the center from

28:23 lightest shop, metabolic tropic is deeply and on center gangly itself is D

28:34 . Now in the light there is glutamate because this is localization, there's

28:41 glutamate. So this is hyper polarization and this is hyper polarization. So

28:51 is an off center gang which means this cell ganglion cell doesn't react to

28:57 center activation, likely reacts to a activation when the light is in the

29:03 region of the center take home And what can I ask you again

29:10 neurotransmitters that are released. The fact you have within it receptors. The

29:16 that you have medical traffic. They're actions. One is signed conserving 11

29:22 signed, inverting the fact that the is hyper polarizing a photo receptors.

29:26 you remember these concepts are going to able to trace down the circuit or

29:31 answer any questions you may have. is the horizontal cells and it's also

29:41 information about horizontal cells. So here's thing is that this is also

29:45 conserving synapse. So in in in the dark this synapses releasing glutamate because

29:52 cells are d polarized. So so that means the retinal ganglion cells will

29:57 always activated in the dark. But happens is that they're also connected to

30:03 cells and they excited horizontal cells the cells said the negative feedback loop or

30:14 feedback in tradition onto the same receptor . So that cell is now not

30:21 deep polarized as being inhibited. So a fine control there through the circuit

30:27 how the cells are reacting to the . Overall darkness and light as you

30:32 if you close the eyes in complete there's uniform certain level of action

30:38 So it will be across the board all of the receptive fields. So

30:44 cells release gaba as the inhibitor They contain got drunk chunks. Uh

30:53 can be responsible for broad area of illumination or control of broad areas of

30:59 illumination and sculpting the aluminum sculpting the because they can inhibit the surrounding clones

31:08 photo receptors and have the uh certain receptors receive more signal, make more

31:15 . Um and the control of of release essentially through this feedback loop.

31:22 you activate the negative inhibitory cells and inhibitory cells project back up to the

31:29 photo receptors and inhibit them back. so this concludes the lecture on the

31:42 transaction on the circuits that we learned photo transaction on these retinal circuits and

31:52 features and of the cells that you're here uh and on and off retinal

32:04 cells that were describing. This is description of receptive field properties. That

32:09 one of the activated when the light shown in the middle clump of these

32:14 are the surround of the photoreceptors. is the only neurotransmitter in this staff

32:28 processing between photoreceptors, bipolar, saw retinal ganglion cell. But then I

32:34 showed you the control of gaba horizontal . Yeah because this is the flow

32:44 information processing is from the photoreceptors. retinal ganglion cells and you can see

32:50 inhibition sculpts it. Remember that these local inhibitor internet, they're not projecting

32:58 sculpting the levels of luminescence and the and the retina. Were you saying

33:06 when it's dark you have people or is a hyper so the other way

33:16 we Yeah but what uh so you you know you can have something really

33:33 fel or not. So contrast fel really bright or something not so bright

33:44 you can sculpt it because you have addition. So you can control the

33:50 of communication in the circuit and how aluminum spreads to the circuit, how

33:56 you inhibit ejaculation in a way uh sculpting is changing the shape of that

34:04 maybe the area and the shape of looters. And also the contract.

34:10 what it's kind of like. Much bright spot versus the light above you

34:22 is much more across and bright area inhibition with control some of this how

34:32 look at things and how you process information, the size of it and

34:40 questions. Okay, so the second in which we distinguish the retinal ganglion

34:45 outputs is by their anatomical and functional , not just receptive field properties which

34:50 a functional feature. And those are . And P. Type and non

34:54 . P. Type p cells are parvo sells their small receptive fields that

35:01 slower conductance. They're less sensitive to levels of contrast. And they're shown

35:07 the small cells and they have uh bushes of the processes, the synaptic

35:16 and therefore they have smaller receptive fields wouldn't be getting as many inputs from

35:21 overlaying photo reception bipolar cells downstream. magno sell so much larger, much

35:30 processes, faster processing and more sensitive low contrast and non Mp types of

35:38 . They don't fall into either parvo . We call them intermediary, we

35:44 them Kanye cellular cells and we call non M. P. Type cells

35:50 in one uh some type of three different descriptions. So the

35:56 If you were connected to the your computer you would see these lighter

36:02 darker spots in the circular patterns. what retina processes when you start going

36:08 into the central processing LG. Will actually still have the same receptive

36:15 properties. There's gonna be collections now retinal gangland south on off center surround

36:22 communicate that information to L. N. But by the time you

36:26 to the primary visual cortex and exhibit lobe were capable of discerning very complex

36:34 , different shapes of patterns, motion depth, color. Uh Very complex

36:42 that comprise our vision. I'm going come back to this example. So

36:46 to 90% of what comes out of retina, 80-90% of the projections that

36:56 out of the retina. They go the lateral nucleus about 10% go detect

37:04 to Sapir curriculum. Spear calculus is for psychotic eye movements. S.

37:11 . C. C. A. . I. C. Psychotic eye

37:15 . And these are the fast jump eye movements that we use in order

37:21 focus on objects as they move in of us. We don't have a

37:25 pursuit. Don't have our eyes moving like like a camera. Instead we

37:33 this. These are the psychedelic If any of you have cats or

37:44 can watch a cat they can sit and sometimes go bounce their eyes like

37:50 eyes at this academy movements or some the most pronounced in in in in

37:56 cats. And that's satirical Oculus From quadra gemini 123% goes to super charismatic

38:06 which is responsible for the Circadian So you'll have retinol outfits coming out

38:14 the nerve crossing over and off the . They're coming off the track off

38:19 track will contain the fibers that cross the nasal fibers that are contra lateral

38:26 the temple fiber center of collateral. know and those projections are gonna go

38:32 the lateral nucleus nucleus. This is stop of the attitude to rig wind

38:36 there and this will become relevant because talk about how engorged pituitary gland can

38:44 start affecting the high asthma. The eye ASM and causing certain types of

38:50 field visual perception losses. So when look at the visual field you have

38:58 and 50 degrees 150 degrees. But lot of it is overlapping between the

39:05 eyes. So both eyes can perceive big big zone which is called binocular

39:11 field. Otherwise it's subdivided into the visual field, right heavy field.

39:19 as you can see that the fibers the temporal side of the retina will

39:24 ipsa lateral and the fibers from the side of the retina will cross over

39:35 the sky as and contra lateral into other side we have projections here the

39:40 optic track left optic tract. And from the lateral nucleus nucleus. The

39:46 are called optic radiations that go into primary visual cortex in the area 17

39:54 the occipital lobe. So let's talk the loss of visual perception and visual

40:03 . If there is uh different accidents potentially can happen, the damage to

40:09 parts of the nerve or the optic or the chi as. Um So

40:16 you have damage to one side, there is a transaction of left optic

40:24 for example, as is shown here Blackwood is illustrated as the loss of

40:31 visual field. This is a visual that you see. And if you

40:36 damage to left optic nerve that means was cut. Transected or something like

40:43 . You would have a loss of the left periphery. You can actually

40:51 it just by closing one eye. one eye you can still see quite

40:57 bit of the territory of that eye is binocular territory. You can still

41:01 the periphery from this I but you're the periphery from the other side.

41:09 you have the loss of the peripheral on the same side. If you

41:13 the nerve or if you damage the fully on that one side. If

41:19 transect left optic tract now you're transacting that are both bilateral and contra

41:30 So if you transect the optic tract lose the fibers that are crossing over

41:38 are nasal and you lose the fibers are staying bilateral which is temporal.

41:48 the best way to visualize is is directness are like cups like this both

41:56 . So if I'm looking in the with this cup, the light that's

42:02 becoming to hear my nasal rattling, nasal retina will be perceiving the preferred

42:12 there. My temporal retina will be over here because it's like a

42:18 Same here, nasal over their temporal be looking over there. So now

42:26 have eliminated the fibers which are nasal the right nasal on the right is

42:37 to the periphery. You lost the and then you're transacting the fibers.

42:46 a lateral which is temporal. Okay side here. I'm looking over here

42:53 looking in the middle so you lose entire right or contra lateral hemi

43:00 Look good. Yeah, that makes . I always think of readiness as

43:07 like that sitting in there and then light is pointing into that cup.

43:11 if you wanted to shine a light this edge of the cup, you

43:14 shine it from here. You would it from there in order to capture

43:19 . That's that's the best way to it now that the damage to the

43:23 eye. ASM it's all of the that are crossing over which are nasal

43:28 where nasal fibers looking at periphery So you have the loss of the

43:36 vision on both sides and you have of the binocular zone. Uh we

43:44 looked at the image that showed this stock of the pituitary gland, which

43:50 a land that controls hormones that controls growth. And uh uh it's possible

44:02 many cases if this gland is if there is enlargement of the pituitary

44:08 that can actually start pushing and pressuring the optic chasm. And one of

44:16 features of that would be loss of peripheral vision of what we call the

44:21 vision. And so in in your , there's a biblical story of a

44:28 between the Philistines and the Israelites between and Goliath. And there's a neuroscientist

44:36 of why David was able to sneak on a Goliath who was considered a

44:43 . Potentially the neuroscientist interpretation is that life was a pituitary giant and had

44:49 tunnel vision. And David was able come up slightly and aside and throw

44:54 stone into his forehead and knock him to win the battle. So the

45:00 explained that his pituitary giant and the vision for the story. Is there

45:06 basis for that? Absolutely. So is pituitary giants and they're giants because

45:13 pituitary gland is larger. It's It means it's producing more, it

45:20 this regulation of hormones, potentially it the growth and make people grow into

45:29 such as andre the giant for is one of the famous giants that

45:34 been in movies and tv shows. they have other issues. Also like

45:41 large faces. A lot of Very large hands and they're very very

45:46 and very very large. So and they also often have the tunnel vision

45:52 of the the to Taiwan. There's neuro scientific explanation to these biblical

45:58 All right. Finally I think I'm almost finished here but I wanted to

46:03 briefly into the lateral nucleus nucleus. lateral nucleus nucleus. We're gonna go

46:09 the new cortex and I'm running out time. Unfortunately I got interrupted by

46:16 recording stoppage and um now I'm just tell you briefly that lateral nucleus nucleus

46:24 a six legged structure. This is missile stain off the lot O.

46:28 nucleus nucleus. This is trans A cross section through the brain.

46:39 dance bands that you're seeing here. very clearly see six den bands represent

46:45 layers of the lateral nucleus. You see that in between these bands there

46:52 dots that hopefully you can see from away on the screen there's a dispersed

46:58 . There's dispersed cells that are located to each of the layers here.

47:06 layers are non mp type or Kanye cells or intermediary selves. The layers

47:17 from midline managed to lateral. So . Each one of these layers is

47:29 ocular. That means that the cells this layer received information from only one

47:35 in this layer from the other eye this layer from the other eye in

47:40 layer from that other eye these arman layers LG. N. If you

47:47 to connect LG. N. Again said what do the relay cells which

47:52 the main subtype of collateral nuclear nuclear relay cells. They're called relay because

47:57 was thought that palamos is passive and relaying the information like in the relay

48:04 . You know I've done my job you relate to the cortex so they

48:09 relay cells relay cells will also have the thalamus and L. G.

48:14 . These concentric centers around receptive field . So in the thalamus the view

48:22 still based on this contrast and luminescence these circular center surround life patterns.

48:31 still no primal sketch on the columns happens in the primary visual cortex and

48:38 understand how that can actually happen from shapes. How can from these

48:42 circular shapes. How can you put shapes? So now the other take

48:50 message is 80 to 90% of everything L. G. M. Receives

48:58 of cortical origin. So most of L. G. M. Only

49:07 of algae in receives input from the and 80 to 90% of that comes

49:14 the cortex into L. G. . That makes sense. So most

49:20 everything that retina gives gives to G. M. Most of what

49:23 G. M receives receives from cortex that's what I wrote that. What

49:28 see with L. G. Has influence on how we feel because

49:32 the primary information gets communicated to the visual cortex it's gonna eventually reach the

49:41 areas in the cortex and it's gonna you that I'm trying to look at

49:48 image but the music I hate the that goes to that image and not

49:52 able to look at that image. just influenced what you see what you're

49:58 at or maybe what you're interpreting what seeing and the focus of that and

50:03 sensitivity of that which basically the visual and input of signal can be controlled

50:09 the level of the L. M. From the projections widely distributed

50:13 from the cortex the visual projections in areas of the cortex that will project

50:18 the L. G. M. we'll leave it at that today and

50:22 we come back we're gonna finish talking L. G. M. Some

50:27 the features of the L. M. Retina toppy and the features

50:33 the cortex. So we will finish Visual system three in the next

50:40 I'll see everybody on

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