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BIOL 4315 & 6315 Neuroscience Mon-Wed 1-2.30 PM - Neuroscience Lecture 17 Visual System III
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00:09 So we covered quite a bit of though, before that, we talked
00:14 the circuit in the retina and the types there, we talked about photo
00:22 . We also talked about receptive field and we discussed how the retina it
00:30 the world best if it is presented these round centers around light source
00:42 And so you have on center and center cells. And we talked about
00:48 photo transduction and the photoreceptors, we about two pathways in the bipolar
00:56 One that is sine conserving mediated through another one sign inverting mediated through metabotropic
01:05 receptors. We discussed that horizontal cells inhibitory cells in the circuit and they
01:14 this negative feedback inhibition uh once they're by the tones. And we talked
01:22 how all of these cells release And the only difference here is that
01:27 it processes through a sign conserving, it processes through metabotropic glutamate is gonna
01:34 sign inverting and will cause the opposite , then the pathways and the central
01:41 will come back to this diagram a later. But we talked how most
01:46 the output most of the things that out of the retina, 80 to
01:51 of it goes to the lateral geniculate . And then 10 to 20% by
01:59 plus uh minus percent go to the colliculus, forya, eye movements,
02:07 then a small portion goes to super nucleus which is responsible for circadian or
02:14 rhythms. Then we talked about how have a binocular zone that means that
02:21 is uh the central zone. If focus right in front of, you
02:27 be perceived by both eyes and the on this side can only be perceived
02:35 the right eye by the same eye the same side. And the periphery
02:41 this side can be perceived by the on the same side. And we
02:47 about how retina was sort of all cups to the bottom of the
02:54 And therefore the nasal retina is positioned look over there. The central retina
03:01 position to live over here and the recognize position to look over that.
03:09 that's why this eye can see the on this side really well. But
03:15 of the nose, this side, side cannot see the periphery on the
03:21 side. OK. So the nasal , the nasal portions of the retina
03:29 the ones that cross over them. remember that and we talked about the
03:36 . So if you have a transaction an optic nerve on one side,
03:42 or right, it's an equivalent of vision in one eye or an equivalent
03:48 just closing one eye that ends up the loss of the peripheral field of
03:54 on the same side to the damaged . And if there is a damage
03:59 the optic tract, now you have realize that optic tract will contain nasal
04:08 that cross over and temporal fibers from same side. So nasal fibers that
04:18 crossing over are damaged. So now don't have this nasal fibers are
04:27 And remember nasal is looking from the over there. So you damage the
04:33 on this side. And the temporal here is the temporal. It's also
04:40 on this side of the binocular Therefore, resulting in a loss of
04:50 of vision from half of the field view essentially on on the opposite
04:55 So left optic track damage, the optic track loss of the right side
05:01 field of view and damage to the tim nasal fibers crossover looking in the
05:10 there in nasal fibers that crossover looking the periphery there. Therefore, you
05:17 the peripheral vision. It's also referred as the tunnel regime. Yeah,
05:24 geniculate nucleus is like we said receives of the output from the retina,
05:32 geniculate nucleus, receives magno and Remember that we have magno power and
05:40 the cellular non N P types or referred to as intermediary cells. And
05:50 when you stain thalamus is a portion the thalamus that contains a lot of
05:56 nucleus nucleus. You reveal with missile that it has very clear six layer
06:05 . And in between of these layers entra to each layer, there are
06:11 cells that can be detected but they not as densely uh packed in therefore
06:17 dispersed quite loosely. These are the MP cell projections that come out of
06:25 non MP subtype of cells of the and carry that information through G M
06:32 the visual cortex. You have six . Each one of these layers is
06:40 . It means that each one of layers receives information only for one time
06:46 parallel processing because as you'll see, there's magnone powerful layers and there's also
06:54 power layers for each eye. So is overlap and there's parallel processing that
07:01 along these layers. Uh the receptive properties just like in retina by these
07:13 centers surround just like they were in . So L G M and
07:27 the cells in retina and the cells L G M. The re the
07:34 properties for the cells found in retina L G N are these concentric on
07:40 off just like you had on and in retina, they're also on and
07:45 in the L G M. So means that if you were to
07:50 as I say, L G M to the computer and say what are
07:54 receptive field properties of the South and G M. Again, they will
07:59 the most action potentials or the least potentials as the retina is being stimulated
08:06 these round spots, lots of light dark, surrounded by light or dark
08:13 the light source. So it's uh similar type of processing in a way
08:18 perception. It's still perceiving. Aldrin still perceiving the world based on luminescence
08:25 based on contrast processing, uh 80% projections into L G N are of
08:35 origin. So if 80-90% of things the I go into L G M
08:44 G N actually receives most of its from cortex. So for L G
08:51 that huge output from retina, 80 90% is also a fraction of what
08:57 G M receives. In fact, receives most of the inputs from
09:02 And that's why we say what we with L G M is influenced by
09:07 we feel. Because cortical processing for , association of vision and a lot
09:15 inputs that go back into L G come from different cortical areas. And
09:22 , it may even influence how you things because it may involve emotional
09:26 So memory areas, association areas that up inevitably a certain emotional response.
09:34 if you look here again, you the right temporal, right,
09:39 left, nasal, left temporal. the nasal fibers are gonna cross over
09:46 when they cross over, they innervate one on the other side, layer
09:53 and layer six. So these are we call contralateral because they're from the
10:01 side, they cross over. So , I will innovate 14 and six
10:08 the ipsilateral side to this G Remember the fibers are gonna stay on
10:16 is gonna stay on the same side ipsilateral is gonna innervate 23 and
10:25 OK. So layers 1 and 2 receive magno inputs. So you will have one
10:40 magno layer, one from gelato magno in green two, it's the lateral
10:49 layer but they're monocular and then you three of the lateral four contralateral Piil
11:01 contralateral. So each eye gets two and one magma layer out of these
11:09 layers on one side of the L M, one side of the
11:16 uh non MP are even to these layers but is a cell you will
11:23 you'll see all diagrams that's gold intermediary . Uh So this is the organization
11:31 the inputs into the lateral geniculate They're called the retina geniculate inputs.
11:39 this is the anatomy or an anatomical layer description of the lateral nucleus and
11:47 thalamus and the cells here are called cells. Yeah, in the light
11:55 nucleus and from the lateral geniculate the relay cells send the information to
12:02 17 which is primary visual cortex or sometimes called area V one or primary
12:12 cortex, V one. If you a monkey brain with a human
12:23 you notice that area 17, which shown here in green in both Midol
12:31 also this lateral views. What you is that area 17. Our primary
12:37 cortex occupies quite a bit of the stays compared relatively to the overall size
12:46 the brain. And the monkeys are well advanced in their visual system and
12:57 rely on the visual system quite a in humans. As you can see
13:02 area 17 or V1 is much, much smaller comparison, relatively to the overall size
13:12 the brain. Again, we are order species than monkeys and higher we
13:22 you go through evolution from rats to to monkeys, to humans. You
13:31 that less and less brain space is to the primary information processing and rather
13:40 and more space in advanced species. in humans is dedicated to secondary tertiary
13:46 areas that each sense will have. visual association areas, auditory association areas
13:54 then cross modal association areas that bind from visual cortex, auditory cortex about
14:03 sensory. And what else might be at that moment? From retina to
14:12 . As I indicated, retina has point here in the retina that's looking
14:18 a point in a visual space over . A point here in the retina
14:22 looking at the visual space over A point in the retina is
14:25 So there's this point by point map the visual field in front of me
14:31 is represented by different photoreceptors and circuits that point by point representation across the
14:40 . OK. So it's called the topic map. And that point by
14:45 representation from retina is in the lateral nucleus and from lao nucleus, most
14:54 the outputs will enter in this case the stride cortex or primary visual
15:02 mostly in layer four, right. even at the primary visual cortex,
15:09 still have a point by point representation this, let's say nine points
15:17 One eye is looking here one through and you'll have one uh through five
15:26 this side and five through nine, represented in point by point in the
15:32 cortex. So it's called the re mop. In the Neocortex or primer
15:38 cortex. We already learned it's a layer structure and we talked about how
15:45 has both layer structure which is laminar also column like structure. We refer
15:54 column, we'll talk about columns today sure. His most superficial neo cortical
16:01 is number one, the deepest one the closest to the subcortical areas of
16:07 brain is six. There's certain organization parameter cells of inter neurons that are
16:15 across these layers. We won't learn lot of the details, but we'll
16:20 a little bit about where the inputs into layer four and how they travel
16:25 the cortex. It's there's a whole within these layers. You have anatomical
16:33 into layers and into columns and you a division of labor uh by cells
16:42 these layers, what they're responsible for inputs they receive, what outputs they
16:47 and within the columns, how that is communicated within the column or structure
16:53 the cortex. So it turns out the reason why primary visual cortex or
17:01 17 is called stride cortex is because some of the early experiments that were
17:08 done with radioactive prolene injections. So this case, the syringe injects one
17:17 , some fibers will cross over the temporal will stay on the same
17:23 . They will go into the lateral nucleus and the lateral geniculate nucleus from
17:29 layers from that one eye, they go into the cortex. And then
17:35 you were to look at the cortex you were to peel layers 123 or
17:40 somehow a microscope to visualize in that plane of las 23, they have
17:47 stride or stride like a appearance. that means that where this dye was
17:54 in one eye, the projections from one eye went into layer 14 and
18:01 . OK. And then from L M, it went into the cortex
18:07 everywhere where you're seeing blue here. are what are called ocular dominance
18:14 This is the information that belongs to eye all in blue and everything surrounding
18:22 stripes and white is the information that being processed and would belong to the
18:29 eye here, right? So they referred to as ocular dominance columns.
18:34 is another visualization. In fact, can visualize them with fluorescent marker
18:41 we can visualize them by visualizing stimulating one eye. So there are
18:48 ways by which we can reveal this interesting ocular dominant structure. That means
18:53 all of the cells and and within black area, this black stripe will
18:59 information from one eye. All of cells in the white area will receive
19:05 from the other eye. So let's it, it doesn't matter which one
19:09 which IPs and contra doesn't matter. for our uh purposes, let's say
19:14 black will call IPs, the wife contra. So all the cells here
19:19 here contra I contra I contra IPs . And this is the anatomical demarcation
19:28 what we call the ocular dominance columns layer four where all predominantly all of
19:35 projections from the lateral geniculate nucleus go the cortex. So now, so
19:42 going on here if these columns and four are receiving information from one eye
19:51 that tells you that layer four cells still monocular. That means that in
19:59 four, all of the cells will be responsive to information from only one
20:05 . And then adjacent ocular dominance column the other eye and adjacent Odoms column
20:11 to the same one eye and so . And so it turns out that
20:16 is a certain circuit and once the from lateral geniculate nucleus innervates, as
20:24 can see here, innervates layer four forms these ocular dominance columns. Information
20:32 layer four gets sent up within the column to layer 2 3. And so
20:42 recordings were made where electrodes were placed position A and position A here is
20:52 centrally located in the middle of the dominance column. But in layers
21:01 and when electrode was, was placed this location, and two eyes were
21:08 in this location. A the electrode receiving signal only from contralateral eye.
21:15 that showed that the cells that are the center and above of these ocular
21:22 columns in layer 23 are still But if you move the recording electrode
21:29 position B and if you know position is in between one ocular dominance column
21:38 to one eye and another ocular dominance belonging to the other eye in this
21:45 B right here. When two eyes stimulated, the cells in position B
21:51 responsive now to both eyes. So says that in these locations that are
21:58 between the ocular dominance columns and above layers 23, the cells are becoming
22:06 . If you move into position which is directly and centrally above the
22:12 dominance column and position c its only to one isa lateral position D
22:21 which is above but in between the ocular dominance columns, the cells there
22:29 responsive. But that tells you that is where in the primary visual cortex
22:34 information from two eyes is finally being together into a binocular picture. And
22:42 is happening not, not in all the layer 23 cells, but in
22:48 layer 23 cells that are located specifically above and in between the ocular dominance
22:56 that are below in layers four. so the inputs that come into the
23:02 from lot of Verni nucleus into the , we call them cortical inputs.
23:09 have M magno, we have P and they predominantly innervate layer four.
23:16 you'll also see that there is another here labeled as I and I to
23:22 , that the non MP cellular cells their projections are also sometimes called
23:30 And that's why this is labeled I intermediary projections note how they bypass layer
23:37 of the Neocortex and instead they innervate layers 23 in the neocortex. So
23:44 of those a few cells that are to each one of those G M
23:50 will be carrying the information to layers three directly. However, most of
23:56 input from MP cells and most of input comes into layer four in ocular
24:04 columns the cells are still monocular But you can see that they're becoming
24:11 in layer 23. So projections from four going to Larus 23 In Las 23,
24:18 are pinal cells that have these long exotic or axons and they stretch far
24:27 outside the stride cortex. They go other extra stri cortical areas. So
24:35 of V one prime into D two visual V three tertiary and into these
24:44 temporal pathways or other pathways with information being communicated. So basically layers 23
24:53 spread that information laterally outside area 17 other adjacent visual information and further association
25:03 that uh that, that that process information as well as layers 2 3,
25:10 that information laterally. They also communicate into deep layers. 5 6 and deep
25:18 six communicates back to the lateral geniculate . So projections from cortex to thalamus
25:28 cortico saam. So these are the and these are cortico thalamic projections.
25:37 as you can see inside you have a loop in the cortex. So
25:44 gets activated by Linus, it sends to 2323, sends it laterally in
25:52 deep layers and 56 layers deep 56 form layer four cells. So this
25:58 is referred to as intracortical loop. other words, the processing of information
26:03 circulation and the projections are happening within cortex. Whereas these are from thalamus
26:09 cortex and these are the cortex back thalamus. OK. So blobs,
26:19 right, blobs are pretty interesting. blobs were revealed when the cytochrome oxidase
26:26 was used. Cytochrome oxidase is an that is involved in energy production.
26:32 what was revealed in the primary visual , especially in layers 23, the
26:38 of these darker blotch like structures in as you can see. Uh and
26:46 they are known as blobs. So you can see Bloss in
26:55 And that indicates that in those there's an increased metabolic processing, there's
27:02 lot more energy production, energy more metabolic activities going on. In
27:09 lists. 23, if you recall intra or cellular cells receive retinal limpid
27:17 from ganglion cells that are non they project primarily into layers 23,
27:23 bypass layer four. It's little that still know about their functional part that
27:30 understand that they're involved in color processing of the color information, maybe
27:38 requiring a different level of metabolic activity energy turnover uh as revealed by the
27:45 staining. OK. So we talked in retina, you had cells that
27:55 responsive to these on off centers around L G M, we said they
28:04 are responsive to these uh shapes And you would have to recreate an
28:11 or sketch of the outside world using shapes only. And now we're in
28:18 primary visual cortex. So what are receptive fuel properties of the cells in
28:25 primary visual cortex. And the way these experiments are done are that an
28:32 is fixating at this blue screen, is the whole field of view an
28:38 can see. So typically in, , in cats or uh in monkeys
28:45 well, microelectrode gets placed in the in one cell in a single cell
28:54 it's recording action potentials. So it's action potentials. That means it's recording
28:59 from one cell. So it takes probably four hours to get to that
29:05 . Experimentally, you have to uh the animal, anesthetize the animal,
29:12 them in the stereotactic. So the is being held and then have them
29:18 at the screen and you have a you're recording from and you are flashing
29:25 of light along the screen. So don't get any responses. So you
29:31 the on off the off center, on center, you don't get any
29:38 in the cell. So that tells that cell is responsive to something
29:44 So, cortical cells are responsive and different receptive fuel properties if you're lucky
29:50 the experiment. And that was the , you start presenting them with different
29:57 . And in this case, a of light was presented and this white
30:02 here is the border of the receptive . And when the experimenter had the
30:09 and passed the bar of life through specific area here, this white
30:15 And when it passed the bar of in this orientation, the cell in
30:21 cortex produced a high frequency barrage of potentials. So that told the scientists
30:29 the cells in the primary visual cortex responsive to bars of light.
30:40 they're no longer responsive and the receptive properties are now best activated. The
30:49 are best activated when you have a of light in the receptive field of
30:55 here and notice that if you change orientation of this bar of white into
31:02 orientation, the response from the cell the cortex is not nearly as strong
31:08 just a few action potentials. And you change it into this orientation as
31:14 is on top, there's no response all from that cortical cell. And
31:20 is all within its still receptive field view of that cell. But that
31:28 says that I prefer not only a of light, but I prefer a
31:35 of light in a specific orientation. . So I am orientation selective cell
31:45 that is called orientation selectivity. I produce most action potentials. If you
31:50 me with a bar of light, other stimulus and I will produce most
31:55 potentials if you present me with a of light and a specific orientation,
32:00 if you change orientation and none, you change it too much. So
32:06 orientation selected cells in the primary visual . Another experiment that was done was
32:16 same experiment where you have a an electrode inside the cell, you're
32:23 action potentials. You have identified the of the receptive field. You now
32:28 that the cells are responsive to bars light in the specific orientation. And
32:35 decided what happens if I pass that stimulus and the cells are most responsive
32:41 the bars of life from this In this case, from left to
32:47 . And as it enters the recept field, the layer, the cell
32:52 you're recording in the cortex and the four boom, boom, boom,
32:55 , boom, boom, boom, , boom, boom responds with a
32:58 of action potentials. Now you OK, what happens if I,
33:04 still recording from the same cell, still the same receptive field. But
33:09 me pass that stimulus and that screen the animal is looking at and its
33:14 field, let me pass it in opposite direction from right to left.
33:19 as the stimulus moves into the receptive , boom, boom boom, you
33:24 a few action potentials and then it silent. So that's told scientists that
33:31 cells in the cortex are not only selective, they're also direction selective.
33:38 they prefer these bars of light to moving into one direction or another in
33:46 specific orientation. OK. So they're selective and orientation selected. You can
33:55 here that you have a patch of patch of retina you have three on
34:03 in this patch of retina, one three, those are three on cells
34:14 those cells will go 1 to 1 AL G N. So that you
34:20 see that the connectivity between retina and G N is 1 to 1.
34:26 then al G N cells can converge the cortical cells in layer four.
34:34 now information from these three cells can . And if you converge information from
34:42 three cells with these receptive field guess what you get, you got
34:50 visual stimulus that resembles a bar of . OK. So this is how
34:58 can put three on centers, you put three off centers, you can
35:04 now on center and off center cells project and you will get different combinations
35:11 in this case bar of light. later on these cells, the simple
35:20 will also project to complex cells. look at this diagram here. So
35:26 G N cells that are concentric retinol that are concentric, that project L
35:32 N cells 1 to 1 that are L G N cells converge OK
35:40 onto these concentric cells. 123 converge simple cells and you can have a
35:48 of light. And then there's another of complexity, simple cells in the
35:54 now can converge on complex cells. now what you get is you get
36:02 of just on center and off you get half oval, on and
36:10 receptive field in simple south of primary cortex, you get middle of the
36:18 off the edges and the lines Ok. So now you're getting all
36:26 these different shapes, the receptive fields are called all in different shapes that
36:41 you can have more like this Mhm All right. Now look what
36:53 can do. This is convergence here get a bar of light. But
37:00 you have that bar of light and of all, in simple cells,
37:05 have these susceptive fuel properties. What you think happens if a cell that
37:10 this property converges with a cell that this receptor field property on the complex
37:19 , it's gonna have a combination of receptor fields in the shape like here
37:25 had a combination of converging cells but it would be a more complex
37:32 OK? Leading to these different receptive properties. And so now this pen
37:41 running out, hopefully this one would have something. Yeah. And so
37:46 if you know, if I was artist, I would say this is
37:51 awesome because I can use these shapes this and like this and then I'm
38:03 go like this. Yeah. Happy this. Yeah, there's another bar
38:18 but like maybe a little things here that little things here with that.
38:25 . And then maybe some small bars a different orientation like that or
38:31 Like that and uh maybe I'll put circle here what I saying? So
38:41 , that's, that's me. that's what we call a, a
38:47 sketch contours contour lines of, of you see. And so in the
38:54 visual cortex, that's what the primary cortex is. If you connect it
38:59 the computer, you will see the sketch, it will have contour lines
39:05 have color because you have color processing have motion because it's reacting to the
39:12 of light or the visual stimulus moving different directions and not just left,
39:18 up and down along all of the open point. So that's kind of
39:24 I was doing on the board And so, you know, you
39:29 have a lot of primal sketches, just at this, you know,
39:33 representation, but you can draw a of different objects using these shapes.
39:40 you have these shapes, the receptive properties, the shapes that these cells
39:45 process in the outside world. And you can see that they can start
39:49 these shapes and it's difficult to do with just on or off center
39:55 Then you're just really talking about dots that's much more difficult to do a
40:00 representation if you were an artist just these two shapes versus having access to
40:07 bars of light and shapes and round and things like that. So,
40:12 that's, that's why as you can you move through the system and retina
40:19 , it converts the light L G processes information it suggests that and
40:24 you have this primal sketch in the cortex. So it's more complex representation
40:31 the visual world in the primal visual , it becomes more complex in
40:36 more complex in V3, eventually involving 1718, maybe 20 different areas in the brain that
40:44 concerned with visual information processing until we complete visual perception that we have of
40:52 of color, of depth, of of motion of and uh stability and
40:57 on and so forth. So uh we're talking about the ocular dominance
41:05 it was Hubble and weasel the two famous scientists that did a lot of
41:11 uh coral systems and atomical descriptions. were doing recordings in the uh in
41:20 uh microelectrode recordings. Uh they spend and days and days. So students
41:28 post docs to record from a single in the cortex with that visual representation
41:34 it's a whole day. So if lucky, you get maybe two cells
41:38 the whole animal three, if you're and you need about 100 to publish
41:43 paper. Uh So and getting data one thing, analyzing data and interpreting
41:51 and measuring and seeing if it is significant is another story and then presenting
42:01 to the to the reviewers. So years and years of work and you
42:05 imagine how many cells el and weasel their students and postdocs had to stab
42:12 the primary visual cortex and what they doing, they were presenting bars of
42:17 and different orientation. So we are these days because we have different dyes
42:25 some of these dyes can record changes the calcium concentration. So we looked
42:32 the calcium concentration changes in pre synoptic and neurotransmitter vesicle fusion. We we
42:41 looked at a diagram that showed calcium dyes. So it can show you
42:46 heat maps or the increased concentrations of . There are also voltage sensitive
42:53 So there are dyes that will penetrate the cells. Imagine these individual cells
43:00 voltage sensitive dyes will report voltage. it's not reporting changes in calcium concentration
43:09 sodium. It's actually reporting changes in membrane potential. So it's voltage
43:17 So therefore changes and these heat maps indicate changes in voltage. So whatever
43:24 you use, obviously, uh what Hubble and weasel determined through these painstaking
43:32 with single cell recordings, microelectrode recordings that there are these micro columns that
43:39 called orientation columns and these orientations approximately to about 100 and 50 micrometers
43:48 So they vary slightly in their But what's interesting is that within these
43:55 columns, the cells are organized in a manner that you can see this
44:02 . That means that all of the in this part of the orientation column
44:07 the six layers of the neocortex are to be optimally tuned or they will
44:13 the most action potentials that will be reactive to a bar of light in
44:20 . And next to it here in orange and then in yellow within this
44:28 of this orientation column, you'll have that are optimally tuned to a bar
44:33 light in a slightly different angle And if you walk around this micro
44:41 orientation column, you have the cells will be optimally responsive for 360 degree
44:50 in this bar of light. So in the middle, the cells
44:55 the middle will be responsive to all . And that's why you have this
45:03 wheel like structure where the cells in middle are responsive to all of your
45:08 . And the cells rating get out the middle and to the edges of
45:13 small orientation column. As you can a processing very specific orientation of light
45:19 the closer they are anatomically next to other, the more similar is the
45:27 that they're processing. So this side the column versus with the further part
45:32 the other side of the column, be processing orientation from a different uh
45:37 uh processing information for a different OK. So voltage sensitive dyes,
45:45 they allowed us is that you can hundreds of cells, you can stain
45:51 of cells and you can represent activity each cell. And you can see
45:57 that all of the cells and uh are responsive to this orientation of
46:05 All of the cells and yellow are to this orientation of light and
46:11 blue, red and so on. each one of these micro columns will
46:16 thousands of neurons that are responsive, orientation of light. And they're organized
46:23 these uh ocular dominance columns. But talked about a lot of things
46:29 we talked about ocular dominance columns. said that there are these columns that
46:35 responsive to information from one eye. I said that you can visualize the
46:42 dominance columns. This is for uh contra I this is contra
46:50 this is IPs C column. So can visualize them with the injections of
46:55 dyes like the radioactive dye. You also visualize them with intrinsic optical
47:05 So this is another very interesting feature speaks again to some of the concepts
47:11 we already started discussing. If we in imaging activity, we're experimental
47:18 we have a lot of different tools image activity, neuronal activity in
47:21 And in vivo, we talk about imaging, functional imaging, noninvasive,
47:27 talk about pet scans and functional magnetic imaging. So in the previous
47:34 we talked about an experimental technique, technique, voltage sensitive dye imaging,
47:39 means you stain the brain, you some dye in the brain and then
47:44 the dye changes its reflective properties, can see which cells are active and
47:50 cells are not, it's vaulted sensitive . But the brain, as we
47:57 about the active neurons in the they will draw more energy, they
48:02 draw more blood, they will consume A T P, eat more
48:07 they will demand more oxygen and the neurons also swell. So if you
48:15 shining a light on the surface of brain tissue, and all of the
48:20 are the same level of activity, won't see much of the difference.
48:27 if you activate one eye flashing information one eye and you look in the
48:33 visual cortex, you don't need any . You can image, you can
48:39 this lighter area right here. This right here. One of the ocular
48:45 columns that was activated and it's called optical signal. There's no dye
48:54 What happens is as the cells swell active neurons, the swell and you
49:00 the same light, the active they change their reflection properties. So
49:05 reflect the light differently from the inactive . And therefore you can reveal the
49:12 domino's column structure using intrinsic tic So you don't need any dye.
49:19 these are all very interesting experimental Neuroscience techniques, calcium sensitive dyes, voltage
49:27 dyes. In this case, no . The fact that you can look
49:31 the surface of the brain and the active circuits are, are gonna appear
49:36 darker and lighter and dependent on, where you're looking in the brain.
49:43 so if we put it all in addition to the ocular dominance
49:48 we have orientation columns. So each of the ocular dominance columns will contain
49:55 orientation columns within it. And we're the middle of the ocular dominus call
50:04 that's where we'll find the blobs. the me metabolically active areas is correlated
50:10 kind of a central portions, middle of the ocular dominance columns. And
50:18 , we have what are called hyper , hyper columns where you have orientation
50:25 uh organization of orientation, select the , ocular dominance contra c contra C
50:34 in the primary visual cortex. And hyper columns are now approximately one millimeter
50:42 . So you have a lot of small orientation columns for orientation processing that
50:49 together and form the ocular dominance column an ocular dominance column. And then
50:56 dominance columns contra and I PC, form these larger hyper columns that are
51:03 your elementary computational modules for processing visual . So they're more complex,
51:12 You can say while you have one , it's a computational module. It
51:17 sure, but that one cell will only one orientation of life. You
51:22 say, well, you can have computational module from the orientation column.
51:28 you do, you know you But in this case, the hyper
51:35 will incorporate several orientation columns and also compare and contrast contralateral and ipsilateral dominant
51:47 . It will already be binocular information it will reveal a lot more about
51:53 visual image. It will have a more information to process by receiving and
51:58 comprised of these different anatomical features. . So you have uh innervation of
52:06 blood vessels. Remember you have in fact, the micro vessels in
52:11 brain, the the the highest, the longest biggest distance between them is
52:17 50 micrometers. So there's no neuron is not few cell bodies away at
52:23 most few cell bodies away from the capillaries. So that's why neurons will
52:32 the blood, will draw the the nutrients and will cause the
52:38 So you can reveal the circular dominance underlying the the overlying the vasculature,
52:46 underlying vasculature uh off the surface of primary visual cortex. And then in
52:53 to these soar dominance columns, you impose smaller orientation columns that you can
53:00 either as hub weasel one cell by cell or using different uh imaging
53:08 functional imaging techniques because you're looking at activity in this case, voltage sensitive
53:15 and voltage activity. OK. And last slide I'm gonna come back to
53:20 that I wanna discuss is this slide this slide talks about several important topics
53:30 wanted to get through the visual It talks about cortico thalamic innovation.
53:35 talks about ocular dominance columns that you understand. And it talks about principle
53:42 plasticity. It's not the plasticity. there are different time periods in our
53:52 and animal lifetimes and developmental stages where of plasticity are also different. So
54:01 younger the animal, the younger the brain, the more plastic it is
54:08 actually at first are born with a more neurons and synopsis that we end
54:14 as adults and everything in our brains sort of interconnected at first. And
54:20 there is anatomical refinement of the pathways the circuits in the brain and their
54:29 and the anatomical refinement into ocular dominance and such. And during this intense
54:36 of plasticity, there is this period critical period of development. During that
54:42 period of development, a lot of are changing. So if we talk
54:49 plasticity in human brains, a good is often foreign language, learning a
54:54 language, you're well, you're much better equipped to learn a foreign
55:02 or to start learning a foreign language the age of 5689, 10,
55:08 , 12 and then 13, 14 after 18 1920 it becomes more and
55:15 difficult. And this is sort of example of human plasticity that were built
55:21 a way where we typically also go school when we're younger. There's nothing
55:26 with, you know, going to in your 50, 6070, that's fine,
55:30 know, but uh we are most of learning, refining the connections in
55:35 brain during the early developmental stages. that critical period of plasticity. It's
55:42 very valuable. Another example is injury uh repair. If a young child
55:52 a traumatic brain injury, they may very little loss of function or maybe
55:59 loss of function at all because they'll a lot of plasticity in their
56:04 this chemical environment and functional environment that allow for the brain circuits to rewire
56:12 themselves and not end up in having loss of function in the brain part
56:18 was injured. If the same part the brain is injured in an adult
56:24 even an elderly person, just like wounds. When you're older wounds take
56:32 time to heal as if you're The same principle, if you have
56:37 or traumatic brain injury in older inevitably it will result in the loss
56:42 function and a lot of times significant of function because it's outside that period
56:48 plasticity where there is a lot of for the cells to rewire, rebuild
56:53 reconnect with each other. So in example, we're looking at rodents in
57:02 . The first month of life is important for the development of the visual
57:09 . And after two weeks of there are eyelids open, they have
57:13 rec axial rays of light. And a lot of restructuring in the 1st
57:19 weeks of life restructuring of retina genicular as well as genicular cortical or thalamocortical
57:28 . And in mature animal, you'll someone with cortical projections that are pretty
57:35 . This is from one axon that extensive branching and innervating layer four of
57:41 neocortex of the falls. And this shows that if you deprive an animal
57:50 vision. So at the end of first month, these animals have their
57:56 sutured and a pirate patch put over sutured eyelid only for three days.
58:05 then three days later, that island open. So it's referred to as
58:10 monocular deprivation, three days. And animal is allowed to recover for a
58:19 . And then one month later, eyes of the animal are being
58:27 left and right eye. And we're from the visual cortex just like we
58:33 about. And we want to know cortical cells still responsive equally to both
58:41 from each eye because one of them closed for three days. And it
58:45 out that yes, the cells in cortex is still processing information from the
58:51 eye, which was closed. But shows also that the cells in the
58:57 are a lot more responsive toward the that are coming from the eye that
59:04 open and was not closed for three . So there's already a change in
59:12 functional responses of the cortex where the is now saying I'm gonna pay more
59:19 to the eye that remained open. nonetheless, you didn't lose ocular
59:26 You just shifted the ocular dominance. biased it toward the open eye in
59:32 cortex. Now, what happens if repeat the same experiment? But instead
59:39 three days, you double the amount eyelid suture and you deprive the animal
59:46 light and vision for six days. of three, you open their
59:53 six days later, you wait for month for them to recover and you
60:00 their contra and their F C I you're recording in the visual cortex.
60:05 you ask the same question, are cells still in the cortex, responsive
60:10 both eyes. And what you find no is that six days during this
60:19 period of development, which can help restructure, but it can also shift
60:24 to the negative effects. Six days deprivation shifted cortical cells to being responsive
60:33 to the eye that remained open and cells on the cortex are no longer
60:39 to the eye that was closed for days. Maybe it will take another
60:45 until some of the cells will become to contralateral eye. Maybe they will
60:51 be responsive to contralateral eye. And is what happens on an anatomical
61:00 This is a normal open eye and are thalamocortical projections from the you can
61:10 clearly see that those axons and the and the complexity of the innovation
61:18 No longer exists. So, thalamic inputs is attrition of thalamic cortical inputs
61:26 cortical cells. So no longer reacted this thalamic cortical MPS following a prolonged
61:32 this case, six day deprivation. . So that will actually end our
61:40 today. I'm wishing everyone good luck the material and I'll see you online
61:48 Wednesday and good luck with the test Monday. Thank
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