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00:00 So this is the final exam or midterm three Neuroscience exam review session,

00:07 we will go over some of the material that we covered and they'll slashed

00:12 section off the course, and we with the visual system. And if

00:17 recall, you had information off light enters into the retina, we studied

00:25 retinal circuit and then the outputs from retina coming into the lateral Jean Nicolet

00:31 of the thalamus from lateral Jean nucleus of the columns that information traveled

00:36 the primary visual cortex V one. subsequently there were two pathways that split

00:42 the dorsal parietal pathway and into the or ventral inferior temporal pathway here.

00:49 we understood the anatomy off the off the lot of genetic alert nucleus

00:55 the primary visual cortex. And we the neocortex. Anatomy of the primary

01:01 neocortex is sort of, ah, for the canonical secretary that you will

01:09 New York cortex and many different parts the cortex. Thio, please recall

01:15 the anatomy of the eye. When light enters, you have the highest

01:20 vision here in phobia, but you the specific anatomy of the eye that

01:26 the light through the pupil into the areas of the retina, which is

01:32 in the very back of the And as the light enters into the

01:39 , encounters retinal circuit. It bypasses all of these cells and the photo

01:47 that convert the signal of light into electrochemical signal. These photo receptors are

01:54 in the very back off the There's cone and rod for the receptors

01:59 are connected to bipolar cells and retinal . South retinal ganglion cell accents them

02:06 the fibers off cranial nerve to or nerve and exit out of the

02:14 Traveling into the lateral Jean Nicolet as well as some other structures that

02:21 retinal input. This synaptic transmission processing this information is also modulated further by

02:30 horizontal on a McCain cells is shown . The two important things this photo

02:40 air the only light sensitive cells and ganglion cells is the only output that

02:45 out off the retina, so the cells will produce the action potentials in

02:52 optic nerve and communicate that information. , the thalamus and columnist, will

03:00 that information to the core attacks. air the layers of the retinal ganglion

03:04 a plex reform in a nuclear outer to form out of nuclear layer photo

03:09 outta segments and pigmented at the This is a very back augmented epithelium

03:15 the photo receptor out of segments. this is the exit point here where

03:20 ganglion cells will actually project the optic output. Here we have different

03:29 rod and cone photoreceptors who please review anatomy. The fact that the Rod

03:35 have free floating disks and we distinguish rod photoreceptors and mostly night responsible for

03:43 vision and our acrobatic and have low acuity. And it is a slowly

03:50 system as opposed to the cones, low sensitivity. But they also process

03:57 acuity, vision and color. But need direct access oil rays of light

04:03 direct rays of light illuminating something penetrating your eye in order to perceive all

04:10 these details and so in the phobia will have the highest concentration of cones

04:16 rods will be dominating in the But the blind spot illustrated here is

04:22 an exit side for all of the ganglion cell fibers exiting out of the

04:28 . This is another representation of the zone where you have this,

04:33 indentation here and the actual structure allowing the light to most directly contact the

04:39 cells that are located in the center the phobia. The three cone receptors

04:45 blue, green and red, uh, they are optimally activated by

04:52 light or green light. What we as green light and the combinations off

04:59 colors come from a very degree of of these three different types of cones

05:06 you can imagine you have color mixing on. And it is really the

05:12 color information that is out there between 100 nanometers of wavelength that we can

05:20 we can perceive. Photo transaction happens the retina. It happens when you're

05:32 , typically with activities you protein coupled and other systems. But in the

05:37 transaction and with light, it's the that activates a G protein coupled receptor

05:44 the effect of enzymes and the mechanism that in the dark, photo receptor

05:52 are deep polarized because there's ample amount cycling GMP which keeps the sodium channel

05:59 and in the light that cycling GMP converted into GMP and you actually have

06:07 high propeller ization. So this is opposite to what we studied excitation in

06:13 way, in the eye excitation excited put off. Visual stimulus means hyper

06:19 off the photo receptors. And so have written all that gets activated by

06:26 light and activation of G protein coupled converts through Fox for the estimated cycling

06:34 into GMP. And in the absence cyclic GMP, the sodium channels are

06:39 . And because there is a decrease sodium or positive current influx, you

06:47 hyper polarization. We also described receptive properties, and the most important take

06:53 message is, is that you have and collections off receptors, photo receptors

06:59 the retina, the process information in visual field and they're receptive. Field

07:07 of these concentric on and off, center, off surround or off center

07:13 on surround receptive field properties, and receptive field properties are created by thes

07:21 of photo receptors that are communicating that to buy all themselves on further down

07:28 the retinal ganglion cells. The take message from this diagram that if you

07:35 on center Sal, the maximal stimulation receptive field would be if the stimulus

07:41 the outside world was focused on a small piece of retina, very small

07:47 of right now that contain these on receptor cells. And it will generate

07:51 of the action potentials when only the of that receptive field that collection off

07:55 photo receptors was activated and in the situation is to surround off center ganglion

08:03 is the most actual potential. Start the surround of the cell of these

08:08 field properties of these cells is We discussed that there's a circuit that

08:17 for the cells to be either signed or sign inverting for the cell synopsis

08:26 exists between the photo receptors and the cells. Most important thing is that

08:31 sand concerning synapses are found in the cells that have kind of a kind

08:37 interceptors, and that simply means that there is deep, polarizing glue domain

08:41 is released by these photo receptors, does glutamate is released as glutamate?

08:47 means excitation in the south means the wonders. Deep polarization of glutamate is

08:53 . It's also going to dip. this cell from the sign conserving synapse

08:59 it has an umpire kind of On the other hand, some other

09:04 cells have medical, tropical, intimate and glutamate and excitation, and the

09:11 release of glutamate actually inhibits activity of cells. But this diagram specifically shows

09:17 center in Europe and the light, what happens in delight is the cells

09:21 proposal arise. And so if this hyper polarized, there is not enough

09:26 . And if it's a sign conserving and this off center bipolar cells hyper

09:31 on this off center ganglion cell is hyper polarized. Now, if you

09:37 the light and the sellers hyper it means you cut off glutamate.

09:40 cell, on the other hand, glutamate is inhibitory because of the

09:45 This on center bipolar cell is actually polarized. And then you have some

09:50 synapses here because all of the retinal cells will have complicated and MBA synapses

09:56 therefore hyper polarization. Hyper polarization. , uh, hyper polarization here means

10:03 polarization and inverted deep polarization and deep here means deep polarization of his gang

10:09 self. So as long as you the concept of all often signed conserving

10:14 Simon averting synopsis and the fact that sign inverting synapses have bipolar cells and

10:20 notable tropical and made receptors, you're to be fine and answering all of

10:25 questions or identifying any of the details only ask of you are in the

10:31 questions. During this exam. The home message of this was that the

10:35 salsa actually inhibitory synapses, so the conserving synapses between photo receptor on the

10:43 cell. So when the photoreceptors deep , the horizontal cell is deep

10:49 but the horizontal cell is in turn these photo receptors. Okay, So

10:57 this horizontal cell is deep polarized and becomes a sign inverting synapse because deep

11:02 of horizontal sell means release of gamma transmit onto the photoreceptors and that means

11:09 polarization of the photoreceptors. Mhm. again you have horizontal cells that have

11:19 . They are very well connected through junctions, bipolar cells, cones that

11:24 glutamate, and then you have horizontal that allow also for broad area retinal

11:33 . It kind of a sharing of information across different receptive fields off the

11:41 . So now we're moving into the processing of the visual information and we

11:49 that there is PNM cells are coming of the retina, and we also

11:53 that there is non MP type cells the projections from the retina. In

12:00 80 to 90% go thio, L m 10% go to superior curricula

12:06 And the fraction of 1 to 3% to super charismatic nucleus, which is

12:10 charge of the circadian rhythms. The from each I cross have a component

12:18 crosses over and has a component that on the same side. Thio,

12:23 that if you injure this area here the chi as um, it gives

12:29 a tunnel vision and one of the exams. There's a question about Goliath

12:35 Goliath was thought to have had um, tunnel vision. And it

12:43 quite, um, often occurring in giants because the sky, as

12:52 is located close to the pituitary So engorged pituitary gland would be putting

12:57 on the chi Azman, causing overtime tunnel like vision and pituitary lines are

13:03 in. People that are very large very large growth hormonal growth,

13:12 growth and are sometimes dubbed this giants . Nikolic Nucleus is a six slash

13:21 . You have to magna lairson for . You have parallel processing because you

13:28 redundancy. And how many layers of information from one eye each one of

13:33 layers is processing information from just And I said, Chairman ocular,

13:38 empty field properties in the algae on very similar thio all on offer something

13:43 property. So we just discussed in retina and l g m receives 80%

13:50 its input from cortex retina sense most its output to the l. G

13:56 . But L G M receives most its input from cortex so concerned not

14:02 with processing the primary visual information, all of the cognitive cortical information that

14:09 communicated back into this major sensory Eso please review the anatomy of the

14:18 and recall that eventually to each we have not as dense collections of

14:25 and these cells are thought to be your cellular or non MP or

14:30 Intra Lonmin ourselves. Um, the 17, as is shown here around

14:36 cultural and Fisher and occipital lobe Primary cortical area, is quite small compared

14:44 macaque monkeys, where the primary visual area again. How much of the

14:48 is dedicated to primary information processing rather cognitive processes? Higher processes that surround

14:57 visual information? We have read no map, and so you have a

15:01 by point representation in the retina that concerned GM along the way to the

15:08 Cortex cortex has six layers, and six layers is in the way.

15:16 anatomically segregated from each other, dividing labor into certain aspects responsible for certain

15:25 . The strike a appear in, , that's referred. Thio Stride

15:32 The primary visual cortex, is referred as a strike cortex because if you

15:38 injections and one eye, you will those projections from one I lighting up

15:44 stride in Layer four off the primary cortex. So these are stride that

15:54 information cortical information processing from one or other. I also referred to as

16:01 dominance columns so that the Layer four South is Stillman ocular, but one

16:07 information gets projected. Them thio more layers to three. Their information already

16:14 binocular. So if you recall you the jalonick inputs, mostly innovating.

16:21 the non NPR intermediary pathways bypassing. , going into learn to three.

16:27 is still, um a cortical inputs cortical lee that information long distances gets

16:33 through lateral excite interconnections and layers to goes toe other extra stride cortical areas

16:39 receives information from other extra stride cortical . That information not only gets spread

16:47 the cortical there 23 longer distances, also gets communicated back in what we

16:53 this filter cortical loop into layers 56 deep layers will actually contact back into

17:02 Solomon. So they're six projections will into the l G m. So

17:06 air called cortical thalamic projections and intra lee. That information is also going

17:12 be communicated onto layer four and therefore have a Philomel cortical input coming in

17:19 have a intra cortical loop 4 to lateral connections. 235642356423 This is an

17:30 cortical loop and finally have the cortical information that is going out of the

17:36 going into the sub cortical areas, as the visual follow most, a

17:40 of ridiculous nuclear's. These are the circus that we discussed the llama cortical

17:46 of cortical thalamic circuits that can engage areas of the cortex that can spread

17:52 between sensory cortical areas, but that can get hijacked by neurological dysfunctions and

18:01 disorders. Reinforcing the negative information or signaling. The south and the cortex

18:11 , um, combinations of what you see in the retina and the

18:16 G M. And so if you at the receptive field properties of the

18:20 visual cortical south to represent the convergent from these more simple concentric on and

18:28 luminescence processing that's coming from the retina the L. G. M,

18:34 you have the cells that are sensitive orientation, you have the south of

18:39 sensitive thio direction, and you have fuel properties that are quite diverse in

18:46 shapes and representations, whereby these receptive of the layer off the simple and

18:52 like South and the primary visual always to create what we call the

18:58 sketch. The Quantrill, Alliance, , color and the fusion of the

19:04 information off the outside world that we the secondary tasks. Tertiary on Mawr

19:12 visual information processing will be performed in two, d three d four.

19:18 finally we blended with information and association . This is again the remind there

19:23 you have orientation columns where in these columns these and Michael columns you'll have

19:29 that live next to each other with columns. So you have both column

19:33 laminar anatomy and the cortex of South live next to each other in these

19:39 process similar type of orientation and the stimulus that's coming from the outside

19:45 So you have pinwheel like structure where cells in the middle will be

19:49 processing information from different orientations. And more you go to the edge of

19:54 micro column, the more specific are to. The cells were going to

19:59 reacting Thio bar of light in a orientation, and these experiments, where

20:09 and performed using well, the sensitive and later in explain to you how

20:15 happens. So you have the orientation that form within the ocular dominance

20:23 And you also have these blobs that responsible for increased metabolic and information

20:30 associate ID with color information processing. for the optical imaging, we discussed

20:38 sensitive dye imaging, which we did on. But an important, um

20:44 matter that we discussed here was this that is shown here. And we

20:51 about how a short term deprivation on sensory input in this case of the

20:56 input with the future of an not even injury to the eyeball or

21:01 to the nerves or anything, simply the animal of the sensory input during

21:07 critical period of development. This is critical period of development for visual information

21:13 rodents is the first month to two of life, and what happens in

21:18 first two months of life will determine term with the connectivity. And the

21:24 is between these cortical networks. And experiment showed that if you deprive animal

21:31 three days, you can still have significant input from the from from the

21:37 I but the deprived I even after short term, three or six

21:42 the deprived I the inputs coming from following us into the cortex are going

21:46 be reduced. Their number of the . There's gonna be attrition off the

21:55 and snap the contacts in that area now dominated by the hips collateralize.

22:01 the projections from the bilateral I, one that remained open will dominate.

22:07 effect can be re, um, back to normalcy the ocular dominance columns

22:15 the deprivation is short. But if deprivation is long for six days during

22:20 first month of development, you can long term off potentially persistent changes and

22:27 anatomy of the cortex and the And how much information will be paid

22:32 to by the cortex if you once that I reopens again. And

22:37 that theme off plasticity, that theme changing circuits and that theme off one

22:45 area map taking over the other cortical continued throughout our conversations in this

22:53 Now we're moving into the hearing just sound just sound molecules coming in 343

23:04 per second traveling through the air and air the compressions and rear factions of

23:08 molecules, the compressed air molecules that oscillating in there for the oscillation of

23:15 speaker can reproduce the compressed air and thes sound waves that are traveling through

23:21 air. Low frequency versus high We just discussed low intensity versus high

23:27 , so it can be the same . But it could be much

23:30 or the tone can change from low , too high pitched tone. Our

23:35 audible range is 20 to 20,000. in the air. We have this

23:41 anatomy, so don't stick a curative into your external auditory me. Eight

23:48 because you may, punk tree, a panic membrane or produce unnecessary stress

23:54 in your obstacles. That's right. have the outer air opinion in the

24:00 canal, going into the air the middle air air drum connected to

24:04 obstacles and the inner air, which connected to the cochlea through the oval

24:10 on the obstacles. And Coakley is part of this tubular cochlear Peratis,

24:16 the cochlear portion of the cranial under , which is Mr Bill cochlear or

24:21 . The stimulant nerve have the institution here, which is the going into

24:27 and is responsible for oppression. Normalization the air and in the oral

24:32 The three obstacles some value sinkers and E's then amplify the vibrations off the

24:39 , Graham and move on to this played off the oval window and the

24:45 of the oval windows. That's off movement of the fluid and the movement

24:50 the fluid and the three shamers through , the stimulus scholar, media scholar

24:56 . The Scholar Media is the one contains the organ of Corti, and

25:01 you were unrolled this cochlear, which about the size of the P,

25:06 would see a particular structure and the Leah. And in the three chambers

25:13 the top chamber of the stimulus on bottom, timpani Paralympic is very similar

25:18 a super spinal fluid that we Another new neurons and end on land

25:23 unusual because it is very high in concentration that is created through the active

25:29 through ST uh, vascular Aris and organ of Corti, where the hair

25:35 are located there. Basil and pictorial are located in this end of the

25:40 environment in the scallop media, just in the retina, you had written

25:46 topic map point by point representation, have the Tono topic. Map This

25:51 a topic map indicates that the highest sounds process the closest to the oval

25:58 and the lowest frequency sound this process hear the apex, also called hilly

26:04 off the cochlea. This tone a map is preserved all the way into

26:09 cortex, and information is included that the fluid movement to set off in

26:15 Paralympic around these two chambers, the of the basilar membrane will display Sicilia

26:23 the direction of the cilia with regard the tutorial, membrane and displacement.

26:28 of bending of the silly into the will cause deep polarization on the bending

26:33 the cilia into the left, and downward will be responsible for hyper

26:40 so the same time of so it'll . Waves now become mechanical sound

26:48 The sound fluid waves move the membranes the Sinus oId fluid waves in code

26:59 of Sinus oId electrical activity in these cells that send receptor potentials, these

27:06 potentials air heard by the spiral ganglion that comprise the auditory nerve portion of

27:13 CBO, cochlear nerve and the spiral cells. Their accents are connected to

27:19 in her hair cells. Wonder of hairstyles and three rows of the outer

27:23 cells. These are McCann a, , transducers. These channels are mechanically

27:31 channels. So in the retina we optically gated channels and these channels,

27:39 were opened by light. And these and the auditory system opened with movements

27:45 their mechanically gated channels. And the of the silly and movement of the

27:50 will open their potassium channels. Remember end. A limp is very rich

27:55 the in the potassium, and the of the potassium will happen here in

28:01 indolent that will cause deep polarization and of calcium. This is the parallel

28:07 . Influx of calcium and the release the excited during neurotransmitters generating the receptor

28:14 . These receptor cells, hair cells the mechanical movement of the fluid into

28:22 polarization and neurotransmitter massacre. Ruiz. of the information that comes out of

28:28 retina off the cochlea comes from the hair cell. So you have most

28:34 the connections from spiral ganglion cells contracting her hair cells and, uh,

28:40 outer hair cells. There's a homework here. What is the equilibrium potential

28:45 in the hair cells? Do you that? What is equilibrium potential?

28:49 ion Haddon Ernst Equation calculating its own potential and that equilibrium potential waas our

29:02 . It has some very interesting things dependent on the concentration on the house

29:07 versus the inside and the RTZ F . And now what? You have

29:12 of very high concentration of the potassium the end, a limp. So

29:17 liberal potential for these cells will be because destined concentration is very high on

29:24 outside as opposed to when we did original nurse equation calculations. And we

29:30 that the sodium was very high on outside and potassium was very high on

29:35 inside. And this is just the . So sound amplification happens in the

29:41 hair cells. They have these very load of proteins and get compressed,

29:44 they actually act like, sort of springs. And they amplifying the movement

29:49 the pictorial membrane, allowing for the hair cell student code. More information

29:54 then ultimately gets sent up, process the auditory pathway, and you have

30:00 the spiraling ganglion cells, connections It's laterally to the ventral cochlear

30:05 There they crossover contra laterally, a of them to the superior olive,

30:10 at the level of the superior olive aural auditory information. Already they travel

30:16 through lateral meniscus into the area off midbrain, where you have the inferior

30:22 sauce in fair curricula. So essentially with processing some of the rudimentary auditory

30:30 before it enters into the media lja nucleus of the thalamus and into the

30:35 auditory cortex. They're still in a map. This frequency map in the

30:41 world that activates on the certain South this Coke Liet organ of Corti is

30:50 all the way through spiral gang themselves the cochlear nucleus and into the primary

30:56 cortex. So this is not your auditory map, but this is the

31:00 auditory map. But we have a auditory map, and we didn't really

31:06 how that comes about. It's a bit more complex, so we talked

31:11 sound localization, and if you we watched the very cool video about

31:16 that showed how incredible they are. organization or one of the aspects that

31:21 had this they had the syringe of that were surrounding the years.

31:27 Imagine if you had two very large behind your ears helping your ears become

31:34 in here better, and that is case with House. Plus, they

31:38 a symmetry in the airs, which some great hunters at night. They

31:44 great depth of sound maps as We talked about sound localization here and

31:51 entrance off signal from one year will certain areas off superior olive earlier than

31:58 signal that, after travels from left , will finally hit the right here

32:02 activate action potentials from that side. , special interests. We're hearing impairments

32:09 us, most of them. Hopefully conduction on some of them are sensory

32:16 such as tinnitus, uh, loss hearing damage to hairstyles. It's all

32:23 neural and in that case is off loss through hair cells. When there

32:29 spiral ganglion cells still preserves. You have cochlear implants, so if you

32:33 , you have a big implant that multiple electrodes, and these electrodes are

32:39 matched to the frequencies of the spiral cells that would process specific frequency at

32:46 specific length off the cochlear, corresponding its tone. A topic map.

32:55 amount of sensors system overview. The processes pressure perception. Temperature came,

33:08 , it's, ah, system that connected to the skin distributed throughout the

33:14 and receptive fields distributed throughout the You have different types of receptors between

33:20 and your puzzle opinion sendings. My score puzzles uh, hair follicle free

33:26 here except the fields. This is point discrimination that showed us that receptive

33:34 are much smaller for sensor information at level of the fingers and mouth and

33:42 . But they're much larger in areas are not a sensitive thio two point

33:48 or sensory discrimination such as casts or or torso. And we have some

33:53 these, uh, receptive fields from score puzzles and petunia in core puzzles

34:03 are rapidly adapting and Marco's discs of finis air slowly adapting. And then

34:09 have some of them that have small , my business and Merkel's small Muslims

34:14 , large Pechiney in Ruffini sendings. is important how you perceive and process

34:24 sensor information that's coming on the The sensor information gets carried by four

34:29 of fibers. The largest ones will off the appropriate exception. Second largest

34:36 McKenna receptors of the skin, the and feeling density changes in the

34:42 The third ones will process pain and , and the slowest wants that Aaron

34:47 ated will be responsible for temperature, and itch. We have dermatologists in

34:53 derma tone from the neck down processes from the skin region that is specifically

35:02 to that one spinal segment on that side, uh, to that specific

35:08 off the body. So Dermot owns the case of the shingles, will

35:13 in one single dorsal root ganglion, , a consequence of reappearance of door

35:20 herpes zoster virus, which causes these uncomfortable and painful itchy rashes and burning

35:29 in just one single dermatology on one of the body. Information from the

35:37 down, anything below the phase is through the spinal cord. It ascends

35:44 the dorsal column nuclei through the dorsal that reaches dorsal column nuclei, which

35:51 located here, OK, at the of the medulla, and that's what's

35:55 matter. Sensor information crosses over Anything that gets damaged below medulla of

36:03 Ghana is going to be on the side and anything that is damaged above

36:09 going to be on the Contra lateral . If there's damage to the spinal

36:13 , it may lack sensations on the side of the spinal cord. But

36:19 there's a damage to the brain stem the billabong, gotta you. The

36:24 is going to be on the contra side. From medulla, information goes

36:29 eventual posturing. It was of the and from there to the primaries amount

36:34 sensory cortex Information from the face is by trigeminal nerve. Five cranial

36:41 Five large mechanical receptor accents innovating to principal trigeminal nucleus, which is located

36:49 here at the level of the and it crosses over and penetrates

36:56 The ventral pastoral nucleus of the columnist subsequently different area face area in the

37:03 somatic sensory cortex. Eso We have map of the whole body and the

37:10 sensory cortex. That's our homunculus. also have a map for digits and

37:14 digit map. You have slowly and adapting neurons, and you have a

37:21 map calling the layer map that represents digit in our brains is a lot

37:26 information that gets dedicated to our hands fingers to our mouth. Lips here's

37:33 here and our general areas, and a amount of sensory sensitive areas.

37:40 this a matter talking that we see map representation is not continues Thio.

37:47 you have generals. Next, two , uh, index finger next to

37:53 , uh, for forebrain, forehead eso. It is a relation to

38:01 body. It's more like a caricature the body and certain parts of the

38:06 . Hands face are mawr important for ? War for appropriation. So matter

38:14 rodents is very different than here. discussed the barrel cortex for each whisker

38:18 whisker pad. Had representation of the like structure in the primary visual cortex

38:24 sensory cortex, and that allows for lot of interesting experimental manipulations where you

38:30 inhibit activity from one of the whiskers see how it effects the map.

38:34 so we over viewed these different changes cortical maps, in this case with

38:41 primary somatic sensory cortex of activation of two whisker and in this case with

38:49 so you have a map for digits loss of one digit determines that the

38:56 areas processing information from a day adjacent before the loss of digit three take

39:03 that area. But the changes in cortical maps don't have to be a

39:10 is lost off the finger or loss arm. It can be just through

39:17 movement or repetitive stimulation of certain vicious certain parts of the body. And

39:22 would see an increased amount of cortex space that is now dedicated to the

39:28 digits on the hand versus inactive And if you recall, as it

39:36 , thio, these different maps brain . We watched a video by Hillary

39:46 Ramachandran, and he described three very syndromes or conditions in that video and

39:56 ways off solving or treating them. please remind yourselves off the Cobb grass

40:05 or crabgrass delusion off the phantom limb or phantom limb delusion and off the

40:17 . Okay, so please review that by Hillary in Ramachandran, it's a

40:22 talk Onda, Please be prepared. , Answer some basic questions about what

40:30 conditions are. What are the parts the brain or the cord assists that

40:37 involved in processing or are damaged in conditions. Mhm What we did.

40:51 also discussed a little bit in greater voltage sensitive dye image ing and uploaded

40:58 for you. And the take home from this is to understand that there

41:03 this vault excessive dies that can be in the membranes of the south and

41:08 they will indicate the voltage change across membrane and that you can image large

41:14 of the brain. You can do image ing. You have to have

41:18 microscope in order. Thio image these windows of activity in the brain and

41:23 can also experimentally correlated to activity that record electrically from a number of south

41:31 from one individual cell. Andi, recall that there are different layers off

41:40 of studying the anatomy and functionality of brain. It goes from macroscopic

41:47 Mesozoic, OPIC, different kinds of in the in the network to circuit

41:54 . How these cells are interconnected. cellular, where different channels located in

42:00 cells and what are different responsibilities off cells are different processes in the communications

42:06 celulas, a synaptic at the level been good experience and access ions.

42:12 so this illustrated also the article that uploaded, that these multiple sensitive dies

42:18 also be genetically encoded, and in case, they become, not

42:23 But genetically encoded voltage indicators and this is very interesting. It discusses the

42:32 of these experimental techniques into practical And what is the future of these

42:39 for very near future clinical application of of the disease or circuit dysfunction?

42:47 ultimately, what neurologists and neuroscientists want get at is understanding non invasively understanding

42:56 , a sub cellular level and understanding activity on a macroscopic level at the

43:02 time. That is the ultimate holy of nurse ons and neurology and non

43:09 image ing off networks of the Overall activity in the brain with ability

43:14 zoom in on two single synapses, three trillion or many trillion of them

43:20 they exist. After discussing a little of vault of sensitive dye, we

43:27 on to this very interesting topic and this is highly relevant and timely

43:35 in 19. How does go that enter into the C N s can

43:40 through nasal cavity. You can enter Valerie Mia blood virus in the blood

43:48 reaches CNN s can enter due to damage where you have compromise of blood

43:54 barrier so you may have inflammation or response or virus in the blood.

44:01 that can affect the blood brain barrier allow for the virus to enter into

44:05 brain. The easiest for the The interest through the nasal cavity.

44:09 important take home message is here in nasal cavity will contain the nerve endings

44:14 nerve endings of penetrate through these administrations the skull that I referred Thio ascribe

44:21 played formation and this crib reform play . You can see these actual ministrations

44:28 the skull that physically allow for the of very small molecules. Infection in

44:34 nose were the virus and creeping up the virus to the crib. Reform

44:40 can in some instances allow that, , infection off the brain, covering

44:46 nose when breathing, not just your , but your announcement. Bringing this

44:52 and preventing not only accumulation of the and the nose or catching the virus

44:57 the nose and enter into the but also ex elation through the mouth

45:04 the nose. And I was out weekend again. I saw almost every

45:09 person with her nose hanging out. I think I'm going to make a

45:15 , Uh, that I'm just gonna in front of people that says aural

45:21 . This is how the virus enters exits. Here's a picture.

45:26 you're not protecting yourself or others, be smart. Now, when the

45:30 enters, it has to hang on something hangs onto the H two receptors

45:37 these H two receptors angiotensin converting enzyme has involved in overall body home,

45:43 , Stasis, information and immune So basically hijacks. H two receptor

45:50 enters into the south and then the . N s. You have these

45:54 receptors that are located on neurons on as well as on the blood

46:02 the brain, the ferial lining that see here and this is where essentially

46:08 have the potential for these viruses to on to is to penetrate itself into

46:14 ethereal self, causing more damage, more information, making the blood brain

46:19 loose, ineffective in infecting potentially glial of the blood brain barrier. And

46:27 it enters into interstitial spaces of infecting neuron Sa's well in the PNS versus

46:35 C. N s, once it into the peripheral nervous system, the

46:40 that the peripheral nervous system and main is a non announced me Andalusia eso

46:48 , off smell and loss of Um, that's because the hair like

46:54 on olfactory tissue, just like you hair cell receptors and the hair

46:57 You have these hair cell receptors, cell protrusions like back there tissue that

47:03 get damaged and die. So the major symptoms of gear on Bar Miller

47:09 syndrome And for the C. N . You have a headache and vertigo

47:15 main, sometimes with the major symptoms in both stroke meningitis, which is

47:23 officer, was spinal food, acute himself philosophy and bleeds, hemorrhaging,

47:32 of the brain, a Dema which swallowing, and with hemorrhaging. You

47:38 have hi coagulation stayed off these blood coagulating and thio into into solidified coagulates

47:51 the brain also binging on the normal of the brain. And this is

47:57 the left. You have mostly came sensory dysfunction in the PNS and then

48:02 C. N s. You have issues such as swelling, cerebral

48:09 compression of brain stem alteration and respiration of this acute necrotic. It's a

48:17 , the on bleeding hemorrhaging in the Onda. Of course, due to

48:24 stress, you can also have neural in the brain, which we discussed

48:28 neurons or some of the most sensitive to hypoxia, a lack of

48:37 So what can happen then? What happen? You have these things like

48:43 blood, brain barrier swelling. You coagulation blood. Um, you have

48:52 , causes a Philip with him, so fill itis and cause lesions in

48:56 brain can lead to coma. ischemic stroke, which is lack of

49:06 . There's a hypoxic stroke where you off the blood supply. Systemic stroke

49:10 is when you have narrowing of the vessels because you have swelling in the

49:18 and there's too much pressure. There blood vessels and they bust open

49:23 causing stroke and blood, uh, in the brain that post infectious neurological

49:32 thio. And you can have also care related neurological manifestations. So the

49:38 home message from this is mostly that can have encephalopathies of Politis ischemic strokes

49:43 these other neurological complications and neurological manifestations intensive care related. You can also

49:51 in our articles review, but I not be asking you detailed questions from

49:59 . They're quickly in the last Novel Review The main take home messages

50:03 the contaminated system that you have major heaven do cannabinoids there synthesizing enzymes,

50:11 they're degrading enzymes. You have cannabinoid expressed widely throughout the body and the

50:18 and influence many different functions. But it seems to be involved in

50:23 You static and fast and slow you static regulation off the brain and

50:28 body in the brain. CB one that are responsible for the euphoric effect

50:35 very heavily expressed in hippocampus, basal , prefrontal cortex, cerebral cortex and

50:42 . But I will not ask you identify parts of the brain where these

50:46 receptors I express. It's more of general understanding that you see that it

50:51 widely distributed through the brain in different and binding off endo cannabinoids or fighter

50:57 to these receptors in different parts of brain can influence different brain functions or

51:04 dysfunctions. This is probably something that worthwhile reviewing. It's the same mechanism

51:11 we discussed again. We have the polarization Exocet, ASUs and on demand

51:18 of Under Cannabinoids that remembering soluble and retrograde fashionable bond to C B one

51:23 C B two receptors. CB one will reduce the influx of calcium and

51:29 transmission for both glutamate and GABA. we'll essentially in a negative feedback

51:34 will control excited during inhibitor neural And in addition in CB two

51:42 When this, uh, under cannabinoids two CB two receptors and Muglia,

51:48 will influence slower processes that are concerned the information from inflammatory Side of Crime

51:55 . Lawless some of the slower household on immune response of the brain that

52:02 mediated by CB two receptors. I this question whether it's actually many and

52:09 cannabinoid systems and the fact that under will bind to CB one CB two

52:14 . But they will also bind to receptors. Trevi receptors P part

52:20 They will influence iron channels. They're different body systems in different organs and

52:28 in this under economic system, and contaminated receptors or the contaminant molecules is

52:34 with distinct syndromes. Now I also questioned your understanding that the endogenous

52:41 such as under economic ones, combined other endogenous receptors such a certain elements

52:46 a strict view receptor. So there's lot of crosstalk between what we call

52:51 cannabinoid and serotonin system between serotonin system other systems in the brain and the

52:58 . This is an important lesson. low THC cannabis industrial home from high

53:07 cannabis, which is medical, recreational from synthetic marijuana sincerity, cannabinoids that

53:15 synthesized in the lab and made from again. You will not be responsible

53:20 answering these questions, but it's very that you know there's difference because Hampus

53:24 legal, you can grow it. researcher that there's products that are made

53:30 CBD that are regulated by state but federally legal. Then you have medical

53:36 recreational cannabis, which is becoming a part of the not only community in

53:41 , but medical community as well. these are the laws that are governed

53:45 each state, um, including State Texas synthetic and avenues. They're completely

53:53 , not regulated on, uh, deadly. Uh, we discuss this

53:59 cone, So please know the word cone, because these are the glandular

54:04 on many plants that will contain some the most important active ingredients. In

54:09 case of cannabinoids cannabis, try Combs contain cannabinoids and will contain other active

54:16 such as Turpin's, um, for medications. You have to realize that

54:22 have synthetic. Do you see since discovery in 1964 it was isolated from

54:28 plant material from hashish or hash in lab in Israel. And then in

54:34 eighties, we had synthetic THC medications were made and still available. And

54:40 in 2021st century saw the production of first plan based medications, such as

54:46 big small sir cannabidiol that are also different conditions for spasms and pain and

54:53 sclerosis. THC and CBD on for activity and Roddy Syndrome and childhood epilepsy

55:02 for the CBD preparation. Um, is an interesting take home message that

55:09 the plant cannabinoids are synthesized a specific . And if you have THC,

55:15 something's the plant will produce THC, CBD A something's the plant will produce

55:21 A and on Lee Heat and do elation will turn this non psychotropic,

55:28 intoxicating THC A into psychotropic THC. cannabinoids, all three of them,

55:34 be expressed by one plant and may a different relationship to CB one

55:39 So THC is an agonist. Activate one receptor C B G is an

55:45 CB one receptor, and CBD is negative al hysteric modulator. So that

55:51 it has a different binding site, it modulates the activity through the CB

55:55 receptor as it gets actively by In addition to cannabinoids and the

56:01 you also have Turpin's and Turpin's volatile volatile molecules on. They give very

56:11 smell, the cannabis plants and the plan. Preparations will contain a number

56:17 cannabinoids. We have over 120 different a number of Turpin's that would be

56:22 , but it all depends on processes which the plant is being processed,

56:28 on the products of being prepared. the take home message from this slide

56:33 not to memorize it, but thio what a complex interaction that is in

56:38 brain between the city cannabinoids, dicker dicker box related mutual cannabinoids, Europeans

56:46 the cannabinoids and the neurotransmitters major excited inhibit their neurotransmitters. And we basically

56:53 about how this CB one system is faster system. Regulating your transmission on

56:58 B two is a slower system regulating and some of the immune responses in

57:04 brain. And I refer to you . This National Academy of Sciences engineering

57:10 Medicine publication, which is publicly available the health effects of cannabis and

57:15 were in 2017. It was already that there is conclusive and substantial and

57:21 evidence for some cannabinoids in cannabis as medicinal blinds and medicinal preparations, and

57:27 is limited and inconclusive evidence for a of it. But in reality,

57:32 have millions of people that have and they're using cannabis, including

57:37 in many different ways, including here Texas, which has ah, compassionate

57:42 program, which is going to be over the next three years, providing

57:48 and jobs in Texas and creating what predicted to be over the next five

57:54 , or $3.2 billion economy in Texas , and we're just talking about medical

58:02 . High THC cannabis here. We're talking about low THC hom CBD,

58:08 is also a huge huge market So as you look into the

58:13 these air some of very interesting things be aware off golden 19 interactions in

58:18 brain and I think politically and biological , uh, renaissance of in the

58:25 system on medicinal cannabis

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