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00:02 | this is neuroscience. Midterm to review also a portion and the ending of |
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00:09 | central visual system processing. And we the connections between retina thalamus and |
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00:20 | We looked at the anatomy of the circuits. We looked at the output |
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00:25 | comes out of the retina. We at the anatomy of the lateral manipulate |
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00:29 | of the thalamus, the sixth layer comprised of magnum carver layers. All |
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00:35 | that information was unoccupied for information we looked at in layer four there are |
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00:42 | dominance columns that are formed but that four cells are still processing Manaka color |
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00:50 | in the primary visual cortex. And at layers 23 the men ocular information |
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00:56 | becomes binocular. So we discussed the of information the llama cortical inputs. |
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01:03 | and I intermediary mp. Going into layer four I bypassing layer for going |
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01:10 | to three. I'm primarily concerned with processing. There's 23 allow for the |
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01:16 | range and intra Colin er and intra connections to take place and spread. |
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01:23 | intra cortical loop between 4-3, five four. Again this is an intra |
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01:30 | loop and then there's the cortical hypothalamic that goes from the cortex into the |
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01:36 | . So recall that there's salama cortical into cortical loop in a certain fashion |
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01:42 | then cortical thalamic outputs. This is going to influence in this case visual |
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01:47 | processing. In many other cases it be dealing with other sorts of sensory |
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01:53 | in different parts of the brain. the color is concerned mostly with Larry's |
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01:58 | . 3. The properties of the . The receptive field properties in area |
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02:04 | . One is that they process A simple cells process bars in certain |
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02:10 | they will produce and be responsive to bar of light and a certain orientation |
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02:16 | a maximum number of action potentials. also have direction selectivity. So those |
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02:22 | in the cortex will prefer a bar light to cross through the field of |
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02:27 | through the receptive field in a certain that will be preferred left to right |
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02:33 | to bottom diagonally and so on. we saw how simple cells and the |
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02:40 | from the retina which are concentric on off cells can converge onto L. |
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02:44 | . M. Cells and how a of L. G. M |
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02:48 | The processes center surround concentric like receptive properties can converge onto the simple cells |
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02:56 | the simple cells can further converge onto cells. So you can get different |
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03:05 | of receptive field properties in different shapes the level of the primary visual |
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03:10 | That, because of the convergence of . G. N. Cells and |
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03:15 | simple cells creating bars, creating various like this. Of the receptive field |
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03:20 | of the primary visual cortical cells and simple cells further converging onto the complex |
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03:25 | . And that is all happening within . One. And with complex cells |
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03:29 | have even the greater variation of this nice um forms and shapes that you |
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03:36 | play with. So if you recall ocular dominance columns, I'm gonna review |
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03:43 | quickly are these projections that if you to look where the projections come from |
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03:52 | , I am to trace them from eye into the L. G. |
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03:56 | layers. And as we discussed you to look and to appeal where those |
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04:02 | in this case of radioactive probing which trans synaptic to it will cross the |
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04:07 | from the retinal ganglion cells until jeon LG installs into primary visual cortex. |
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04:13 | in the primary visual cortex will get stripes or striatum. These are ocular |
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04:18 | columns. So one of these blue in layer 23 belongs to one eye |
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04:24 | the white column belongs to that I this is where you still have the |
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04:29 | ocular vision and then leads to three molecular vision becomes binocular vision. Now |
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04:36 | this course, I'm going to go to one slide here that we didn't |
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04:41 | in this course, we've emphasized the of plasticity and we said that during |
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04:48 | there is critical period of development during very early age where there is the |
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04:53 | chemistry, the right factors in the environment for the synopsis to form and |
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04:59 | for the synopsis to be trimmed and connections to be specified. And so |
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05:05 | is an experiment that tells you something this critical period of development and if |
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05:11 | is sensory deprivation during that critical period development. This could be likened. |
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05:16 | example if a newborn child somehow was of census during some early stage of |
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05:23 | , how would that affect the anatomy the brain. And obviously anatomy or |
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05:29 | means function too. And if you this is an experiment that can be |
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05:34 | in rodents And in rodents you can one eyelid and you would perform this |
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05:43 | at the very end of the first of life. So the first month |
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05:47 | life is really this period that we critical period of development where there is |
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05:52 | lot of plasticity, a lot of and in this case the animal is |
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05:59 | off the visual input. That's why wearing a pirate like patch here on |
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06:03 | eyes. You have sutured island And island is only suited for three |
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06:10 | And then three days later the sutures . The animal is allowed to recover |
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06:17 | a whole month and a month later experiment was performed where both eyes of |
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06:24 | stimulated the left and the right And it turns out that there is |
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06:29 | slight bias and this is number of that are responding from the iptc lateral |
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06:36 | . And the itsy lateral. I the one that remained open and there |
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06:41 | a bias of response In Layer In these ocular dominance columns toward the |
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06:49 | that remained over. It's not much you can see that the blue problems |
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06:54 | the number of cells have shifted. over the red ones. Now if |
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07:01 | repeat the same experiment but instead of the eyelid for three days The island |
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07:07 | future for six days. And it sutured all the way until the basically |
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07:14 | of this first month where the critical of development also ends. Animal is |
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07:22 | to recover for a month. And two eyes, the sutured I hear |
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07:28 | lateral and the open eye of being and it is now very obvious that |
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07:36 | cells and therefore in the primary visual are only responsive to the eye that |
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07:43 | open. They are no longer responsive the eye that was closed. That |
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07:51 | that if you have short term deprivation three days there might be a small |
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07:58 | in the functional structure. But if have a prolonged deprivation in this case |
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08:04 | six days without vision. In one you can have a permanent reconstruction of |
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08:10 | connections from the cortex and therefore the loss of function. And if you're |
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08:17 | that critical period of development where there a lot of plasticity, you may |
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08:22 | be able to rebuild that function a or two months later forever. So |
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08:29 | the short term deprivation there's obviously a loss of function to the eye that |
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08:35 | closed and the bias toward the eye was open. And if you look |
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08:39 | the fibers. These are the These are the thermometer cortical projections into |
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08:45 | four coming in. This is following term binocular deprivation. This is an |
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08:51 | eye and below here is deprived dot what that tells you that that I |
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08:59 | that was not receiving the inputs, Kalama particle processing of that information which |
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09:05 | conscious perception. Right? First the sketch and later the whole visual |
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09:12 | You already have lost a significant number inputs and synapses. You have rearranged |
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09:19 | you have structurally changed the connections in anatomy in the primary visual cortex. |
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09:25 | obviously that reflects very much on either or prolonged period of visual deprivation and |
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09:33 | full loss of function. Okay, that's that's really important to to keep |
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09:40 | mind again this plastic period how such is so important. How deprivation during |
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09:47 | development during this critical period of development long term deprivation can result in long |
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09:55 | um functional loss for prominent functional So we walked through the anatomy and |
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10:04 | ended up on this slide last lecture I said I'm gonna put this all |
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10:10 | of it together for you and here have these columns and you can see |
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10:17 | these bars here are shown in different and this color here has nothing to |
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10:22 | with actually color processing but this color represents a different orientation of the bar |
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10:28 | light. And so we said that this primary visual cortex itself responsive. |
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10:35 | prefer certain orientation or orientation selectivity. these are referred as the orientation of |
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10:43 | columns where the cells that are in within the yellow part of the |
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10:50 | It will be responsive to a bar light that is at a certain |
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10:55 | The cells that are located within the column, it will be responsive to |
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10:59 | bar of life in a different And if you sort of a circle |
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11:04 | this column and sample and this micro , the cells Here, you will |
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11:09 | able to find the south that will responsive all the way 360° maximum and |
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11:15 | to those bars of light and the that process similar orientation. So |
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11:22 | dark, orange or red would be orientation. This versus this. They're |
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11:27 | located closer to each other within the of this micro column. Now, |
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11:33 | you were to look in the middle this call, in the middle of |
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11:36 | column looks sort of like a pinwheel from which you have orientation specific cells |
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11:42 | out of that central pinwheel. And central pinwheel will contain south that will |
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11:47 | responsive to pretty much all orientations because really the collection of the cells that |
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11:52 | coming from the uh from the bigger of the outer boundaries of this micro |
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12:00 | centering into, into this pinwheel like . So these micro columns will find |
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12:06 | individual cortex of monkeys of other animals well. It's called orientation columns Hubble |
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12:14 | weasel where the scientists have studied it micro electorate recordings. Imagine how many |
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12:21 | electrode recordings you have to make to out how this brain circuit actually processes |
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12:27 | orientation columns. So now we have complex cells, we have concentric fields |
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12:35 | we also can use techniques like both sensitive diets. So instead of using |
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12:40 | electrodes we can actually image single cells numbers of cells within these micro |
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12:47 | That's a huge huge advantage because we image potentially 10,000 cells versus making a |
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12:54 | electorate recording from one or two And when you use voltage sensitive dye |
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13:00 | it's a functional type of imaging. voltage sensitive dives communicates membrane potential |
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13:08 | So you can see if the cell d polarized if its hyper polarized. |
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13:12 | if you stimulate the vision right, stimulate the retina. You're looking in |
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13:17 | cortex. Now you can look at whole window in the cortex and see |
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13:20 | cells are active to this orientation, cells are active to this orientation and |
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13:25 | on. And by doing that now can describe all of these. You |
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13:30 | see this is a much larger chunk the visual cortex but within that you |
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13:34 | see a number of these orientation micro that are about 3200 and 50 micro |
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13:41 | wide and neocortex is about two millimeters or so you can see that these |
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13:49 | be individual cells. For example each of these dots is an individual cell |
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13:54 | on top of these dots and then apply this color coded pattern which the |
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13:59 | coded pattern really represents orientation selectivity. this is how we know. Not |
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14:06 | poking endlessly. You have to record how many of two million cells |
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14:15 | Well you can image two million cells one experiment and if you have good |
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14:21 | resolution you can resolve it in a cell level. If you don't you |
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14:24 | see sort of a circuit level Now these orientation columns is just a |
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14:33 | of the largest structure, bigger what call hyper columns. If you think |
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14:38 | hyper columns and even orientation columns that some way are very elementary computational |
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14:46 | And these hyper columns are also somewhat because these hyper columns would still be |
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14:52 | closing only limited information processing within uh structure of the brain like the |
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14:59 | So but they're still interconnected. And the elementary computational modules interconnect, they |
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15:08 | more complex. When they interconnect multiple with multiple modules in another brain structure |
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15:17 | also becomes more complex hierarchically functionally and processing of the information in the higher |
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15:27 | centers. What you have here is you remember ocular dominance columns, Ocular |
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15:33 | columns here are shown by these So C stands for contra lateral I |
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15:39 | stands with bilateral area. This is a lateral area. So within these |
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15:46 | ocular dominance columns. That's what we early on basically. There is a |
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15:50 | more specificity and there are other hyper and orientation columns that are located |
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15:58 | So what this shows that within the of the ocular dominance columns you will |
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16:04 | multiple of these beautiful pinwheel like color . Which means that within each ocular |
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16:11 | columns you have multiple selectivity, selectivity micro columns. You can see |
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16:21 | these are the blobs. So this the side of chrome occident, see |
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16:26 | and you can see that it's somewhat the center of the ocular dominance |
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16:32 | It's concerned with colour information processing. you have the blob like structure especially |
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16:38 | layers 2, 3. And then is another type of really interesting |
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16:44 | So we talk about both extensive I'm gonna in the next section show |
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16:50 | a little bit more about that. what's really interesting is you can actually |
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16:55 | activity of the brain without applying any . And it's called intrinsic optical signal |
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17:01 | . When we talked about F. . R. I. Or pet |
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17:04 | we said what what is the functional really represents? It represents metabolic |
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17:10 | It represents changes in the oxygen glucose levels represents how much those neurons |
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17:18 | demanding the oxygen of workouts and when get active and they demand oxygen and |
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17:24 | and they fire a lot of action and they d polarized what happens to |
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17:28 | . They also swell to act in circuits. The south that are very |
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17:34 | on fire, they become slightly larger they swell. And what happens when |
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17:38 | swell? The plasma membrane stretches a bit. And as a consequence of |
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17:45 | you have changes of the reflective properties the tissue. And this is called |
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17:51 | optical signal or intrinsic optical signal meaning its intrinsic because there is no |
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17:58 | that is being track there. And you are looking only at the |
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18:04 | activity to these kinds of experiments with optical signal may actually show you if |
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18:10 | have the surface if you can get layers four, that's one thing. |
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18:14 | on the surface you can see the and darker shades And that's because when |
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18:19 | stimulated one I one of the cells cells to responsive to that I would |
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18:25 | swelling. And there was like with would be slightly different. So you |
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18:30 | to employ multiple methodologies, experimental neuroscience . Multiple sensitive dye imaging, imaging |
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18:38 | voltage or imaging calcium fluctuations is another way of tracking activity. Or intrinsic |
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18:45 | signal imaging which is reflective properties of the south based on the self |
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18:51 | That one particular number in potential ion calcium tracing. Of course the fact |
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18:59 | the matter is you have sophisticated vasculature innovates the cortex and innovates the primary |
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19:06 | cortex and the micro capillary is the distance that you would find in the |
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19:12 | between the micro capillaries is only 50 apart. That means that only five |
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19:19 | Mazz 10 micrometers in diameter. Maximum so moses away is the further station |
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19:27 | 2.5 so much is because five and so 2.5. So much away. |
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19:31 | is micro vasculature of blood, oxygen nutrient supply going into the brain. |
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19:38 | with intrinsic optical signal. If you the correct set up, you can |
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19:44 | visualize the ocular dominance signals and you visualize the preferred orientations using another imaging |
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19:53 | and then you can put it all together. These are my small orientation |
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19:58 | . Those small orientation columns go into ocular dominance columns. These larger ocular |
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20:06 | columns make larger hyper columns which will information from both eyes, contra lateral |
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20:15 | . So this is really the true . So this is kind of a |
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20:20 | all of the central processing together Within circuits. And this indicates that hyper |
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20:29 | is about 1 mm in in So we talked about 5240 50 micrometers |
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20:37 | orientation selectivity calls. So you can the math that it will include about |
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20:44 | or so orientation. Uh selectivity Poor ocular dominance columns or so. |
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20:52 | this is the structure. This is anatomy that underlies the function the function |
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20:58 | the representation of the primal sketch that discussed. And so there's of course |
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21:03 | anatomical structural properties. Then there's orientation as cellular or um receptive field properties |
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21:12 | which the information that we generate visual is built on. So this concludes |
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21:19 | information on the visual system. This now the review for midterm too. |
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21:30 | I'm just continuing as a part of lecture and end of in this |
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21:37 | In the initial lectures we talked about discovery of chemical neuro transmission. We |
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21:44 | about how water polo, we used vagus nerve stimulation which you now know |
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21:51 | cranial nerve 10. And you know that vagus nerve released the single Colin |
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21:57 | that acetylcholine was inhibitory on the cardiac and that there are two types of |
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22:04 | that we know chemical and electrical and synopsis allow for very fast flow of |
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22:13 | and small molecules like secondary messengers and Synopsis is very important for synchronization of |
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22:21 | networks themselves. And I refer to gap junctions. In the last reference |
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22:28 | gap junctions we made was in the circuit When we talked about horizontal cells |
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22:34 | are inhibitory cells that contain gap junctions them. And that should indicate that |
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22:41 | how the broad areas of luminescence in retina or sharper areas are created through |
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22:50 | the gap junction signaling in the You have the pre synaptic components with |
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22:58 | zones and the pasta nappy components with past synaptic densities have a variety of |
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23:05 | . The excitatory synopsis are asymmetrically synoptic post synoptic with round vesicles, inhibitor |
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23:14 | . If you were to look at microscope imagery would have these flattened vesicles |
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23:20 | symmetric synopsis. Then we spent quite bit of time talking about neuro muscular |
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23:26 | . So we talked about how the that come out from motor neurons in |
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23:31 | spinal cord and we use this neuro junction because it is simple, there's |
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23:36 | one neurotransmitter acetylcholine and when the civil is released it will guarantee acetylcholine receptors |
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23:44 | the civil choline receptors will generate this potential that we call and play potential |
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23:49 | will always result inactivation of both educated and calcium channels deeper within these junction |
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23:58 | falls which will be responsible for the of the action potential skeletal muscle action |
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24:06 | . And in this case the seal is excitatory because its skeletal muscle and |
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24:12 | also excitatory because the past fanatical you have I on a tropic nicotine acetylcholine |
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24:20 | . It's only only one neurotransmitter acetylcholine it's only excited for boston ethically for |
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24:27 | gated receptor channel. You only have acetylcholine receptor. There are certain criteria |
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24:34 | neurotransmitters that have to be synthesized there to be transported into vesicles really |
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24:41 | Re synthesized. Re transported, buying applicant caused post synaptic effect, activate |
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24:49 | trophic cascades and we'll come back to slide because we talked about different neurotransmitter |
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24:57 | and different neural transmitter system types. and we highlighted the amino acid neurotransmitters |
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25:05 | glutamate and glycerine gaba and glutamate uh major excitatory is glutamate the major inhibitor |
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25:14 | gaba in the brain. And the inhibitory neurotransmitter in the spinal cord is |
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25:20 | . But we also talked about licensing co factor in excitatory N. |
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25:27 | D. A. Dramaturgical transmission in C. N. S. It's |
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25:35 | function of the molecule depends on what it binds and what what part of |
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25:40 | receptor it binds. Yes. Or you repeat the question? But for |
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25:59 | holding like excited for a home in guarantee the reversal potentials for different |
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26:07 | We discussed as uh for acetylcholine it's also zero melon balls. It's |
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26:13 | employee potential. Yeah it's the same for ep sp also. Well for |
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26:20 | . P. S. Speed is and I PSP if you're looking at |
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26:24 | Gabba A it's chloride reversal potential dependent B. Is potassium. But if |
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26:32 | don't mind, let me get through of those sections because those themes are |
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26:36 | up ahead and then I'll pause in 10 minutes or so and see if |
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26:41 | have any questions about that. We discussed the meaning neurotransmitters and different |
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26:47 | Acetylcholine dopamine norepinephrine histamine norepinephrine serotonin. talked about peptides but only how they |
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26:55 | different in the sense of their synthesis and storage in comparison to the neurotransmitters |
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27:02 | neurotransmitter vesicles that are located mostly optical and inside this box we inserted |
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27:09 | neurotransmitters. So I urge you to this unusual neurotransmitters such as gasses nitrous |
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27:17 | carbon monoxide such as endocrine adenoids such our economic asset and A. |
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27:25 | P. So mentions of these may up on the exam but in general |
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27:32 | pre synaptic neurotransmitter vesicles to fuse. have to have pre synaptic deep polarization |
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27:38 | is the action potential influx of An influx of calcium is necessary to |
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27:44 | the protein protein complex fusion so that can be a neurotransmitter molecules release. |
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27:52 | it can be in the C. . S. This really is going |
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27:55 | be partial or full which doesn't happen the muscle. So you can have |
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28:00 | partial command if partial contraction that means if something is wrong. And so |
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28:07 | the C. N. S. potentials the E. P. |
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28:10 | P. S. Are much smaller on the order of only half a |
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28:14 | volts as opposed to in the neuro junction, 17 million volts. So |
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28:18 | need many many different synopsis and neurotransmitter fusions in order to activate the cns |
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28:28 | . So the PSP is generated when is released and binds to glutamate receptors |
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28:35 | there is this deep polarization. The is generated when Gabe's released. It |
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28:41 | to gather a suffers and causes the polarization in the form of IPs there's |
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28:47 | a tropic signaling versus metabolic tropic signaling tropic signaling. You can see the |
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28:53 | of the ligand never opens a But instead it actually activates the g |
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29:00 | complex which can activate enzymes and downstream messenger. Then we use the single |
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29:06 | in system sort of exemplary system for that the means signaling. All |
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29:12 | And we really talked about amino assets great degree glutamate and gaba and dopamine |
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29:19 | . But we refer to immune And we talked in great detail about |
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29:25 | synthesize the sudoku and choline with chat , acetyl transfers loaded up into vesicles |
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29:34 | in the cns. We distinguish as C. N. S. Acetylcholine |
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29:39 | you have on a tropic which is academic acetylcholine receptors and you have metabolic |
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29:44 | acetylcholine receptors as well, not as as neuromuscular junction. Once a single |
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29:50 | is released, you remember neuro muscular and here you needed to acetylcholine molecules |
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29:55 | bind to the receptor in order to it. Once a single covid has |
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30:00 | , it binds to the receptor temporarily then it gets degraded by a cyclical |
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30:09 | . Once it gets degraded by into and acetic acid Colin gets re transported |
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30:18 | through the sodium co transporters and Colin re synthesize acetylcholine with the help of |
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30:25 | and re uploaded into the vessels. we discussed that going back to your |
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30:32 | medications slide acetylcholinesterase inhibitors, some of most common alzheimer's medications because the acetylcholine |
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30:45 | is impaired since an early pathology of disease. So by blocking a pseudo |
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30:52 | degradation. You know, I'm making simple coding more bio available within the |
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30:58 | where it still exists. So still will be an agonist to both nicotine |
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31:04 | Mascarenas. Acetylcholine receptors. Nicotine will an agonist nicotine, it must korean |
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31:12 | tonic and they will have their own , cure ari from little poison frog |
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31:17 | atropine. So for example, if put your are in the neuro muscular |
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31:23 | , you would block acetylcholine receptors and you block the silicone and receptors you |
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31:28 | block the end plate potential. And you block downplayed potential you would block |
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31:33 | action potential and the skeletal muscle. if you block the action potential you |
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31:37 | not see a contraction of the Okay. To an antagonist blocking the |
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31:43 | receptor here, it would basically resolved no deep polarization in the muscle. |
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31:49 | also talked about other means such as , l dopa dopamine norepinephrine, |
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31:57 | I said that you do not have know they're into intermediary uh enzymes here |
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32:03 | synthesis but you do need to know details of acetylcholine but it does follow |
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32:08 | similar Cascade here that we discussed. three update and we discussed how the |
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32:17 | that degrades catacomb means is located on membranes off the mitochondria, I mean |
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32:28 | and so the therapies that would be cata column immune systems can also be |
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32:35 | A O inhibitors. So you would inhibiting the enzyme that is degrading the |
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32:41 | column and this is another strategy therapeutic . You can have something that goes |
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32:45 | the synapse and blocks of degrading a Colin asteroids in the studio collection system |
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32:51 | you can have something that's inside the and maybe inhibiting this enzyme around the |
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32:56 | mitochondria that's responsible for degrading catacomb. thereby prolonging uh by a little ability |
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33:05 | more violent available. Also blocking the . I mean with amphetamines or cocaine |
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33:14 | cause if you think about norepinephrine, is like nor adrenalin or adrenaline of |
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33:19 | brain that would cause a speed That's why they're called, What are |
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33:26 | called? Not the speed drugs but uh uppers uppers. It's it enhances |
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33:33 | signaling within these pathways but it can be highly addictive a negative effects as |
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33:42 | . Uh Those are illegal substances that talking about. We're not talking about |
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33:47 | substances. Glutamate, glycerin, glutamate synthesized with God turns into Gaba |
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33:58 | into neurons. Serotonin an interesting Each one of these systems deals with |
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34:06 | different. Norepinephrine, Abramoff rana's fight flight response. Serotonin mood, |
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34:15 | sleep learning a different response. Serotonin . PROzac which is pharmaceutical medication will |
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34:23 | controlling the re uptake of serotonin from synapse. So start o'nan is in |
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34:27 | way a happier mood molecule. And will see certain logic treatments and cases |
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34:33 | depression and the cannabinoids are different because they can adenoids are synthesized on demand |
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34:39 | synaptic quickly. They're not stored in vesicles there. The number is |
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34:44 | They will use this retrograde mechanism to back into the pre synaptic side where |
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34:51 | receptors are located. So if you receptor activation prison africa we will activate |
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34:56 | G protein complex which will shut down channels by shutting down please sign up |
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35:03 | calcium influx and the cannabinoids will regulate release of both excitatory and inhibitory |
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35:09 | So there is deep polarization induced suppression inhibition when there's a lot of deep |
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35:16 | . There's going to be under cannabinoids of that release of inhibition or that |
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35:22 | of excitation essentially balancing the release of to inhibitory neurotransmitters. Delta nine THC |
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35:30 | is a molecule that is found in plant. It's a psychotropic psychoactive molecule |
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35:37 | causes the high effect THC DELTA nine will be acting through CB one receptors |
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35:44 | it's a natural substance that is synthesized cannabis plant. And if you are |
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35:49 | my other course the graduate course, just finished talking about how DELTA eight |
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35:54 | which you find advertisements for around different shops and gas stations and baby shops |
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36:01 | . Delta H. THC is a synthetic cannabinoid that doesn't come from the |
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36:06 | . The process that turns DELTA eight from another can avenue it's called CBD |
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36:12 | is not the cleanest process. There's medicinal benefits that are known to DELTA |
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36:18 | THC. There is very many accepted and medicinal benefits for DELTA nine |
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36:27 | We don't know exactly the methods each uses to produce after a THC And |
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36:35 | . People have really strange reactions to eight and once they've used Delta nine |
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36:41 | also report they have very strange reactions Delta eight. So it's not because |
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36:45 | tried something that is new psychotropic away that's something to be aware of. |
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36:50 | these molecules interact with the cannabinoid system also interact with other systems in the |
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36:57 | . You know is the chemistry and hybridization of the two common techniques but |
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37:02 | you can label neurotransmitters. One uses , another uses the radioactive the label |
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37:09 | of nucleic assets engaging neurotransmitters or neurotransmitter . We discussed that if you are |
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37:17 | neurotransmitter in the fluid you would have significant dialysis. And so if you |
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37:22 | to study very precise activation of single you would use something like engaging of |
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37:28 | and laser photo license in order to very precise areas or single synapses along |
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37:35 | down right? So you can study the currents flow along the done dr |
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37:41 | have different types of synaptic integration. we talked about how you produce a |
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37:46 | ep sp and we'll look into the of that E. P. |
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37:49 | P. And if you have spatial where three accents are activated at the |
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37:54 | time you will have the maximum response will some overtime at the same |
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37:59 | And if it's summed over over Sorry but if it's summed over |
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38:04 | Like in temporal summation you can see the PSP is going to be much |
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38:09 | than just by producing a single action to producing three action potentials. You |
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38:15 | grow on this deep polarization. It not be as maximal as spatial estimated |
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38:21 | , but it will be longer in actually. And that is important. |
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38:28 | as we look at the concept of voltage lambda, which is the length |
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38:35 | . And dendrites that are non myelin structures that are non myelin ated were |
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38:41 | will leak out over distance. It's doesn't have the cable installation like the |
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38:49 | do. And if you insert the and produce the maximum current here, |
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38:57 | at this Area, right here, distance away from that area, that |
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39:04 | is going to die down and at point it goes to 37% of maximum |
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39:10 | at the injection side. This distance space is referred to as the length |
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39:17 | . So the cells that have a length constant this will persist over longer |
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39:23 | . The cells that have short line are leaking. This curve would be |
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39:30 | in much steeper fashion. In order the cell to generate the action |
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39:37 | you have to have many synapses that active. Each synapse is half a |
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39:42 | evolved And the threshold for action potential -45. So you have to have |
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39:49 | of excitatory synapses activated and then you inhibitory synopsis and those inhibitor synopsis are |
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39:55 | to cancel out part of this excitatory a lot of times inhibitory synopsis are |
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40:00 | to be located closer to the That's just by design. And cns |
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40:05 | they have this control of the paris region so there's strong control but remember |
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40:11 | outnumbered only 10 to 20% in the will be inhibitor in generals. They're |
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40:18 | very diverse and the population many different of inhibitory cells and they have a |
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40:25 | of targeting mostly these para somatic regions controlling mostly the integrative properties, how |
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40:31 | cell is going to integrate all of inputs coming in. And so if |
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40:36 | is an activation of excitation and inhibition the same time at the level of |
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40:41 | soma you may not see any response maybe it's essentially will cancel each other |
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40:46 | . Part of the current will leak . Part of the current will get |
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40:49 | through this inhibitory currents to And so have to have very significant activation on |
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40:56 | down director of the selma significant input order to have the cell generate the |
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41:02 | potential. Uh metabolic tropic signaling is referred to as modular. A torrey |
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41:10 | because it modulates downstream cascades. It also modulate downstream channels and it can |
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41:17 | so by force for relating them with kindnesses. Or it can do so |
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41:22 | defrost, correlating them using phosphate So this is the point we say |
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41:30 | . This is what we're referring to that's switched. These are our major |
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41:45 | again repeated here. This is the I really want you to know all |
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41:50 | the details on. So I showed live five times maybe six times in |
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41:57 | contexts. So you can expect at five or six questions along these systems |
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42:02 | we're talking about. A single And so Mascarenas. Acetylcholine signaling would |
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42:08 | linked to the g protein cascade. you can see that in some cases |
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42:13 | call this g protein signaling shortcut That means that the g protein complex |
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42:18 | is going to bind to a nearby which in this case is potassium channel |
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42:23 | going to open potassium channel, opens channel positive charge is going to be |
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42:31 | the cell. Therefore activation of this . Acetylcholine receptor is going to cause |
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42:38 | hyper polarization of the plasma mom. . So we talked about the fact |
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42:43 | nicotine nick acetylcholine receptor will cause an of sodium and potassium sodium D polarizing |
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42:51 | cell and masculine IQ will cause the of potassium channel downstream, causing the |
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42:57 | polarization. So they that the central system synopsis, they act in opposing |
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43:04 | . As far as the numbering deep hyper personalization assets are different from uh |
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43:13 | mean neurotransmitters assets are produced everywhere in brain. So you will find assets |
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43:18 | different neurons and brain stem throughout brain and the C. N. S |
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43:22 | the cortex. Primary visual cortex and is very intricately involved in control of |
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43:31 | glutamate can be imported into glia with . Santa's turned into glutamine and then |
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43:37 | imported back into neurons with contaminates. synthesize into glutamate and reload it back |
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43:44 | . And post synaptic aly glutamate receptors also iron, A tropic and metabolic |
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43:50 | . I don't know why I jumped catacomb and start Tony Already reviewed |
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43:55 | This is another system and metabolic tropic . In this case you have norepinephrine |
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44:03 | which is stimulatory and produces cyclic GMP turns on the production of protein |
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44:09 | And you have alpha two receptor which inhibitory will reduce the general cyclist production |
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44:15 | control protein kindness by reducing its So unlike the amino assets that we |
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44:22 | be coming back to in a But we're finishing with the means |
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44:25 | Those means are expressed in very specific . So rafi nuclei will express serotonin |
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44:32 | the projections from the stone Amos of neurons that produce produce serotonin will project |
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44:40 | lee throughout the cortex of cortical areas into the preference of the spinal |
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44:45 | No more referendums producers and not a locus Aurelius. Acetylcholine is produced in |
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44:55 | couple of nuclei here. Uh This this is uh you can't really read |
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45:04 | the slide. Uh Let me see I can larger though but so be |
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45:11 | to answer the questions. For example which nucleus is producing norepinephrine which nucleus |
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45:17 | producing serotonin which nuclei are producing a Colin. So please please review |
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45:24 | It can be a labeling question can just a simple multiple choice questions related |
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45:29 | this. The big difference here is you have these nuclei. So if |
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45:33 | were to take out local civilians like remove local civilians there would not be |
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45:40 | made in the brain anymore. So if you were to take out one |
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45:45 | hemisphere of the cortex you would still a lot of glutamate Gaba and all |
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45:51 | the amine acid neurotransmitters that are being produced everywhere. And the cannabinoids are |
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46:00 | and also nitrous oxide, carbon monoxide also not stored in the vesicles. |
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46:05 | acid is also number insoluble. These the major endocannabinoid anandamide and two |
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46:10 | G. And the two mechanisms or the polarization to suppression of the |
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46:17 | the polarization of the suppression of This retrograde negative feedback mechanism by which |
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46:23 | cannabinoids act in the brain. Just uh glutamate. Gaba also has transporters |
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46:32 | gets uploaded into vesicles and gets released . We focused on iona tropic and |
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46:40 | tropic signaling a little bit mostly on tropic, ample kind nick and India |
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46:45 | they have each own agonists and We talked about the fact that once |
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46:52 | is released it will bind to ample NMDA receptors and ample receptors will open |
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46:59 | and ample receptors are responsible for the the rising phase of this excitatory post |
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47:04 | potential and then M. D. receptor is have a magnesium block and |
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47:09 | order to alleviate that magnesium block and . D. A receptor has to |
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47:13 | glutamate. Mountain also has to detect polarization. Is the initial deep polarization |
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47:18 | happen to ample receptors which will kick the magnesium from an M. |
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47:23 | A receptors and then an M. . A receptor will be responsible for |
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47:26 | late portion of this E. S. P. And will also |
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47:32 | large amounts of sodium and calcium inside south. So AMp A cane has |
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47:39 | conductance of about 20 Picasso demons and D. A. Has a conductance |
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47:43 | 50 P. Cosima. So it's to open that channel. It needs |
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47:47 | have both pre synaptic and post synaptic . That's why it's referred to as |
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|
47:52 | detector coincidentally it detects pre synaptic glutamate post synaptic deep polarization in order to |
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47:59 | . Once it does we will conduct times more current causing that prolonged deep |
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48:05 | in the PSB al pacino and have own antagonists or blockers. Just CNN |
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|
48:11 | . X. And N. D. A. Has its own |
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48:13 | HPV. And that comes up when talk about the ivy properties of amber |
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|
48:18 | an M. D. A receptors be a tropical intimate receptor is not |
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48:25 | any way in an M. A receptor NMDA receptor is on a |
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48:30 | just blocked with magnetism don't confuse it metabolic tropical element receptors. Measurable tropical |
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48:36 | and receptors well again actively the G cascade, just mostly acting through possible |
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48:43 | . They see signal. This is experiment which shows that in normal physiological |
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48:50 | $1.2 million magnesium, there is very of an M. B. |
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48:56 | Current and hyper polarized potentials that the potential for an NBA receptor occurrences zero |
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49:03 | volts reversal potential for ampara receptor currency also zero million balls, which makes |
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49:11 | reversal potential for MPS B also zero vaults because CPS P is a combination |
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49:19 | Tampa and N. M. A. Signaling and these potential the |
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49:23 | potential. So you can see that receptors are quite active. Now if |
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49:28 | remove magnesium. So if you eliminate from the solution, extra cellular |
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49:35 | then at these negative holding potentials minus hyper polarized potentials. You will be |
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49:42 | an M. D. A So that proves that magnesium is blocking |
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49:45 | M. D. A receptor. is not enough to open this receptor |
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49:50 | hyper polarized potentials. But if you magnesium glutamate is enough to open an |
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49:57 | . D. A receptor and this abnormal conditions. So if you have |
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50:01 | in the levels of magnesium, you have the excitability of the cells go |
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50:07 | because there will NMDA receptors will be lot more responsive to even ambient levels |
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|
50:13 | of glutamate and the zero magnesium can used as a model to induce abnormal |
|
|
50:20 | and even seizure like activity and also be used as a model for |
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|
50:27 | There are some similarities physiologically between the that happens in the cellular circuits during |
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|
50:35 | and the one that happens during a attack. These are the I. |
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|
50:40 | . Plots for an app and an . B. A channel. So |
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50:43 | you measure this early component, which already know is an ample component and |
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|
50:48 | follow this first race line just a milliseconds after the stimulation And you hold |
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|
50:53 | number in potential at different voltage levels -40 plus 20. You can have |
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|
51:00 | ivy block for this early component. can see how much current is flowing |
|
|
51:04 | different numbering potentials. And this will the early component plot which turns out |
|
|
51:09 | be linear. So ampara ivy plot linear and an M. D. |
|
|
51:15 | . I. V. Plot which measured at the second line, which |
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|
51:18 | the late component here and represents really blue area under the curve here. |
|
|
51:24 | is an M. D. A and you can see that there is |
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|
51:27 | blue area under the curve under hyper potential. So it's nearly zero. |
|
|
51:32 | when you do polarize the salad you see a little bit of an NMDA |
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|
51:36 | here in late component and you can recording this. These are the closed |
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|
51:40 | as the cell D polarizes the number potential D polarizes the minus 40 and |
|
|
51:46 | start seeing significant NMDA receptor current and current reverses its zero mil evolves just |
|
|
51:54 | the ample current and it prefers to in the opposite direction, in the |
|
|
51:59 | direction. Physiologically of course the cell potential is going to be fluctuating only |
|
|
52:07 | resting membrane potential around resting membrane firing action potentials and coming back hyper |
|
|
52:14 | a little bit. So it shouldn't sitting there constantly locked at positive, |
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|
52:19 | of positive 40. But this is voltage clamp experiments that we can do |
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|
52:24 | order to define the curves the V . So NMDA is nonlinear current And |
|
|
52:32 | is one. The other portion of experiment applied a PD which is an |
|
|
52:37 | . D. A receptor blocker. you can ask a question. So |
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|
52:41 | a PV affect the early current. just told the Ap D specific to |
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|
52:45 | M. D. A. And it doesn't. But you can prove |
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|
52:49 | and you can closed or open It's in the presence of a PV |
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|
52:54 | without a PV. It's not going affect the ivy plot for the sample |
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|
53:00 | something. If you put a PV you were tracing this late current, |
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|
53:05 | second line then this blue area under curve would disappear. This is without |
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|
53:12 | PVS. The top line. This with a PV. This is without |
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|
53:17 | P V. Bottom line and this with a PV and what it |
|
|
53:22 | These are the open circles. Now got this almost flatline which indicates that |
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|
53:27 | no flux through N. M. . A channels. There's no late |
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|
53:32 | current here. So this proves that PV only blocks the late component which |
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|
53:39 | an MD. A compartment interestingly if have a single amino acid substitution in |
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|
53:48 | M. Two trans membrane segment of emperor receptor you can have that cell |
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|
53:55 | one condition with are with Q. is Letterman it will conduct calcium. |
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|
54:01 | if you substitute glutamine with arginine are cell and that sorry that channel receptor |
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|
54:10 | is not going to be conducting calcium . Apple receptors. So we distinguish |
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|
54:15 | fact that all of them the receptors calcium but some emperor receptors will conduct |
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|
54:22 | and the ones that will have the and MD. A receptors are only |
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|
54:27 | at early developmental stages and that's why talked about silent synapses, meaning that |
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|
54:34 | you have glutamate release and you only an NBA receptors, the synopsis will |
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|
54:38 | silent. So there will be different that will be activating excitation during the |
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|
54:44 | developmental stages. And NBA receptors have sub units and these subunits during the |
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|
54:50 | and they also reshuffle and different subunits dominate during different parts of this critical |
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|
54:57 | of development. Post critical period of into adulthood, ample receptors are very |
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55:05 | So they can move from extra synaptic that are located outside the synopsis into |
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|
55:10 | synopsis and they can move across plasma . Micrometers within milliseconds. Member tropic |
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|
55:19 | for glutamate is this P. P. To breakdown through possible |
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|
55:24 | P. C. Into a membrane diacetyl glycerol D. A. |
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|
55:31 | Which can then activate protein chinese sea into the new hospital triphosphate which binds |
|
|
55:38 | I. P. Three receptor channels are calcium permeable. And so it |
|
|
55:45 | call up on the intracellular calcium stores cause the release of calcium from cytoplasmic |
|
|
55:54 | , smooth ectoplasmic meticulously kindnesses and phosphate . And there's a balance of these |
|
|
56:03 | someone specific that will control the phosphor and the phosphor relation of these |
|
|
56:09 | Gaba signaling amino acid channel. Gaba . This is where Gaba binds and |
|
|
56:15 | a chloride channel but other substances alcohol, then there are the as |
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|
56:23 | uh which are anti epileptic medications, , sedatives and there are steroids that |
|
|
56:33 | have their own targets in these So when you think about agonists and |
|
|
56:38 | but some of them will be competitive . And when you hear a stable |
|
|
56:42 | agonist that means the two molecules are for the same binding side on this |
|
|
56:48 | channel. Non competitive means that one its own binding site. Neither has |
|
|
56:52 | own binding site. So these molecules lot of them will have their own |
|
|
57:00 | sites and sometimes they can be competing for the binding sites activation of Gaba |
|
|
57:06 | receptor tra will result in the influx fluoride and hyper polarization activation of Gaba |
|
|
57:13 | receptor boston optical, it will open channels and will also cause hyper polarization |
|
|
57:21 | present optically it will close calcium channels can control neurotransmitter vesicles release this similar |
|
|
57:31 | mm hmm. Um push synaptic Similar mechanism to the endocannabinoid. It's |
|
|
57:41 | similar mechanism. This mechanism of closing synaptic calcium here that we're seeing is |
|
|
57:48 | found with a denizen stimulation. And reason why I'm mentioning this to you |
|
|
57:53 | there's a redundancy in control of neurotransmitter and the cannabinoids can control neurotransmitter |
|
|
57:59 | But so there's Gabby can control neurotransmitter and so can a dentist in |
|
|
58:04 | There are transmitters abilities and they can it through these pre synaptic mechanisms we |
|
|
58:09 | do through the post synaptic mechanisms. I really like the slide and I |
|
|
58:15 | that if you have the slide in of you can understand everything in the |
|
|
58:18 | and add your own details to That this is a really good way |
|
|
58:23 | review things about neural transmission. So we talked about in the slide is |
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|
58:30 | there's inhibitory synapse and there's excited to synopsis. This inhibitor synapse will the |
|
|
58:40 | Gaba. So it should stay in God. So you can add that |
|
|
58:46 | . You know it's staying for Alright now Gaba gets released and pastrnak |
|
|
58:53 | you can put this as Gaba a is formidable to chloride is going to |
|
|
58:59 | polarize and boston optical. you also Gaba B. And activation of Gaba |
|
|
59:07 | . Through G protein complex right through jew protein cascade will open potassium channel |
|
|
59:15 | cause more hyper polarization. So you put chloride means that this channel will |
|
|
59:21 | to reach acqua Librium potential for chloride is about -17. This channel potassium |
|
|
59:28 | will hyper polarize the cell will try reach the equilibrium potential for potassium Which |
|
|
59:34 | -80 -90 and themselves will be causing polarization. Now that same Gaba synapse |
|
|
59:45 | also contain pre synaptic Gaba B And prison optically you can see that |
|
|
59:51 | same Gaba B receptor is linked to too. So posten optically this do |
|
|
59:58 | complex targets potassium channels but prison optically calcium channels and what it does it |
|
|
60:06 | blocks calcium channels. These voltage gated channels that are necessary for the |
|
|
60:12 | bicycle fusion and neurotransmitter release. So does God would do? Well if |
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|
60:17 | is Gaba that is spilling over retrograde back onto its audio receptors. Order |
|
|
60:25 | released gable and I am binding to own order receptors here. I'm going |
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|
60:29 | control my own Gaba release Mhm. now nearby you have an excitatory |
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|
60:39 | Senators and house will target ample and receptors posting typically this is an |
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|
60:44 | D. A receptor that have shown is a significant source of calcium not |
|
|
60:49 | deep polarization of calcium and guess what discussed that calcium also as a secondary |
|
|
60:56 | . So there's calcium cal module and and that kind of is can affect |
|
|
61:06 | B. That are located fast synaptic in the excitatory synapse since and also |
|
|
61:14 | affect these channels through potentially phosphor relation channels in both cases doing what in |
|
|
61:25 | cases opening a potassium channel and causing of positive ion and hyper polarizing these |
|
|
61:37 | . So there's glutamate coming in deep through AMP and NMDA the cell and |
|
|
61:42 | calcium rushing in through NMDA on the stage of the PSP activists secondary messenger |
|
|
61:51 | . And through the interactions with Gaba . And potassium channel hyper polarizes the |
|
|
61:59 | . That has nothing to do with release, has everything to do with |
|
|
62:03 | metabolic tropic intracellular signaling. And the of Gaba B receptor is post in |
|
|
62:08 | and excited to the synopsis. So glutamate is here and then in addition |
|
|
62:15 | that if this Gabba allergic synopses very , then there's a spillover of |
|
|
62:22 | Remember it will diffuse through this interstitial in between the cells you have a |
|
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62:28 | of Gaba Gaba b receptors are also preseason optical and excitatory synapses and their |
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62:37 | receptions. Because these synopsis don't produce So Gaba binding to these gaba receptors |
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62:45 | shut down calcium channels and will shut glutamate release. So now through this |
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62:53 | mechanism Gaba and activation Gaba B receptor topically can control glutamate release and that |
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63:05 | uh fairly significant to the same mechanism calcium channels present topically under cannabinoids control |
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63:15 | channels through their own g protein coupled Denison also controls calcium percent catholic channels |
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63:24 | its own g protein cascades. So targets through multiple medical tropic cascade |
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63:31 | This is an example in many synopses will see in the initial deep |
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63:36 | this E. P. S. . That is followed by Gaba ai |
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63:42 | . And then the late component of will be gone by BP SP I |
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63:47 | which is going to be even more polarizing because it is driven by potassium |
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63:52 | is very briefly. We discussed it protein signaling and the variety of all |
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63:58 | the jew protein receptors that we have notice that all of the means except |
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64:06 | a single a single coding has an receptor. But most of the other |
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64:14 | that you're seeing here and receptors are metabolic tropical. There's a huge variety |
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64:18 | these metabolic tropic receptors, the seven member in segments. They are different |
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64:24 | the transmitter gated channels. We reviewed Sistine locally in channel structure briefly and |
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64:31 | said that there's different subtypes of these . Alpha, beta delta gamma and |
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64:35 | you can have like a mixing of sub units in order to produce proteins |
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64:42 | have slightly different functions. So what you have to know from this |
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64:46 | Acetylcholine everything. Okay, Norepinephrine. functions of alpha and beta receptor, |
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64:54 | they're different glutamate everything. Yabba you to know Gaba, A chloride, |
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65:04 | b potassium and we only talked about eucalyptus gaba antagonist but I may ask |
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65:10 | a question as ethanol and agonists. . Okay 80 P. Again |
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65:17 | T. P. Is an agonist also dennison is an agonist. So |
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65:22 | should know that and caffeine is an and you should know it because you |
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65:27 | consume it every day. So if will block those present at the calcium |
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65:34 | and block glutamate release caffeine is an to dentists and channels and it will |
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65:42 | keep the calcium channel open and will glutamate release. This is the cascade |
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65:49 | amplification that you have through the chemical transmission of activating multiple downstream cascades. |
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65:56 | it's different from electrical because only a of electrical signal transfers. But immediately |
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66:02 | synaptic transmission and chemical transmission you have delay whether you can activate these downstream |
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66:08 | that can multiply the effect and then review that you have all sorts of |
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66:14 | divergence convergence redundancy of parallel streams between receptors transmitters and and their downstream of |
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66:24 | . This concludes our review session and out of time for this lecture as |
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66:32 | . But I will be happy to any questions. I'm just going to |
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66:36 | the recording so it starts |
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