| 00:06 | this is neuroscience. Midterm to review also a portion and the ending of |
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| 00:12 | central visual system processing. And we the connections between retina thalamus and |
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| 00:23 | We looked at the anatomy of the circuits. We looked at the output |
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| 00:28 | comes out of the retina. We at the anatomy of the lateral ridiculous |
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| 00:33 | of the thalamus, the sixth layer comprised of magnum carbon layers. All |
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| 00:38 | that information was molecular information we also at in layer four there are ocular |
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| 00:45 | columns that are formed but that layer cells are still processing Manaka color information |
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| 00:54 | the primary visual cortex and then at 23 the man ocular information actually becomes |
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| 01:01 | . So we discussed the flow of Kalama, cortical inputs Mp and I |
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| 01:08 | mp. Going into the layer I bypassing layer for going in to |
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| 01:14 | . I'm primarily concerned with color There's 2 3 allow for the long |
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| 01:20 | and intra columnar and intra Cortical connections take place and spread. There's intra |
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| 01:27 | loop between 4-3, five and Again this is an intra cortical loop |
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| 01:34 | then there's the cortical hypothalamic outfit that from the cortex into the thalamus. |
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| 01:40 | recall that there is still um cortical into cortical loop in a certain fashion |
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| 01:45 | learn cortical thalamic outputs. This is going to influence in this case visual |
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| 01:50 | processing. In many other cases it be dealing with other sorts of sensory |
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| 01:56 | in different parts of the brain. the color is concerned mostly with Larry's |
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| 02:01 | . 3. The properties of the . The receptive field properties in area |
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| 02:07 | . One is that they process A simple cells process bars in certain |
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| 02:13 | they will produce and be responsive to bar of light and a certain orientation |
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| 02:19 | a maximum number of action potentials. also have direction selectivity. So those |
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| 02:25 | in the cortex will prefer a bar light to cross through the field of |
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| 02:30 | through the receptive field in a certain it will be preferred left to right |
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| 02:36 | to bottom the diagonal and so So we saw how simple cells and |
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| 02:43 | cells from the retina which are concentric and off cells can converge onto |
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| 02:47 | G. M. Cells and how number of L. G. M |
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| 02:51 | of processes center surround concentric like receptive properties can converge onto the simple cells |
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| 02:59 | the simple cells can further converge onto cells. So you can get different |
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| 03:08 | of receptive field properties in different shapes the level of the primary digital |
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| 03:13 | That because of the convergence of G. N. Cells and the |
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| 03:18 | cells creating bars, creating various shapes this. Of the receptive field properties |
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| 03:23 | the primary visual cortical cells and their cells further converging onto the complex |
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| 03:28 | And that is all happening within One. And with complex cells will |
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| 03:33 | even the greater variation of these really um forms and shapes that you can |
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| 03:39 | with. So if you recall the dominance columns, I'm gonna review very |
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| 03:47 | are these projections that if you were look where the projections come from one |
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| 03:55 | and to trace them from one eye the L. G. On |
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| 04:00 | And as we discussed you were to and to appeal where those uh in |
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| 04:06 | case of radioactive probing which is trans to go across the synopsis from the |
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| 04:11 | ganglion cells until jeon from LG installs primary visual cortex. And in the |
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| 04:16 | visual cortex will get these stripes or . These are ocular dominance columns. |
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| 04:22 | one of these blue columns in layer belongs to one eye and the white |
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| 04:28 | belongs to that I so this is you still have the men ocular vision |
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| 04:33 | then leads to three that molecular vision binocular vision. Now in this |
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| 04:40 | I'm going to go back to one here that we didn't discuss in this |
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| 04:46 | , we've emphasized the theme of plasticity we said that during plasticity there is |
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| 04:52 | period of development during this very early where there is the right chemistry, |
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| 04:57 | right factors in the neuronal environment for synopsis to form and also for the |
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| 05:03 | to be trimmed and the connections to specified. And so this is an |
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| 05:10 | that tells you something about this critical of development and if there is sensory |
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| 05:16 | during that critical period of development. could be likened. For example if |
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| 05:20 | newborn child somehow was deprived of census some early stage of development, how |
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| 05:27 | that affect the anatomy of the And obviously anatomy or structure means function |
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| 05:34 | . And if you look this is experiment that can be done in rodents |
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| 05:40 | in rodents you can suture one. live and you would perform this experiment |
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| 05:46 | the very end of the first month life. So the first month of |
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| 05:51 | is really this period that we call period of development where there is a |
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| 05:55 | of plasticity, a lot of reorganization in this case the animal is deprived |
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| 06:02 | the visual input. That's why they're a pirate like patch here on their |
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| 06:07 | . You have sutured island And this is only suited for three days. |
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| 06:13 | then three days later the sutures removed the animal is allowed to recover for |
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| 06:20 | whole month and a month later an was performed where both eyes being |
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| 06:29 | the left and the right guy. it turns out that there is a |
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| 06:33 | bias and this is number of cells are responding from the IFC lateral |
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| 06:39 | And the itsy lateral I was the that remained open and there is a |
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| 06:45 | of response In Layer four. In ocular dominance columns forward. The eye |
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| 06:52 | remained over it's not much but you see that the blue columns and the |
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| 06:58 | of cells have shifted. Mhm. the red ones. Now if you |
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| 07:04 | the same experiment but instead of suturing eyelid for three days The island is |
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| 07:11 | for six days. And it is all the way until the basically end |
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| 07:18 | this first month where the critical period development also ends. Animal is allowed |
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| 07:25 | recover for a month. And the eyes, the sutured I hear contra |
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| 07:32 | and the open eye of being stimulated it is now very obvious that the |
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| 07:40 | and layer for in the primary visual are only responsive to the eye that |
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| 07:46 | open. They are no longer responsive the eye that was closed. That |
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| 07:54 | that if you have short term deprivation three days there might be a small |
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| 08:01 | in the functional structure. But if have a prolonged deprivation in this case |
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| 08:07 | six days without vision. In one you can have a permanent reconstruction of |
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| 08:13 | connections and the cortex and therefore the loss a function. And if you're |
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| 08:20 | that critical period of development where there a lot of plasticity, you may |
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| 08:25 | be able to rebuild that function a or two months later forever. So |
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| 08:32 | the short term deprivation there's obviously a loss of function to the eye that |
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| 08:38 | closed and the bias toward the eye was open. And if you look |
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| 08:43 | the fibers. These are the These are the thalamus cortical projections into |
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| 08:48 | four coming in. This is following term binocular deprivation. This is an |
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| 08:55 | eye and below here is deprived dot what that tells you that that I |
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| 09:02 | that was not receiving the inputs, Kalama particle processing of that information which |
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| 09:08 | conscious perception, right? Or first primal sketch and later the whole visual |
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| 09:15 | . You already have lost a significant of inputs and synapses. You have |
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| 09:22 | and you have structurally changed the connections the anatomy in the primary visual |
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| 09:28 | And obviously that reflects very much on partial or prolonged period. The visual |
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| 09:36 | and the full loss of function. , so that's that's really important to |
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| 09:43 | keep in mind again this plastic period such information is so important. How |
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| 09:50 | during the development during this critical period development can long term deprivation can result |
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| 09:56 | long term um functional loss for prominent loss. So we walked through the |
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| 10:07 | and we ended up on this slide lecture and I said I'm gonna put |
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| 10:13 | all kind of together for you and you have these columns and you can |
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| 10:20 | that these bars here are shown in color and this color here has nothing |
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| 10:24 | do with actually color processing but this here represents a different orientation of the |
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| 10:31 | of light. And so we said in this primary visual cortex itself are |
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| 10:38 | . They prefer certain orientation or orientation . So these are referred as the |
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| 10:46 | micro columns where the cells that are yellow within the yellow part of the |
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| 10:53 | , it will be responsive to a of light that is that a certain |
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| 10:58 | . The cells that are located within blue column, it will be responsive |
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| 11:02 | a bar of life in a different . And if you sort of a |
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| 11:07 | around this column and sample and this column, the cells Here, you |
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| 11:12 | be able to find the cells that be responsive all the way, 360° |
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| 11:17 | and responsive to those bars of And the cells that process similar |
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| 11:23 | So orange, dark orange or red be similar orientation. This versus |
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| 11:30 | They're also located closer to each other the boundaries of this micro column. |
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| 11:36 | , if you were to look in middle of this call, in the |
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| 11:39 | of this column looks sort of like pinwheel structure from which you have orientation |
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| 11:44 | cells radiating out of that central And that central pinwheel will contain south |
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| 11:50 | will be responsive to pretty much all because it's really the collection of the |
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| 11:55 | that are coming from the uh from bigger arches of the outer boundaries of |
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| 12:02 | micro column centering into, into this like structure. So these micro columns |
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| 12:09 | find them in the visual cortex of of other animals as well. It's |
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| 12:16 | orientation columns Hubble and weasel where the have studied it using micro electorate |
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| 12:23 | Imagine how many micro electorate recordings you to make to figure out how this |
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| 12:28 | circuit actually processes the orientation columns. now we have simple complex cells, |
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| 12:37 | have concentric fields and we also can techniques like voltage sensitive dyes. So |
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| 12:42 | of using micro electrodes we can actually single cells or numbers of cells within |
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| 12:49 | micro columns. That's a huge huge because we can image potentially 10,000 cells |
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| 12:56 | making a micro electorate recording from one 2 cells. And when you use |
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| 13:01 | sensitive dye imaging it's a functional type imaging. So voltage sensitive dyes communicates |
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| 13:09 | potential changes. So you can see the sellers d polarized if its hyper |
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| 13:15 | . So if you stimulate and the right you stimulate the retina. You're |
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| 13:20 | in the cortex Now you can look the whole window in the cortex and |
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| 13:23 | which cells are active to this which cells are active to this orientation |
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| 13:28 | so on. Somebody doing that. you can describe all of these. |
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| 13:33 | can see this is a much larger of the visual cortex but within that |
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| 13:37 | will see a number of these orientation columns that are about 3200 and 50 |
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| 13:44 | meters wide and neocortex is about two deep or so you can see that |
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| 13:52 | could be individual cells for example each of these dots is an individual cell |
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| 13:57 | on top of these dots and then apply this color coded pattern which the |
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| 14:02 | coded pattern really represents orientation selectivity. this is how we know. Not |
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| 14:10 | poking endlessly. You have to record How many in two million cells |
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| 14:19 | Well you can image two million cells one experiment and if you have good |
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| 14:24 | resolution you can resolve it in a cell level. If you don't you |
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| 14:28 | see sort of a circuit level Now these orientation columns is just a |
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| 14:36 | of the largest structure, bigger what call hyper columns. If you think |
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| 14:41 | hyper columns. And even orientation columns in some way are very elementary computational |
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| 14:49 | . And these hyper columns are also elementary because these hyper columns would still |
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| 14:55 | in closing only limited information processing within One structure of the brain like the |
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| 15:02 | . So but they're still interconnected. when the elementary computational modules interconnect, |
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| 15:11 | become more complex. When they interconnect modules with multiple modules in another brain |
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| 15:19 | that also becomes more complex hierarchically uh and intellectually processing of the information in |
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| 15:29 | higher cortical center. So what you here is if you remember ocular dominance |
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| 15:35 | , ocular dominance columns here are shown these lines. So C stands for |
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| 15:40 | lateral I hear stands with the lateral . This is it's a lateral |
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| 15:47 | So within these four ocular dominance That's what we saw early on basically |
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| 15:53 | is a lot more specificity and there other hyper columns and orientation columns that |
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| 16:00 | located here. So what this shows within the boundaries of the ocular dominance |
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| 16:06 | you will have multiple of these beautiful like color wheels. Which means that |
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| 16:13 | each ocular dominance columns you have multiple , orientation, selectivity michael Collins. |
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| 16:23 | can see that these are the So this is the side of chrome |
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| 16:27 | , see stain and you can see it's somewhat within the center of the |
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| 16:33 | dominance columns. It's concerned with color processing. So you have The blob |
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| 16:40 | structure especially in Larry's 2, And then there is another type of |
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| 16:46 | interesting imaging. So we talk about extensive damaging. I'm gonna in the |
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| 16:52 | section show you a little bit more that. But what's really interesting is |
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| 16:58 | can actually image activity of the brain applying any die and it's called intrinsic |
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| 17:03 | signal images. When we talked about . M. R. I. |
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| 17:07 | pet scan we said what what is functional imaging really represents? It represents |
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| 17:13 | changes. It represents changes in the levels, glucose levels represents how much |
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| 17:20 | neurons are demanding the oxygen of workouts when neurons get active and they demand |
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| 17:26 | and glucose and they fire a lot action potentials and they d polarized what |
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| 17:31 | to them. They also swell. active neuronal circuits the south that are |
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| 17:37 | active on fire. They become slightly than they swell. And what happens |
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| 17:41 | they swell? The plasma membrane stretches little bit. And as a consequence |
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| 17:47 | that you have changes of the reflective in the tissue. And this is |
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| 17:53 | intrinsic optical signal or intrinsic optical signal , meaning its intrinsic because there is |
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| 18:00 | die that is being track there. . And you are looking only at |
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| 18:06 | surface activity to these kinds of experiments intrinsic optical signal may actually show you |
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| 18:13 | you have the surface if you can two layers for that's one thing. |
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| 18:17 | on the surface you can see the and darker shades. And that's because |
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| 18:22 | you stimulated one I one of the responsive cells to responsive to that I |
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| 18:28 | be swelling. And there's likely properties be slightly different. So you have |
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| 18:34 | employ multiple methodologies, experimental neuroscience Multiple sensitive dye imaging imaging. The |
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| 18:42 | of imaging calcium fluctuations is another common of tracking activity or intrinsic optical signal |
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| 18:49 | , which is a reflective properties of cells based on the cell swelling. |
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| 18:54 | one particular number in potential or ion calcium tracing. Of course the fact |
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| 19:02 | the matter is you have sophisticated vasculature innovates the cortex and innovates the primary |
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| 19:09 | cortex and the micro capillaries. The distance that you would find in the |
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| 19:15 | between the micro capitalists, only 50 apart. That means that Only |
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| 19:22 | Selma's 10 μm in diameter. Maximum . So moses away is the further |
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| 19:30 | really 2.5 so much is because five five. So 2.5. So much |
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| 19:34 | . There is micro vasculature of oxygen and nutrient supply going into the |
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| 19:41 | . And with intrinsic optical signal. you have the correct set up, |
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| 19:46 | can actually visualize the ocular dominance signals you can visualize the preferred orientations using |
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| 19:55 | imaging technique. And then you can it all anatomically together. These are |
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| 20:00 | small orientation columns. Those small orientation go into larger, popular dominance |
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| 20:07 | These larger ocular dominance columns make larger columns which will contain information from both |
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| 20:16 | , contra lateral collateral. Okay, this is really the true hypochondria. |
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| 20:22 | this is kind of a putting all the central processing together Within these |
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| 20:29 | And this indicates that hyper columns is 1 mm in in size. So |
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| 20:36 | talked about 5240 50 micrometers of orientation columns. So you can do the |
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| 20:43 | . But it will include about eight so orientation uh selectivity columns. Poor |
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| 20:53 | dominance columns or so. But this the structure. This is the anatomy |
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| 20:58 | underlies the function the function and the of the primal sketch that we |
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| 21:04 | And so there's of course there's anatomical properties. Then there's orientation such as |
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| 21:12 | or um receptive field properties in which information that we generate visual information is |
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| 21:19 | on. So this concludes our information the visual system. This is now |
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| 21:30 | review for midterm too. So I'm continuing as a part of this |
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| 21:38 | And in the in the section in initial lectures we talked about the discovery |
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| 21:44 | chemical neuro transmission. We talked about little, oh we used this vagus |
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| 21:52 | stimulation which you now know as cranial 10. And you know that that |
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| 21:58 | nerve released acetylcholine and that acetylcholine was on the cardiac muscle. And if |
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| 22:06 | are two types of synopsis that we chemical and electrical and electrical synopses allows |
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| 22:12 | very fast flow of ions and small like secondary messengers and electrical synopsis is |
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| 22:21 | important for synchronization of large networks And I refer to as gap |
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| 22:29 | In the last reference to gap junctions made was in the retinal circuit where |
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| 22:36 | talked about horizontal cells that are inhibitory that contain gap junctions between them. |
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| 22:43 | that should indicate that that's how the areas of luminescence in the retina or |
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| 22:50 | areas are created through partially the gap signaling in the retina. You have |
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| 22:58 | pre synaptic components with active zones and pasta synaptic components with the past synaptic |
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| 23:06 | of a variety of synopsis. The synopsis are asymmetrically synoptic to post synoptic |
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| 23:14 | round vesicles, inhibitor synopsis. If were to look at electron microscope imagery |
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| 23:21 | have these flattened vesicles and symmetric Then we spent quite a bit of |
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| 23:27 | talking about neuro muscular junction. So talked about how the axons that come |
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| 23:33 | from motor neurons in the spinal cord we use this neuro muscular junction because |
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| 23:38 | is simple. There's only one neurotransmitter and when the civil Colin is released |
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| 23:45 | will guarantee acetylcholine receptors and the civil receptors will generate this massive potential that |
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| 23:51 | call and play potential that will always inactivation of both educated sodium and calcium |
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| 23:59 | deeper within these junction all falls which be responsible for the generation of the |
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| 24:06 | potential skeletal muscle action potential. And this case the ceo Colin is excitatory |
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| 24:13 | its skeletal muscle and it's also excitatory the past fanatical you only have I |
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| 24:19 | a tropic nicotine acetylcholine receptors. So only one neurotransmitter acetylcholine and it's only |
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| 24:27 | for boston ethically for ligand gated receptor . We only have nicotine acetylcholine |
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| 24:36 | There are certain criteria for neurotransmitters that to be synthesized there have to be |
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| 24:42 | into vesicles really degraded re synthesized. transported, buying post synaptic cause post |
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| 24:50 | effect, activate metabolic trophic cascades and come back to that slide because we |
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| 24:58 | about different neurotransmitter systems and different neural system types. Um and we highlighted |
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| 25:06 | amino acid neurotransmitters, gaba glutamate and gaba and glutamate uh the major excitatory |
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| 25:14 | glutamate the major inhibitory neurotransmitter gaba in brain and the major inhibitory neurotransmitter in |
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| 25:21 | spinal cord is slicing. But we talked about licensing being co factor an |
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| 25:30 | mm D. A good dermatologic transmission the cns. It's the function of |
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| 25:39 | molecule depends on what receptor it binds what what part of the receptor it |
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| 25:44 | . Yes. Right. Can you the question? The reversal potentials for |
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| 26:09 | receptors we discussed as uh for civil receptor it's also zero melon balls. |
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| 26:16 | for employees potential. Yeah it's the as for E. P. |
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| 26:21 | B. Also. Well for P. S. Speed is different |
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| 26:25 | I PSP if you're looking at the A it's chloride reversal potential dependent Gaba |
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| 26:33 | . Is potassium. But if you mind, let me get through some |
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| 26:37 | those sections because those themes are coming ahead and then I'll pause in about |
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| 26:42 | minutes or so and see if you any questions about that. We also |
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| 26:48 | the meaning neurotransmitters and different classes acetylcholine norepinephrine, histamine norepinephrine serotonin. We |
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| 26:56 | about peptides but only how they are in the sense of their synthesis transport |
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| 27:02 | storage in comparison to the neurotransmitters and vesicles that are located mostly precision |
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| 27:10 | Then inside this box we inserted unusual . So I urge you to review |
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| 27:17 | unusual neurotransmitters such as gasses, nitrous , carbon monoxide such as endocrine adenoids |
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| 27:25 | as? Our economic asset and a p So mentions of these may come |
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| 27:33 | on the exam. But in general pre synaptic neurotransmitter vesicles to fuse. |
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| 27:39 | have to have pre synaptic deep polarization is the action potential influx of |
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| 27:44 | An influx of calcium is necessary to the protein protein complex fusion so that |
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| 27:51 | can be a neurotransmitter molecule release. it can be in the C. |
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| 27:57 | . S. This really is going be partial or full which doesn't happen |
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| 28:01 | the muscle. So you can have partial command if partial contraction that means |
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| 28:07 | if something is wrong. And so the C. N. S. |
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| 28:12 | potentials the E. P. P. S. Are much smaller |
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| 28:15 | on the order of only half a volts as opposed to in the neuro |
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| 28:19 | junction 17 million volts. So you many many different synopsis and neurotransmitter vesicles |
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| 28:26 | in order to activate the cns So the E. P. |
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| 28:33 | P. Is generated when glutamate is and binds to glutamate receptors. Under |
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| 28:39 | this deep polarization the I. S. P. Is generated when |
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| 28:42 | is released. It binds to gatherings and causes the hyper polarization in the |
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| 28:48 | of IT PSP there's iron, A signaling versus metabolic tropic signaling metabolic tropic |
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| 28:55 | . You can see the neurotransmitter of ligand never opens a channel but instead |
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| 29:01 | actually activates the g protein complex which activate enzymes and downstream secondary messengers. |
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| 29:08 | we use the single component system sort exemplary system for understanding that the means |
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| 29:15 | right. And we really talked about assets to great degree glutamate and gaba |
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| 29:21 | immune signaling. But we refer to signaling and we talked in great detail |
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| 29:27 | acetylcholine synthesize the sudoku and choline with choline. Acetyl transfers loaded up into |
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| 29:35 | released in the cns. We distinguish a cns acetylcholine signaling. You have |
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| 29:42 | a tropic which is an academic acetylcholine and you have metabolic tropic acetylcholine receptors |
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| 29:48 | well. It's not as simple as junction. Once a single column is |
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| 29:55 | , you remember neuro muscular junction and you needed to receive incoming molecules to |
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| 29:59 | to the receptor in order to open . Once a single covid has |
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| 30:03 | it binds to the receptor temporarily and it gets degraded by a cyclical |
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| 30:12 | Once it gets degraded by into clothing acetic acid Colin gets re transported back |
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| 30:21 | the sodium co transporters and Colin gets synthesize acetylcholine, the help of chat |
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| 30:29 | re uploaded into the vessels. So discussed that going back to your Alzheimer's |
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| 30:37 | slide a cyclical industries inhibitors, some the most common alzheimer's medications because the |
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| 30:47 | signaling is impaired since an early pathology Alzheimer's disease. So by blocking a |
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| 30:55 | Colin segregation. You know, I'm a civil code more bio available within |
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| 31:00 | synopsis where it still exists. So Coleman will be an agonist to both |
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| 31:07 | and Mascarenas. Acetylcholine receptors. Nicotine be an agonist nicotine. It must |
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| 31:15 | muscular tonic and they will have their antagonist, cure ari from little poison |
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| 31:20 | and atropine. So for example, you put your are in the neuro |
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| 31:25 | junction, you would block acetylcholine receptors if you block the silicone and receptors |
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| 31:31 | would block the end plate potential. if you block the in place potential |
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| 31:35 | would block the action potential in the muslim. If you block the action |
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| 31:40 | , you would not see a contraction the muscles and to an antagonist blocking |
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| 31:46 | acetylcholine receptor here, it would basically and no deep polarization in the |
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| 31:53 | We also talked about other means such tyrosine, l dopa dopamine, |
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| 31:59 | epinephrine. I said that you do have to know they're into intermediary uh |
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| 32:06 | here with synthesis but you do need know the details of acetylcholine but it |
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| 32:11 | follow a similar Cascade here that we . Release three update and we discussed |
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| 32:19 | the enzyme that degrades catacomb means is on the membranes off the mitochondria. |
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| 32:29 | mean oxidants and so the therapies that be targeting cat akal immune systems can |
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| 32:37 | be m a o inhibitors. So would be inhibiting the enzyme that is |
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| 32:43 | the cata column and this is another therapeutic strategy. You can have something |
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| 32:48 | goes in the synapse and blocks of a student Colin asteroids in the studio |
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| 32:53 | system here, you can have something inside the cell and maybe inhibiting this |
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| 32:58 | around the matter mitochondria that's responsible for catacomb means thereby prolonging violet availability, |
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| 33:08 | more violet available. Also blocking the . I mean re uptake with amphetamines |
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| 33:15 | cocaine would cause if you think about , norepinephrine is like nor adrenalin or |
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| 33:22 | of the brain. That because a up that's why they're called, what |
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| 33:29 | they called? Not the speed drugs whatever uppers uppers it's it enhances they're |
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| 33:37 | within these pathways but it can also highly addictive a negative effects as |
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| 33:45 | Uh Those are illegal substances that we're about. We're not talking about therapeutic |
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| 33:51 | . Glutamate, glycerin, Gaba, synthesized with God turns into gaba and |
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| 34:01 | neurons. Serotonin an interesting system. one of these systems deals with something |
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| 34:12 | . Norepinephrine, abramoff, rana, or flight response. Serotonin mood, |
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| 34:18 | , sleep learning a different response. system. PROzac, which is pharmaceutical |
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| 34:26 | will be controlling the re uptake of from the synapse, the star tonin |
|
| 34:30 | in the way a happier mood And you will see certain logic treatments |
|
| 34:35 | cases of depression and the cannabinoids are because and the cannabinoids are synthesized on |
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| 34:42 | . Personal. Typically they're not stored the vesicles. Their numbers soluble, |
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| 34:48 | will use this retrograde mechanism to travel into the pre synaptic side where cannabinoid |
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| 34:55 | are located. So if you want activation precision optical you will activate the |
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| 34:59 | protein complex which will shut down calcium by shutting down free sign up the |
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| 35:06 | influx and the cannabinoids will regulate the of both excitatory and inhibitory molecules. |
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| 35:13 | there is deep polarization induced suppression of . When there's a lot of deep |
|
| 35:19 | . There's going to be under cannabinoids of that release of inhibition or that |
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| 35:25 | of excitation, essentially balancing the release excitatory inhibitory neurotransmitters. Delta nine THC |
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| 35:33 | is a molecule that is found in plant. It's a psychotropic psychoactive molecule |
|
| 35:40 | causes the high effect THC DELTA nine will be acting through CB one receptors |
|
| 35:47 | it's a natural substance that is synthesized cannabis plant. And if you are |
|
| 35:52 | my other course the graduate course, just finished talking about how DELTA eight |
|
| 35:57 | which you find advertisements for around different shops and gas stations and baby shops |
|
| 36:04 | . Delta H. THC is a synthetic cannabinoid that doesn't come from the |
|
| 36:09 | . The process that turns DELTA eight from another can avenue. It's called |
|
| 36:15 | actually is not the cleanest process. no medicinal benefits that are known to |
|
| 36:21 | eight THC. There's very many accepted and medicinal benefits for DELTA nine THC |
|
| 36:30 | don't know exactly the methods each lab to produce DELTA eight THC. And |
|
| 36:38 | people have really strange reactions to DELTA . And once they've used DELTA nine |
|
| 36:44 | also report they have very strange reactions DELTA eight. So it's not because |
|
| 36:48 | tried something that is new psychotropic away that's something to be aware of. |
|
| 36:54 | these molecules interact with the cannabinoid system also interact with other systems in the |
|
| 37:00 | . Um You know is the chemistry insider hybridization of the two common techniques |
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| 37:05 | which you can label neurotransmitters. One antibodies, another uses the radioactive the |
|
| 37:12 | sequence of nucleic assets engaging neurotransmitters or mimicry. We discussed that if you |
|
| 37:20 | applying neurotransmitter in the fluid you would a significant dialysis. And so if |
|
| 37:25 | wanted to study very precise activation of synopsis you would use something like engaging |
|
| 37:30 | neurotransmitters and laser photo license in order activate very precise areas or single synapses |
|
| 37:38 | the dendrite. So you can study the currents flow along the dendrites. |
|
| 37:44 | have different types of synaptic integration. we talked about how you produce a |
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| 37:49 | the PSP and we'll look into the of that E. P. |
|
| 37:52 | P. And if you have spatial where three accents are activated at the |
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| 37:57 | time you will have the maximum It will some overtime at the same |
|
| 38:02 | . And if it's summed over over sorry but if it's summed over |
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| 38:07 | Like in temporal summation. You can that the PSP is going to be |
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| 38:11 | larger than just by producing a single potential to producing three action potentials. |
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| 38:21 | can grow on this deep polarization, will not be as maximal as spatial |
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| 38:28 | signal, but it will be longer duration actually. And that is |
|
| 38:33 | Especially as we look at the concept lambda voltage lambda, which is the |
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| 38:41 | constant. And dendrites that are non ated structures that are non myelin ated |
|
| 38:47 | current will leak out over distance. it doesn't have the cable installation like |
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| 38:55 | axons do. And if you insert electrode and produce the maximum current |
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| 39:03 | 100% at this Area right here, distance away from that area, that |
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| 39:11 | is going to die down and at point it goes to 37% of maximum |
|
| 39:17 | at the injection side this distance and is referred to as the length |
|
| 39:24 | So the cells that have a long constant. This will persist over longer |
|
| 39:30 | . The cells that have short line are leaking this curve would be declining |
|
| 39:37 | much steeper fashion. Yeah. In for the cell to generate the action |
|
| 39:44 | , you have to have many synapses are active. Each synapse is half |
|
| 39:49 | million volts And the threshold for action is -45. So you have to |
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| 39:55 | tens of excitatory synapses activated and then encounter inhibitory synopsis and those inhibitor synopsis |
|
| 40:02 | going to cancel out part of this signal a lot of times inhibitory synopsis |
|
| 40:07 | going to be located closer to the . That's just by design and cns |
|
| 40:12 | they have this control of the paris regions so there's strong control but remember |
|
| 40:18 | outnumbered only 10 to 20% in the will be inhibitor in generals, they're |
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| 40:25 | very diverse. And the population many subtypes of inhibitory cells and they have |
|
| 40:31 | strategy of targeting mostly these para somatic in controlling mostly the integrative properties, |
|
| 40:38 | that cell is going to integrate all the inputs coming in. And so |
|
| 40:43 | there is an activation of excitation and at the same time at the level |
|
| 40:48 | the soma you may not see any and maybe it's essentially will cancel each |
|
| 40:53 | out. Part of the current will out, part of the current will |
|
| 40:56 | shunted through this inhibitory currents to and you have to have very significant activation |
|
| 41:03 | the downright or the selma significant input order to have the cell generated the |
|
| 41:09 | potential uh metabolic tropic signaling is also to as modular. A torrey signaling |
|
| 41:17 | it modulates downstream cascades. It can modulate downstream channels and it can do |
|
| 41:25 | by force correlating them with protein kindnesses it can do so by default correlating |
|
| 41:31 | using phosphate Asus Okay, so this when we say modulation, this is |
|
| 41:37 | we're referring to. Well let's switch . These are our major systems again |
|
| 41:53 | here. This is a system. really want you to know all of |
|
| 41:57 | details on. So I showed this five times maybe six times in different |
|
| 42:04 | . So you can expect at least or six questions along these systems that |
|
| 42:10 | talking about a cdo calling And so acetylcholine signaling would be linked to the |
|
| 42:16 | protein cascade. And you can see in some cases we call this g |
|
| 42:21 | signaling shortcuts athlete. That means that g protein complex itself is going to |
|
| 42:27 | to a nearby channel which in this is potassium channel is going to open |
|
| 42:31 | potassium channel. It opens potassium channel charge is going to be leaving the |
|
| 42:40 | . Therefore, activation of this Acetylcholine receptor is going to cause the |
|
| 42:46 | polarization of the plasma mom works. we talked about the fact that nicotine |
|
| 42:52 | acetylcholine receptor will cause an influx of , the potassium sodium d polarizing the |
|
| 42:59 | and muscular clinic will cause the opening potassium channel downstream, causing the hyper |
|
| 43:05 | . So they at the central nervous . Synopsis to act in opposing directions |
|
| 43:11 | far as the numbering. Deep polarization personalization. Yeah, assets are different |
|
| 43:18 | uh I mean neurotransmitters assets are produced in the brain. So you will |
|
| 43:24 | assets in different neurons and brain stem the brain stem and the C. |
|
| 43:29 | . S in the cortex. Primary cortex and glia is very intricately involved |
|
| 43:35 | control of glutamate. Glutamate can be into glia with glutamine santa's turned into |
|
| 43:44 | and then re imported back into neurons contaminates. Re synthesize into glutamate and |
|
| 43:50 | it back up and post synaptic aly receptors are also iron. A tropic |
|
| 43:55 | metabolic tropic. I don't know why jumped the catacomb and star Tony. |
|
| 44:01 | reviewed that this is another system and tropic signaling. In this case you |
|
| 44:09 | norepinephrine beta which is stimulatory and produces GMP and turns on the production of |
|
| 44:15 | kindness. And you have alpha two which is inhibitory will reduce the general |
|
| 44:21 | production and control protein kindness by reducing levels. So unlike the amino assets |
|
| 44:29 | we will be coming back to and lot of that we're finishing with the |
|
| 44:32 | here. Those means are expressed in specific nuclear. So rafi nuclei will |
|
| 44:38 | serotonin and the projections from the selma's these neurons that produce produce serotonin. |
|
| 44:46 | will project diffuse lee throughout the cortex cortical areas and into the preference and |
|
| 44:51 | board no more but not friendless not the nucleus locus Aurelius. Uh |
|
| 45:00 | is produced in a couple of nuclei . Um uh This is this is |
|
| 45:10 | can't really read on the slide. me see if I can in the |
|
| 45:16 | but so be prepared to answer the for example of which nucleus is producing |
|
| 45:24 | , which nucleus is producing serotonin which are producing seal Colin. So please |
|
| 45:30 | review this. It can be a question. It can be just as |
|
| 45:34 | multiple choice questions related to this. big difference here is that you have |
|
| 45:39 | nuclear is so if somebody were to out local civilians like surgically removed locus |
|
| 45:45 | there would not be norepinephrine made in brain anymore. So but if you |
|
| 45:50 | to take out one full hemisphere of cortex you would still have a lot |
|
| 45:56 | glutamate Gaba and all of the amine neurotransmitters that are being introduced produced |
|
| 46:05 | And the cannabinoids are different and also socks that carbon monoxide are also not |
|
| 46:10 | in the testicles. Orthodontic acid is number insoluble. These are the major |
|
| 46:16 | anandamide and two A. G. the two mechanisms or the clinicians the |
|
| 46:23 | do suppression of the division, the to the suppression of excitation. This |
|
| 46:27 | negative feedback mechanism by which under Canavan act in the brain just like uh |
|
| 46:37 | . Gaba also has transporters also gets into vesicles and gets released glutamate. |
|
| 46:44 | focused on iona tropic and miserable tropic a little bit mostly on iron, |
|
| 46:49 | tropic, ample kind nick and India they have each own agonists and |
|
| 46:55 | We talked about the fact that once is released it will bind to ample |
|
| 47:02 | NMDA receptors and ample receptors will open . Then ample receptors are responsible for |
|
| 47:08 | early the rising phase of this excitatory synaptic potential and then M. |
|
| 47:13 | A receptor is have a magnesium block in order to alleviate that magnesium block |
|
| 47:19 | M. D. A receptor has have glutamate. Mountain also has to |
|
| 47:23 | deep polarization. So initial deep polarization happen through ample receptors which will kick |
|
| 47:29 | the magnesium from an M. A receptors. And then mm dia |
|
| 47:32 | will be responsible for the late a of this E. P. |
|
| 47:36 | P. And will also conduct large of sodium and calcium inside the |
|
| 47:43 | So AMP A canaanite has a conductance about 20 Picasso demons and India has |
|
| 47:49 | conductance of 50 P. Cosima. it's harder to open that channel. |
|
| 47:54 | needs to have both pre synaptic and synaptic activity. That's why it's referred |
|
| 47:58 | as coincidence detector coincidentally it detects pre glutamate and post synaptic deep polarization. |
|
| 48:05 | order to open Once it does we conduct 2.5 times more currents causing that |
|
| 48:12 | deep polarization. In the PSP al have their own antagonists or blockers which |
|
| 48:18 | CNN Q. X. And M. D. A. Has |
|
| 48:20 | own blocker. HPV. And that up when we talk about the ivy |
|
| 48:24 | of amber and the FDA receptors. tropic limitless after. Is not in |
|
| 48:33 | way in an M. D. receptor NMDA receptor is on the tropical |
|
| 48:38 | blocked with magnetism don't confuse it with tropical element receptors. Measurable tropical storm |
|
| 48:43 | receptors well again actively the g protein and just mostly acting through possible |
|
| 48:50 | They see signaling. This is an which shows that in normal physiological conditions |
|
| 48:59 | million magnesium, there is very little an M. B. A. |
|
| 49:03 | and hyper polarized potentials that the reversal for an NBA receptor occurrences zero million |
|
| 49:12 | reversal potential for ampara receptor currency is zero million balls, which makes the |
|
| 49:19 | potential for E. P. B. Also zero mila vaults. |
|
| 49:24 | CPS B is a combination of Tampa N. M. D. A |
|
| 49:28 | and these potentials positive potentials. You see that NMDA receptors are quite active |
|
| 49:35 | if you remove magnesium so if you magnesium from the solution, extra celery |
|
| 49:41 | solution, then at these negative holding minus 60 hyper polarized potentials. You |
|
| 49:48 | be activating an M. D. receptor. So that proves that magnesium |
|
| 49:52 | blocking NMDA receptor. Glutamine is not to open this receptor to hyper polarized |
|
| 49:58 | . But if you remove magnesium then is enough to open an M. |
|
| 50:04 | . A receptor and this is abnormal . So if you have drop in |
|
| 50:08 | levels of magnesium you will have the of the sales go up because there |
|
| 50:15 | an NBA receptors will be a lot responsive to even ambient levels of of |
|
| 50:21 | and the zero magnesium can be used a model to induce abnormal synchrony and |
|
| 50:28 | seizure like activity and also can be as a model for migraines. There |
|
| 50:34 | some similarities physiologically between the phenomenon that in the cellular circles during seizures and |
|
| 50:42 | one that happens during a migraine These are the I. D. |
|
| 50:47 | , for example in an M. . A. Channel. So if |
|
| 50:50 | measure this early component, which we know is an ample component and you |
|
| 50:55 | this first race line just a few after the stimulation and you hold the |
|
| 51:00 | in potential at different voltage levels minus minus 40 plus 20. You can |
|
| 51:07 | an ivy block for this early You can see how much current is |
|
| 51:11 | at different numbering potentials. And this be the early component plot which turns |
|
| 51:16 | to be linear. So ampara ivy linear and an M. D. |
|
| 51:22 | . I. V. Plot which measured at the second line which is |
|
| 51:25 | late component here and represents really this area under the curve here. This |
|
| 51:31 | an M. D. A. and you can see that there is |
|
| 51:34 | blue area under the curve under hyper potential. So it's nearly zero. |
|
| 51:39 | when you do polarize the salad you see a little bit of an |
|
| 51:42 | D. A current here in late . And you can start recording |
|
| 51:46 | These are the closed circles as the D polarizes the number of potential D |
|
| 51:52 | the minus 40. And I start significant NMDA receptor current and that current |
|
| 51:59 | its zero mil evolves just like the current and it prefers to conduct in |
|
| 52:04 | opposite direction, in the outward Physiologically of course, the cell numbering |
|
| 52:11 | is going to be fluctuating only between membrane potential around resting membrane potential, |
|
| 52:18 | action potentials and coming back hyper polarizing little bit. So it shouldn't be |
|
| 52:23 | there constantly locked at positive, plenty positive 40. But this is the |
|
| 52:29 | clamp experiments that we can do in to define the curves the V |
|
| 52:34 | So an M. D. Is nonlinear current and Apple is |
|
| 52:40 | The other portion of this experiment applied PV which is an M. |
|
| 52:44 | A receptor blocker and you can ask question. So does a PV affect |
|
| 52:49 | early current. I just told the V specific to an M. |
|
| 52:52 | A. And no it doesn't. you can prove yourself and you can |
|
| 52:58 | or open triangles. It's in the of a PV or without a |
|
| 53:03 | It's not going to affect the ivy for the Apple. If you put |
|
| 53:08 | PV and you were tracing this late , the second line then this blue |
|
| 53:15 | under the curve would disappear. This without a PVS. The top |
|
| 53:21 | This is with a PV. This without a P V bottom line and |
|
| 53:26 | is with a PV and what it . These are the open circles. |
|
| 53:31 | you get this almost flatline which indicates there's no flux through an MD. |
|
| 53:36 | channels. There's no late component current . So this proves that HPV only |
|
| 53:44 | the late component which is an A. Compartment Interestingly if you have |
|
| 53:52 | single amino acid substitution in this M2 membrane segment of the Emperor receptor, |
|
| 54:00 | can have that cell in one condition are with Q. Which is |
|
| 54:07 | it will conduct calcium. But if substitute glutamine with argentine are that cell |
|
| 54:14 | that sorry that channel receptor channel is going to be conducting calcium anymore and |
|
| 54:20 | receptors. So we distinguish the fact all of them the receptors conduct calcium |
|
| 54:26 | some Emperor receptors will conduct calcium from ones that will have the queue and |
|
| 54:32 | . D. A receptors are only at early developmental stages. And that's |
|
| 54:38 | we talked about silent synapses, meaning if you have glutamate release and you |
|
| 54:43 | have an NBA receptors, the synopsis be silent. So there will be |
|
| 54:47 | mechanisms that will be activating excitation during early developmental stages. And NBA receptors |
|
| 54:54 | the sub units and these subunits during intelligent and they also reshuffle and different |
|
| 55:01 | may dominate during different parts of this period of development. Post critical period |
|
| 55:06 | development into adulthood, ample receptors are fast so they can move from extra |
|
| 55:14 | spaces that are located outside the synopsis the synopsis and they can move across |
|
| 55:20 | membranes. Micrometers within milliseconds. Many the tropics signaling for glutamate is this |
|
| 55:29 | . I. P. To breakdown fossil I. P. C. |
|
| 55:33 | a membrane bound diacetyl glycerol D. . G. Which can then activate |
|
| 55:40 | chinese sea and into the hospital triphosphate binds the I. P. Three |
|
| 55:47 | channels that are calcium permeable. And it can call up on the intracellular |
|
| 55:56 | stores and cause the release of calcium cytoplasmic smooth smooth into plasma in particular |
|
| 56:06 | and phosphate oasis. And there's a of these especially somewhat specific that will |
|
| 56:12 | the phosphor relation and the phosphor relation these channels. Gaba signaling amino acid |
|
| 56:20 | . Gaba. A. This is Gaba binds and it's a chloride |
|
| 56:25 | But other substances ethanol, alcohol, , which are anti epileptic medications, |
|
| 56:36 | , sedatives and there are steroids that have their own targets in these |
|
| 56:42 | So when you think about agonists and that some of them will be competitive |
|
| 56:48 | . And when you hear a stable agonists, that means the two molecules |
|
| 56:51 | competing for the same binding side on receptor channel noncompetitive means that one has |
|
| 56:58 | own binding site. Now that has own binding site. Okay so these |
|
| 57:04 | a lot of them will have their binding sites and sometimes we can be |
|
| 57:09 | also for the binding sites activation of . A receptor tra will result in |
|
| 57:15 | influx of fluoride and hyper polarization activation Gaba B receptor boston optically. It |
|
| 57:23 | open potassium channels and will also cause polarization and present optically it will close |
|
| 57:31 | channels and can control neurotransmitter vesicles release similar mechanism. Mhm. Um percent |
|
| 57:42 | to collect similar mechanism to the It's also similar mechanism. This mechanism |
|
| 57:51 | closing pre synaptic calcium here that we're is also found with a denizen |
|
| 57:57 | And the reason why I'm mentioning this you because there's a redundancy in control |
|
| 58:02 | neurotransmitter release and the cannabinoids can control release but so does Gabby can control |
|
| 58:08 | release and so can a dentist in . There are transmitter release and they |
|
| 58:13 | do to these pre synaptic mechanisms they do through the post synaptic mechanisms. |
|
| 58:19 | I really like the slide and I that if you have the slide in |
|
| 58:23 | of you you can understand everything in slide and add your own details to |
|
| 58:29 | . That this is a really good to review things about neural transmission. |
|
| 58:35 | what we talked about in the slide that there's inhibitory synapse and there's excited |
|
| 58:41 | our synopsis. This inhibitory synapse will synthesizing Gaba. So it should stay |
|
| 58:49 | for God. So you can add detail. You know it's staying for |
|
| 58:56 | . Alright now Gaba gets released and synaptic lee. You can put this |
|
| 59:02 | Gaba a blue. It's permissible to is going to hyper polarize and boston |
|
| 59:09 | you also have Gaba B and activation Gaba B through G protein complex right |
|
| 59:17 | this jew protein cascade will open potassium will cause more hyper polarization. So |
|
| 59:24 | can put chloride means that this channel try to reach acqua Librium potential for |
|
| 59:31 | which is about -17. This channel leaving will hyper polarize. The cell |
|
| 59:37 | try to reach the equilibrium potential for Which is -80 -90 and themselves will |
|
| 59:46 | causing hyper polarization here. Now that Gaba synapse can also contain pre synaptic |
|
| 59:54 | B receptors and prison optically you can that the same Gaba B receptor is |
|
| 60:01 | to calcium channel. So posten optically do protein complex targets potassium channels but |
|
| 60:08 | and optically targets calcium channels and what does it actually blocks calcium channels. |
|
| 60:15 | voltage gated calcium channels that are necessary the neurotransmitter. Classical fusion and neurotransmitter |
|
| 60:22 | . So what does Gaba do? if there is Gaba that is spilling |
|
| 60:26 | retrograde lee back onto its order Order I released Gabba and I am |
|
| 60:34 | to my own order receptors here. going to control my own Gaba |
|
| 60:40 | Mhm. So now nearby you have excitatory synapse, senators and house will |
|
| 60:48 | ample and NBA receptors posting typically this an M. D. A receptor |
|
| 60:52 | is shown. This is a significant of calcium not only deep polarization of |
|
| 60:58 | and guess what we discussed, That also as a secondary messenger. So |
|
| 61:04 | calcium cal module and canines and that is can affect Gaba B. That |
|
| 61:14 | located fast synaptic aly in the excitatory since and also can affect these channels |
|
| 61:25 | potentially phosphor relation potassium channels in both doing what in both cases opening a |
|
| 61:36 | channel and causing flocks of positive ion hyper polarizing these membranes. So there's |
|
| 61:45 | coming in deep polarizing through AMP and M. D. A. The |
|
| 61:49 | and then calcium rushing into an D. A. On the latest |
|
| 61:52 | of E. P. S. . Activists, secondary messenger cascade. |
|
| 61:58 | through the interactions with Gaba B. potassium channel hyper polarizes the self. |
|
| 62:06 | has nothing to do with Gaba release everything to do with the metabolic tropic |
|
| 62:11 | signaling and the presence of Gaba B is post in optical and excited to |
|
| 62:16 | synopsis. So this glutamate is here then in addition to that if this |
|
| 62:24 | ergic synopses very active and there's a of gaba. Remember it will diffuse |
|
| 62:32 | this interstitial spaces in between the You know the spillover of Gaba Gaba |
|
| 62:37 | receptors are also located preseason ethical and synopsis and their hetero receptions. Because |
|
| 62:45 | synopsis don't produce gamma So Gabba binding these Gaba receptors will shut down calcium |
|
| 62:54 | and will shut down glutamate release. now through this spillover mechanism Gaba and |
|
| 63:03 | gap will be receptive present topically can glutamate release and that is uh fairly |
|
| 63:15 | to the same mechanism controlling calcium channels topically under cannabinoids control calcium channels through |
|
| 63:23 | own g protein coupled cascade. A um also control scouts super synaptic channels |
|
| 63:31 | its own g protein cascades. So targets through multiple metabolic trophic cascade |
|
| 63:38 | This is an example in many synopses will see in the initial deep |
|
| 63:44 | This E. P. S. . That is followed by gaba ai |
|
| 63:49 | . And then the late component of will be gobbled Bps P I P |
|
| 63:54 | P. Which is going to be more hyper polarizing because it is driven |
|
| 63:58 | potassium conductance is very briefly. We the g protein signaling and the variety |
|
| 64:05 | all of the jew protein receptors that have and notice that all of the |
|
| 64:11 | , except for a single a single has an academic receptor. But most |
|
| 64:18 | the other molecules that you're seeing here receptors are all metabolic tropic and there's |
|
| 64:24 | huge variety of these metabolic tropic the seven trans member in segments. |
|
| 64:30 | different from the transmitter gated channels. reviewed the Sistine locally in channel structure |
|
| 64:37 | and we said that there's different subtypes the subunits alpha, beta delta gamma |
|
| 64:42 | that you can have like a mixing these subunits in order to produce proteins |
|
| 64:49 | have slightly different functions. So what you have to know from this |
|
| 64:53 | Acetylcholine everything. Okay, Norepinephrine. functions of alpha and beta receptor, |
|
| 65:01 | they're different glutamate everything. Yabba you to know gable A chloride Gaba b |
|
| 65:12 | and we only talked about black eucalyptus antagonist but I may ask you a |
|
| 65:18 | as ethanol and agonists. Gaba A . T. P. Again |
|
| 65:24 | T. P. Is an agonist also dennison is an agonist. So |
|
| 65:29 | should know that and caffeine is an and you should know it because you |
|
| 65:34 | consume it every day. So if will block those present at the calcium |
|
| 65:41 | and block glutamate release caffeine is an to dentists and channels and it will |
|
| 65:49 | keep the calcium channel open and will glutamate release. This is the cascade |
|
| 65:56 | amplification that you have through the chemical transmission of activating multiple downstream cascades. |
|
| 66:03 | it's different from electrical because only a of electrical signal transfers. But immediately |
|
| 66:09 | synaptic transmission and chemical transmission you have delay but you can activate these downstream |
|
| 66:15 | that can multiply the effect. And please review that you have all sorts |
|
| 66:20 | uh divergence convergence redundancy of parallel streams the receptors transmitters and their downstream of |
|
| 66:31 | . This concludes our review session and out of time for this lecture as |
|
| 66:39 | . But I will be happy I'd happy to take any questions you may |
|
| 66:47 | . I don't see anything in the except will you be uploaded today's video |
|
| 66:53 | ? Professor will try to do so can not that will be uploaded before |
|
| 66:59 | weekend. So you have plenty of to review the material until next |
|
| 67:07 | And I think |
|
