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00:03 | This is Lecture five of neuroscience and have just having a great discussion here |
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00:09 | class that for those of you that just watching the videos you missed out |
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00:16 | it. And if you're just watching videos, we're almost halfway through, |
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00:22 | be more than halfway through the first of the course is this is a |
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00:27 | to face course. You should be the lectures taking notes and reviewing videos |
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00:40 | as a supplementary material. So, is only the next term. It's |
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00:46 | the primary source of learning and I encourage you to take a lot |
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00:51 | questions in class and advantage of sitting classes that you hear all of the |
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00:57 | . Uh, if I don't repeat on the video, advantage of sitting |
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01:03 | classes, seeing everything that I write uh wide board, which does not |
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01:10 | unfortunately as well on the videos. so that's basically my message that if |
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01:19 | want to do well, you should on the material that we discuss in |
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01:24 | lectures. Of course, definitely the is you should use your book. |
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01:30 | there's some information in the book that in greater detail than what we discussed |
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01:34 | the course. There's some information in course that we discuss in greater detail |
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01:40 | it is discussed in the book, my questions on the exam will be |
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01:46 | accordingly to how much time we spend the materials during the lectures and not |
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01:53 | what is in the book. okay, so make sure that you're |
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02:00 | yourselves that you're attending and learning all the material. if you want to |
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02:05 | yourselves where you left off last time we had lecture for and we finish |
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02:12 | lecture by talking about neuronal networks and about how different cell subtypes are different |
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02:22 | different parts of the brain. And spent quite a bit of time on |
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02:26 | diagram and there is a class supporting documents that has a paper in it |
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02:32 | hippocampal circuit inhibitory neurons in your folder the blackboard that you can review and |
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02:41 | the figure legends. But I will you what I would like for you |
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02:46 | know about this diagram on the but this is where we ended up |
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02:50 | time. So this is it here this is what is labeled as lecture |
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02:59 | . And today we're gonna go through and then we're gonna go into lecture |
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03:05 | , kind of a word ends here pick up with glia. So we'll |
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03:09 | glia and then we'll cover the simple arts in the south and the south |
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03:16 | within the outside of the spinal So when we talked about this |
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03:26 | we talked about structure called McDonough uh . Oh, hippopotamus campus. |
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03:54 | is that gonna make it help you it? Hippocampus. Okay, so |
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03:59 | is the things that I would like you to know about the slide came |
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04:05 | campus. What did we say about for campus? It is our key |
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04:09 | which means it is predominantly three layer . So Arky cortex and archy park |
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04:17 | for archaic. So ancient cortex. hippocampus and this this particular section we're |
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04:29 | at is only a portion of the . So this is a circuit within |
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04:34 | hippocampus that we're setting on the And if we were to stay in |
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04:40 | of the cells with glutamate in the , so all of the cells that |
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04:47 | be expressing and releasing glutamate, Which excitatory cells, we will realize that |
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04:58 | of all of the neurons in the in this area that we're looking at |
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05:05 | excited to glutamate sounds. So we can repeat the same question what is |
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05:13 | proportion or the ratio of the inhibitory , inhibitory cells in hippocampus that release |
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05:21 | as the major inhibitory neurotransmitter in the Gaba will account approximately the other 10 |
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05:32 | 20% of neuron. Oh, so so now what is the big difference |
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05:43 | the excitatory cells and the inhibitory cells the circuits that we're discussing. We're |
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05:49 | about the fact that the excitatory cells are parameter cells, they can talk |
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05:55 | each other within local circuits but there are excitatory projection cells. Therefore they're |
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06:03 | project into the adjacent circuits that will contain sad story and also inhibitory |
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06:11 | Now, inhibitory cells can also talk each other and they can talk to |
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06:19 | excitatory cells and inhibitory cells gather releasing but their local network into neurons and |
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06:30 | cells do not have projections that come of the networks, but the excitatory |
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06:38 | have the projections that come out of networks. The reason why I'm explaining |
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06:47 | circuit to you is because this circuit what we call a canonical circuit, |
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06:53 | means that we will find similar type arrangements. The ratio of excitatory versus |
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07:01 | cells. Right? And also the that the diversity here is the cellular |
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07:09 | population starts from the diversity and the cells in particular. So this is |
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07:16 | going to be a theme in the cortex or neocortex, which is a |
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07:22 | cortex, which is a six layer . Now, some of the important |
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07:29 | that we talked about when we looked the slide is that we can distinguish |
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07:35 | cell subtypes using a variety of different and the take home message is that |
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07:41 | modern day neuroscience we have to use techniques in order to actually prove the |
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07:51 | , prove ourselves, prove our audiences we are studying a particular subtype of |
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07:59 | . It's not so difficult with excitatory in the hippocampus or even in the |
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08:05 | . Because excited to the parameter which will projection cells and they'll project |
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08:11 | axons out of this hippocampal network. , these excitatory production cells are very |
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08:20 | to each other morphological e essentially We also started talking about the dialects |
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08:29 | neurons in the sense of the patterns action potentials they can produce. So |
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08:33 | particular parameter all cells will also produce patterns of action potential, so identical |
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08:42 | . It's also indistinguishable and the only that can definitively determine the difference between |
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08:49 | different cell types are some inter cellular specific markers that are present in certain |
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08:56 | of parameter self C. B. and others are C. B. |
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09:02 | because essentially expression of molecules expression of binding proteins or other enzymes and such |
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09:11 | the cell also indicates a different function that cell. Even if it cannot |
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09:16 | observed outwardly through morphology or even inwardly their dialect they're speaking, they may |
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09:24 | be different subtypes of cells even if speak the same dialect. That's what |
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09:29 | getting at. Now when we look the inhibitory cells that we said that |
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09:37 | about 21 different subtypes of inhibitory cells destruction. The Hippocampus inhibitory cells can |
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09:44 | discerned one from another based on the based on their cellular location. But |
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09:50 | the end, the fact of the is that some of these inhibitory cells |
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09:55 | have the same dendritic morphology and the and these yellow cups that you remember |
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10:02 | are the synaptic contacts and the locations the synaptic contacts with the respect of |
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10:07 | Samata access to the programmable cells. these axons from number to number four |
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10:16 | target the same regions of the parameter cells again to distinguish between them. |
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10:22 | would need to use cell specific markers would distinguish these two different subtypes itself |
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10:32 | another thing that we talked about hippocampus we mentioned is that hippocampus is very |
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10:40 | for semantic memory. Okay, learning memory. So if you're memorizing |
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10:48 | you're learning something, if you're learning facts, the faces, the |
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10:52 | the stories of when Luigi Galvani, used the laden jar to stimulate the |
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10:58 | leg. You're learning this through hippocampal to do these circuits that you're looking |
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11:06 | . And so it's really the major of semantic memory or it's also involved |
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11:12 | emotional response and emotional information processing. inevitably a lot of the memories, |
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11:21 | sharp memories that we have retained and with us for a long time or |
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11:27 | have to do with a heightened emotional rather than just block things happening around |
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11:34 | . So these inhibitory cells then they the excitatory projection cells locally within the |
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11:45 | Because of the variety of the inhibitory . You have a variety of dialects |
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11:51 | can be recorded in this case, looking at the neocortex. This is |
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11:57 | layered structure Neocortex and the parameter sounds be producing this type of dialect |
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12:05 | but other cells with the same input actually produce very different frequencies and very |
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12:13 | patterns continues versus bursting patterns versus certain , very different patterns of action potential |
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12:24 | , action potential in the end results the release of the neurotransmitters. So |
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12:29 | frequencies and the patterns, electrical patterns result in different frequencies and patterns and |
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12:37 | release of the neurotransmitters in the Yes. What accounts for the difference |
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12:44 | the territory in why is that why that the case? Because it is |
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12:58 | just in these specific circuits like in Hippocampus and Neocortex, you would see |
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13:04 | dominated number of cells and in particular certain layers, 80, parameter cells |
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13:12 | the much lesser numbers inhibitory cells. the parameter cells are pretty much the |
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13:18 | Ortho logically and functionally and the inhibitory are very different. Now there are |
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13:24 | in the brain and nuclei in the that will not have any excited to |
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13:28 | . So when we study, for , following us in the brain which |
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13:33 | all of the sensory and information. has different nuclei and some of these |
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13:42 | will have the ratios and the proportions excitatory cells to inhibitory cells in the |
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13:47 | way. And then you learn about other nucleus called the particular formation and |
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13:52 | polymers that is all inhibitory. So , canonical in the sense that you |
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13:58 | see this ratio proportion why it is a way if you think about |
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14:05 | the diversity and communication, it comes the inhibitory self. So that's the |
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14:11 | that I can sometimes use an analogy if you uh have a switch on |
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14:21 | is excited to herself and the light comes on. It's pretty boring. |
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14:27 | want to have the dimmer function. want to be able to turn them |
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14:31 | and on as fast as you want and that's what the diversity of these |
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14:36 | cells provides. And later as we'll about other neurotransmitters apart from glutamate gaba |
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14:44 | today we'll learn about slicing but we'll about a mean neurotransmitters that are located |
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14:50 | very specific areas of the brain. will be adding color to the light |
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14:55 | . So it's in a way that then then uh there's certain networks that |
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15:02 | to encode the information that they will in a very robust way and maybe |
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15:08 | why they excited to ourselves. so dominant, especially in the interconnected |
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15:13 | that need to be engaged in order perform a given task. Yes, |
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15:27 | meant that you will find these arrangements of the cells and certain types of |
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15:34 | in which these cells communicate on their and with each other in different parts |
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15:38 | the brain. I have a question with this with this, Not |
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15:45 | but uh, I just, I know if it's a question but since |
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15:49 | conferences related. So one of the functions like that is important in learning |
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15:54 | memory for that. It's not that or that long term pronunciation. |
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16:02 | forgetting that will be like needed. have a high number of for which |
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16:09 | so okay, so, so what , what, what you're mentioning is |
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16:19 | cellular process called long term potential And this cellular process is like a |
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16:25 | substrate for learning and memory. So will get into that a little bit |
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16:32 | into potentially ation. But it is to what we already talked about is |
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16:36 | plasticity. And in order to encode new information in order to learn |
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16:42 | It's not necessarily that only hippocampus has potential patient and you only need to |
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16:47 | locally in another potential chemicals only in is for any of the new connections |
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16:53 | be strengthened. They have to be ated. They have to be made |
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16:59 | . And there's a number of chemicals are involved and there is chemicals are |
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17:03 | to be different. Different parts of brain. Sometimes they're reliant on |
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17:07 | sometimes reliant on dopamine and different rules different encoding information will rely different chemical |
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17:15 | . So uh it's it's it's it's little bit complicated. But you're you're |
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17:23 | thinking is uh and the question is silly. It's actually maybe advance for |
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17:30 | we are at the moment in the . But we'll touch on these things |
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17:35 | later in the course, we'll talk plasticity, potentially a shin at the |
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17:41 | to describe to you the plasticity is ability for the cells to form new |
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17:45 | , strengthening connections lose those connections when say L. T. P. |
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17:49 | potentially ation. You also know that L. T. D. Which |
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17:53 | depression which means you have to get of the synopsis. So as you're |
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17:58 | new information you're potentially shedding all information different times of the year, different |
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18:05 | and different decades of your life. may prioritize certain types of learning and |
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18:09 | types of information at an expense of things because we have in the end |
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18:18 | adults finite number of synapses. And despite the variety of the cells will |
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18:24 | have only 150, sub tasks which be even more different ways of processing |
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18:34 | . So uh yeah we always have think about that. That potential |
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18:41 | strengthening, building this synopsis also comes an expense potentially weakening, shedding old |
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18:47 | once as well. So but we'll back to some of these topics later |
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18:53 | the course. Uh Sure. So people do these kinds of recordings, |
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19:01 | they try to record from neurons and can try to record from individual |
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19:07 | So we can if you recall we visualize neurons and we can visualize neurons |
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19:12 | infrared microscopy. And the neuron on left and you're on the on the |
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19:17 | . This is a cross diameter about micrometers diameter of this pie path path |
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19:24 | about one micro meter too. And these cells receive identical input but they |
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19:31 | a completely different output in the patterns their action potentials to sell on the |
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19:36 | is very fast frequency of firing the on the right is slow and in |
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19:41 | when we look at the diversity of dynamic range, how fast or how |
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19:48 | neurons can fire. Some neurons will fire maximum up to 57 herds which |
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19:55 | 5 to 7 spikes a second. so fast. And then on the |
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19:59 | range we have neurons that will produce of 600 hertz of 600 spikes the |
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20:06 | . And that's because our sensory stimuli at different frequencies for us to create |
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20:12 | unique thoughts paintings writing in our Motor output requires different frequencies slow and |
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20:21 | but these neurons will receive identical They'll have very different output during these |
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20:28 | which are called whole cell or patch recordings. The pipettes can also contain |
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20:33 | . So in this case it contains dye called neurobiology and the bios |
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20:38 | After the experiment you can reconstruct the of these cells that you reported |
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20:44 | You're not using Golgi stain because in stain is 1 to 3% of non |
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20:50 | neurons that are going to pick up stain and reveal the morphology using your |
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20:55 | . And then histology so that you inject dye and sells your reporting from |
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21:01 | reconstruct them more ecologically. So when alcohol was doing cellular reconstructions using camera |
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21:09 | . This microscope with the armed and to reconstruct the neurons. This is |
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21:16 | day done with the neural lucida software with a pretty intensive and engaged human |
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21:25 | of that software. So it cannot be an automated reconstruction of the south |
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21:30 | still a human element involved. And after you do the recording so you |
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21:35 | the electrical activity. You know what cells look like. You know their |
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21:40 | , you know their morphology precisely. see some of the parameter cell and |
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21:45 | action going out. This is actually out to be number seven cell which |
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21:53 | oriented molecular. I don't get Orients layer all the way to look |
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21:59 | the molecular larry because it has these axons that go all the way |
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22:04 | And then finally to convince the reviewers had to cross stain it or the |
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22:10 | marker histology for Samantha status of these are positive for Samantha status. And |
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22:16 | then reviewers said, okay, your is not good enough and that wasn't |
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22:20 | this was not the point of the . This was the point of the |
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22:26 | and these multiple recordings. But people enough like me for years sitting under |
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22:32 | microscope to do these brain slice recordings operation. It takes about an hour |
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22:38 | a half to two hours in the . Then you have to have a |
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22:42 | bit of coffee with the slices recover then you go for it. So |
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22:47 | 10 30 11 and it's like sort growing into a submarine and you may |
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22:54 | somebody distracts you for lunch like around 32 PM. Or maybe you don't |
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23:00 | that the sunset since already six PM you're still poking and stabbing cells under |
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23:06 | microscope. So but the reason why want to do these multiple recordings is |
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23:12 | the reason why you would want to all of these techniques is not just |
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23:16 | say I recorded from this subtype of . I already knew I was targeting |
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23:21 | number seven And parameter all cells. that was nothing new. This was |
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23:27 | in 2000. Mm I want to maybe nine or something like that. |
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23:35 | paper. This is my research But that wasn't the point. I |
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23:41 | there to do all of the immunity the chemistry, electrophysiology reconstruction of cell |
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23:49 | . Just to say God, Cell seven, just like five. Guys |
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23:52 | me already showed the morphology. We answering a different question and we were |
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23:59 | multiple cells at the same time. question was which cells are responsible for |
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24:07 | epileptic seizures? Is it excited to ? Is it inhibitory cells? Which |
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24:15 | of the cell? Is it number or is it number two? |
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24:20 | How is it connected to each How do they talk to each other |
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24:24 | normal environment? How do they talk each other when the brains become a |
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24:31 | optic? Like? Okay, so was the question. So we would |
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24:35 | multiple cells and we have to describe for the reviewers. We have to |
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24:40 | through all of these techniques to prove we recorded from cell number 74 10 |
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24:46 | . It'll sell to prove. But wasn't again just to do that. |
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24:50 | was to show which cells were And we discovered the inhibitory cells would |
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24:57 | more active at first and synchronizing seizures certain types of seizures. And what |
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25:03 | discovered in the slices in the And we took three years to prove |
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25:09 | the reviewers two years later was found humans, similar patterns of activity. |
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25:18 | the fact that in epilepsy and humans cells synchronized first to start the |
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25:27 | So that was really rewarding because that my postdoc work and you always want |
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25:32 | do whatever you're digging around on the or and tested or in a Petri |
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25:37 | eventually want to know that you're contributing you're relating to something that is happening |
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25:43 | humans or that maybe it's going to applicable uh service for cure for for |
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25:53 | some disease that you are interested So these are pretty sophisticated recordings managed |
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26:00 | do multiple at the same time. was my rig, we call it |
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26:05 | in texas rig can be different if in oil, there's oil rigs and |
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26:10 | fishing this fishing rigs and if you're electrophysiology there, electrophysiology rigs and so |
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26:18 | sophisticated. This was George Mason University I did my second postdoc and we |
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26:24 | interested in Apple, etc. And different cell subtypes contribute to initiating seizure |
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26:33 | sometimes we'd run out of equipment. you know this this is a pen |
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26:38 | then using it as a holder because other more expensive holder broke and I |
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26:43 | in the on the role, so speak. So I had to replace |
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26:47 | with just depend and continued the experiments took a picture of that. I |
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26:50 | it was pretty fun. Anyways, concludes our discussion on neurons. You |
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26:57 | a lot to learn about different sometimes neurons, you're going to still learn |
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27:02 | about neurons at the very end of lecture. But right now we're gonna |
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27:06 | into now when we talk about Glee the very beginning of this neurons and |
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27:18 | collection of I had difficult race at very beginning I said that Glia Again |
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27:32 | about 90 of the cell populations in brain and neurons comprised about 10%. |
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27:45 | I said neurons are like chocolate chocolate in the cookie and glee is like |
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27:50 | dough. In reality you cannot have normally functioning brain without having the dough |
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27:56 | the chocolate chips. So, and lot of science because neurons produce action |
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28:04 | and you don't, we have communicated slower waves through calcium. So neurons |
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28:13 | the fast ones, neurons can fire hertz a second, we communicate within |
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28:18 | of milliseconds to seconds. So we two different temporal scales of processing neurons |
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28:27 | uh few hurts a second to hundreds hertz a second and glia two |
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28:34 | Essential. Okay, glia for a time we thought to serve a support |
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28:40 | insulation function and that meant that they not may be looked at as importantly |
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28:50 | neurons and so that is not the . Glia is very actively involved in |
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28:59 | different functions in the brain. From development to control of blood brain barrier |
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29:06 | control the formation of the synopsis to of plasticity and aging. In the |
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29:12 | , we is very intricately involved in . So today we're gonna learn about |
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29:18 | types of glia and we're going to primarily on these types of glia microglia |
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29:26 | of legal Diandra sides. And also is not shown here that is prevalent |
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29:31 | early development is radial glial cells. micro glial cells are the smallest and |
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29:37 | most mobile units in the brain that involved in scavenging and repair following the |
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29:43 | . And also that immuno inflammatory They control the release of cytokines in |
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29:50 | brain. So when you talk about 19, for example, even on |
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29:55 | radio, you turn on NPR people talking about cytokine storms in the middle |
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30:01 | the crisis with covid 19 and cytokines a normal process of evolving inflammation and |
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30:09 | response to that inflammation in the body the brain. However, it is |
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30:14 | , It is off balance. It also be detrimental and causing abnormal pathology |
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30:20 | the brain. Now astra sides are intricately involved in the control of what's |
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30:26 | at the synapses. So they're involved the synapse formation and synaptic genesis. |
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30:31 | involved in neural transmission or communication between and a lot of funds they viewed |
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30:39 | as a third part of the synapse synapse where two neurons are communicating with |
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30:45 | other and astra acidic cells are actually in this communication. There are also |
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30:53 | . The glial cells are involved and the amount of the excitatory glutamate neurotransmitter |
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31:00 | the brain. So they in a control the amount of excitation that is |
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31:06 | for neurons. The amount of excitatory that is available for neurons to communicate |
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31:14 | . They're also having their end feet the capillaries here becoming a part of |
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31:21 | we call the blood brain barrier. we'll discuss that in a few slides |
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31:25 | well. Ah Legal tender sides in central nervous system are responsible for forming |
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31:32 | violent segments and insulation of the Recall that axons are insulated, not |
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31:40 | rights nor are the selma's and the are specifically insulated using illegal dendrites sides |
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31:48 | the C. N. S. you will see that in the |
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31:51 | M. S. It's a different of cell that is called Schwann cell |
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31:56 | at that in the second. Then have a pen dermal cells here that |
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32:00 | separating the spinal ventricular spaces from the spaces here in dependable cells are thought |
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32:07 | be potent, which means that the may become other types of glial cells |
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32:18 | developed into the other cells listed here for a lot of the information that |
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32:28 | discussing. For example, there is supporting lecture materials. And if you |
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32:33 | to that folder there these videos and some of these videos lead you to |
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32:40 | videos with some commercials that are not for But the content of the videos |
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32:46 | I wanted to pay attention to not advertisement for commercial. And what you |
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32:51 | see in this video is this dock represents an injury and all of the |
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32:58 | and processes here are micro glial So the staying here specifically stains microbial |
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33:07 | in their processes. And what is evident here is this is a temporal |
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33:13 | in minutes. This is 10 micrometers space. That's the scales. You're |
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33:18 | at. What is very evident is following the injury, you immediately see |
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33:27 | the processes of the micro glial cells extending themselves physically. Talk about the |
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33:34 | of the injury and that is happening 15 minutes. So, minutes following |
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33:42 | injury. And then at some point actually with this time lapse what you're |
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33:49 | is the soma of these cells that located further away now are migrating in |
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33:58 | the side of the injury. that's where they're going to help with |
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34:03 | inflammatory immune response repair and damage to brain tissue. Okay. And they're |
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34:11 | most mobile elements out of all of cellular subtypes the most mobile, they |
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34:19 | move through brain tissue from the surrounding in this case forward the side of |
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34:25 | injury. And that injury could be physical traumatic brain injury. That injury |
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34:31 | be a rupture of the blood that maybe stroke. That injury could |
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34:38 | infection affecting more of a specific area the brain over the other areas. |
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34:45 | this is the micro glial cells and video shows the micro glial cell function |
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34:54 | well. You can see that within this side of the injury is engulfed |
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35:01 | the micro glial cells that have migrated so much and processes to it. |
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35:08 | this is a during early development you another type of self called radial glial |
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35:16 | . And these radio glial cells are arms. They're like lattices for neurons |
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35:24 | travel along when during early development the circuits are forming in the brain |
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35:33 | assembling itself into different nuclear hippocampus and cortex. There's only a few areas |
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35:40 | the brain. When neurons are That means that that neuron that processes |
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35:47 | information and the back in the occipital and the primary visual cortex. It |
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35:52 | not born there. It was born very specific internal areas of the brain |
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35:59 | we don't really talk about the birth migration or the migration of neurons but |
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36:03 | migrate to their final destinations. So neuron that was born. Sub cortical |
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36:09 | going to migrate into cortex is going migrate into the occipital cortex and it's |
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36:17 | find this location maybe in layer And that is gonna be its final |
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36:22 | destination within the network. So to that migration they will use radio real |
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36:29 | and there's actually a cytoplasmic continuity that and this primordial tissue to clean these |
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36:37 | . One of them which essentially is the other one to climb belong to |
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36:43 | its destination. So this is the that is happening during early development. |
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36:51 | then when I said when you're born happens is that you have everything connected |
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36:55 | everything you have a lot of synopsis then personally you're going through this refinement |
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37:00 | connectivity and development of specific talents and and such. So now this is |
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37:10 | the party going on over here. migration party. Yeah. And this |
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37:19 | what's happening in the in the early brains that one can observe And again |
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37:25 | will find these in your supporting Lecture documents these links to the different |
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37:32 | and I can see that maybe some them are hidden from you right |
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37:37 | So I'll make sure that I will these as an additional resources you can |
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37:41 | for themselves. Some of them will figure legends as well. So I |
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37:47 | activate this for you to view and you will find these in the supporting |
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37:51 | lecture documents. All right so radial cells. Glial are also involved in |
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37:59 | factor release growth slow growth factor released control of that. And astrocytes are |
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38:06 | in blood brain barrier so but no potentials. But rather calcium waves. |
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38:13 | for the mile information in the N. S. You have a |
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38:18 | Denver sites and illegal denver sites in C. N. S. One |
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38:24 | of one arm of the cell will a single myelin segment on the axons |
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38:30 | neurons. That means that a single tender side with its multiple processes can |
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38:37 | multiple segments on different neurons that are the vicinity of this illegal deandra |
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38:44 | Okay so there's a cell to cell that happens. And then once the |
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38:50 | says okay you're a legal tender side we can dance together. Then the |
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38:55 | tender side starts wrapping around that accident the periphery and the periphery. Again |
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39:02 | is peripheral nervous system, everything outside spinal cord, everything in your |
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39:08 | All the nerve endings coming out of brain stem that's outside the CMS proper |
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39:14 | the periphery. You will have my by Schwann cells And in this case |
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39:20 | single Schwann cell is a single axon in my eliminating that peripheral neuron. |
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39:33 | this is a cross section through it astrocytes. Still most of the space |
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39:40 | the brain that is not occupied by and blood vessels. So you can |
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39:44 | how much of a of a massive exercise. No decides if you were |
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39:51 | make a cross section in this case optic nerve fibers that are coming out |
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39:55 | the retina. You will see again my inclination is really compaction of the |
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40:02 | and then wrapping of the smiling around the proper installation of the excellence. |
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40:09 | in between each one of these myelin you have a note of run |
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40:15 | A note of run dear functionally will action potentials and will contain high levels |
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40:21 | what is to come in the next lectures, voltage, gated sodium and |
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40:25 | educated potassium channels to reproduce this action . So the point being is that |
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40:32 | amplitude of the action potential that gets here at the axon initial segment by |
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40:36 | selma. It's the same as when arrives at the each note of run |
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40:42 | and as it reaches its final terminal final destination. So very important for |
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40:52 | communication. Right? What happens if lose insulation around wires? It's called |
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40:59 | circuit things start burning up and light start burning up and stuff like |
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41:05 | Right? So now inst installation is important for precise current conduction and which |
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41:16 | precise communication between cells or between cells muscles. So this slide actually talks |
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41:27 | some of the diseases that we started as they relate to Myelin specifically here |
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41:35 | the condition that is known as D Nation. So, for this myelin |
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41:40 | form there's a number of proteins myelin proteins that are involved in this process |
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41:46 | the myelin compaction and the proper formation take place. There's about seven related |
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41:57 | . Examples of such proteins is like associated glycoprotein, which is important for |
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42:04 | to cell recognition and initiation of myelin . That means that there are other |
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42:09 | that will be involved in compaction and of how much of it gets |
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42:15 | So it's a complex network of proteins is involved in regulating the normal Violin |
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42:23 | and compaction of Myelin around the Uh this is an example where you |
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42:31 | full mile Island nation here And in case this is an animal model of |
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42:39 | we call a shiver mutant in this model is created via genetic mutation particular |
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42:48 | 18. That leads to the myelin and that leads to shivering to traumas |
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42:57 | convulsions and the reason why we're talking this animal model here is this animal |
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43:04 | is a model of multiple sclerosis. , this is another neurological disorder. |
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43:10 | you can add on to your list disorders. We've already discussed Alzheimer's |
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43:17 | We also discussed fragile X syndrome under spectrum disorders. Okay, today we're |
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43:26 | talk about multiple sclerosis. And I in this course, will remind you |
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43:34 | about this disease, what it conjures in your mind, you when you |
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43:39 | about multiple sclerosis, are you thinking young developing Children, adults, middle |
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43:46 | adults or aging population and multiple sclerosis is typically in the 30s. So |
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43:55 | a it's an adult. It's a adult disease. Typically with the onset |
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44:00 | the 30s, it is not to that there's no early onset Alzheimer's which |
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44:05 | before 55 and before 15. So not to say that there's no early |
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44:11 | of of multiple sclerosis. But for most part you will see the symptomology |
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44:17 | and the diagnosis of this disease In 30s systems. It's very different from |
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44:23 | acts. It's very different from Alzheimer's as far as the onset the time |
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44:28 | onset, typical onset of this It's an auto immune disorder. And |
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44:36 | have to have in one of the in the genes. You have to |
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44:41 | two bad aliens in chromosome 18. it's recessive. It's autoimmune. Which |
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44:49 | that it is killing its own It is dim eliminating because it is |
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44:59 | myelin, this is in the central system. Multiple sclerosis is in the |
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45:04 | . N. S. We will about a disorder and PMS called shark |
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45:08 | marry tubes. This is in N. S. Illegal Denver sites |
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45:15 | what is happening in multiple sclerosis and is also similar to tremors. You |
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45:27 | tremors and you have spasticity and muscle and sometimes convulsions and multiple sclerosis because |
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45:36 | illegal underside myelin is being recognized as foreign invader and immune response is to |
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45:46 | the myelin causing the auto de Myelin . Right. Uh This shows a |
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45:55 | pectin normal genes. So this is gene trance faction of gene therapy if |
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46:00 | may where you can recover partially some that myelin that is lost due to |
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46:06 | genetic mutation. And so when we animal models, typically we want animal |
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46:13 | to be really good models of what's in humans. There's a lot of |
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46:18 | we cannot test in humans ethically, we can try to understand in animals |
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46:24 | testing animals. And so animal you want to have the same mutations |
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46:30 | humans would have in the same You want to have the same symptomology |
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46:39 | or spasms and multiple sclerosis. And then it becomes a good |
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46:45 | And then you can start testing therapies it's a gene therapy or chemical therapy |
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46:51 | some sort. And seeing if first all an animal, if it improves |
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46:55 | condition and hopefully taking into clinical trials see if it improves in humans. |
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47:01 | there was a question in the back me. So like that's a great |
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47:10 | . I mean, so one thing I haven't mentioned it at the very |
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47:14 | of this slide is that there's multiple that the imagination can happen. And |
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47:20 | way is that you can cause with infection and super myelitis and through information |
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47:28 | can lead to do my elimination. some of the infections in the brain |
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47:34 | syphilitic infections that are severe and cannot controlled. For example, they could |
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47:40 | to the Myelin Nation. And in infections for example there are ticks that |
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47:49 | as a colitis. And in certain certain countries in certain areas during breeding |
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47:56 | , it can be really dangerous actually hospitalization of quite a few people with |
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48:01 | . And it just depends what the is, the individual's immune response, |
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48:06 | far the infection, the load of virus and so on. So uh |
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48:13 | . Um if you have neural degeneration have everything you have d my elimination |
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48:22 | neuro degeneration. But this is unique the sense that it is autoimmune. |
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48:27 | there's multiple ways that this demolish nation a term But not multiple sclerosis is |
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48:36 | the genetic component is inherited and I there's both sporadic and inherited and this |
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48:52 | not only location for this mutation in 18, there's other mutations that are |
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48:57 | with MS2. This is just an of it. Um Or so I |
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49:20 | confess I have really poor hearing. have partial hearing loss and in one |
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49:26 | my ears. So I didn't hear first part and that's why I asked |
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49:31 | to repeat. I'm not being alright, walk up closer. I |
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49:35 | want to intimidate you but I just hear very well. So I |
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49:39 | The first thing is my elimination, constant process is the renewal of my |
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49:48 | nations. A great uh question there outgrowth of new axons. But that |
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49:58 | mostly during the development. That there's just maintenance of that myelin in the |
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50:05 | . Oh okay. Let me move to the next of these. Which |
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50:12 | shocked about married to. And in case and when we talk about these |
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50:18 | basic proteins, it's not that it's lack of protein. Therefore there's a |
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50:22 | of myelin. This is an example there's too much of peripheral Myelin |
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50:28 | Otherwise known as PM 22. There's duplication of chromosome 17 producing too much |
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50:36 | this program which also leads an abnormal Nation. Now when we talk about |
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50:42 | attack, marry tooth disease, the and the outward expression of the disease |
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50:51 | quite noticeable. The person that has severe Charcot Marie tooth disease. They |
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51:00 | their legs that are deformed and typically outwards and they're walking is not gonna |
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51:10 | as much of a forward motion but sideways motion is difficulty in controlling your |
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|
51:17 | and balance as you're walking. This in early development in Children. If |
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51:25 | have this mutation they will have D Nation and the peripheral nerves and D |
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|
51:33 | elimination loss of Myelin around the peripheral . What happens if you cannot send |
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51:38 | signals, you cannot activate the If you cannot activate the muscles, |
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|
51:44 | body is you're developing and forming your are growing and your muscles are |
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|
51:49 | But if your muscles are not activated by the nerves, they will not |
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|
51:54 | the bones and the side of the skeleton, not the side of |
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|
52:00 | the skeleton. The bones properly. the only way to try to fix |
|
|
52:07 | is uh well we're not actually talking therapies right now. But the only |
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|
52:12 | for multiple sclerosis or for alzheimer's. haven't talked about therapist. This is |
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|
52:17 | non chemical therapy. You can put person in braces and if you do |
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52:21 | early enough and this is specifically really the lower limbs. If you can |
|
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52:28 | a person in the braces and lower and adjust those braces during early development |
|
|
52:33 | may preserve more of the proper symmetrical structure and allow them to have more |
|
|
52:39 | the forward motion. So that's uh Marie tooth disease. And so |
|
|
52:46 | S. You're talking about effects at central nervous system. So all the |
|
|
52:53 | undersides and here you are talking about nervous system. So she wants. |
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53:02 | . I think I just did you this is due to the violation? |
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53:08 | . Yes. It's too much of protein. But like I said, |
|
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53:12 | doesn't mean too much. It's too of myelin. Too little. Too |
|
|
53:15 | myelin the protein levels. The ratios the interactions are more complex than |
|
|
53:21 | In this particular case it's actually overproduction the protein that leads to this |
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|
53:29 | Okay, so here's the cast of of the glial sauce that we've reviewed |
|
|
53:35 | far. Let's talk about the blood barrier for a little bit here. |
|
|
53:43 | as the sides we talked about blood barrier when we started discussing the COVID-19 |
|
|
53:51 | and we said the blood brain barrier the themselves and have tight junctions. |
|
|
53:59 | things kind of pass through these junctions type parasites surrounding them and then you |
|
|
54:04 | the astro glial processes. So the site empty is the other checkpoint here |
|
|
54:10 | the molecules to pass from the blood the brain. So we have this |
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|
54:16 | here. So small molecules fat soluble because they can cross the plasma membranes |
|
|
54:23 | can pass through molecules that have their and facilitated scope transporters molecules have combined |
|
|
54:31 | certain receptors and chemicals they are going be able to find their way into |
|
|
54:37 | brain. We talked about if you lose blood brain barrier that happens if |
|
|
54:46 | have significant even infection with covid you have inflammation, you have infection |
|
|
54:52 | epithelial cells in the blood. That the blood brain barrier gets loose. |
|
|
54:58 | also talk about how hypoxia a lack oxygen and also contribute to this abnormal |
|
|
55:04 | brain barrier leakage and so the blood barrier lose blood brain barrier becomes leaky |
|
|
55:11 | and allows for things to be more be transferred from the block into the |
|
|
55:20 | . It's a good thing that we blood brain barrier because you know, |
|
|
55:24 | have things that go into the not all of them will go into |
|
|
55:27 | brain, even infections and things like , you know, chemicals or even |
|
|
55:33 | you consume something is food and a of that chemical could be harmful in |
|
|
55:38 | brain, but it will be staying the body not crossing over maybe. |
|
|
55:43 | it's also a challenge. It's also you're thinking about Uh drugs, so |
|
|
55:50 | challenge you in this course to start about things that you will be doing |
|
|
55:54 | the next 20 or 30 years. , how do people take typical neuron |
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|
56:01 | for depression and anxiety or epilepsy or ? They swallow a pill? There's |
|
|
56:09 | like you don't open the box in brain, put it on clothes, |
|
|
56:12 | know, different boxes for different parts pretty neat, you know? But |
|
|
56:16 | you swallow a pill and then what to that pill? It goes into |
|
|
56:21 | esophagus drops into your stomach ph 3.3 , starts digesting, it goes into |
|
|
56:32 | gut micro villa starts absorbing it goes the secondary liver metabolism, all of |
|
|
56:40 | things happening later. Right? When take a typical uh painkiller like |
|
|
56:48 | ibuprofen or acetaminophen, Do you expect your headache or minor pain to go |
|
|
56:54 | within seconds or you know, it's , 20 minutes. So that drug |
|
|
56:58 | to go in, go through this , get into the blood and |
|
|
57:02 | you know, pain is here obviously going to be affecting in the |
|
|
57:07 | Now if you want the neuro drug drug from the blood has to cross |
|
|
57:10 | the into the brain and it becomes challenge. And so you will hear |
|
|
57:16 | Tv for example or any pharmaceutical drug if you see them for example for |
|
|
57:22 | or depression, like well if you this drug, you know, be |
|
|
57:26 | of the side effects which is constipation or pain swelling and rashes on |
|
|
57:35 | stomach. And and that is because a fraction of that drug that you |
|
|
57:40 | will get into the brain. But there's common targets between the brain and |
|
|
57:45 | body. So if you're trying to something in the brain, it's better |
|
|
57:49 | very specific that crosses the blood brain and a very efficient fashion but also |
|
|
57:56 | something that specifically in the brain. , the less specific molecules are targeting |
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|
58:00 | brain, you're getting into the the more of the systematic or general |
|
|
58:05 | effects that drug may cause in the . So that's not the best way |
|
|
58:11 | get drugs into the swallowing. We about the virus can find its way |
|
|
58:16 | the nasal passages. The silken drugs small molecules. So there are some |
|
|
58:23 | sprays and there aren't even nasal sprays seizure but they're not very popular because |
|
|
58:28 | creatures of habit and comfort. Another way to get things in the blood |
|
|
58:35 | through suppositories, anal vaginal suppositories, we're creatures of habit and that's, |
|
|
58:42 | know, takes a lot more effort do that. But that goes directly |
|
|
58:46 | the blood, bypasses liver metabolism, the digestion. What else? Inhaling |
|
|
58:54 | in your lungs, it goes into lungs, goes into the blood, |
|
|
58:57 | doesn't get digested. So the time takes for the drug to take |
|
|
59:03 | If you're swallowing something, you're looking minutes, 10 minutes, sometimes an |
|
|
59:08 | if you're inhaling or suppository, you're at much faster time where the drug |
|
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59:15 | take effect. But in the end a fraction of what you swallow will |
|
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59:20 | into the brain. And this is you will hear so many associated side |
|
|
59:24 | with the brain medications and vice versa of the shared targets. You're taking |
|
|
59:30 | in the periphery to, you help your pancreas and there's a depression |
|
|
59:36 | is developing because there's similar signaling molecules receptors that are involved in in |
|
|
59:43 | in this whole system that's called the and the brain. Okay, so |
|
|
59:50 | future is yours in developing really precise specific drugs to treat neurological conditions. |
|
|
60:00 | in mind the blood brain barrier and in mind all of these unique formats |
|
|
60:07 | medications but which maybe it can be more effectively and maybe it can become |
|
|
60:14 | comfortable that we can have a different of delivery of these medications to be |
|
|
60:22 | . Okay, so this concludes our and glia. And we are moving |
|
|
60:28 | our next lecture which is 45. some of these slides at the beginning |
|
|
60:34 | over a lot because typically do a bit of the review. But we |
|
|
60:39 | finished this material and I'm a little behind like half an hour in this |
|
|
60:44 | or so. So I'm gonna try make it catch up the time. |
|
|
60:51 | we're gonna study neuronal number and addressed member and potential and the action |
|
|
61:01 | And you understand everything and more than wanted to understand about action potentials. |
|
|
61:06 | you understand how there's a different way understanding action potentials also. But in |
|
|
61:12 | all the action in neurons is at level of the plasma membrane, plasma |
|
|
61:18 | has an equal distribution of charge and the outside is possibly charged on the |
|
|
61:24 | of the membrane, it's negatively you want to call the outside environmental |
|
|
61:29 | zero neutral, no charge and miller or bowls and to sink an electric |
|
|
61:35 | the zero into the cell. Your meter which show immediately a drop of |
|
|
61:41 | minus 65 million. So with respect the outside the inside membrane of these |
|
|
61:47 | is negatively charged because of the accumulation of charge that will be discussing in |
|
|
61:55 | next and unequal distribution of charges will discussing in the next couple of |
|
|
62:01 | So, as we discussed, this action potentials were recorded in 1939 and |
|
|
62:06 | , there were very fast 1 to milliseconds and we needed to develop fast |
|
|
62:11 | in order to pick up that activity display that activity on the fastest |
|
|
62:16 | A lot of the action potential recording the circuit development came together with some |
|
|
62:21 | the U. S. Military and Navy uh developments that were taking |
|
|
62:26 | In fact in electrophysiology lab where I you all of this electrodes going in |
|
|
62:31 | and in the slice we use B C. Cable student to connect the |
|
|
62:38 | and different pieces of equipment and B C case. This is not on |
|
|
62:43 | test. It stands for british Navy Navy cable that was adopted between the |
|
|
62:49 | , the americans and the brits. was developed further during World War two |
|
|
62:56 | even more sophisticated circus that we could use in the lab. Okay, |
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|
63:00 | action potentials are very fast, 1 2 milliseconds. That's what we needed |
|
|
63:04 | very fast circuits. And today before talk about resting membrane potential and before |
|
|
63:10 | talk about other things, we're going very briefly. Not so briefly, |
|
|
63:15 | we'll try to understand the circuit which the reflex arch, simple reflex or |
|
|
63:22 | the simplest kind of reflex pathway. also referred to as major stretch or |
|
|
63:29 | tendon reflex. And it's really simple understand. But this is good information |
|
|
63:34 | I'm going to ask you to know the test. So if you understand |
|
|
63:38 | signaling here, you can understand how cell subtypes will contribute to growth and |
|
|
63:48 | in this particular circuit. So if going to doctor's office and uh like |
|
|
63:54 | yearly checkup or if you're having some in the lag or if you have |
|
|
63:59 | neurological condition quite often the doctor may your knee. Okay this patella tendon |
|
|
64:07 | so they sit you down just like person and they tap it with a |
|
|
64:11 | mallets. And if you have good tendon stretch reflex, your leg will |
|
|
64:19 | up after the tap. So this a stimulus and this is the response |
|
|
64:23 | the stimulus and the input is this mallet. And then we have the |
|
|
64:29 | nerve endings that are in the muscle are in the in the joints and |
|
|
64:34 | . And they will feel this mallet the on the attendant. And through |
|
|
64:42 | muscle spindle will take up that information the dorsal root ganglion cells. So |
|
|
64:49 | . R. G. Songs, dorsal root ganglion cells are pseudo unit |
|
|
64:56 | salts, morphological E dorsal root ganglion will release excited glutamate and dorsal root |
|
|
65:06 | cells will have their selma's located outside spinal cord proper forming this bundle or |
|
|
65:13 | ganglia of the selma's of the dorsal cells. So here you have the |
|
|
65:18 | axon carries that information. This is integrated unit as the selma which is |
|
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65:24 | outside the spinal cord and then it a central axis that will innovate through |
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65:29 | dorsal side of the spinal cord, back of the spinal cord into the |
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65:34 | cord and it can contact a motor . Okay, so modern Iran and |
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65:44 | exciting modern neuron, this dorsal root cell by exciting modern neuron, which |
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65:51 | a multipolar cell morphological e motor neurons acetylcholine and motor neurons will project that |
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66:02 | onto the muscle, releasing acetylcholine and the contraction of the muscle. So |
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66:09 | sensory cells are a parent. They're information from the periphery into the spinal |
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66:19 | proper and the modern neurons are They're going from the central nervous system |
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66:31 | cord proper into the periphery. So kind of activation is reported as Mona's |
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66:38 | and it's this most simple kind of . Now this reflex means that if |
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66:45 | sensory neuron is activated and it excites motor neuron, this motor neuron will |
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66:50 | the muscle and cause the contraction of quadriceps of the extensive muscle. So |
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66:56 | muscle can contract with once and as activated monos in africa activation. But |
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67:03 | do we know about muscle function If are contracting biceps? What's happening to |
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67:09 | triceps? It's relaxing If you're contracting triceps, what's happening to your biceps |
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67:15 | relaxing. So for this reflex and the leg kick to be a proper |
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67:23 | . What you need is you need make sure that this muscle is relaxed |
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67:28 | this is your opposing muscle, hamstring . A flexor muscle is opposing to |
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67:33 | extensive muscle. In this case that dorsal root neuron is going to have |
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67:42 | not only on the mona motor neuron also on this black cell which is |
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67:49 | inhibitory into neurons inhibitor into neurons which also multiple ourselves. And these neurons |
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68:00 | release glycerine which is inhibitory neurotransmitter. this is the exception that we talked |
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68:07 | . The major inhibitory neurotransmitter in the as gaba. Except for the spinal |
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68:13 | where the major inhibitory neurotransmitter in these neurons, local network inhibitory cells here |
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68:22 | gliding. So if the sensor neuron excited it's going to excite motor neuron |
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68:28 | going to excite muscle cause the contraction dorsal root ganglion cells, excited is |
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68:36 | to excite the inhibitory neuron which is to inhibit the modern neuron and assure |
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68:45 | this hamstring is relaxed and the proper tendon stretch reflex and kick can take |
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68:54 | . So for the task you'll actually responsible for dorsal root ganglion cells with |
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69:00 | sido, una polar polar multipolar motor and interneuron. The neurotransmitters that they |
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69:07 | and the best thing that you can is mark around the circuit and try |
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69:12 | draw the circuit on your own without at the notes and then you will |
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69:16 | really well prepared to answer all of questions. In reality you can have |
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69:22 | of synaptic reflex and contraction of this but it has to involve multiple synopsis |
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69:30 | Synaptic to be fully functional and fully to this stimulation here in the form |
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69:36 | the maori and in the body we other reflexive behaviors. So also when |
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69:42 | say reflexive behavior, this is a which you cannot control, meaning that |
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69:47 | you sat there with your leg like and the doctor and the mallet and |
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69:54 | said I'm not going to move the , I'm not gonna let the leg |
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69:57 | , I'm not gonna let there's no power over reflex. It's going to |
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70:04 | right? You may be able to it while it initiated and started happening |
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70:09 | you're not gonna be able to stop initiation of that. It also means |
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70:15 | if something is reflexive it doesn't mean it's not conscious to proceed. We |
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70:20 | to have fast action potentials. We to have this reflexive behavior because if |
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70:25 | step on the nail, the last you want to do is contemplate about |
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70:28 | doesn't hurt. No, not that . Not that part of the foot |
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70:32 | would really hurt. So when you about it. But if you immediately |
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70:37 | withdraw your foot from that bad stimulus that pain, what do you |
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70:43 | You're consciously aware. So these signals ascend up the spinal cord through the |
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70:50 | pathways and to the higher surface of brain and will inform you that this |
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70:56 | what happened. The reflex and then have conscious perception of that and then |
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71:00 | will happen then will happen response that no longer reflects it. And the |
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71:06 | is going to be pretty complicated. going to initiate a complex motor pattern |
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71:11 | bending over to make sure that the that your foot is not damaged by |
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71:17 | nail. You're gonna put a band , you're gonna call the doctor's office |
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71:22 | make sure that there's no infection or so that's not reflective. But this |
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71:27 | will be happening reflexively. Most of reflexes we have in the body of |
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71:32 | . So an example of a complex synaptic reflex is the gag reflex when |
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71:39 | you are when you're nauseous when that is created by either emotional or chemical |
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71:48 | . That's a complex reflexes involved multiple in the brain and multiple centers in |
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71:54 | brain to have that response over Is that the? Yes, |
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72:15 | Inter neurons are interacted with with with nerves, two glasses. So actually |
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72:22 | gonna end here today and when we back, we're going to delve into |
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72:26 | nice membrane biophysics selectivity of the No ernst equation baldwin equations, |
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72:35 | So you may want to remind yourself some of this good biophysics stuff but |
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72:40 | than that, have a good rest the week and I will see you |
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72:45 | on monday. See you all on so that you can be ready for |
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72:51 | |
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