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00:00 | So welcome back. This is lecture off neuroscience and we will be wrapping |
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00:09 | talking about neural transmission and hopefully beginning talk about, um, central nervous |
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00:19 | , different parts and functions of the . Still admitting a couple of people |
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00:24 | in late. Now, if you , we talked about different systems and |
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00:29 | pointed out that the interesting thing about I'm allergic systems and me and societal |
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00:36 | histamine, dopamine and acetylcholine norepinephrine, is that they're expressing these very specific |
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00:44 | along the brain stem and the days forebrain and that their projections and go |
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00:50 | the neocortex, the cortical matter, cortex into the columnists and the cerebellum |
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00:56 | well so. This is in contrast the and the cannabinoids that have produced |
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01:02 | and the South there produced on And there is a couple of |
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01:06 | How can it be deep polarization? suppression of inhibition If you're suppressing excited |
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01:11 | signaling so within the cannabinoids will discuss they regulate both but the inhibitory |
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01:17 | If it is a gap allergic synapse will inhibit release of in condition, |
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01:22 | too much inhibition. They will control . There will reduce inhibition. If |
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01:27 | exciting ter synapse and it's too much . They will control excitation. |
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01:34 | in a way, being one of systems and this negative feedback fashion retrograde |
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01:39 | from post synaptic cells where they're produced pre synaptic Lee, where their respective |
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01:44 | receptors are this retrograde fashion and controlling synaptic transmission both excited Torrey and Gob |
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01:51 | synopsis and inhibitory excited her in the the glutamate ergic synopsis and military activity |
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02:01 | the Gabba Logic synapses for glutamate It's that you really believe the whole glutamate |
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02:08 | the cycling of glutamate we distinguish between I am a tropic kinds of glutamate |
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02:14 | sampa NMDA and kind of glutamate Um, we talked about the fact |
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02:22 | the early phase of the E P P is due to the ample receptors |
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02:26 | upon the release of glutamate binding of to the emperor receptors opened immediately. |
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02:32 | in order for the late phase of E p s p to be contributed |
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02:38 | these NMDA receptors, plasma numbering is deep polarized and so magnesium block will |
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02:44 | . The cell will leave the channel channel. Now you can have the |
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02:49 | off positive. Current and re polarization happen through the flux of potassium |
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02:56 | the flux of potassium through both emperor NMDA receptors. So we talked about |
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03:03 | M D A receptors as, having called being called coincident detectors because |
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03:10 | , coincidentally detecting the glutamate release and made binding and lice into a factor |
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03:17 | as well as deep polarization, which pasta? Not so. It's confidentially |
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03:21 | the pre synaptic activity on the posson activity. Where's the Amper or non |
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03:27 | ? Ample kinda channels Glutamate binding. sufficient to open these channels. Interesting |
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03:32 | of potential and with an M A receptor magnesium will leave when |
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03:39 | when when the number of potential D magnesium block will be alleviated. There's |
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03:45 | to be flux of ions through an D. A channel, and it |
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03:49 | , ah, higher conduct its channel Amper channels or not an MBA Ampang |
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03:55 | near channels. Uh, these, , Tampa and an M D A |
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04:00 | will also have their respective blockers are . Tampa Kaine. It will be |
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04:06 | by sea and Q X chemical called and Q X and NMDA receptors are |
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04:12 | by chemical called a PV. Uh . When we talk about the |
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04:17 | these air, the fast glutamate Iona channels are the ample channels As soon |
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04:24 | glutamate binds open and responsible for the phase of the PSP and an M |
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04:29 | . A channels are responsible for the phase of the E P S |
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04:33 | and they are slow, and they're because deep polarization needs to happen in |
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04:40 | for these channels to open. um, we talked about a binding |
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04:47 | for a PCP and M Kato one PCP. It's ah list of drug |
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04:53 | the streets on and is referred to angel dust a lot of times. |
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05:00 | one thing is that some of these that are out there are so potent |
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05:06 | so powerful that they can, permanently of the brain function. And so |
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05:14 | is known thio induced hallucinations. It induce acute schizophrenia where somebody essentially goes |
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05:22 | a psychotic state of mind and doesn't for weeks and potentially go into a |
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05:27 | state of schizophrenia from just a single of some of these substances. |
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05:35 | J. Lo one is a very substance that binds only open and then |
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05:42 | air receptors on again. That's for to start thinking about. Why only |
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05:48 | ? Because the configuration the three dimensional of the channel, has changed. |
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05:54 | confirmation of the channel has changed, now open channels can be bound by |
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05:58 | substances. Is supposed thio channels that closed because they opened up this new |
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06:05 | acid binding sites on the protein the number tropic glutamate receptor site differently |
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06:12 | non mdn NMDA receptors, the actor protein complexes and M D A. |
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06:19 | . If you were to recorded minus million balls, Interesting member and potential |
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06:24 | the presence of glutamate would be almost present. Minus study. You will |
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06:30 | opening of an M D A Channels M D A. Current through an |
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06:34 | D channels will reverse zero million volts will flow in the opposite direction when |
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06:39 | cells are de polarized and in this , held at the positive holding paternal |
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06:46 | eso in the presence of regular which is 1.2 million Mueller. On |
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06:51 | outside of the cells, you have blockade of an M D channels and |
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06:56 | the presence off glutamate and magnesium release glutamate. But magnesium blockade thes channels |
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07:03 | not open. But in the experiment the right, you're recording the same |
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07:08 | through an M d receptor. But really is glutamate and you remove extra |
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07:13 | magnesium so there is no magnetism and cellular solution. There's no magnesium |
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07:18 | and in that case you demonstrate that can open an MBA channels and there |
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07:23 | be conducting a lot of current interesting close to resting member of potential proving |
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07:29 | point that magnesium is was blocking the on this on the leftist. Proving |
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07:35 | point that deep polarization is what helps the channel. I eat removed the |
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07:41 | block. Okay, so these air experimental conditions on the left this regular |
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07:47 | concentration extra cellular, 1.2 million Mueller the presence of glued in a There |
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07:52 | not much current that these potential student receptor in the same experiment you have |
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07:58 | , but now you remove Eszter Salamon . And now you have the current |
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08:03 | on opening of this and then be receptor channel. So if we recall |
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08:10 | the first block, we discussed ivy and these air the current voltage |
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08:16 | And we said that the amount of depends on their on the change in |
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08:22 | voltage. So in this case, looking at to currents here. |
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08:30 | we're looking at a compound GPS speed . Mhm. But we're looking at |
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08:37 | recordings. One of these recordings of 80 million volt holding potential. Your |
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08:43 | clamp is holding the cell of minus million bowls from the second situation. |
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08:48 | cell membrane potential is held at minus million volts de polarizes cell. And |
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08:54 | the third here on the top. cell is how the positive 20 million |
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09:01 | . You're taking two measurements. During experiment, you're releasing glutamate, and |
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09:07 | taking two measurements. Glutamate release are to re stimulation. Corresponds to |
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09:14 | uh, lying right here. Come here. This is this is |
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09:21 | Or maybe or good image stimulation or made application. And you're taking two |
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09:27 | . You're taking the early measurement. this is this dash line. The |
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09:33 | dash line on the left is the measurement. And then this is a |
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09:39 | scale of 50 milliseconds and some 20 Later. 20 milliseconds later, you're |
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09:46 | a second measurement. Each of these measurement points you're measuring the strength of |
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09:53 | current at three different holding potentials minus minus 40 plus 20. So when |
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10:01 | trace what is happening, Thio the measurement at the first dashed line here |
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10:09 | the left, you record straight You get a linear ivy blonde in |
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10:20 | linear TV plod corresponds to the early of the E p s b, |
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10:26 | corresponds Thio the Ampara. Sabra. this graph has two plots the linear |
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10:34 | that is shown in black. And you have these, uh, |
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10:42 | here. These triangles represent current measurements the on the Y access and the |
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10:50 | access is your voltage s o minus million volts minus 18 million balls. |
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10:57 | had a current of about minus 200 amp airs. True, at minus |
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11:06 | million volts, you had a current about 100 negative people out. There's |
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11:12 | 25. You had about negative 50 empire. So this early component shows |
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11:19 | is a linear ivy plot. So shows that the Ampara receptor channel has |
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11:27 | linear ivy plot. Things get a bit more complicated when we look at |
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11:34 | second line here which measures the lead in the current. The amount of |
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11:42 | that is present at the late component what it measures is now in |
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11:48 | In particular. We're looking at the circles where minus 100 million volts and |
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11:55 | 80 million volts. You don't see current If you look at the late |
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12:01 | , there is not no current There's recover at monos 80. You |
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12:06 | get the fast excited Torrey Potential that's by an m d by Ampara But |
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12:13 | don't have any measurement. Here is zero million valves recurrent nearly zero p |
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12:19 | in Paris. When you dip rise the cell and you dip Polarize |
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12:24 | Positive 40 Where this circle is Now seeing a significant late current that you're |
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12:31 | here. This slave current is shown blue so anything that you see in |
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12:38 | is the late current on that late and blue corresponds to NMDA receptor and |
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12:45 | shows that it opens it about minus minus 40. It's conducting P come |
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12:53 | , it reverses. It starts starts decreasing so you d polarize the |
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13:00 | minus 20 it starts decreasing and notice the circles and the triangles both reverses |
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13:08 | millennials. So this is the reversal for both Ampara NMD air separate channels |
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13:17 | then, as you increase the potential positive 25 million volts. Now you |
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13:23 | a significantly the current shown here because now you're tracing the second line to |
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13:31 | this current, and it shows that the d polarized potentials positive 40 2050 |
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13:39 | volts an MBA receptors are preferring to in the opposite direction. So physiological |
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13:47 | for an MBA function, of are in the negative ranges. But |
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13:53 | illustrates that you have a reversal for empire and an MBA. Zero mil |
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13:59 | that the early component, measured through first dash line, represents Ampara, |
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14:05 | it's a linear I V plot that second late component measured by the second |
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14:12 | line, is nonlinear here, and shows a reversal of zero. It's |
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14:17 | linear and represents an M d a . It's non linear because until you |
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14:22 | deep polarization, you have magnesium So you have nearly zero people hunters |
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14:28 | current being conducted here, and then current increases as you alleviate the magnesium |
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14:34 | and then there's no magnesium and conducts lot. Finally, we have, |
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14:41 | , open triangles and we have open . So and the in the in |
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14:49 | in the in the situation where we're looking at the neuro pharmacological manipulation as |
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14:57 | mentioned that each one of these receptors m d A and ample receptors will |
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15:02 | their own respective blockers. So a is a blocker for an M B |
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15:10 | . So in this situation, you're not just measuring the early and live |
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15:16 | . Now think about how much you now, using a voltage climb your |
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15:22 | the potential and different holding potentials. are applying glutamate or you're stimulating |
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15:29 | No matter. GIC fibers, you're the early components the current some five |
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15:38 | following stimulation and the component 25 milliseconds stimulation approximately. No, you understand |
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15:48 | the early component is the linear I plot was just ample channel. That |
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15:52 | component is nonlinear and envy. A . Now you're using nerve pharmacology. |
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15:58 | applying a PV which is an M a receptor blocker. So this blue |
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16:04 | , which represents an M. D current. I think it's blocked by |
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16:09 | PV. So this line, the line here and gets reduced to the |
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16:14 | line and the bottom line gets Thio no current here and this is |
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16:19 | these open circles indicate. So in presence of a PC in the presence |
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16:25 | V. P V. If you this late and m d component you |
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16:29 | really see, it maintains itself close zero line. It doesn't mean that |
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16:35 | linear ivy plot. It just simply that it is close Thio zero that |
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16:41 | no current is flowing through an D. A. With south |
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16:45 | There's virtually no leave current that's being in the presence of NMDA receptor |
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16:52 | And if you want to prove how specific is this blocker to an |
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16:57 | . D a receptor? How specific this blocker Teoh to the late |
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17:04 | Then you do the measurements in the component in the presence of a PV |
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17:12 | , and in this case you have triangles. What you have is that |
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17:19 | triangles still show you a linear plot you still measure significant amount of karm |
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17:26 | the early component. So this proves a PC does not affect emperor receptors |
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17:33 | does not affect the early component off E. P s p A PV |
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17:38 | is a blocker. A PV instead a blocker of NMDA receptors and by |
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17:48 | virtue blocks the late an m d current. So again, Alfa is |
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17:56 | , and M d A is not PV receptor blocks. The late component |
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18:00 | not affect the early component. This really good. Exam crashes to so |
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18:09 | gated channels you have We're gonna talk calcium from Tajani or development of these |
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18:18 | and cellular location. So first of , what's interesting is we talked about |
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18:23 | channel. So we said that ampoule , unlike an M D A. |
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18:29 | therefore amenable to sodium and potassium, they're not always permeable to calcium. |
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18:34 | there are ample channels. There in fact, promotable to calcium |
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18:40 | Okay, And that all depends. go back to the building blocks off |
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18:45 | amino acids and amino acid sequences. , the primary, the secondary, |
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18:52 | treasury sequences. And this is quite that if you look at this membrane |
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19:00 | two sub unit in the calcium what you see is that in one |
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19:08 | , if you have glutamine in the of amino acids, if you have |
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19:15 | , which is a cube in the , then that Ampara receptor general can |
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19:23 | the passage of calcium if you have . But if you have an edited |
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19:31 | of that Ampara receptor, and you both versions basically that get expressed naturally |
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19:38 | that immersion you have Argentine in a amino acids. Substitution all of a |
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19:46 | makes this entire protein structure impermeable to . So if you go to the |
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19:55 | days of this course and the history we discuss Roderick MacKinnon trying to understand |
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20:02 | one of these sequences is important now have to think about which one of |
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20:10 | Amina acid building blocks is important. , it's It's a break. You |
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20:21 | one brick to the other, then of a sudden you're doors. Don't |
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20:26 | for your doors only let in certain that's again very, very powerful. |
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20:33 | if you have home ology now, sequences and you can identify the sequences |
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20:38 | individual I mean our assets and substitution delusion of individual. I mean our |
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20:44 | . Somehow, by manipulating the and you can achieve quite significant |
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20:53 | just geological changes of the level of channel. Um, so this is |
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21:01 | experiment where you have a Q where have glutamine and you're recording sodium current |
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21:10 | ample channel you're applying. L glued name l glutamate eso You're stimulating essentially |
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21:18 | glutamate channel, and you are recording current, and you're also recording calcium |
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21:24 | through that channel, and you have second version, the edited version of |
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21:30 | channel. Now you replace this glutamine with Argentine are and you stimulated with |
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21:40 | . And you, of course, record sodium currents. The channel is |
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21:44 | permissible to sodium, but all of sudden no, the child was no |
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21:50 | preventable. Thio Calcium, single amino substitution or editing of a single amino |
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21:59 | can be quite profound, because calcium again may not be contributing as |
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22:05 | Here to the member in potential change ah, as opposed to the influx |
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22:11 | calcium is very, very important. cellular downstream mechanism, secondary cellular secondary |
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22:21 | mechanisms and such who Tajani um in structures and quite a few brain structures |
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22:31 | early developments that we're already starting to now about brain structures and early |
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22:38 | The synapses at First Express only an D a. Receptors. Very, |
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22:44 | interesting. So then you would say if they express an M D |
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22:50 | And what happens if gloomy? Maybe released. Well, those synapses air |
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22:56 | silence synapses if glutamate gets released on synapses that air during early developmental |
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23:05 | have only NMDA receptors possum optically. is no Boston optic deep polarization. |
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23:13 | what they're called silence and absence. you have tohave ample receptors, an |
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23:21 | receptors will dipaula rise the membrane and will open up in MBA channels. |
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23:26 | until you have expression during the development ample receptors in these synapses CNS |
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23:33 | those synapses remain silent. But they're silent all of the time, and |
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23:39 | can actually produce very large waves of and developmental stages that will produce Parson |
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23:47 | deep polarization. But they're called silent there will not be activation of Amper |
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23:54 | , and you will have to have lot in a lot of activity and |
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23:57 | polarization in order to activate them, just blue made for leads. The |
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24:02 | interesting thing that we talked about sub and there's a sub unit composition shift |
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24:08 | M D A. Receptors. Because the FDA, receptors are coincident detectors |
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24:14 | Do you receptors are very much involved the plasticity and mediating and ah, |
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24:22 | of forms off. Synaptic plasticity are we call in India, a sector |
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24:29 | . So if an M D receptors properly will have that synaptic plasticity. |
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24:34 | not, it can affect many different of learning and synaptic plasticity. Doing |
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24:42 | development. You also have some unit shifts, so on em dia receptors |
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24:49 | have subunits and R two and R b, and you will have the |
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24:54 | of these subunits shift during the Also changing the function of these receptor |
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25:01 | . So this sort of ah shift the sub unit composition or editing off |
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25:06 | channels can happen as a normal part the development. Normal part of the |
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25:12 | . Any of these channels and synapses from silent, where just in India |
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25:18 | with now with ample receptors, they active synopsis, and it's very important |
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25:25 | you have activity, dependence and cellular where these channels are expressed. So |
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25:36 | have a lot of changes in the of these channels with age. During |
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25:41 | early development, you have shifts in composition of the sub units, the |
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25:47 | patterns and with age and activity. , um, remember that AMP. |
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25:55 | and M D heiress address again? cells will strategize. Were put these |
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26:00 | , they will put them pasta. , Piccoli in the synapses are the |
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26:06 | on initial segment the nose of ranveer with ample on an M d. |
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26:10 | . With opera. Snow cells have receptor. They have different channels are |
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26:17 | , potassium, calcium channels, pre Aly amping and the pasta in |
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26:23 | Remember, we talked about the fluid model of the plasma membrane, and |
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26:28 | said that these pro dance move through membranes and the travel. So ample |
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26:35 | , in particular very fast Emperor receptors be located extra cellular early, and |
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26:41 | all of a sudden they flow in the extra synaptic Aly and then all |
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26:45 | a sudden from these extra synaptic spaces they don't get much access to |
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26:50 | they position themselves through plasma membrane through movement into the synapses. So both |
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26:59 | when an M D A. and this dynamics of the receptor insertion |
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27:05 | internalization expression level, also good in perceptions will very much contribute to long |
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27:10 | potential ation. Too many different forms learning and memory. Now, when |
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27:17 | talk about I am a tropic glutamate , it's one thing on medical tropical |
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27:23 | receptors. What we see is when activate medical tropical with them interceptor it's |
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27:29 | to G protein coupled, uh, . And it's linked in particular Thio |
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27:40 | prosper in Arsenal P I p. die false faith and activation off possible |
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27:47 | pace. See, uh, an at the level off the membrane, |
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27:54 | then converts P I p two into A G, which is the vessel |
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28:01 | , and that SL glycerol will target kindly see at the level of the |
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28:08 | the second part of this pathway the of this pathway activation and the break |
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28:15 | of P. I. P. in D. A G, which |
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28:18 | membrane bound and into I P which stands for a new hospital |
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28:24 | I'd be three, will act as secondary messenger and it will bind to |
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28:30 | channels that are expressed on the surface under plasmid particular. Um, and |
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28:37 | from smooth er. You'll have a release of calcium from smooth and so |
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28:45 | particular into the side of plaza, you can essentially raises the level. |
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28:52 | cytoplasmic calcium by activating Netivot, tropic protein coupled receptor. And we discussed |
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29:00 | you know you have very important kindnesses as calcium, ical module and kindness |
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29:06 | Kindness is important, important in memory learning, and we also mentioned that |
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29:13 | is certain levels of kindnesses which force a late molecules and proteins they eyes |
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29:21 | . For group, there's a certain of phosphate ASIS, which deep us |
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29:26 | a late this abstract appeal for group lot of times forced correlation Press relations |
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29:31 | channels may influence their function, but relation may be very important. Thio |
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29:37 | and keep the Amper channel functioning and properly. And when you have deepest |
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29:44 | of these channels by phosphate ASIS, can reduce the function of certain |
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29:49 | Okay, so the expression of these protein kinase c, other kindnesses calcium |
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29:56 | module on Chinese, which could be by intracellular calcium levels and interactions of |
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30:03 | Chinese is and foster tasteless, locally cellular early by the pieces of the |
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30:09 | and regulating phosphor relation of the channels molecules. It's all a part of |
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30:15 | intricate post synaptic cellular machinery that keeps function off the cells intact and allows |
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30:25 | certain mawr things to happen when they're in tact. Gabba signaling. So |
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30:33 | pretty much now finished with talking about , signaling. We understand that you |
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30:39 | glue dermatologic signaling I on a I understand I V curves and dynamics |
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30:46 | the metal tropic signal we look at . First we talked about GABA and |
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30:52 | understand that binding of GABA we'll open Gabba a receptor. This is the |
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31:00 | on a tropic Gabba receptor. The of the Gabba. Every chapter will |
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31:04 | the influx of chloride. Okay, Gaba receptor is essentially also can be |
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31:13 | the gala gated chloride channel. Gabon this channel when Gabba binds to this |
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31:19 | , chloride flocks us through the We also have very important molecules neuro |
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31:28 | storing molecules that bind to Gabba And that's why when you're on steroid |
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31:35 | , that tells you not to do things. It tells you don't consume |
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31:42 | because alcohol is ethanol. Ethanol also through GABA. A receptors binds to |
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31:50 | receptors, okay or operate heavy If you're taking benzodiazepines, bend those |
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31:59 | the as opinions or benzos. A of times are some of the most |
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32:05 | anti epileptic medications, so by stimulating receptor, you stimulate inhibition and |
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32:14 | You have abnormal amounts of excitation. called hyper excitability. There's too much |
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32:20 | in one way in which you can that X citations by increasing inhibition. |
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32:27 | . You have benzodiazepines that combined to receptors and open the GABA ah receptor |
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32:36 | the same way the Gabba molecule barbiturates or sedatives also have a binding |
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32:46 | on the GABA receptor. So in eyes of being, for example, |
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32:51 | the popular uh, literatures referred to Valium, it was sedatives. Barbiturates |
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33:00 | also sedatives. When you're taking these , you have to be very careful |
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33:06 | if you are being treated for that you're not consuming nothing. All |
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33:10 | your being treated for steroids for co , you're not consuming alcohol that you |
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33:17 | that these molecules can have interactions that single receptor and then you have different |
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33:28 | . First of all, with It's interesting because with ethanol in first |
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33:35 | in the addition. Okay, now gonna translate it and Teoh a happy |
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33:44 | situation. Uh, one or two keeps you pretty inhibited. One |
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33:54 | one drink you just yourself because you're addition. Then what happens is that |
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34:00 | you overstimulate the inhibitor of receptors, no longer responsive, so there's no |
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34:08 | any ambition. So after three or drinks, the shirt is coming off |
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34:14 | jumping on the table. There's gnome inhibition because a little bit of ethanol |
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34:21 | you. Elated ambition keep normal. of gabba activated. A lot of |
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34:25 | will flood the brain. Well, eventually the cortex, I'll say |
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34:31 | too much of this inhibitory, agonists here, ethanol mine ambition is |
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34:38 | up inhibition has a half life. these receptors, they can, |
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34:44 | potentially ate their function, or Bagan their function. So these agonists, |
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34:52 | different molecules can overtime depress the function these receptors. Where there you need |
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34:58 | , Maura, Benzodiazepine, amore, off a certain pharmacological drug to see |
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35:06 | effect. Okay, they get You have sensitization. So now the |
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35:14 | is binding thio the Gabba receptors, there's no longer any conditions. That's |
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35:19 | you're standing, dancing on the You lost all of their divisions. |
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35:24 | gon everybody's your best friend, so is just puts in sort of a |
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35:30 | life situation. But these out of benzodiazepines game. For example, if |
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35:36 | are a severe epilepsy case and you status of Galactica's, which is, |
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35:42 | , Grandma's seizure, you have about minutes to exit out of the seizure |
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35:48 | you can cause permanent damage to the , brain, tissues or even |
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35:55 | So benzos benzodiazepines would be administered in case very fast, especially in Children |
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36:04 | have status of Galactica's. It would a suppository administered through anise, because |
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36:12 | where you have the highest circulation and the person is experiencing a severe seizure |
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36:19 | that has a tonic Kalanick component, means it has motor component off |
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36:26 | and it's very difficult maybe to access mouth of that person for them to |
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36:32 | a pill. So that's why it presented in the form of PSA Posit |
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36:37 | . It's the rescue situation to bring person out of the seizure Now, |
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36:43 | regular days, that person who has might be consuming a combination of different |
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36:54 | as a benzodiazepines and some other anti drugs that might be acting through different |
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37:02 | , not through Gabba Channel. But you have to understand, is that |
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37:08 | air psychotropic, pharmacological drugs and when person takes a certain amount of these |
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37:18 | , they can be loopy with Children that have to take pretty high |
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37:25 | of benzodiazepines to maintain the brain activity they don't go into seizure activity. |
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37:33 | can present themselves almost like drunk like and like drunk because advances the same |
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37:41 | that that presents a similar type of like behavior. Okay, so this |
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37:47 | Gabba Channel, Gloria Channel and You didn't think it made so much |
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37:53 | to you every day. Whether you a drink of beer or wine or |
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38:00 | interested in pharmacology or taking steroids or , roids are are familiar in one |
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38:09 | or another, with benzodiazepines and Welcome, Thio Neuroscience, where now |
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38:16 | here trapped for good. It's great be here so Gaba Receptor will allow |
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38:24 | chloride. Channel gap would be a . It's the same Gabbert that will |
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38:29 | to gather be a receptor Gabbert being again will like through Geep Rodin's and |
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38:36 | look what it can do. It close calcium channel posson optically, and |
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38:41 | can open potassium channel. Guess what when you open potassium channel and potassium |
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38:47 | leaving the cell. There is the of potassium. There is a there |
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38:52 | hyper polarization. Mhm. So what is when there's Gabba released on, |
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39:00 | gonna be synopsis that will contain gabba gabby receptors both. When gabby binds |
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39:07 | gabble receptors, there will be influx chloride. There will be initial hyper |
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39:11 | polarization. Gabba binding to gabble Bureau with a certain delay off 10 milliseconds |
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39:19 | . So activation of this Jeep road couple complexes and the flux of potassium |
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39:25 | contribute to further high propeller ization of plasma membrane. So Gabba is I |
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39:32 | a Tropic with Gabby is measurable, . Let's try to put this all |
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39:38 | this context and let's see you can . This is this is a lot |
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39:43 | things in here that we're discussing. at the look at the keys |
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39:49 | PSD stands for Boston optic density blues A receptors, Right? Green is |
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39:59 | Dearest chapters. Then you have potassium . You have calcium channels. You |
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40:08 | NMDA receptors. Mhm. So first all, let's talk about this. |
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40:15 | is what we're talking about Is there this This is glitter Matar GIC synapse |
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40:20 | on the right. And with you glutamate in flex and calcium is |
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40:27 | Calcium is necessary to control the glutamate . What is shown here is Gabba |
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40:32 | receptors prison optical. He can control calcium influx. So if you have |
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40:38 | view receptors pre synaptic Lee, they control vesicles release. Okay, these |
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40:45 | glue dermatologic synopsis But the same can in Gabba Allergic synopsis. Okay, |
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40:55 | remember Gabba be activation and the cannabinoid can also control calcium can also control |
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41:02 | secular early release in both little mate goblets in absence. Uh, now |
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41:08 | have glutamate release here and you have of calcium through an m d A |
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41:14 | . So there you have activation off Chinese too. And then it shows |
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41:19 | this calcium kind a student can now the activity of Gabba be receptors. |
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41:25 | , These Galibier receptors open potassium channels Matic. Um, okay, so |
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41:34 | understand that. Okay, So this our hyper polarization through God would be |
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41:42 | . What about here? So this this is this is Boston optically there's |
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41:47 | gabble binding here. This is through call module and activation of Gabba B |
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41:53 | . But you can also have gathered binding. So here is strong that |
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41:58 | , when you have these synapses, the excited or inhibitory, most of |
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42:03 | neurotransmitter chemical will be in the special . But some of them it is |
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42:08 | to spill over. All right, is called still over a gabba. |
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42:13 | is Ambien, Gabba Gabba binding to , but they will open chloride |
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42:20 | Gabba binding to Gabba V will open channels. This is a mechanism that |
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42:25 | understand so causing initial hyper polarization and causing more hyper polarization for potassium |
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42:35 | And then if there is spillover from synapse here into the exciting Terry |
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42:41 | Now, if you activate Gabba beach and excited Terry Synapse because of the |
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42:46 | of inhibition, now you can control synaptic activity. Good. So once |
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42:57 | , you can read the description but the taking of messages for you |
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43:01 | start putting these together. All of signaling molecules that we're talking about |
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43:07 | particularly here, excited their inhibitory signaling and glued in eight and in this |
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43:14 | , gather a signaling chloride and gather signaling, which effects potassium channels. |
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43:19 | it can also affect calcium channels, we saw in this diagram here, |
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43:25 | it can affect calcium channels pre synaptic and control the circular release the parson |
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43:33 | . It can affect potassium channels by potassium channels and can cause pasta, |
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43:39 | , hyper polarization, even the inhibitory or through the spillover. Even in |
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43:45 | excited Torrey synapses. Spillover happens when is a lot of gabba being released |
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43:52 | and here order receptors referred Thio. cell that releases GABA pre synaptic Aly |
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44:00 | also have GABA receptors located pre synaptic . That's what the order receptors referred |
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44:07 | . The same synapse. The same that releases Gabba also has the receptors |
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44:13 | gabble or header or synaptic gap would receptors hetero receptor. So you have |
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44:20 | from the inhibitory synapse, and you gap will be receptors located in other |
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44:26 | . So these air the gap would header receptors versus auto receptor. What |
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44:32 | tells you is GABA release can control so on. Release through on your |
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44:40 | . Gabby, released in this pre molecule, can control its own |
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44:44 | released by controlling calcium, shutting down influence. Or it can control release |
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44:51 | nearby synapses through the spillover mechanism. , right? Everybody's on board with |
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44:59 | . Excellent. So now I'm gonna to you some of my early |
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45:07 | Not so early, but it's about years back. The publication that we |
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45:13 | in The Journal of Neurophysiology with my mentor, William Guide Oh, who |
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45:21 | later become a chair off Virginia University Virginia and their science department. We |
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45:29 | studying inhibitor and excited her responses. so I'm using this diagram is an |
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45:36 | thing. So here you have an of Gabba. A gaba is |
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45:42 | Gabba is trying to reach the goal potential for chloride of about minus |
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45:49 | This lady inhibitory component is Gabba be was Gabbert. Be component is due |
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45:58 | potassium channels. Opening potassium makes it more hyper polarized because it's trying to |
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46:04 | the membrane potential to that delivery. , potential for potassium and So what |
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46:09 | have here is you have a synapse the thalamus and part of the brain |
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46:14 | the thalamus, where activation produces excitation excitation. That's followed by the early |
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46:23 | through Gabba ai on a tropic receptor and laid inhibition through g protein coupled |
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46:32 | off potassium channels through, Yeah, receptors. Uh huh. And you |
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46:39 | read about it in more detail. is the only take home message I |
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46:42 | show you is an A. But did really, really cool experiments and |
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46:48 | showed that if you apply by, and see if you apply by |
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46:54 | which is Gaba receptor antagonist, you the same stimulation when you get inhibition |
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47:02 | you applied by jubilant. Now you massive excitation. So this is a |
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47:11 | here that you see, that's followed e p s p you have e |
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47:16 | s p. That is followed by ai PSP and Gabba B I p |
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47:21 | p If you blogged gabba. what happens is that this eh PSP |
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47:27 | becomes massive, massive excited to Nah, pick response with firing of |
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47:33 | potentials. So it's telling you that this this synapse excitation is being shocked |
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47:40 | inhibition through both I on a tropic middle the Tropic gather receptors now G |
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47:49 | structures air different. You have G coupled receptor, which is a seven |
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47:56 | membrane alfa hell exists. 1234567 that on intracellular side and member inside attached |
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48:05 | this Jew protean. And this is the G protein signaling happens. And |
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48:11 | have a lot of different G protein receptor subtypes, too. So for |
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48:18 | Rennick, remember we talked about Mouskouri . It'll Colleen, you have on |
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48:25 | Maybe because this diagram and the stable from a few years back. |
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48:34 | Medical tropical intimate receptors on glue are through 12 12 different subtypes of these |
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48:43 | tropical automate receptors, which means that have a slightly different structure and association |
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48:49 | different G proteins. It could be I gee, inhibitory geek pro |
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48:55 | different G protein complexes, serotonin five 15 ht 25 ht four or five |
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49:03 | . Five Alfa data Oh, a dopamine. 1234 nor up Enough. |
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49:10 | remember, we sent push flow mechanism have to. Not from data is |
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49:15 | person Alfa is the Paul? You have Alpha one Alpha to beta |
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49:20 | data to beta three and they expressed different levels in different cells in different |
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49:27 | of the brain. Okay, These protein coupled receptors that correspond to the |
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49:33 | of norepinephrine Ron or dopamine or serotonin different parts of the cortex. Cannabinoid |
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49:40 | , C B one and C B . So we haven't even discussed CB |
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49:46 | receptor, but you have to g coupled receptors and potentially G p r |
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49:53 | 55 which is a third emergent cannabinoid . Okay, so you have two |
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50:01 | of G party, a couple cannabinoid . Then you will understand that the |
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50:06 | CB two receptors, mostly it is in neurons, but it is mostly |
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50:12 | highly expressed on glial cells, especially glia CB two receptors. CB one |
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50:21 | control neural transmission, CB two receptors information, an inflammatory side of kind |
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50:29 | and signaling. Okay, so these receptors g protein coupled receptors at different |
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50:38 | , too. They're expressing different subtypes cells, different parts of the |
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50:42 | and they have different functions. you have a T p a one |
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50:48 | two a two b A t p . Remember, Is this a Dennison |
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50:54 | ? So the molecule 80 p will be signaling through g protein. This |
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50:59 | all G protein coupled neurotransmitters. This all G protein. Remember that they |
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51:05 | have I on a tropic signaling as . This is a transmitter structure of |
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51:12 | signal Colleen receptor, and this is receptor channel. And he is shows |
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51:19 | in order for the channel to you have to binding size for a |
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51:22 | coleene and that acetylcholine has to bind , Alfa and Alfa. You have |
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51:28 | alfa subunits beta, gamma and And each one of these will |
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51:37 | uh, for trans membrane segments called one through M four. So each |
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51:43 | of these subunits will have four trans in segments, so you can see |
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51:49 | you have gabba a receptor and this the code basically for for for different |
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51:57 | . But they take home message here that these structures are very different. |
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52:03 | trans membrane subunits structures that air channels the G protein coupled receptor that her |
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52:09 | and their combinations, it can almost to be like endless. So if |
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52:16 | talking, for example, about acetyl now let's compare uh, Colin ergic |
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52:24 | continent receptor his eye on a tropic and nicotine caradhras antagonists. Musk arena |
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52:32 | after g protein coupled receptor agonist is antagonist. It's a trap in |
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52:40 | norepinephrine, when you talk about norepinephrine A, they're both g protein |
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52:46 | So you have to start knowing some these details. Glutamate happen. |
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52:51 | They're both I on a tropic with own respected agonists and antagonists. Gabba |
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52:58 | Yeah, Gaba is an agonist. also have chemical agonist Muslim alarmed by |
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53:03 | . We just looked at the bike two slides back. Http. |
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53:10 | P two accident A type receptor subtypes you have agonist today type receptor as |
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53:16 | Dennison and antagonists Caffeine. This is highly relevant. I probably assume close |
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53:27 | 90% of you consume caffeine in the of coffee or tea, cheers or |
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53:37 | other form. So it acts through Dennison receptors and it influences glutamate. |
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53:42 | on the Dennison shuts down widow mate . So Dennison will be expressed in |
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53:47 | evening and at nighttime help you sleep and you drink in the morning. |
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53:53 | you wake up and stay awake is glutamate release. Okay, let's play |
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54:00 | games. Gabai ev receptor subunits You're all human calculation robots total |
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54:10 | How many Gaba A receptors. Can we have if you have Alfa |
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54:19 | through six. Data 71 through four 71 through four. No, the |
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54:26 | serve units. How many combinations can come up with? Well, none |
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54:34 | us are robots. The nature does own place. The fact of the |
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54:38 | here is that you have these slight in these actual sub units comprising these |
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54:47 | in these receptor channels and combinations are , the world not particularly completely |
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54:57 | But possibilities are there for us to discovering new and new channels and new |
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55:02 | combinations of the sub units and slide and their amino acid composition slide variations |
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55:10 | their functions and their downstream signaling What these systems do is they amplify |
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55:20 | in the gap junctions and the electrical , you have immediate transfer of ions |
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55:25 | transfer of small molecules to that it . But a small amount of that |
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55:31 | there was no amplification of the chemical . No transmitter binding. The one |
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55:37 | can activate multiple G boat in, , complexes. They can stimulate multiple |
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55:46 | . Is kindness is possible. Cases of production of secondary messengers. The |
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55:53 | messengers can produce kindnesses. Prospectuses that secondary messengers from college economy system fostered |
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56:01 | can influence the function of downstream channels as potassium channels can force for late |
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56:09 | channels and help them keep open. you have massive amplification through the system |
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56:15 | the neurotransmitter entering into the cell and the channel opening. But activating g |
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56:22 | coupled complexes at the level of the membrane. So you have amplification. |
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56:28 | also have divergence. You have a neurotransmitter that combined to three subtypes of |
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56:37 | . Vampire an, M, D and kind eight. Okay, and |
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56:43 | D. A. Was scepter, example, can have different effective |
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56:48 | Three effective systems inside the cells y and Z. You can also |
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56:54 | convergence. You can have convergence on same factors. System transmitter. A |
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57:02 | from one receptor will get to President may see, but so will transmitter |
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57:07 | acting through B receptor, and so transmitter see acting to see receptor. |
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57:11 | may all converge and influence one defector . They may all influence the levels |
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57:18 | calcium. They made all target calcium . One targets calcium channels and the |
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57:25 | well, Khloe's calcium channels and so gather be receptors will close calcium channels |
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57:30 | same effect er system. Okay, neurotransmitters, different receptors. You also |
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57:38 | redundancy and the redundancy and in the that this relates thio parallel streams of |
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57:46 | parallel streams of processing that are at level in this case, off transmitters |
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57:52 | receptors Parallel streams of processing at the off the brain function in general. |
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58:03 | what we have is we have transmitter that can buy into a one receptor |
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58:09 | a two receptor in one receptor can a factor. Three transmitter be through |
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58:20 | years after the different receptor can also and activate affected three. Uh |
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58:31 | There is redundancy here. This this in this redundancy in parallel streams, |
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58:38 | two affected effects effects affected too. have their own distinctive factors and they |
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58:45 | overlapping of factors too. Through these . So is you don't have a |
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58:56 | receptor any longer you may lose access affect her too. With affected 3 |
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59:05 | serve a similar function to affect her . So you have a redundancy. |
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59:09 | of these defectors will serve similar Also, what happens if you lose |
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59:14 | one receptor? Can you still get affect your three? Yes. So |
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59:19 | can, through B receptor and transmitter so this affect your three doesn't sees |
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59:24 | functions inside the cells. If something array with a one receptor to this |
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59:30 | and parallel streams of processing a very of keeping the overall brain function, |
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59:38 | injuries and loss of specific neurotransmitter systems relate thio specific function losses and also |
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59:48 | expressions the respectively. Okay, so we're finished with synoptic transmission. Now |
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60:00 | understand how individual neuron with individual neurons made off, how they function and |
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60:09 | they communicate thio each other and what glial cells play in the maintenance of |
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60:17 | function, as well as in maintenance brain activity and synaptic transmission, with |
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60:24 | cycling and with buffering off the ions many other functions of glia play. |
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60:33 | now that we understand how the cells the action potentials, other cells released |
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60:39 | and communicate two other Selves. Let's ourselves back onto the macro scale and |
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60:48 | ourselves about the structure of the central system about major parts of the central |
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60:56 | system and major functions off these different of the CMS. So, first |
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61:03 | all, on the left, you brains that are shown to scale. |
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61:10 | you have a rat brain which about centimeter rapid brain A few centimeters, |
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|
61:18 | brain Japan's a human dolphin brain. . Uh, now this is this |
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61:29 | this image is not to scale on right. The image on the left |
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61:34 | to scale. So if foreign ologists correct and they said that the size |
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61:41 | the muscle being things, all things equal represents the strength, therefore the |
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61:50 | off a certain area of the brain a certain ability. Then again, |
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61:55 | know, dolphins would be telling us to dio and so with elephants, |
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62:01 | their brains are bigger than ours. the complexity and the structure and the |
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62:08 | of the brain is what determines that walk on 2 ft and rule the |
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62:15 | . Or at least we think Until we get hit by nature and |
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62:20 | that we are part off the nature the world. And dolphins developed different |
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62:27 | of the brain and rats developing at parts of the brain to survive in |
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62:32 | respective environments. Was there body their sensory body structures and sensory brain |
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62:44 | . You can see a rat and and lizard brains would be flat. |
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62:50 | are no imaginations there, no self gira on the surface that you would |
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62:56 | seeing on the higher order species. you can see that it gets very |
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63:01 | when you come up to the humans you have a lot of salsa. |
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63:05 | right, which increase the complexity of network structure, increases the surface area |
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63:13 | the ability for the complexity of processing these brains. So you hear a |
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63:20 | lizard brain. It refers to somebody smooth brain. That means it's a |
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63:29 | insult, but it refers to the that these brains air not very complex |
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63:34 | notice and rats. You see these bulbs sticking out in the front and |
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63:39 | rat it too. Guess what those are. Those air olfactory evolves for |
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63:46 | . Now look at the humans. barely see them. They actually buried |
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63:52 | the front here. So we have bulbs, but we don't nearly realize |
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63:57 | on the sense of smell. Is other animals doing their four other parts |
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64:01 | the brain in us is a lot sophisticated and much more developed. |
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|
64:08 | so now let's look at the Let's look at some anatomy and symptoms |
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|
64:14 | the anatomy because this is our Somehow we name brain structures, and |
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|
64:21 | also identify the location of different brain . So first we have dorsal. |
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64:27 | already know dorsal is the doc. is a sensory neurons in the dorsal |
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64:33 | . Ventral side is our motor neuron on the ventral side, the front |
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64:37 | the spinal cord. Well, look the top. Midline corresponds to closer |
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64:44 | midline. You are even the brain the whole animal body. The structures |
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64:50 | called medial structures, and the further you are from MEDLINE to the outer |
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64:57 | of the animal, the brain. you're laterally located laterally and most of |
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65:03 | brain. The front is referred to interior or all rest role, and |
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65:12 | tail cardinal called it eyes posterior You have cuts that are defined in |
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65:24 | of the brain, such as agile cuts, horizontal and kurono |
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65:29 | A little cots are made. Ross to coddle from the front. If |
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65:35 | made to the tail, Rasta wrote cardinal, and it's made along the |
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65:42 | plane. He's in the sagittal Horizontal cots are made along the |
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65:50 | Okay, Kurono cuts are trance verse made perpendicular to the brain structure perpendicular |
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66:00 | horizontal cuts. The major parts of brain again is the cerebral cerebellum, |
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66:07 | and spinal cord serie broom divided into cerebral hemisphere, less cerebral hemisphere. |
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66:16 | in rats, uh, separated by massive satchels, Fisher, the sagittal |
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66:23 | separates the two hemispheres one from The two hemispheres are interconnected with a |
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66:30 | powerful bundle of fibers. This is agile view. So if you want |
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66:35 | make this cut, Ross wrote to , you would then reveal the inside |
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66:41 | sagittal view off the brain. So cerebral, Um, and Serena's our |
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66:52 | and cerebral hemispheres. So first of , cerebral mom is New York or |
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67:00 | , right? Cerebral hemisphere left cerebral . When we talk about the function |
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67:08 | the hemispheres. Our function is contra sensory motor functions and censor information crosses |
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67:19 | and motor information. If it is in the right side of the |
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67:24 | it will control left side of the left side of the brain controls right |
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67:29 | of the body. Sarah Ballon, the other hand, is it still |
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67:36 | ? So Senator Belem is very much in control of the movement of the |
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67:42 | . But it will control the movement cerebellum on the left side. Rights |
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67:46 | on the right side, Brain stone many significant functions. It has massive |
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67:56 | that connects the re broom to cerebellum through brain stem across cerebral cerebellum pathway |
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68:02 | Bella cerebral pathways. There's also served cerebral serverless spinal that way. And |
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68:12 | the brainstem will control major vital body such as breathing consciousness and control of |
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68:20 | temperature. It will also express this cool Raffi nuclei. You like the |
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68:29 | ? I mean, the twist question on the Raffi nuclei norepinephrine. Some |
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68:34 | you got the question on the Nora Locusts, Aurelius nuclei. They're all |
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68:41 | in brains, town, brain. will have cells that dictate and control |
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68:49 | breathing rate. If you injure brain , you can lose consciousness too, |
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69:02 | control of many, many different additional , not just body temperature. |
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69:09 | so we're just starting here today. when we come back, we're going |
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69:15 | talk a lot about different parts of brain. We will talk about the |
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69:20 | of the brain. We will talk CNN's development and how it comes |
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69:26 | And then the next lecture, you find out a lot about different brain |
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69:32 | and their functions, as well as site of architecture of the cortex. |
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69:37 | I believe that we're probably going to all of this material in the next |
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69:44 | trip. Then we will review the . And you should be well prepared |
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69:49 | on your way to take the term . So we'll end here. |
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69:56 | I will see you all in the |
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