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00:03 | this is neuroscience. Midterm to review . We spend about a third of |
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00:11 | second section of the course, focusing the neural transmission. When we talked |
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00:18 | neuro transmission and neurons and the N. S. We discussed that |
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00:22 | are two types of synopsis, electrical chemical have distinct features distinct anatomy. |
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00:27 | electrical synopsis or connections that form the junctions that allow for the passage of |
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00:33 | molecules and ions across freely. It's instantaneous activation across the gap junctions of |
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00:39 | population that allows for neurons to synchronize large populations so they can produce a |
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00:45 | effect downstream into the interconnected networks. then most of the rest of the |
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00:51 | we spent talking about the chemical neural . And when we started talking about |
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00:56 | neural transmission, we actually first focused neuro muscular junction. And we talked |
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01:02 | how neuro muscular junction is a fairly it's a very large synapse. The |
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01:08 | has so many different ramifications, forms templates. And when these synapses are |
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01:15 | will contract muscle fiber that they're projecting . And so uh whenever you have |
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01:24 | of a single clothing from neuro muscular This is a neuro muscular junction. |
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01:31 | will cause the end plate potential. is the end plate potential is this |
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01:37 | portion and this is the muscular action . So the in place potential is |
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01:44 | going to be about 70 million balls size and it will always reach the |
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01:50 | value for the action potential generation. a very powerful sin ask. It |
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01:57 | has nicotine acetylcholine receptors because it has acetylcholine receptors and has no other signaling |
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02:05 | inhibition then uh it's only excited for . Okay, nicotine acetylcholine receptors are |
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02:14 | close to the synaptic flat and deeper you have all the educated sodium calcium |
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02:20 | potassium channels. And so this is to produce a very long muscle |
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02:27 | Very long action potential in the It's in the water of about 300 |
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02:33 | for more. Okay, these are simple synopsis they're very efficient. Synopsis |
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02:39 | have the ability to recruit a few from the spinal nerve and move one |
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02:45 | . A few more fibers move two for a lot of fibers. It's |
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02:49 | recruitment but actively release these nerve vascular . You can recruit the whole arm |
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02:55 | the whole shoulder and so on attached them. So these are systems neurotransmitter |
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03:01 | , the seal cove, inn is of these neurotransmitter systems. So you |
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03:05 | that there are different neurotransmitter systems. have classical amino acids which is glutamate |
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03:12 | and glazing. We have the means we discussed and some of them we |
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03:17 | in great detail like acetylcholine and we about peptides and the differences between synthesis |
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03:24 | release of neural peptides versus transmitters. in addition inside these boxes we added |
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03:31 | the cannabinoids and we added the metric oxide and monoxide and also academic |
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03:38 | said that those are different. They're stored in the vesicles, they're not |
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03:42 | in the Secretary Granules like peptides would rather they remember insoluble they're synthesized on |
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03:49 | and they function and reprogrammed faction will that in a second. There are |
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03:55 | are synthesized more when there's heightened levels activity stored in Secretary Granules and released |
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04:01 | not as specifically as neurotransmitter vesicles would which arm mostly released and serviced at |
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04:08 | level of the pre synaptic terminal. the pre synaptic vesicles fuse and release |
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04:13 | . You need the action potential. deep polarization prison optically which now opens |
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04:19 | gated calcium channels and the influx of is the second thing that is necessary |
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04:24 | the protein protein complex to be activated the vesicles membrane to fuse with the |
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04:29 | membrane to cause excessive doses following which will have the psychosis of the |
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04:34 | Talk about how there was an interest understand which part of the membrane |
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04:40 | which elements proteins and such to visualize junctions to visualize the fusion of the |
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04:46 | . And also we mentioned an interesting . It's a die and it's imaging |
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04:50 | the dye that is sensitive to So we talk later about different imaging |
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04:56 | in the clinical settings such as pet and F. M. R. |
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04:59 | . We also in the visual Talked about more experimental imaging such as |
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05:04 | sensitive dye imaging intrinsic optical signal And this is also an experimental technique |
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05:10 | you can image the fluctuations. The temporal dynamics. The spatial and temporal |
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05:16 | the concentration dynamics in this particular case calcium ions. So this is calcium |
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05:22 | dye and imaging most of the end psychosis and recycling of the neurotransmitters is |
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05:28 | here at the pre active pre synaptic zone. Sometimes vesicles will be re |
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05:37 | into early under some and reprocessed um acetylcholine signaling which uh acetylcholine obviously will |
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05:49 | a bicycle. Your translator will be there in this case a meeting and |
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05:55 | have botulinum toxins that are produced by botulinum that will target this protein protein |
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06:00 | complex. So we talked about how are pharmaceutical drugs and there are also |
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06:07 | of abuse and also there are chemical nature and toxins that can impede with |
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06:15 | systems with the release of the With bio synthesis of neurotransmitter with the |
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06:22 | of neurotransmitter with the binding of neurotransmitter optically all along this different chain of |
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06:28 | neurotransmitter systems. We also talked about and how organophosphates cyclical industries inhibitors. |
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06:36 | welcome back to that when we highlight in the next slide. So unlike |
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06:42 | neuromuscular junction which just has nicotine acetylcholine just has the potential uh N. |
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06:50 | . N. S. First of when we talk about acetylcholine, we |
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06:53 | about nicotine IQ and Mascarenas. Acetylcholine . Okay so we know that nicotine |
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06:59 | uh and muscular nick and the same . The cns will have a different |
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07:06 | effect. Now when we talk about and c n s we talk about |
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07:13 | . P. P. S. in the neuro muscular junction and plate |
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07:18 | is not excited words and plate E. P. S. |
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07:23 | Is excitatory post synaptic potential. And C. N. S. Apart |
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07:32 | excitation, we also have inhibitory post potentials. Unlike the employee potentials, |
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07:40 | E. P. S. S. A very small in size |
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07:42 | order of a fraction of the And so in order for the membrane |
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07:49 | to reach the threshold value for the potential in the C. N. |
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07:53 | . You will have to have summation activation of multiple excitatory synapses in order |
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07:59 | reach the threshold, which is not case at the neuro muscular junction. |
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08:04 | you will have not only excitation but will also have inhibition which will be |
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08:09 | hyper polarization in the system and potentially the deep polarization levels that would generate |
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08:17 | action potential and the action potential is the duration of about two milliseconds. |
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08:23 | is in contrast all to the what seeing at the level of the |
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08:28 | So, so, an interesting For example, if I'm telling you |
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08:33 | the fiber recruitment for the muscle one finger or move the finger versus |
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08:38 | the whole finger or the hand, it versus one finger then in other |
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08:45 | . For example, the cardiac muscles that doesn't typically happen because you wouldn't |
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08:50 | to just partially open the valve or close it, that would cause a |
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08:55 | serious cardiac problems. So E. . S. P. S. |
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08:59 | are mediated by glutamate mediated by the of positive ions such as sodium and |
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09:06 | to some extent. And the P. S. P. |
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09:08 | Which are gaba mediated by the influx the an ion chloride inside the |
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09:15 | And there are two components, the I. PSP. In the late |
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09:18 | . PSP. Because we have here tropics signaling. In some instances mental |
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09:26 | signaling neurotransmitters will activate. G protein receptor, G protein will immediately affect |
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09:35 | nearby channel. So we'll talk later this as a shortcut pathway. There's |
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09:40 | intermediaries between the decoding coupled receptor the protein channel and there's sometimes enzyme activation |
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09:48 | downstream secondary messenger activation. And creation other intermediaries such as highnesses and hospitals |
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09:55 | then affect the adjacent ion channels. for acetylcholine, I encourage you to |
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10:02 | everything. The synthesis of acetylcholine, acetylcholine ester is the fact that most |
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10:09 | the alzheimer's medications are cyclical unnecessary is . So by inhibiting the cyclical |
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10:16 | make more civil coding available here in synopsis. There are cooling transporters that |
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10:23 | transport molecules back to pre synaptic Re synthesize to prepare them for the |
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10:31 | . Again, we talked about the that each one of the nicotine will |
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10:37 | an agonist from nicotine IQ and must will be an agonist for most |
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10:41 | So equally each one of them will their own antagonists such as curare and |
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10:47 | for civil code in the clinic and subjects. You should know that for |
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10:51 | exam as well. Then we talked other types of means and there were |
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10:56 | tables that showed you how certain means precursors to other means such as |
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11:02 | precursor of norepinephrine, norepinephrine as They slightly have, they different |
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11:08 | They have the same type of signaling the fact that they released and they're |
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11:14 | broken down or recycled back in the of the cattle colonies and the pre |
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11:18 | terminals and they're broken down there by . I mean oxidizes in the prison |
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11:25 | terminal. So regulating mono amine oxidase also another level of regulating the amount |
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11:32 | cata column means blocking the re uptake cattle colonies, blocking the re uptake |
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11:38 | serotonin is also a strategy for both drugs but also elicit street drugs such |
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11:45 | cocaine. Uh Now you don't need know the synthesizing intermediaries for these molecules |
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11:53 | you should probably focus on knowing the that we discuss on certain types of |
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12:00 | . Again for assets. An interesting to know is glutamate gets converted into |
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12:05 | with the help of atomic acid, box delays. And so all of |
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12:09 | inhibitor inter neurons that release Gaba will positive for God with one of the |
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12:16 | that we discussed um you know history for in situ hybridization, for |
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12:21 | Uh serotonin when we had some descriptors we said wait a second. Some |
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12:26 | these things mood appetite sleep learning. then we also have mood regulation by |
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12:32 | cola means. Yes there's some overlapping . Their serotonin again. Uh five |
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12:38 | . T. Will be recycled back the trend. Sport is so |
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12:43 | Antidepressant medications that you see on the they will be referred to as serotonin |
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12:49 | uptake inhibitors sa rise and this is re uptake. This is a re |
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12:57 | of serotonin and you're inhibiting serotonin re of one of the classic uh depressant |
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13:04 | brand name PROzac. There's also involvement M. A. O. |
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13:08 | And degradation of these amine molecules. so there's also medications that controlled |
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13:14 | A. L. S. That pretty significant antidepressant medications. It's interesting |
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13:19 | with some of these things it takes three weeks to see an effect on |
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13:25 | like M. A. O. . That are involved in in the |
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13:29 | and metabolism of these elements. And cannabinoids are different. We talked about |
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13:35 | fact that the cannabinoids produced when there very high levels of activity. Pre |
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13:43 | lee even excited for inhibitory South will production under freely across the plasma |
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13:49 | Retrograde fashion that will go from boston the pre synaptic size bind to g |
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13:54 | coupled receptors close the calcium channel and the release of both excited for and |
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14:03 | governor transmitters. The two most common in the cabinets and lander mind and |
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14:10 | our aka donald glycerol and the most and demonized broken avenues that comes from |
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14:17 | plant also buys the CB. One is delta line tetrahydrocannabinol delta nine |
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14:25 | So you know the differences between and hybridization, antibodies versus strength of |
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14:33 | R. N. A. Uh situ hybridization versus the immunity chemistry which |
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14:38 | antibodies. Remember that another technique to neurotransmitter activity of study neurotransmitter activity on |
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14:46 | Southeast neurotransmitter mimicry. And we also UNQ aging of the neurotransmitters. So |
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14:53 | difference is that in this type of you're applying the fluid and then uncaged |
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14:59 | of the neurotransmitters. They're actually cage chemical cages and your photo allies ng |
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15:04 | light those cages and you can get lot more of the spatial and temporal |
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15:10 | dimensional specificity using uh the caging of rather than these more classical older techniques |
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15:20 | infusion which will lend itself to laws diffusion and will spread accordingly from higher |
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15:29 | zones and low concentration zones. Making not as specific as an caging of |
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15:34 | neurotransmitters. Uh in order for this to reach the action potential threshold neurons |
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15:43 | certain responsibilities and some of these responsibilities some of these strategies are that they |
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15:51 | spatial and temporal summation And neurons that been dirty cables of course they |
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15:58 | And we know that the dirty cables not insulated. That means the current |
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16:02 | going to leak out over the inverted . So we talked about the life |
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16:07 | neurons that have a long lead That means from a maximum 100% of |
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16:12 | current located here. It will take long distance For it to die down |
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16:18 | 37% of its maximum value which is the λ or the length constant value |
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16:26 | this neuron. So length constance, sells a very long length constants. |
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16:32 | great for especially temporal summation. And we talked about the fact that uh |
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16:41 | receive excitation of addition. And if receive excitation distantly in the dendrite and |
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16:49 | approximately there is an inhibitory input at level of the soma. You may |
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16:54 | detect any difference at all because there be active inhibition. There will be |
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16:59 | of the current through the shunting And so you need to really activate |
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17:04 | lot of the excitatory synapses and then in order for the selma to see |
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17:11 | small response because a lot of the recall. So you have to recruit |
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17:15 | lot of synapses 40 50 60. synapses for the soma to reach the |
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17:21 | for the action potential generation. This uh an interesting diagram which shows norepinephrine |
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17:28 | norepinephrine through the production of a dental and cyclic GMP produces protein kind they |
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17:35 | . And this protein kind they say really potassium channel and actually open the |
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17:44 | channel and this is a similar mechanism we see with medical tropical acetylcholine |
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17:50 | And so there are similarities, there's molecules that we discuss that actually can |
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17:55 | through medical tropic cascades potassium channel such medical tropic acetylcholine norepinephrine gaba B |
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18:06 | Okay, so there's some redundancy that talking about in targeting either the synaptic |
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18:12 | channels or the pre synaptic. Both calcium channels for example, we'll come |
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18:18 | and talk about that in a Okay, I think this ended this |
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18:27 | . We moved into the next This is one more quick review for |
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18:33 | of all of the neurotransmitter systems. that girl I seen is a major |
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18:41 | in neurotransmitter in the spinal cord glycerine actually involved in the excitatory receptor signaling |
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18:48 | receptor signaling in the brain. Uh is just a little bit more review |
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18:55 | continued mascara in it. This is masculinity. Acetylcholine receptors that go through |
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19:02 | shortcut tackling. So instead of what say through the intermediary faculty with more |
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19:06 | an upfront with medical tropic, the is the same potassium channel. But |
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19:13 | you don't have an intermedia is that protein subunit that's catalyzed now uh can |
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19:20 | this potassium channel. So in academic receptor activation. CNS will cause a |
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19:27 | polarization. Most chronic activation by opening channel positive charge. Leaving the cell |
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19:33 | have the opposite effect will have a polarization. So we see that in |
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19:37 | cns you can have the car and tropic versus metal tropic signaling with the |
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19:42 | molecule cause two different effects on the cell. Um we call that with |
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19:51 | assets and with glutamate when we talk communication between two excitatory synapses in particular |
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19:59 | talk about tripartite synapses neuron one pre neuron to post synaptic and the third |
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20:05 | of the synapses. We, because only neurons have intimate neuronal transporters, |
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20:13 | release and exerts its Bhasin optic Get transported back to synaptic reloaded into |
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20:20 | but also we ourselves have the glial transporters and they're capable of picking up |
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20:27 | turning it into glutamine and then giving back to neurons convinced emphasize glutamate out |
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20:35 | glutamine using contaminants. So here you a very clear demonstration of how the |
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20:42 | of excitatory neurotransmitter glutamate is quite tightly and modulated by the astro glial cells |
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20:51 | particular and not just by neurons and can decide it's getting more or less |
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20:57 | decided. I mean let's say it alter the function of its transport, |
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21:02 | may alter the function or the speed the breakdown of the molecule for it |
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21:07 | return into neurons And so we definitely excited for neural transmission and then we |
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21:15 | back and talked about cattle common means some of their functions. This is |
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21:21 | some of the review and and since discussed that I am a tropic and |
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21:26 | tropic and have opposing the actions And said well can to medical tropic have |
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21:31 | actions and we looked at this just norepinephrine activating basically turning on the production |
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21:38 | protein kinda say. And it's going do it if it binds the debate |
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21:42 | receptor which is linked to G. . A. Stimulus authority protein |
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21:47 | But if that same molecule norepinephrine binds alpha two receptor that's linked to the |
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21:53 | . I. Division and this molecule going to basically increase the amount of |
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22:03 | . So in this case we're talking downstream secondary messenger effects protein, chinese |
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22:10 | , hospitals production. Remember that kinesis correlate at P. 04 group hospitalizations |
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22:16 | defrost for a late protein channels for . And so this is referred to |
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22:22 | push pull system. This is pushing produce more cycling and p including finance |
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22:27 | pulling the system away from producing more the sporting finding saying So now you |
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22:33 | an example of how to medical tropic can have an opposing different effect on |
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22:40 | downstream signaling within the south amines are . And unlike the immune assets which |
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22:47 | widely expressed throughout the brain the means their own specific nuclei where they have |
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22:54 | soma the nucleus ford or local civilians going to be selma's of neurons that |
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23:02 | these are all of the projections and arrows, external projections that will innovate |
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23:08 | and also sub cortical regions going all way into this final cord wrapping nuclei |
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23:13 | serotonin and then you have to see lateral fundamental nuclear magnet seller of basal |
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23:23 | . So small populations of mirrors that these mean transmitters but they diffuse distribute |
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23:32 | throughout the brain. Is very non innovations that are cortical and also sub |
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23:39 | . So when we talked about when cannabinoids I had this D. |
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23:43 | I. And then later said well S. I. Stands for equalization |
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23:47 | compression position. And so the actions under cannabinoids and actions of THC was |
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23:53 | discovered in in neurons by neurophysiologist and Because Canada's gets people high. So |
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24:00 | they thought probably the receptors are not the stomach and the brain. So |
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24:04 | gonna go look for effect there. discovered the control inhibition and then later |
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24:09 | DsC was added because also experiments were where there was a clear example of |
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24:15 | Canavan was also regulating levels of excitation it's regulating levels of excitation through regulating |
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24:23 | pre synaptic, low educated calcium channel neurotransmitter release. And that's also a |
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24:29 | story among some of the other neurotransmitters we looked at. Just like |
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24:34 | Gaba also has its own transporters into pre synaptic terminals has transported into the |
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24:39 | and everything along the lines of the . The synthesis their delegations transport and |
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24:47 | synaptic receptor effects can be potentially pharmacological glutamate for anna tropic signaling functions through |
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24:58 | and NBA incarnate receptors with their respective as soon as glutamate is released and |
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25:04 | bind to receptors and binding of glutamate enough to open up the receptors and |
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25:09 | the initial D. Polarization. So the E P. S. |
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25:14 | S are produced in the C. . S. They had the early |
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25:31 | and this early component is ample component they have the lead component. This |
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25:38 | component of G P. S. . Is an M. D. |
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25:42 | receptor components. So as soon as binds ample receptors it starts D |
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25:47 | The plasma membrane magnesium is blocking an . D. A receptor. And |
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25:52 | deep polarization from rust to more D levels will alleviate the magnesium block and |
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25:58 | up an M. D. A that's going to be responsible for the |
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26:02 | uh component. Late currents of the . P. S. P. |
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26:08 | not an M. D. A . They are activated fast but once |
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26:13 | NBA receptors are activated they will conduct lot more 50 Pecos emails of card |
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26:18 | takin it will have their own antagonists is seeing Q. X. And |
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26:23 | . D. A receptor will have antagonist A PV. And we discuss |
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26:26 | when we look at the ivy plots AMP and an M. D. |
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26:29 | receptor currents an M. D. receptor is referred to as coincident detector |
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26:34 | it's coincidentally needs to detect glutamate binding release prison optically glutamate binding and deep |
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26:42 | personality. So if it's just deep and M. D. A receptor |
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26:47 | not going to open if it's just it's not going to open. But |
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26:51 | it's glutamate and deep polarization is coincidentally detecting pre synaptic synaptic activity will bind |
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26:58 | two and will have a significant Glycerine acts as a co factor that |
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27:04 | the presence of YC. Glutamate binds NMDA receptor and promotes full act the |
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27:09 | of an M. D. A . And NBA receptors are all formidable |
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27:13 | sodium calcium and potassium and has multiple sites. So it has binding sites |
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27:19 | the neurotransmitters. Some of the neurotransmitters also be competing with some of the |
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27:25 | that are exogenous molecules. So when two agonists are competing for the same |
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27:30 | on the protein to bind to the called competitive agonists antagonists are competing for |
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27:35 | same lock. The two keys sit the same lock um They're gonna be |
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27:42 | antagonists in that respect. And there's binding sides. PCP which is uh |
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27:51 | a drug can cause significant effects of M. D. A receptor that |
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27:55 | be long lasting effects. So besides accurate hallucinations or bouts of psychosis, |
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28:01 | systems can actually buy one or two activation. But some of the list |
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28:05 | drugs can break and you may have chronic cases of psychosis and schizophrenia that |
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28:12 | from crystal methane use and some other hard addictive drugs and cato one we're |
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28:18 | his antagonist in NBA receptors that once is bound to an M. |
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28:22 | A receptor that an NBA receptor is , it also changes its confirmation and |
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28:28 | opens new holes for new keys to new laws and new keys to come |
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28:34 | and say okay to one will bind the NMDA receptor only if it's open |
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28:39 | means that it can be floating around it cannot bind anywhere. But an |
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28:43 | . D. A receptor opens and a new crevice amina assets for that |
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28:48 | to bind. It can then bind the NMDA receptors. Remember NMDA receptors |
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28:53 | not medical traffic so meta but tropics . And we looked at very briefly |
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29:00 | then uh glutamate inedible tropic signaling. then we came back and talked about |
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29:04 | tropic glutamate signaling and bipolar cells in retina. All searches this diagram shows |
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29:09 | if you use voltage clam and you the number of potential from different holding |
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29:14 | from minus 60 plus 60. It several things. First of all this |
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29:19 | is you have glutamate but you also the last have normal physiological concentration of |
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29:24 | which is $1.2 million minus 60. don't see much of an NBA cars |
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29:29 | 30. You start seeing them and currents reverses zero million volts. So |
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29:34 | ample as we saw in the So it is the holy PSP. |
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29:39 | does the CPP they all reverse zero volts. And the I PS PS |
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29:45 | would reverse IT chloride reversal potential which give minus 70 million volts. Now |
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29:50 | you remove the magnesium from the extra solution. So you have this experimental |
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29:55 | . Now you illustrate that in the of magnesium, even if the hyper |
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30:00 | resting membrane potentials and receptor will be will still reverses zero million volts. |
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30:06 | that proves that magnesium indeed is blocking the reception, the absence of magnesium |
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30:12 | is enough to activate. That an . D. A receptor. When |
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30:15 | studied the curves and we described this in which there was a stimulation and |
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30:21 | was released and there was a post response recorded in the current. So |
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30:25 | is voltage clamp recording and two measurements taken the early component, the early |
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30:30 | and the late current. And we that the early current which is ample |
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30:34 | is linear. And we voted zero balls. I say it's a vessel |
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30:40 | because it's multiple ions flux into ample such as an M. D. |
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30:44 | . Receptor also. And these closed open triangles is the response of this |
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30:50 | component which is linear component, not M. D. A component measured |
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30:54 | at the first line closed triangles and triangles in the presence or in the |
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31:01 | of a P. V. Which an M. D. A receptor |
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31:04 | . And this is an occurrence. says the early currents are not affected |
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31:08 | an M. D. A receptor and they shouldn't be because a tv |
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31:12 | and M. D. A And these circles the closed circles show |
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31:18 | an M. D. A. is nonlinear. So you don't have |
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31:21 | in India current at negative potentials. you have an M. D. |
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31:24 | . Current that increases when the cells deep polarized. A number of potential |
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31:28 | of minus 15 minus 45. You persistent in M. D. |
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31:33 | Currents that reverse them zero miller balls and prefer to conduct in the opposite |
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31:38 | . So an M. D. . Chart here. This I. |
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31:41 | . Plot is taken from the second line which measures the late component of |
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31:45 | E. P. S. And M. D. A. |
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31:47 | is this whole blue area under the . And so if you apply to |
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31:52 | Tv would essentially block this hole area the curve that is blue. And |
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31:57 | are the open circles in the presence a P. V. And |
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32:01 | D. A. Currents. Except some little residual currents. And these |
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32:04 | circles are blocked and are staying at zero PICO ampere value. So that |
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32:11 | that a PV does not affect the component and it's a linear component. |
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32:16 | M. D. A. Is nonlinear component in the presence of an |
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32:20 | . D. A. You will zero in the presence of a |
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32:23 | D. Which is antagonist for an . D. A. You will |
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32:25 | zero current flexing through that receptor. you recall all of the N. |
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32:31 | . D. A receptor channels are to sodium calcium and potassium and |
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32:38 | Some of them are permeable to Others are not. But this is |
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32:42 | significant example that shows that within these dimensional protean channel structures, substitution of |
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32:50 | single immuno asset and thousands of amino can now determine whether that channel is |
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32:57 | to be permeable to calcium or So we saw that the substitution here |
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33:02 | argentine are will now block the flux calcium for an M. B. |
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33:07 | . Through ample receptions are early in development only an M. D. |
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33:12 | receptor of present. So they're called synapses because there's not much of the |
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33:20 | synaptic deep polarization that are happening ample are not there. There are other |
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33:25 | by which in India receptors get Apart from emperor activation and the developing |
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33:32 | and also the subunit composition that comprises different receptors. They may shift during |
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33:37 | development. So in an M. . N. M might be a |
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33:41 | ratio of subunits at one stage of versus later stage of development. And |
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33:47 | is very important for L. P. Which stands for long term |
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33:51 | for long term potentially ation because of coincident detective pre synaptic post synaptic activity |
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33:58 | properties and M. D. A serve very well positioned for mediating and |
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34:04 | of the calcium in mediating the plasticity the pre synaptic and post synaptic connections |
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34:10 | therefore their effects on an M. . A receptor can be very significant |
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34:15 | many different perspectives, ample receptors they most mobile from these glutamate receptors and |
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34:22 | can actually enter into the synaptic space the extra synaptic spaces through this fluid |
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34:29 | model of the plasma membrane. But a very fast fashion micrometers in |
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34:36 | So medical tropical intimate receptors when we as we study the breakdown of |
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34:41 | I. P two by activation of I. K. C. And |
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34:45 | the divergence of the cascade into P. Three activation of I. |
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34:49 | . Three recep calcium channels that are into plasma particular and the member inbound |
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34:57 | which states and can activate another molecule remember that what what is going to |
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35:02 | is that these timings and foster cases going to modulate the phosphor relate and |
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35:09 | correlate different proteins and protein channels. there is a significant regulation of these |
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35:15 | inside the cells. This is an of how metabolic tropics signaling would be |
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35:19 | place. And that is not to confused with an M. D. |
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35:22 | receptor which is ion tropic but it delayed activation and it has a magnesium |
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35:29 | . When we talked about inhibition we about Gaba and Gaba a receptor in |
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35:36 | which allows for the flux of Gaba A receptor also has multiple binding |
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35:41 | who decides Gaba which is an endogenous in the brain, ethanol alcohol will |
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35:47 | to Gaba receptors. Benzo dad barbiturates, no steroids will also bind |
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35:53 | Gaba A receptor agonists. Most of substances that actually all of the substances |
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35:59 | seeing here that agonists Gaba A So binding of gaba gaba a receptor |
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36:04 | increase inhibition. It's a sedative. increase inhibition, its anticonvulsant, anti |
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36:13 | , it's a sedative barbiturates, Okay, it's all increasing inhibition, |
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36:20 | one or two glasses is sedative beyond you lose inhibition. So then it |
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36:25 | something something different. Now Gaba You can see signaling through chloride and |
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36:32 | B past synaptic aly signaling potassium So we talked about the two components |
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36:38 | inhibition. Gaba A, which is by chloride and chloride is coming |
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36:45 | And Gaba B, which is mediated metabolic tropic opening of the potassium channel |
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36:54 | very similar to what we talked about muscular acetylcholine receptor. So now, |
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37:00 | in this review because we're going so master stuff, you actually can connect |
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37:05 | things and see some of the redundancy the systems and the functioning of these |
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37:10 | in this case it's potassium is going be going out. Both of these |
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37:15 | hyper polarizing effect. So unlike nicotine locally versus most chronic, they had |
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37:22 | effects on the membrane. You can additive effects hyper polarization through iona tropic |
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37:28 | A and more hyper polarization through medical Gaba B receptor and three cinematically because |
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37:36 | talking about voltage gated calcium channels located synaptic Gaba B receptor can also block |
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37:42 | gated calcium channels which will control neurotransmitter . I use the slide here and |
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37:48 | said hey this is a really good . You can actually erase the figure |
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37:53 | if you want to copy the image put all of the notes that you've |
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38:00 | . For example this is gather be spots, synaptic potassium channel. |
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38:07 | And what else opens part synaptic fashion about perceptive. So you can put |
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38:14 | your nose yourself a similar mechanism. here you can label yourself instead of |
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38:20 | at the key, you can sort Gaba A. Because it's chloride Gaba |
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38:25 | . Because it's potassium. And what talked about here, we talked about |
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38:29 | you have an inhibitory synapses can release cause inhibition through Gaba A. Cause |
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38:34 | inhibition through Gaba. D. But can also regulate its own release through |
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38:39 | auto receptors. So Gaba B receptors are located on the pre synaptic inhibitory |
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38:45 | , they will essentially shut down the through regulation of voltage gated calcium channels |
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38:52 | they will self regulate the Gaba However there is a lot of Gaba |
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38:57 | Gaba spills over. It also has cis optic receptors on the adjacent excitatory |
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39:02 | and activation of the Gaba B. the pre synaptic terminal of the glutamate |
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39:08 | can now regulate dramaturgical elements. We talked about how Gaba B can also |
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39:14 | located post synaptic aly on these excitatory and that. Although glutamate is being |
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39:21 | here through calcium influx and through the messenger cascades. You can actually activate |
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39:29 | B receptor. And that Gaba B will open. potassium channels will cause |
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39:34 | hyper polarization. That will basically start an M. D. A channel |
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39:42 | opening by causing the hyper polarization. you can see these really nice interactions |
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39:48 | between the inhibitor and excited synopsis. complexity that you see here that you |
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39:52 | see in the neuromuscular junctions. Okay like I said this is a really |
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39:57 | slide to take notes about what's happening what you've learned about. And when |
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40:03 | talk about inhibition this is Gaba and B. So when you stimulate this |
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40:09 | lateral nuclear itself and the relay cells the lateral nuclear nucleus. So when |
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40:15 | stimulate an optic nerve and optic tract this case optic tract input into the |
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40:21 | . G. M. You get followed by inhibition. If you block |
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40:27 | A. With bike you colon, is with Gaba A. You can |
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40:32 | excitation followed by inhibition. Small excitation you blow Gaba A. And you |
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40:38 | the same stimulus boom, you produce abnormal excitation in these cells. So |
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40:44 | does inhibition do? It really sculpts C. P. S. |
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40:47 | S. It sculpts the excitation levels deep polarization levels in the south G |
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40:54 | coupled receptors. We reviewed our seven membrane the receptors that are linked to |
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41:00 | G protein complexes multiple different muscular We just mentioned one but there are |
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41:06 | of masculinity and 12345 medical tropic glutamate through 12, maybe 14 since I |
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41:14 | last time. Uh dopamine same Opioid cannabinoid CB one we talked about |
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41:20 | one. CB two are mostly on wheel cells, will come back and |
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41:24 | about it a teepee which buys the and receptors and we looked a little |
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41:28 | in the ligand, trance mitigated channel and has these M one through M |
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41:36 | trans member in segments. And there some similarities between some of the segments |
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41:42 | some of the coding. And these are usually coming in different flavors. |
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41:47 | alpha alpha, this is nicotine. receptor has five subunits to alpha |
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41:53 | That's where the two molecules of acetylcholine going to buy the number, you |
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41:57 | to buy two molecules in order for uh receptor channel to open. So |
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42:03 | for this diagram you should know acetylcholine step dives agonists and antagonists acetylcholine |
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42:12 | You should know the push pull system alpha and beta receptor systems for |
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42:20 | You should know everything to an M A and an M. B, |
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42:23 | C. And Q. X. a PV. For Gaba, you |
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42:27 | know that there's Gaba, a laura b potassium. We only mentioned by |
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42:32 | colon as an antagonist for Gaba A for a T. P. We |
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42:36 | to Dennis and track prostate will also as a neurotransmitter. So that's another |
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42:42 | that I left off of that initial were added under cannabinoids, orthodontic acid |
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42:48 | and a denizen triphosphate. Denizen triphosphate also bind the denizen receptors. A |
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42:55 | receptors. What they do a denison of the denizen receptors will close present |
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43:02 | the calcium channel and excited to a . So dennison will reduce the amount |
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43:08 | glutamate. It's an agonist but it activate the G protein and will close |
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43:15 | channel. So it will activate G caffeine is an antagonist. So by |
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43:22 | this pathway calcium channel. Stay open the calcium channel stay open and glutamate |
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43:28 | getting the proper release and that's what you up in the morning when you |
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43:32 | a cup of coffee and then we a significant amplification through neurotransmitter systems and |
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43:39 | have the systems that can divert the that can converge systems that can work |
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43:43 | parallel overlap and target the same effective we just saw that you can target |
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43:49 | potassium channel through gotta be masculinity You can even target through norepinephrine but |
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43:55 | a slightly different pathway that leads to in different defector. And uh let's |
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44:06 | this actually concluded our neuro transmission So if there is any questions in |
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44:14 | or on zoom, I'm running really on time but I would be happy |
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44:20 | take a couple of questions. If I'm gonna take a couple of sips |
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44:26 | water and continue with the C. . S. You guys missed your |
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44:42 | couple of questions. Sleuth 400 blue fly high with an M. |
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44:59 | . D. A. Receptor. is the neural transmitter. Glycerin is |
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45:04 | co factor. So binding of licensing the proper binding of glutamate, proper |
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45:09 | of an M. D. Receptor. The studies that are being |
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45:12 | to what extent can you open an . D. A receptor and reducing |
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45:16 | amount of glycerin or in the absence it. But for it to be |
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45:20 | functioning it's a co factor that has co binding to a different site than |
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45:25 | . It's not competing for the same in order for that an M. |
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45:29 | . A. Receptor to properly Okay. C. N. |
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45:34 | Uh We have about 10 minutes. C. N. S. So |
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45:40 | your medical terms location? Centerior posterior, caudal dorsal, ventral, |
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45:46 | sagittal, horizontal kurono. We talked how you have development of the brain |
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|
45:55 | that. We discuss the three men said dura arachnoid and the PM. |
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46:00 | talked about subdural hematomas that can happen maybe the brain trepidations were also used |
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46:05 | alleviate the damage from subdural hematomas. production of cerebrospinal fluid and cord plexus |
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46:11 | gets circulated throughout the cNS and the cord that we're talking about and some |
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46:19 | If there's overproduction of the fluid needs be drained if it is not it |
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46:24 | cause a bad shape of the skull the brain. This condition called |
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|
46:30 | We then looked into how you have primordial tissues and the meso ecto derm |
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46:35 | how the neural plate and the neural formation happens from the extra term. |
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46:41 | you have this process of no relation during this process of no relation. |
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46:46 | there is a dysfunction in roster, may end up with anencephaly dysfunction with |
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46:52 | folding of the neural tube may lead spin bifida bifida be surgically corrected. |
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|
46:59 | then from this neural tube you have process formation of forebrain, midbrain, |
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47:05 | brain and further differentiation of forebrain into talent cephalon phallic vesicles and diane cephalon |
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|
47:12 | is thalamus and hypothalamus optic vesicles. we traced the differentiation of midbrain for |
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47:20 | into corporate quadra gemini, this superior and Nero caligula pointed out the major |
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47:26 | in the in cephalon thalamus hypothalamus, connectivity here through corpus callosum of the |
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47:32 | hemispheres. The projections from the thalamus, cortical and cortical thalamic through |
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47:36 | internal capsule. And here is the large lateral ventricles for the cerebrospinal fluids |
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|
47:44 | there will be a lot of labeling . Uh Mostly I think labeling questions |
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47:49 | come from C. N. From this portion and some from the |
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47:55 | system. But when you're learning something labeling you should learn it in |
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48:01 | So not for that specific image but a different image also. And you |
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48:06 | quiz yourself online if you can label different parts of the brain here, |
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|
48:10 | introduce the cortical organization in the cortex we said it's a laminar structure but |
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48:15 | also a columnist structure. Okay. we introduce the new die here. |
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48:21 | wider stain that is axon specific and clearly shows these vertical projections that are |
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48:26 | within the cortex across the lamb in in a vertical fashion. And then |
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48:31 | also touched upon the fact that in brains the primary sensory areas are very |
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48:37 | compared to the rest of the size the brain and the lower order |
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48:40 | including cats and some other animals like . They're all concerned about the primary |
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48:45 | processing which I also see what I for the visual cortex but not necessarily |
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48:51 | you interpret what I see or how I feel about what I see? |
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48:54 | really about what I see rather than it and making a bigger picture overall |
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|
48:59 | other senses which happens in the association . Look at the division's major divisions |
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49:06 | the spinal cord, signal number, , cervical brainstem and midbrain attached cerebellum |
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|
49:14 | the back we talked about different functions these structures. We talked about service |
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49:20 | example, force and range of learning motor skills which is procedural |
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|
49:24 | We talked about basal ganglia as motor initiation and some of the complex motor |
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|
49:32 | patterns that are being stored and initiated basal ganglia, zebra hemispheres and |
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|
49:39 | in addition to basal ganglia. We talked about hippocampus and amygdala. So |
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|
49:45 | we talked about hippocampus and amygdala I there was an image maybe somewhere |
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49:51 | This is amygdala, this is the . We talked about the hippocampus is |
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49:55 | for semantic memory, places, spatial memory and spatial navigation, encoding |
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50:02 | that memory and recall of that So that's different from procedural memory that |
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|
50:07 | just discussed with cerebellum. Amygdala is fear center. Also Magdala will have |
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50:13 | very special area that recognizes emotions in faces. So it can tell you |
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50:18 | digital cortex can tell you're looking at face, this is what it looks |
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50:23 | amygdala eventually through complex communications will say an angry face, stayed away or |
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50:30 | they're happy you know, don't go them. So complex activities in the |
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50:37 | we don't think about them but many parts of the brain are involved. |
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50:41 | we're doing simple tasks. We talked dan cycle and talentless different nuclear and |
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50:47 | processing different sensory functions for L. . N. S. Provisions. |
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50:51 | media is for auditory GPL ventral posterior is for the summer to censor information |
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50:57 | it goes into cortex and surrounding these which have their own circus society and |
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51:02 | circuits within these nuclei surrounding these nuclear the radical Islamic sheet economic nucleus which |
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51:10 | another layer of inhibition that controls activity the Islamic nuclei and they're not |
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51:17 | So they have their own functions and gating the incoming sensor information hypothalamus we |
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51:24 | is involved in the neuro endocrine system super charismatic nucleus which is a part |
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51:29 | the cephalon is the control of the rhythms and a small portion of our |
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51:35 | . Gay, angry and sell outputs the retina, innovative, super cosmetic |
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51:40 | , a few percentages of all of original fibers and innovate here is the |
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|
51:45 | callosum that we discussed in a different . That's what I said. Don't |
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|
51:49 | where corpus callosum is. Um One , because I may ask you about |
|
|
51:52 | callosum in another slide that that is the one that you learned in. |
|
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51:58 | it's better just to learn where the are. Talked about the cerebellum. |
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|
52:02 | if you remove the cerebellum you expose corporate corporate Germania, superior curricula here |
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|
52:08 | we discussed in the visual system and psychotic eye movements so they will get |
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52:12 | small portion of the retinal ganglion cells into the superior caligula to inform them |
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|
52:17 | there's light outside. This is the ventricle going into the spinal canal for |
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|
52:22 | ventricle system and then we talked about cranial nerves and I said that with |
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|
52:28 | cranial nerves I use the pneumonic you have to use the pneumonic. I |
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|
52:33 | that pneumonic but what I asked you I asked you to know six of |
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|
52:38 | nerves. One which is all factory which is optic three which is ocular |
|
|
52:44 | . We saw these beautiful muscles that attached to the eyeball. Popular |
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|
52:49 | So this is the control of the movement of the eye. Trigeminal, |
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|
52:55 | largest nerve you should be able to its stock optic nerves that should recognize |
|
|
53:00 | often track should be pretty easily for . So five trigeminal than eight vestibular |
|
|
53:06 | because we'll come back and talk about especially the cochlear to component of the |
|
|
53:11 | cochlear nerve when we talk about the system and 10 is the vagus nerve |
|
|
53:17 | runs very extensively through this. So of the cranial nerves will be controlling |
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|
53:21 | lot of the census and motion around face, head and neck. And |
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|
53:25 | of the cranial nerves will have broad throughout the body. Vagus nerve is |
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|
53:29 | example of that Vegas nervous, innovating heart. That's where auto low we |
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|
53:35 | between the nerve and the cardiac muscle the acetylcholine is a neurotransmitter and there |
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|
53:43 | is an inhibitor neurotransmitter because most of receptors in the heart are masculine IQ |
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53:51 | receptors and it's really very sympathetic control your body sympathetic. Everything is up |
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|
53:58 | rate up higher sympathetic down. So is through vagus nerve and settle Colin |
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54:03 | the heart. That's the mechanism that civil coding that we really discovered. |
|
|
54:10 | then we moved into the spinal We walked through the anatomy and said |
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|
54:14 | you have seven cervical vertebra you have thoracic five lumber. And you have |
|
|
54:21 | which within each one of these Within vertebral column you have a spinal |
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|
54:25 | that's associated. But for cervical you'll eight cervical nerves. Uh and then |
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|
54:31 | have 12 thoracic nerves coming in a lens. The proper spinal cord is |
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|
54:35 | start with number 23 and number 23 becomes caught a quien and surprise into |
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|
54:41 | fibers and innovate the lower portions of body. If somebody has a brain |
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|
54:46 | for example such as meningitis, they undergo spinal tap and the spinal tap |
|
|
54:51 | is typically going to be between Two and three, inserting a needle |
|
|
54:56 | the meninges and trying to sample the spinal fluid without damaging the spinal cord |
|
|
55:01 | . And if you sample the cerebral fluid here that seems to the spinal |
|
|
55:06 | is bathing your brain. So if detect infection here, bacterial or |
|
|
55:10 | it is in in the in the the severe room as well. So |
|
|
55:15 | way of looking at it. Epidural anesthesia that is done to anesthetize the |
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|
55:21 | portion of the body. Epidural is typical anesthesia that some women choose to |
|
|
55:26 | during the birthing process to alleviate the from the contractions in the lower body |
|
|
55:34 | . So now in uterus. Now spinal nerves are comprised of the sensory |
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|
55:40 | motor component. You have the ventral dorsal horns. The dorsal horns with |
|
|
55:46 | sensory component is going to come Ventral horns is where you have motor |
|
|
55:51 | that are located there that will send axons out. Okay. And then |
|
|
55:55 | have these major ascending sensory pathways. as you can know the dorsal column |
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|
56:00 | the major sending sensory pathway and also you to remember that ascending sensory descending |
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|
56:07 | not sensory, descending his motor because is descending is descending down into the |
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|
56:13 | cord ultimately the output of the spinal is not to think about stuff but |
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|
56:19 | execute the contraction of the muscle and motor movement. Okay. And then |
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|
56:24 | course you know the cranial nerves are now that I'm speaking you know moving |
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|
56:28 | tongue and speech areas and communication with of that and waving my hands through |
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|
56:35 | cortical spinal and the llamas spinal outputs so on. So I didn't ask |
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|
56:41 | to remember the descending but I asked to remember the descending of motor but |
|
|
56:45 | ask you to know that dorsal calling major sending sensory pathways to innovation through |
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|
56:52 | peripheral nervous system. We mentioned briefly talked about imaging techniques that we said |
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|
56:56 | our static imaging techniques, X ray scan. And then there is a |
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57:01 | imaging techniques and these are clinical functional techniques and we compared pet positive emission |
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|
57:08 | which tracks the oxy glucose neurons that active from consume a lot of glucose |
|
|
57:15 | neurons that are active also consume a of oxygen FmR. I functional magnetic |
|
|
57:21 | imagery will be tracking the levels of oxygenation. So you can actually produce |
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|
57:26 | measurements of these brain maps and these maps. These hotspots will show you |
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|
57:32 | active areas of the brain as a who's performing certain tasks. Just like |
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|
57:37 | looked at at the very first two of this course and also mentioned that |
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57:42 | procedure can be quite difficult to young or to elderly patients or patients that |
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57:47 | claustrophobia especially for head and neck And I also mentioned that Patton Fmr |
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57:53 | also be used outside head and neck diagnosing different things such as cancerous activities |
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57:58 | cancer cells in different parts of the . Okay so this concluded the pretty |
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58:07 | the um C. N. And I would recommend for you to |
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58:13 | major parts and functions of the N. S. Again maybe I |
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58:18 | take that diagram that I was just you with different divisions of spinal |
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58:24 | brain stem and C. N. . And I would use that maybe |
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58:28 | a as a note taking I would like cervical, 12 cervical Uh sorry |
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58:37 | cervical nerves, 12 thoracic nerves. we put c. seven which means |
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58:44 | are seven cervical vertebra. But then would put C nerve eight has eight |
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58:51 | . So you can take notes on . Then for example brainstem when it's |
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58:55 | down the duo of long gotta write the function and then you're gonna be |
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58:59 | really good shape for this section to visual system will discuss the properties of |
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59:06 | anatomy of the eye. In general walked all the way from the |
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59:11 | from the eye into the primary visual and we ended there in the primary |
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59:16 | courthouse. So we did talk about there are streams that are going to |
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59:21 | into the parietal areas and the temporal that will process different parts of this |
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59:26 | information. But when we stop you the primary visual cortex we actually have |
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59:31 | primal sketch what we call that the world. So please review the anatomy |
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59:37 | the eye. That phone is a security region located very centrally. This |
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59:43 | circuit of photoreceptors, bipolar cells, ganglion cells, the processing of |
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59:49 | And when attempts to that, we about how photo receptors are responsible for |
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59:55 | transaction ganglion cells will be the only from the retina. You have these |
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60:01 | layers. There's major differences in the segments of the photo receptors where the |
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60:06 | are very sensitive and they have free discs that are loaded with photo pigments |
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60:11 | different systems, rises from night Very high sensitivity combs is for chromatic |
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60:16 | three types of cloners and for direct of light and high acuity. So |
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60:23 | are expressed in the central areas of phobia of the retina laws are concentrated |
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60:28 | the periphery and because you have these types of cones, you can undergo |
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60:33 | we call color mixing and producing a of different colors and use that we're |
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60:40 | . So uh if you recall in dark, the photo receptors actually d |
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60:46 | because there's influx of sodium in the of cycling GMP in the light. |
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60:51 | photo transaction is such that this retinol from trance turns into cysts in the |
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60:57 | and actually activates the G protein which decreases the presence of cyclic |
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61:03 | And in the absence of cyclic the sodium channels closed. Therefore |
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61:08 | they're actually hyper polarized in the When we talked about the receptive field |
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61:13 | of the south. And we said if you were to connect to the |
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61:16 | ganglion cell newer to stimulate retina. is this retinal ganglion cell is going |
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61:21 | be most responsive to and we found it's most responsive to these circles of |
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61:26 | that have center and surround light center lights around dark center or dark |
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61:32 | That's what Britain is most responsible This is the anatomy. It is |
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61:36 | to groups of photo receptors. This what retinas processing. We later saw |
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61:41 | L. G. M. Is seeing the same point by point representation |
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61:44 | these concentric centers surround receptive field properties only in the primary court actually had |
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61:50 | convergence of these receptive field properties in different shapes that allowed us to produce |
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61:55 | primal sketch of the outside world. looked at the circuit and a lot |
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62:00 | people are confused about the circuit but are several things that I wanted you |
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62:03 | know about the circuit despite the fact there's light or dark. Just remember |
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62:09 | in the dark, neurons are d in the light are hyper polarized. |
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62:14 | these photoreceptors can be enacted to either is going to be excited. So |
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62:22 | the cell is excited this cell is to be excited because it's acting through |
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62:28 | a tropic receptors glutamate acting through medical receptors and some bipolar cells will express |
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62:34 | tropical receptors eliminate these metal tropic receptors gonna be inhibitory. So this is |
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62:40 | inverting it doesn't mean that inhibition is . This is the same neurotransmitter |
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62:45 | But if it goes here deep polarization in the light, it's what hyper |
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62:52 | sign, conserving hyper polarization Simon servant polarization. That means this cell is |
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62:59 | reacting to the cell in the likely reacting to the cell is going |
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63:03 | be this around. That's why it's center. It's not reacting to the |
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63:08 | in the light. This is hyper . If there is no blue to |
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63:12 | this is hyper polarized. Inverting is do what D polarizing. This is |
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63:17 | polarization. So this polarized, the is on center game. Okay so |
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63:23 | this details that there's sign conserving sign . So I'm conserving island tropic |
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63:29 | inverting is metabolic tropic signaling. the light in the dark. I |
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63:33 | ask you questions like the light was off set yourself. It's connected to |
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63:39 | medical tropic bipolar cell you know. I want you to know that this |
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63:44 | tropic on the tropic that you can essentially to the same which has been |
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63:49 | to cells can have a different effect of the ganglion cells. And also |
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63:55 | you to know that Gaba or inhibition produced by horizontal cells. So there's |
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64:01 | when we talk about negative feedback if excite, the cell is assigned conserving |
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64:06 | going to excite this horizontal cells but horizontal cell is inhibitory Gaba and it's |
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64:12 | to project back from the same cells excited and what projects Gaba onto this |
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64:17 | receptive and hit the suspect. And there's this horizontal lot of control basically |
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64:24 | is inhibitory control. Otherwise the entire here is just glutamate. I'm not |
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64:31 | it's all excitatory because we have signed burden but it's all glued dramaturgical signaling |
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64:35 | this direction going down to the horizontal . So the ones that introduced this |
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64:40 | allergic or inhibitory levels of signaling. but you having fun yet can we |
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64:50 | this in three minutes. Sign inverting in conserving. This was an interesting |
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64:57 | . We talked about critical period of . Critical period of plasticity. We |
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65:01 | in animals like rodents is the first of life in humans depends for what |
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65:06 | we learn different things at different stages life, it is typically into the |
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65:11 | when we are most susceptible to learning best and recovery from injury the best |
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65:16 | well because of the chemistry and because the connectivity and plasticity that is still |
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65:22 | . And so we saw an example how short term deprivation, sensory deprivation |
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65:26 | vision in one eye. And these during the critical period of development can |
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65:32 | the projections into the cortex. Most them will come into layer form |
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65:38 | This will change the function so the will not be as responsive to images |
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65:43 | the eye that was closed. And you prolong this deprivations to longer period |
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65:48 | time you can forever change the anatomy the functionality of the cortex where it's |
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65:54 | ignoring all of the stimulation coming in the side doesn't mean that the circuit |
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65:58 | the eye is destroyed but the cortex not responsive to the activity coming from |
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66:02 | . I kind of forgot that it important during this critical period of development |
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66:08 | now there is no regain or recovery function. So when we talk about |
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66:15 | visual field deficits is a great exam too. When you talk about damage |
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66:19 | one nerve on one side and equivalent that is closed you online, that's |
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66:26 | damage that you will see on the field. When you talk about damage |
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66:31 | the optic tract. You're talking about that crossover contra and it's a lateral |
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66:37 | that stay on the same side. that retina collect cups. They're not |
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66:44 | . If your retina was flat and portion would be looking here. This |
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66:49 | will be looking here and this portion be looking here. This will be |
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66:53 | here. Retina is not flat. this portion is looking here. This |
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67:00 | is looking here. This portion is at So put your two hands like |
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67:06 | and verte and tell me where your retinas are looking in the periphery. |
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67:12 | we're looking at the periphery nasal retinas the ones that cross over you cause |
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67:19 | to nasal retinas to the chi as over. You lose peripheral vision. |
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67:25 | tunnel vision. So do this exercise you're having difficulty and of course you |
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67:30 | memorize what it does to the optic but now if you know which one |
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67:33 | it in concert is going to be to do this exercise. Close one |
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67:37 | for one nerve damage and remember that writing these kinds of cops. This |
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67:42 | looking over there and now flat the is not flat like this. Okay |
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67:49 | is the damage. We have six . We have this written the |
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67:53 | Point by point representation from the retina the L. G. M. |
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67:57 | have the magna and the powerful We have very small primary visual cortex |
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68:02 | 17. This point by point representation all the way to the visual |
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68:07 | We have very specialized anatomy and layer where the projections come from the |
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68:12 | We have the stride cortex which are dominance columns. Australia belongs to activation |
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68:18 | only one eye. So the signal mine. Ocular that signal starts becoming |
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68:23 | . In layers 23 there's salama cortical that come in mostly to layer |
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68:28 | Except for the intermediary that bypass layer directly into layers 23. There is |
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68:34 | inter cortical loop that communicates information from to 3 passes it along laterally through |
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68:40 | to three communicates it back to deep and outside from cortex and the thalamus |
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68:45 | also completes this loop layer. Force llama cortical inputs of inter cortical loop |
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68:51 | the cortex have cortical thalamic outputs. so most of the L. |
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68:55 | M. What it receives is cortical and therefore L. G. |
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69:00 | Is really listening and following with cortex to say the blobs which is cytochrome |
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69:08 | increased metabolic activity found in letters to . The south. We asked that |
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69:13 | question we ask the question how can maximally activate right now ganglion cells relay |
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69:19 | and it turned out with the circular Concentric patterns. And then we ask |
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69:24 | can we maximally activate primary visual cortical and it was no longer circles it |
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69:29 | now bars of light and it was activated when it was in a specific |
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69:35 | , specific angle or in a specific of movement, left to right, |
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69:41 | to left up and down diagonally all the 360°. And then we comprised these |
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69:48 | receptive fields and these receptive fields gave different shapes to work with. And |
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69:53 | convergence of simple cells and complex styles us even more shapes to work with |
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69:58 | comprising out of these shapes, what call the primal sketch, which is |
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70:04 | and motion and color that you would on the outside world. We talked |
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70:09 | voltage sensitive dye imaging technique and we in this case that die sensitive to |
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70:13 | in voltage and that was a great to use to delineate these orientation |
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70:19 | These are the smallest units, orientation 31 50 let's say 100 micrometers in |
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70:25 | . And we said, how do fit? These are micro processing units |
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70:29 | south located adjacent to each other, similar orientation to go around this |
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70:34 | You will process orientation all the way 360 degrees. And then we |
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70:40 | let's put this all together, we the blogs and layer 23. We |
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70:44 | the boundaries of the ocular dominance We have these hyper columns. These |
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70:50 | columns, we have the ocular dominance . The blobs within each ocular dominance |
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70:56 | will have multiple of these orientations column . And we finally discussed elastic |
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71:01 | which is the intrinsic optical signal. said that there's no die here. |
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71:05 | no eye on down the drain will reflect its properties and the cell will |
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71:10 | reflecting properties as a function of So this light wide that you're sitting |
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71:16 | in faith represents this zone here, is this contra lateral zone, Oculus |
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71:24 | zone. You can actually visualize on surface of the brand. So this |
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71:27 | more of an experimental technique again about sensitive dyes both and the intrinsic optical |
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71:33 | rather than the clinical application. But is something you should know that active |
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71:38 | will not only consume glucose oxygen, will swell and they will change the |
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71:44 | properties because their membranes are becoming thinner least neurons well. And we ended |
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71:51 | . So for the sake of saving lecture and uploading it, I'm gonna |
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71:57 | the recording here and happy to take few questions for about five minutes until |
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72:04 | have to clear out of this I'm wishing everyone good luck on |
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72:09 | I'm hoping everyone is registered. I'll this review session now. It was |
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72:14 | better than yesterday's and I didn't have interruptions. So thank you, thank |
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72:19 | . That was being on zoom and will see everyone in person next week |
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72:25 | the |
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