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BIOL 6397 CELLULAR NEUROSCIENCE Mon-Wed 4-5.30 PM - Cellular Neuroscience Midterm 2 Review
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00:02 So this is uh my two review I'm gonna do it a little bit
00:11 . I'm gonna go through the video and remind you that all of this
00:17 is on in the video points. we discussed some important uh concepts of
00:30 in our first lectures. And we about in particular the rate code and
00:39 talked about the spike timing code. when we talked about rate code,
00:49 talked about the fact that when you the cells, that stimulus of conditioning
00:57 we looked a lot of and C one of the hippocampus can change
01:04 Synoptic elasticity can strengthen synopsis called called potentiation or facilitation. If it's short
01:14 , it's facilitation. If it's long , it's long term potentiation or it
01:19 cause short term depression or long term . Uh And so what we saw
01:28 that there is a particular rate code that rate code typically low frequencies and
01:36 particular along the uh Shaffer collateral projections the hippocampus that VCA 1 area of the
01:47 , uh low frequency stimulation can cause and repeated high frequency stimulation can cause
01:56 term P Preti now within the actual stimulus, which can come in different
02:06 . So you can produce 100 Hertz , 10 Hertz trains, 50 Hertz
02:12 within that stimulus. What you'll see that you'll see that you'll have during
02:19 stimulus. If there's summation and the P S BS are increasing in amplitude
02:26 you have facilitation and in some you have temporary facilitation followed by short
02:33 depression. So we said that this one way by which the brain circuits
02:42 the information and learn the information uh by this rate code. Uh And
02:53 we looked at some of the explanations how it's possible that in some instances
03:03 have L T D in other you have L T P. And
03:07 saw that it's an MD A receptor , it is dependent on calcium
03:12 And in general, this plasticity can presyn optic and synoptic. So you
03:16 have changes on the preoptic level and level that are both going to be
03:23 to either potentiation. In this if we're talking about um uh
03:30 uh you will have insertion of new optically and an MD A receptor in
03:37 glutamate and MD A receptors as coincident are very important in plasticity. And
03:44 also understand that we can generate new , we can insert new proteins in
03:51 synopsis. So we can cycle new with spines and the synaptic spaces and
03:57 synaptic spaces and they can laterally travel the synaptic spaces here into the synaptic
04:04 . So upon demand, there's more that can be recruited into the
04:12 Now, long term changes inevitably will require activation of the cellular processes.
04:22 And even transcription factors, short term could be related to the changes here
04:30 the level of the synapse, the during the stimuli. Um following the
04:38 , longer term changes and long term can last days and weeks. Uh
04:45 are associated with intracellular changes. And we can see that in this
04:55 we saw how imaging will demonstrate that then we moved on to talk about
05:01 timing, the dependant plasticity. So addition to the rate code, we
05:06 about how the timing of when the cell fires an action potential and the
05:13 to when the postsynaptic cell is not producing an E P S P,
05:19 when the postsynaptic cell is stimulated enough produce an action potential, that's when
05:26 have the presynaptic stimulation and post synaptic . So if you have pre synoptic
05:36 post synoptic and it's very tightly linked time within 10 to 20 milliseconds,
05:44 cells will bind the activity. Pre poop activity will cause potentiation, spike
05:52 , dependent plasticity L T P. if you reverse the water, so
05:57 synoptic cell is firing before pre synoptic . You may see the opposite effect
06:04 it computationally the communication is not making for the pre synoptic cell because the
06:13 cell is firing first, not in to the input but uh in response
06:18 some other input to, to this cell, the relationship with the postsynaptic
06:24 gets weakened. So you have this that you have L T P and
06:31 shorter the window between the pre synoptic potential and synoptic response, the the
06:38 uh level uh of efficacy there is . If pontic, before pre synoptic
06:46 L T D also the closer in they're associated, the larger depression you
06:52 see in that sys in reality, we also learned is that these curves
07:00 be shifted. So you can have degree of potentiation or higher degree of
07:07 . And you can also have uh windows and longer windows for plasticity,
07:17 potentiation or depression. And we also about how with neuromodulatory substances such as
07:24 mean agonous and antagonist, it can reshape what you call the spike timing
07:32 plasticity. Classical curves in B and , you can alter these curves where
07:39 post synoptic signaling before pre synoptic signaling also in some instances cause potentiation.
07:47 rule again are closer in time pre posts or post pre still stands
07:54 these altered curves for the classical climbing plasticity curves on modulated curves. So
08:03 talked about um neuromodulation uh and uh in diseases and how there are neurodegenerative
08:16 and neurodevelopmental disorders and addiction disorders where may have impaired plasticity and in particular
08:25 spike timing, depend on plasticity. So I pointed you to, to
08:33 article to view for your viewing which is attached on your uh class
08:43 literature documents. And that's where you find it. And uh we talked
08:53 uh this diagram there again that showed prepose stimulation that we discussed and showed
09:01 example of modulation of spike timing dependent . OK. And after that,
09:17 started talking about imaging techniques and we . So this is where kind of
09:25 talk ends. Although imaging is also to imaging plasticity in the synopsis.
09:31 this is just a brief overview of plasticity. If there is no
09:37 I'm gonna move on to the imaging . So this is the functional
09:45 When we say experimental, it's obviously the basic sciences category and the advantage
09:53 basic sciences that we can image at of these different levels from subcellular cellular
10:03 centric meso scopic and macroscopic levels. we talked about genetically encoded voltage indicators
10:16 and so you can express indicators in cells. And when those cells change
10:23 voltage, when the membrane potential changes those cells, you could actually see
10:29 as a change in an optical signal is expressed by the cells in the
10:36 of these uh voltage indicators. So uh dyes uh do do not have
10:47 be genetically expressed, they can also added. So voltage sensitive dyes not
10:56 genetically encoded but voltage sensitive dyes. the advantage of voltage sensitive dyes again
11:03 that you can see from single cell multiple cells to this mass cop and
11:11 level. And you can sample very fast speeds. That means you
11:18 image activity, voltage sensitive dyes and genetically encoded voltage indicators are very
11:25 So you can image that activity in very fast fashion. Mhm I think
11:32 gonna come back and talk about this a little bit later. But here
11:38 talked about uh how you have static functional imaging. And in functional
11:46 we're looking in intrinsic activity imaging is , blood flow metabolism, ions,
11:55 and potentially receptor movement that can OK. So then we uh where
12:04 we here? Yeah, then we to talk about cortical organization but we
12:11 back and talked about this example again we looked at the visual system and
12:18 organization and the ocular dominance columns. what I wanted to share with
12:29 it is the following movie that was by me and my graduate student.
12:39 called epileptic brain waves. And can see this blue screen that says optic
12:46 waves? No, we can't. , interesting. So I'll show you
12:58 of what voltage sensitive di imaging looks in this movie. I'm gonna play
13:05 the movie and explain to you and should understand everything that I say here
13:10 . Mhm. 30 Hertz period, means you're reducing your policies. Recall
13:31 . The this I'll see you guys side. See sir, transfers if
13:54 a serious and this is from So I'm stimulating Gyrus and seeing the
14:02 spread now the same stimulation, 40 Hz stimuli. But now we've created see
14:14 difference in the out. It's the same stimulus, exact same the we
14:28 the space has become wider. You , doctor, we can't hear all
14:41 the, that's what show is Yeah, Kevin to experiment individual
15:01 When we're looking at little uh collections of cells down, this is
15:12 stimulation. This is C3 right signal traveling through shop of collaterals into
15:22 C. This is uh basically it's that were created that show how these
15:33 bursts can start forming. So you really start sensitive. Um What is
15:41 formal signaling? What is was a temporal pattern? And the what is
15:53 ? This is really neat. What see is you'll see that this is
15:57 a cross section or coronal slide through . Neocortex. We're looking, I
16:05 here in the visual cortex, this deep layer six and this is superficial
16:11 one. So if you remember when talked about the visual system, we
16:15 about the circuit and the projections. so here you'll see the formation of
16:23 bursts in the deep layers, they up into layers 23, they spread
16:29 distance along layers 23. It's an wave in this case again, it's
16:35 activity but it shows it's very uh C how this to pieces here.
16:58 this is a contour map slash edge of I is what you previously here
17:19 multiple sensitive guys, the most dominant of signal that you see here in
17:28 representation that's really cool. And then talked about rip. So we talked
17:37 it's very super fast oscillation sitting You see emission, excitation and emission
17:43 of waves of excitation spreading across the actually turned out to be an
17:51 But other labs have demonstrated that in tissue, this particular example turned out
17:57 be a and of the decision. , exactly. Of course, is
18:37 presenting. So this is a really demonstration of uh of this uh Doctor
18:57 Yeah. Oh my God, you hear us. OK? Um
19:01 sorry, we're talking in the None of us can hear you for
19:06 whole thing. Your video plays super music. And so we've missed like
19:11 of it basically. Yeah. hopefully it will be on the
19:20 I hope somebody would have uh interrupted . I couldn't hear you for some
19:27 if you're trying. Yeah, we'll . I think it's going to be
19:41 your recording because it's on, it's my screen. So I'm hoping the
19:48 time. It didn't uh didn't, show up. Um I don't want
19:57 stop the recording now and save it then restart it because this will kind
20:02 uh eat up the rest of our . So I'll just move on as
20:09 demonstration of all of these different, sensitive dyes and the pathways that you
20:16 are familiar with uh in the hippocampus what they appear like with visual sensitive
20:25 , uh molted sensitive dice. For clinical noninvasive functional imaging, we
20:40 two techniques patent F MRI. So should know the difference between the x-ray
20:46 C T scans that are static MRI that are static and pet positron emission
20:56 . F MRI. Inevitably imaging changes metabolism changes in oxygenated hemoglobin levels in
21:06 case of F MRI and the ability reveal these activity maps in the brain
21:16 . Although as we discussed, the the procedures for this are are are
21:21 fairly difficult um and almost impossible for of the patients for a number of
21:29 . OK. There was a supplement also that you can download that talks
21:37 these imaging techniques in addition to to slides that we discussed and then we
21:45 ourselves into the visual system. And the visual system, we talked about
21:54 transduction that happens in the photo receptors the mechanism for photo transduction. We
22:02 about neuronal circuit in the retina from , bipolar cells to retinal gang cells
22:10 well as horizontal and amrine cells. talked about receptive field properties of the
22:19 and the retina and L G M on center or off center. So
22:27 like representations of luminescence at the level the retina and L G M,
22:34 also discussed the fact that in the in the retina. So glutamate and
22:42 the difference between uh glutamate exciting certain and glutamate inhibiting other cells is the
22:53 that's expressed by bipolar cells and ate would excite those bipolar cells. And
22:58 they express some GR- 6 glutamate would actually those cells and lack of glutamate will
23:09 depolarization just the opposite. So if can recall the principle that in the
23:18 , the cells are actually depolarized and the light, the cells are hyper
23:24 because there's no influx of sodium through mechanism here. And if you can
23:30 that a is signed conserving the metabotropic is sign inverting. You should be
23:37 to understand the circuit and answer some the questions. I may have horizontal
23:44 as we talked about are inhibitory. express gabber with these gabba and they
23:49 this negative feedback like circuit onto the cells. Uh We talked about uh
24:00 that exit out off uh off off the retina. OK. Uh
24:13 uh go into the higher processing So we talked about retinal gang cells
24:21 are on off, that are distinction on receptive field properties. And then
24:27 have projections from MP and non MP that is anatomical functional distinctions. And
24:36 , before we ventured into the uh we spend significant amount of
24:45 Uh speaking about the retina geniculate And if you recall, there is
24:54 information that was included about retina genicular . OK. So if you go
25:04 to your lecture folders under the content your lecture reading supporting materials.
25:20 we have this information here. Single networks, neuromodulation of synoptic plasticity,
25:32 , neuronal activity, and faction and illness, which relates to olfaction and
25:41 illness. And I thought that here have the long cortical circuit vision review
25:50 we also have the retina genicular OK. So I highly recommend that
25:58 review. In this case, we about the refinement of retinal projections into
26:07 geniculate nucleus. Uh We talked about connectivity and uh and this period of
26:17 uh critical period of plasticity um and field structures that you would see in
26:25 retina and algae and how the activity from retinal waves that are spontaneous into
26:35 visual responses. After P 12 P 14, that's when the eyes open
26:40 get direct a rays of light. there is retinal convergence? At
26:45 a lot of inputs coming into the cells and then that gets refined to
26:51 you have 1 to 1 connectivity between and al G M and you also
26:57 this feed forward inhibitory circuit here. Synoptic activity that we discussed also changes
27:06 you will have a lot of A lot of these staffs will be
27:11 of many of these different synopsis. in adults, you would see only
27:16 or two E P SPS indicating just or two excited inputs, mostly one
27:22 well as the sub the field structure you will see both in the retina
27:28 the algae on. So now this also a diagram that we discussed where
27:34 retina projections will go into the L N. But L G N also
27:40 a lot of input from cortex. It receives input from Sue Colliculus.
27:47 receives input from brain stem as well it has this thalamic particular nucleus around
27:55 thalamus which is inhibitory on the thalamus has a specific circuit in the cortex
28:02 that information is communicated from the thalamus communication goes into uh layer four.
28:10 this, the core of the higher levels like 23 and one from
28:16 shell of the thalamus. And these are going into the primary visual cortex
28:24 it's also receiving from the cortex. these going into the cortex of thalamic
28:31 from cortex into thalamus or coral And there's also cortical projection into the
28:37 R N thalamic reticular nucleus to inhibit here uh at the level of the
28:44 the shell and the core of the . So this is important if you
28:51 at the circuit and understand that you can look at the anatomical
28:56 So you can look at these circuit representations of refinement of retinal convergence uh
29:07 the projections that go from the thalamus the cortex. Yeah. Uh There
29:15 also another um article that is attached and that is actually work that I
29:33 as a graduate student that I'm describing . But I described it to you
29:38 different terms of how we did these and filled the relay cells and the
29:44 G N and stimulated them and saw cells are contralateral of lateral. How
29:51 of them were monocular? How many them are binocular? And we saw
29:55 at first, a lot of the are binocular and later after the P
30:00 , p 14, most of the now become monocular responsive in the in
30:08 thalamus. So at first, they're input from both eyes as it was
30:12 the other diagram. So this is another representation of how you would do
30:17 uh experiments with stimulation. You have one step, two, step 333
30:22 , 44444, 55555, you're increasing with stimulus, but you are seeing
30:29 responses that allows you to count how synapses you have onto a given
30:35 So this was really cool work that did I did as a graduate
30:41 And uh it was some of the glory days. Uh when I did
30:47 phd and uh town of New Orleans the Louisiana State University Medical Center.
30:59 we look then at the kind of development of the visual system from thalamus
31:05 cortex. So I'm not gonna go the details of the anatomy, the
31:09 contra the connectivity, but I'd rather these articles and we looked a little
31:16 about uh expression or overexpansion of area one as uh a part of the
31:30 essentially where we can see that a of the inputs used to be in
31:39 order animals projecting into the superior And by the time you get to
31:45 higher water cats and the cats, very little input going to the superior
31:51 , which is responsible for uh this tic eye movement for focusing. And
31:59 more and more inputs are going into thalamus, which is the perception,
32:05 perception of the visual construct. Uh is a number of L G N
32:16 and V one area expansion. So the number of neurons and how much
32:22 the uh V one area is present different animals. OK. So we
32:30 this almost uh like a perfect linear here between the number of L G
32:36 neurons and the area V one. I think that we talked about how
32:44 lot of neurons will be born and will migrate to their final destination.
32:51 This is some of the lateral contralateral that we talked about. And then
32:58 we talked about the visual field of , we talked about the binocular versus
33:05 field of view and the evolution of . So our binocular field is here
33:12 general, our monocular fields shown in and monocular field in yellow, we
33:20 see um 100 um 50 typically degrees visual field. And we have a
33:32 large binocular zone. Some of the have their eyes placed on the size
33:39 their head. So they actually see 360° such as rabbits or rodents,
33:45 their binocular zones are very small. it also tells you that the higher
33:51 species, uh you have more of binocular vision. You lose uh overall
34:00 to see all around in 360°. But gain a lot more of the binocular
34:11 , which I think is, is is better for for us and
34:16 more advanced way of perceiving visual OK. So these are the articles
34:26 we discussed as a part of the system. Of course, the other
34:32 that we discussed in the visual system the receptive field properties of different
34:40 We talked about ocular dominance columns and how monocular deprivation can actually alter the
34:50 of the cortical cells to the stimuli the deprived eye. OK. And
34:57 talked about the fact that the primal is made in the primary visual
35:07 Uh And in this primary visual you get the construct of the outside
35:16 with the color and with the And so this is where we end
35:21 talking about the uh visual system. I presented it here, this review
35:27 little bit differently for the visual system uh as I said, you have
35:34 notes that have more of the And this is more of the original
35:40 that we uh discussed uh as a of our lecture material. And after
35:48 visual system, we had two more , although we covered the visual system
35:54 two lectures. OK. So sort a lot of it was structure
35:59 receptive fields. And then we talked the red genicular development uh to great
36:07 . And then after that, we about the faction and the olfactory circuits
36:14 how one creates the perception of perception of odors. And after the
36:23 system covered, then the cannabinoid So if you look then for the
36:31 , you have 123456 lectures and about questions. So you can expect somewhere
36:48 seven or so questions per each section we discussed. OK. And uh
36:58 there are quite a few articles on timing dependent plasticity on the re genicular
37:05 refinement, you may want to review figures and you may want to review
37:12 videos where I discuss the figures. if I ask you any questions,
37:18 articles are pretty extensive, especially the article that talks a lot about different
37:25 , but we just focused on the zone and that's what I would
37:30 I would open the article open that , read the figure legend. If
37:36 not explanatory enough, I would find figure figure five big six big
37:44 whatever it is in the text and that 1 or 2 paragraphs associated with those
37:52 If you're having a hard time understanding , time dependent plasticity, I think
37:57 that's kind of a one of the difficult concepts I would say. Uh
38:05 I would try to read up a bit more from those articles. Uh
38:12 I think in principle, if you the difference between what the rate code
38:19 versus what the spike timing, pre versus post synoptic, the rules or
38:27 rate codes and basic rules, frequency rules, calcium dependent and MD
38:34 Uh And then you have spike timing rules on modulation where the curves can
38:42 . And that's what enables us of types of learning and in different
38:48 you learn things differently. And that's those curves, the spike to dependent
38:54 curves change. OK. So do guys have any questions? I apologize
39:03 uh the vaulted sensitive dye imaging part didn't see and I'm hoping it's on
39:10 video that I recorded. But if is not, it was just an
39:15 that I'll repeat again in class and will not ask you uh questions on
39:21 video. Anyway. So it was to reinforce what I was explaining about
39:25 Sensitive Dye imaging in general. good. Thank you for being here
39:41 in time because I forgot to connect computer to charger. And it's saying
39:47 about to run out of battery just into battery saver mode. My screen
39:51 getting dim so we'll conclude our review . Good luck studying. Please use
39:58 sample questions. Expect similar questions and 40 of them on your exam on
40:07 Wednesday. Good luck and I'll see back in class next week. Take
40:14 everyone. Thank you, Doctor Appreciate
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