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BIOL 4315 Neuroscience Mo Wed 4-5.30pm - NEURO Lecture 03 Neurons and Glia 1
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00:00 according now this is cellular, this neuroscience. Lecture three and we're going
00:08 start talking about the major cell subtypes cellular composition of the Cns. Most
00:16 the studies that you see on the , on the CNN esses down on
00:20 own. And only a fraction of is done on glia. When you
00:27 in the brain, the most abundant subtype and the brain is glia.
00:31 90% of glia and neurons comprised by only 10% of the self. So
00:38 glial cells are way more abundant number neurons. Most of the people who
00:44 studied neurons only as of last decade so. Glia came into picture as
00:53 type of cell that everybody wants to more about the type of cell that
00:57 believe is very actively involved in neuronal , neurons are like chips in a
01:03 chip cookie. Glia is like the or the glue. The original name
01:09 Julia comes from google. You cannot a chocolate chip cookie without having either
01:14 dough or the chocolates. The chocolates the cookie a lot more interesting.
01:22 in order for us to understand the of the brain and how we have
01:27 breakdown of 10% of neurons, 90% we have to visualize them and in
01:33 to visualize the brain we have to stains. So that's why I have
01:36 gain in the brain is mainly in stain like the rain in spain is
01:41 in the plane and we talked about types of stains used to label
01:49 One of them was Golgi stain and stain revealed, the fraction of neurons
01:56 when those neurons picked up Golgi they reveal the entire anatomy. Their
02:01 , dendritic processes, the axonal processes the selma precise anatomy and morphology of
02:07 cells and the second type of state we talked about which you should review
02:12 missile state And unlike Golgi stain and will stand stands all of this
02:18 It was really good for describing side , tonic and cider architecture of the
02:24 distinguishing neurons between from glia but not used. This oil stain is not
02:30 used to distinguish and describe the precise and morphology. At first glance,
02:38 look like any other cells or other that you have studied at the Soma
02:44 the nucleus. They have all of organ analysis. You're familiar with mitochondria
02:50 apparatus polarized. Somo complexes rough on plasma in particular Ribosomes, three floating
02:59 . So it looks like other cells you have studied and then you look
03:03 and neurons than have some unique features themselves. So first of all,
03:08 have these dendrites and dendrites have these protrusions coming off of them that we
03:13 dendritic spines. They're also contacted by neurons via axons and axons have these
03:21 nation sheets surrounding the axon which prevents the electrical currents to leak out of
03:28 axon. So once the actual potential generated over here by the axon initial
03:35 , it will be the same amplitude it reaches the external terminal here to
03:40 the neurotransmitter vesicles fusion the neurotransmitter released this. Not the class. Those
03:47 some unique features this axon hillock or initial segment, that's where neurons will
03:53 the action potential which is going to the subject of discussion in the next
03:57 lectures again, at a glance, about the same thing. You
04:03 nucleus nucleus have genetic code. All this also in the body have the
04:08 genetic code but you have many different of cells, the liver cells,
04:14 cells and neurons will have the same code but they will express a subset
04:20 genes that will transcribe and translate the of genes That will make themselves different
04:27 one And not just neurons different from but in fact there is over 150
04:33 subtypes of neurons in the brain. different types of neurons in the
04:41 So this is basic concepts that you're familiar with. You have gene transcription
04:48 transcription. You get translation. transcription creates RNA. RNA then gets
04:58 . M. RNA transcript gets transported the nucleus. With these shuttles transported
05:04 Cida Plaza and the trans cida It gets translated into a program.
05:11 during this process you have a promoter intron exon antron and you have the
05:19 process which produces the R. A. And as Arnie's produced the
05:24 messenger RNA? The non coding regions removed through a process of splicing.
05:31 so we have what we know is variants. And during this process there
05:36 be slight variations in the splicing and what makes normal splice variants. Different
05:45 or different molecules acting slightly differently. there are also pathological supplies. So
05:51 this process of splicing the incorrect regions the code are removed and the translated
06:01 may be abnormal such as a protein pathological activity inside itself. With some
06:08 concepts that we all know about cells rather than the plastic ridiculous. Um
06:13 ribosomes also has polio ribosomes conflicts. it also has Golgi apparatus and there's
06:23 fates mostly two states that the proteins they're translated from M. R.
06:30 . A. Their newly created proteins are cytoplasmic, they float inside of
06:36 or the proteins that become numbering associated and they can be trans membrane channels
06:42 trans members embedded proteins that are not but all right linked to g
06:49 These are the two major pathways that proteins get finalized to take place.
06:57 this slide describes to you that we in a post genomic era. That
07:02 we understand the code and we understand sequence of the genetic code. And
07:08 of you may have heard them. there are these gene micro race
07:13 So what is the micro rate And are you doing gene micro very studies
07:17 why would this technique be useful for the brain and studying the neurological disorders
07:24 abnormalities and brain tissue. The micro is this plate. It's actually a
07:31 plate that you place under a And that microscopic plate contains even smaller
07:38 wells. And each one of these is loaded with synthetic DNA with a
07:47 or gene specific sequence. So these that you have on the micro
07:53 They can number in thousands. They number 10000s. They can number
07:59 You want to study thousands of Why would you want to study thousands
08:04 James? I'm not only interested in . Well, Micro rays give you
08:08 really good bird's eye view of what the major changes across this selection of
08:16 genes. So if the brain cells 30,000 genes or so you want to
08:22 what is going on with these 30,000 in the brain. That's brain
08:27 And let's say it's normal brain and to that is epileptic brain for abnormal
08:34 . Its brain that has neurological The way these experiments are done is
08:40 you have a vial of M. from brain one you will have a
08:44 of M. RNA from brain to of these vials is labeled in
08:50 So it has red color. Another is labored in green. So whenever
08:57 see gene with reduced expression and brain the walls are going to be dominated
09:03 brain. One gene material, which in rare, whenever there is gene
09:11 that's reduced from brain one, you see the green color dominating. But
09:18 that gene expression didn't change, that that the gene expression didn't produce in
09:23 brainwashed or brain. To then the colors blue and red and green would
09:29 equally in producing the yellow color, indicates genes with equivalent expression in both
09:38 . So just like you can see this microscopic slide, how does this
09:43 actually pick up the information? So have a specific sequence of DNA sitting
09:48 each well and then the messenger RNA to match the opposite and precisely matching
09:55 synthetic sequence of DNA that you implanted his mind for a while.
10:00 so there's a lot of that gene going to be there. There's more
10:04 that gene. That's going to be . Or if there is a reduction
10:08 that genus has shown in this there's going to be reduced expression of
10:13 . Alright, so you came to lab and you did an experiment,
10:17 compare normal brain and epileptic brain through methodology micro rate and you get the
10:23 back, Let's say you started 30,000 200 of the genes went up An
10:32 brain and 200 of the genes went an epileptic brain, which ones are
10:39 . The next thing you're gonna see some of these have numbers. You
10:46 see negative numbers and you can see numbers. So if you're seeing a
10:51 number, negative 1.79 there is a of that gene. If you're seeing
10:57 positive number like .46 or one 03 an increase in magic. So now
11:06 can look at which of these genes the highest decrease or the highest increase
11:13 out of those 200 that went up 200 going down and say Okay I
11:17 that 10 of them went up radically tell them that went down also by
11:24 lot. Then you should say maybe these are important genes and you could
11:29 studying or you could say I'm only in apple aficionado. These 10 genes
11:34 went up, only five of them known to be involved. And then
11:40 in order to do your undergraduate or even a PhD dissertation, your mentor
11:46 come up and tell you that out these five epilepsy genes, My lab
11:51 interested in this gene. So you spend your PhD Studying this gene or
11:58 . Take home message. Is it to mommy Karen this micro race allow
12:02 to really get a nice bird eye and understanding what genes have changed and
12:07 not tell you where they changed unless isolate a specific brain structure. But
12:11 you take overall brain homogenize it and it into solution or a big chunk
12:16 the brain, you may not know those specific genes but if you take
12:21 very specific area of the brain loses balance compared to the other cerebellum,
12:26 might be getting down to more and and more specific data until you identify
12:32 of Eugene's that are very important this and the alterations of those jeans you
12:37 experimentally proved actually do contribute enough. know that things that go up will
12:43 down the most sometimes they're not the important. Just that's the way life
12:48 . It's not linear systems if we're with organelles smooth in the plasma in
12:54 where you have protein folding and calcium . So you have smooth er which
12:59 loaded with calcium inside the cells. apparatus which does post translational processing and
13:06 sorting, deciding whether these proteins are be cytoplasmic membrane bound proteins and you
13:14 know about mitochondria and the crab So I learned Krebs cycle in high
13:18 . I learned Krebs cycle in I learned Krebs cycle in graduate school
13:24 I still need to learn crop There's a lot of details. There's
13:28 lot of arrows of course electron transport . All the good stuff that is
13:34 here for the purposes of our It's very important to know the mitochondria
13:38 is the main source of energy in body but also in the brain,
13:43 mitochondria and take the dietary and stored sources protein sugar is fat, sol
13:49 glucose. They take those glucose sugars the castle turned into pyro picasa in
13:55 . And you have these inner membranes outer membranes and these imaginations called the
14:02 where there's a conversion and oxidation of tick acid and production of a teepee
14:08 c. 0. 2. And of energy in the brain is very
14:13 important because in the brain there is need for a lot of energy.
14:23 . The brain comprises only a few of the total body event. So
14:29 brain weighs about £3.5. I don't . Okay and how the how much
14:41 the body way? So of course weight is very different but Let's say
14:52 3 1/2. Because the brain, the total nice of the brain compared
15:00 the mass of the body. It's a fraction. It's only a
15:07 Okay. Only one to few And the brain consumes 20 of the
15:19 body energy. Think about it. that you eat that you drink Is
15:29 of it is consumed by the So so eight ep and production of
15:36 teepee is very important for the N. S. And the more
15:40 the neurons and the more active the circuits. The more oxygen the more
15:48 and fats are going to draw and to themselves in order to satisfy this
15:54 demands. I also say that it's system that's driven outside of the linear
16:00 . It's a nonlinear system Because if head weighed, if my brain weighed
16:06 2% would consume 2% of total But it is not, it's driven
16:11 the equilibrium and 2% consumes upwards of of the total body energy of metabolism
16:17 everything that's dedicated to the function of brain. And it is not quiet
16:21 night, you disconnect your motor activity your brain and the consumption of energy
16:26 the brain continues throughout your sleep neurons like other cells have possible lipid
16:34 . But when we talk about neurons when we talk about the plastic processes
16:38 the dynamics that are happening in a fast basis in the brain. Because
16:43 compute things, you think about things produce speech, You listen to things
16:48 you can multitask at the same motor and sensory information. And it's
16:53 just that this membrane is rigid. membrane is very fluid, So the
16:59 lipid bi layer, which is the hydra filic head group consisting of killeen
17:05 and glycerol here, and the non polar tales that come together
17:11 forming the inside of the plasma There's a possible if it by learning
17:15 has cholesterol embedded in it has trans proteins, some of them are channels
17:22 will allow the passage of islands like proteins, carbohydrates some of the trans
17:28 proteins from membrane associated proteins that are channels also and right underneath the number
17:34 you have the side of skeletal elements the side of skeletal elements is really
17:38 structural elements that are supporting and providing the shape of the outer boundaries of
17:44 plasma membrane. So how fast can molecules move? Do plasma membrane very
17:52 in the brain? Remember that neuron about 10 μ m in diameter and
17:59 of the trans membrane proteins can move in milliseconds on demand. So the
18:08 of molecules in the plasma membrane is fast and there's also a rearrangement of
18:14 skeletal elements that can happen underneath because side of skeletal elements chains, polymer
18:22 can become longer and shorter. And you're talking about is the building materials
18:27 long big sticks to build a house short little sticks to build a
18:32 Um there's a whole strategy and these skeletal elements changes in the cyber skeletal
18:38 can change the shape of the plasma and the fluidity properties of the plasma
18:43 as well. So this is a short video that basically describes the fluidity
18:54 the mosaic composition of the planet. is no audio by the way.
20:06 as you see the movement of these of these trans membrane proteins, membrane
20:12 . We're not talking about cytoplasmic elements are moving through the side.
20:15 But actual protein mediums that are moving this possible lipid violators. Right,
20:50 . It's a simple video but I it has a great explanation and visualization
20:55 the fluidity and the mosaic composition. it's a mosaic because different types of
21:01 will have slightly different proteins, black, a proteins, sugar coated
21:09 that will make them different And in , as I mentioned, an important
21:14 is that these trans membrane proteins can very fast within the number of um
21:20 of skeletal elements that underlie the overall , the underlying structure of the cell
21:29 the plasma membrane of the cell. subtypes Micro tubules are the largest elements
21:36 20 nm in diameter comprised of turbulent , then the medium size of neuro
21:44 that are also referred to as intermediary . So it's easy neuro intermediary,
21:50 10 nm in diameter and the smallest of skeletal elements are micro filaments and
21:57 filaments are comprised of active molecules, nanometers in diameter and the micro filaments
22:08 they have active molecules are also the to prelim arise and two prelim arise
22:13 form longer chains and shorter chains of micro filaments. If you look at
22:18 diagram on the right, what is is an electron microscope image that is
22:25 cross section through an axon m here for myelin But if you look inside
22:33 axon, the myelin is surrounding this . You can see these sheets of
22:39 like lines because we ourselves will wrap around repeatedly to form this installation in
22:45 form of violence. If you look inside the axon though, you see
22:51 almost like spaghetti looking strands. And these spaghetti looking strands are actually
22:58 tubules. A lot of counselor reports micro tubular highways because there is a
23:05 amount of transport and exonerate transport that place from soma into the periphery and
23:17 of the distal regions, out of peripheral regions of the south back into
23:21 centralized region of the Soma. With image illustrates very nicely are two different
23:31 of skeletal elements. The jubilant, is shown in yellow and active,
23:37 shown in blue. Now these two of cells, these two cells that
23:42 shown here are fibroblast cells. So not the best type of cell to
23:50 to to really talk about when you about neurons. But it's a great
23:56 of standing in these cells. And you're seeing first of all in
24:01 you have the nucleus. Remember to , micro tubules, tubules and you
24:08 see the turbulent and micro tubules are at the very core of the inside
24:15 inside of the cell and smallest molecules molecules that are part of the micro
24:23 here. The smallest elements there stained blue. And you can see that
24:28 mostly densely fact that the most outer of the plasma number. And so
24:33 are the most dynamic side of skeletal . These are the side of skeletal
24:38 that can change. And by problem . Deep alarm arising, building longer
24:44 shorter chains of active molecules. They change the shape, the overall change
24:52 shape of the overall plasma member. this is also a dynamic process,
24:57 that the plasma membrane changes its shape on the activity and dependent on the
25:04 of the silo skeletal elements that arrived the plasma member to resume the
25:14 And we're going to talk right now Alzheimer's disease. Okay, so this
25:21 the first neurological disorder that we And this is a good point to
25:27 it because we're talking about cyber scalable and there's an involvement and effect of
25:34 disease. So what I would like you to do in this in this
25:41 is actually if you have a notebook if you have notes that you're taking
25:45 I'd like for you to make a on Alzheimer's disease. So you can
25:51 a new page in Alzheimer's disease and tell you why because we will go
25:56 several diseases in the scores and we be adding information about these diseases throughout
26:03 course. And so what you learned about Alzheimer's disease, you will learn
26:07 new maybe in the second section when study other parts of the Alzheimer's
26:13 Okay, so it's important that you this page and that we start developing
26:19 of a language and how we talk this season. So first of
26:24 what is Alzheimer's disease in plain Do you know what Alzheimer's diseases?
26:32 it normal part of aging? Is a neurological disorder as a neuro degenerative
26:40 ? What is it? I can't them. Is that all? What
26:46 the most basic definition of a It's a form of seen our
26:54 It's a form of dementia. It's a part of normal aging. It
26:59 a disease. Plenty of people die very old age without Alzheimer's disease.
27:04 it's not that because you live so you end up getting Alzheimer's disease.
27:10 definition of this dimension when there's a the prevalence. See does it start
27:21 in early development? Does it happen teenage years Now the provenance of the
27:30 starting from the 50s years of age older increases. So you have an
27:37 in Alzheimer's disease with older age. the prevalence of Alzheimer's then when a
27:46 walks in with Alzheimer's disease or the suspect they have Alzheimer's disease or the
27:53 one suspect to have Alzheimer's disease. come into a doctor's office and they
27:58 I have an Alzheimer's disease pathology doctor my brain is that what happens now
28:05 come in and usually either the white or the patients say that I'm having
28:10 remembering things. I am confused. very anxious. I am getting confused
28:19 the time I am spatially disoriented. don't know which room I am in
28:27 how to get to the next drum I should be in. What are
28:32 things? That's not pathology, This symptomology. So these are symptoms
28:39 being anxious, being spatially disoriented, disoriented in time, afraid not
28:50 just not remembering who the person not remembering who the name is or
28:54 the person is period. Very, scary. These are the symptoms and
29:01 the disease progresses the symptoms get worse worse and worse and worse. So
29:06 may start out the symptoms with the of short term memory that you just
29:11 somebody. They I told you their and then you forgot about it.
29:17 happens all the time. Right? then you can't remember any names or
29:21 happened yesterday. So things that happened term, I don't remember what happened
29:26 . But oh yeah, when I a kid I was going through this
29:29 and doing this. You remember everything long term memory story. Maybe initial
29:35 is a loss of short term anxiety, being worried about. I'm
29:41 saying the right thing or understanding who talking to, maybe remember who you're
29:46 to and then of course there's progression the disease and there's progression of symptomology
29:52 that means that the condition is getting . The drugs on the market right
29:58 . There are no drugs that can can cure Alzheimer's disease, you can
30:05 stop the progression of sort of and are the mechanisms of action or what
30:13 the pathology? Okay, so this all very great terms that will appear
30:18 your exam and can appear on your to prevalence. Developmental disorder has dementia
30:26 is more prevalent elderly. What is basic symptomology and of Alzheimer's disease.
30:33 are the hallmarks of pathology? And there are two pathological hallmarks that are
30:40 in this live on the cellular And there's one that is shown on
30:44 gross anatomical level. If you look the severe Alzheimer's brain and the gross
30:49 level, you see massive shrinkage of cerebral hemispheres, massive shrinkage of the
30:57 and the white matter. Also, neural degeneration that means the cells are
31:03 , the cells are dying, the are dying and they're not regenerating their
31:09 . So there's a significant cell significant shrinkage of the brain tissue loss
31:15 summers as well as the connectivity So this is on the gross anatomical
31:23 . Can you see this with noninvasive scans of severe Alzheimer's pathology can actually
31:31 on the scans because you will see abnormalities from the cns and the brain
31:36 the cortical structure. However, on more microscopic cellular level, there are
31:42 hallmarks of alzheimer's disease. One of is amyloid plaques was also referred to
31:47 beta amyloid Flags Flags or senile It's an abnormal aggregation uh peptides and
31:58 and causing this plaque formation and And as these flags warm they start
32:07 larger and they actually migrate throughout the and multiply and these plaques aggregate this
32:15 collections of junk and they start physically the cells from the outsides of extra
32:24 early and the part of the cell neurons that produces action potential action.
32:30 hillock is exquisitely sensitive to the amyloid . And so if the amyloid plaques
32:37 in the vicinity, they can start the processes such as downright such as
32:41 is what they can also start it a dysfunction Where one neuron cannot communicate
32:50 another. Inter cellular communication is impaired these plaques are infringing on the axons
32:57 are generating action to control inside the . You have neuro february really
33:06 And remember we were talking about side skeletal elements and we're talking about neurofibromatosis
33:12 we're talking about sino skeletal elements. talking about the micro tubular highways.
33:25 . So what happens if there's a production of protein in this case it's
33:30 protein inside the south and the tangos the highways that we're looking at what
33:38 in the city. If all of highways get basically. There's no directionality
33:45 the highways. And there's no transportation it's all rearranged all of the way
33:50 you know how to come to Of H campus. All of a
33:53 has changed. So there is no inside the cell. You can use
34:01 cell as a city and this city to communicate to another city. So
34:05 you put the plaques on the outside the cell, it starts causing problems
34:10 inter cellular communication. If you have opinion really tangled inside the cell,
34:15 causing all sorts of problems that will associated with intracellular and with axonal transport
34:22 anything that relies on the transportation and things get transported in the south are
34:28 just for fun, it's nutrients, all of the necessary elements to keep
34:32 cells alive. The most advanced the most severe advanced stages of Alzheimer's
34:42 resolved and death. Because it is thing when the centers of the brain
34:48 are responsible for memory and dying. it's another thing when the centers of
34:52 brain that controls swallowing, eating and are dying and eventually then the death
34:59 because the brain cannot take care of and the body any longer. And
35:05 in the course, you will learn there is a chemistry involved that there
35:09 certain chemicals that are impaired in Alzheimer's and that there are certain therapeutic approach
35:16 is most common to Alzheimer's disease. for today's lecture for today's notes on
35:22 stage that you started from Alzheimer's These are all of the things that
35:26 have to put and then leave space other things that you can add throughout
35:31 course of the semester. Okay, we're replacing this hallmarks of Alzheimer's disease
35:40 the slides that I just showed Let's move further along and understanding the
35:48 and how they're different. You have . We talked about the critics
35:51 they have axons, there's axons formed and they ran the fire where they
35:58 they're called axon hillock or axon initial . This is where the action potential
36:04 generated. Axon terminals is where the terminal acts on bhutan or button will
36:12 terminal axonal projections. But on the to the terminal external projection you may
36:17 these collaterals and you will have these and present. Or synopsis that formed
36:23 facade and of course where Axiron approaches cell. Typically in the dendrite and
36:31 find you have a location of the . Pre synaptic alie you can see
36:36 the axons you have mitochondria. So need a lot of energy in order
36:40 these vesicles diffused to the plasma number deposits of psychosis of the neurotransmitters.
36:47 unethically and Pastrnak typically you have what called post synaptic densities and these would
36:52 densities of the receptors that are located the plasma member and post synaptic aly
36:58 objects supposed to these axonal terminals. synaptic clock is an actual space between
37:10 and the other neuron them. And another neuron. Okay. And
37:16 transmission is a process where these basic and neurotransmitters are released and Europeans literally
37:25 will bind to the receptor spots. inducing a possum africa response. Then
37:30 will know a lot about your transmit a special image. Second section of
37:35 scores, acts of plastic transport. is why it's very important because if
37:41 tangle up these side of skeletal highways side of skeletal structure, you start
37:47 the membrane shapes, you start destroying synapse shape and the dendrites and also
37:52 cannot deliver goods. So you have intracellular delivery of goods in case of
37:59 tangles. But in general you have ectoplasmic transport which regularly was studied with
38:06 some dye in the maximum tying it one end and seeing How long is
38:11 gonna take for that die to travel the axon. So it's 1-10 mm
38:16 then there's also fast axl plasma transport labeled the clinic assets can be injected
38:22 axons and they revealed that fast ectoplasmic is 1000 millimeters a day or a
38:29 a day. The interrogated direction which from the summer months of the periphery
38:34 will have these innocent motor arms like like little motor engines going along the
38:42 tubules and passing the knesset passing the or the nutrients or the proteins stop
38:51 along the micro tubular highway sort of handing it off with one contestant to
38:58 and the retrograde transport will have another dynamic. So Vanessa will travel one
39:04 against micro tubules and dining will go direction. Now, what happens if
39:09 tie up this highways? Obviously you the transportation of goods. The gain
39:18 the brain is mainly in the And one of the good ways in
39:22 we can take advantage of staining the is by having tracers or dyes that
39:29 retro gravely transported. And that's really our advantage because things that are reaping
39:34 and transported, that means that they come from the distal parts of the
39:38 from the periphery and they will be into the summer. And so this
39:43 an example of a retrograde transport. can inject the horseradish peroxide as you
39:47 for example. Want to inject it the patch of the skin and see
39:52 nerves are connected to this patch of skin. Or you want to inject
39:56 to patch up the brain and say accents are going to pick up this
40:02 from this patch of the brain and gonna reveal me what network of
40:06 HR be labeled neurons that are processing , receiving information from this area of
40:11 brain. So horseradish for oxygen's or be staying. You're gonna inject HR
40:18 stain is used for retrograde transport Herpes viruses capable of retrograde transport.
40:27 means it's capable of going from the into the syllables of the neurons rabies
40:34 . We will later in the course about shingles when we talk about herpes
40:39 virus and that virus has the ability travel in both directions. Answer greatly
40:45 then retrograde. Yeah. Um so viruses can also be taken advantage for
40:54 purposes because if the virus travels from axon from the purpose to the
41:00 that means you can tag that you can tag that virus within markers
41:03 as fluorescent marker. And as you that privacy recognition marker, you can
41:09 precisely anatomy at the south of communicating have been taken out from this area
41:14 as is transported by the virus. rides are also quite unique and especially
41:24 spines are unique to neurons. These and dendritic spines are the most plastic
41:31 in the brain and the shape, size, the number and their
41:37 Whether they're strong or weak functionally will on the activity and will depend on
41:44 environment that they are surrounded by this . We call activity or environment dependent
41:53 that these spines are very much responsive what is going on in the
41:59 During early development. We are born a lot more synapses and dendritic spines
42:05 we have in the adulthood and during process of the development there is refinement
42:11 connectivity in the brain. There is of certain synopsis there's establishment and strengthening
42:18 certain dendrites and dendritic spines and there's and reduction of the spines and the
42:25 that are not being used. So is shown here is an electron microscope
42:31 showing you this boston aphid densities. is where the british spine is.
42:36 also have mitochondria and the 10 dr to the red cell which is axons
42:43 contained these red vesicles and these red containing neurotransmitters. And this space the
42:51 all of space that is here is 20 nm apart. This is another
42:56 spine here that has mm hmm. no plasma critical um storing calcium stores
43:03 synaptic density. And there's another Now here's a very extensive spine.
43:09 they all have different names. The study beast in spine. This c
43:15 is called the mushroom shaped spine and can see it has three parts synaptic
43:20 . So it can have a much communication coming from this the synapse that
43:27 talking to this axon here. The was talking to this synaptic neuron
43:33 In addition inside the sponsor, you find synaptic parlor over some more complex
43:40 that's important. So now you have teepee you have sources of calcium scr
43:47 you have side uh synoptic polarized personal in the spine which makes the spine
43:55 biochemical independent from the rest of the from the soma because they can locally
44:02 spoiler about soma complexes to translate things need to translate and use the stores
44:08 energy. A teepee and calcium to and modulate things locally here within the
44:14 spine independently from the rest of the . These spawn's are the most plastic
44:22 that can look and think of them leaves on the trees. So every
44:26 the tree doesn't die. Instead it its lead, it's not evergreen and
44:32 showed some ranchers and then it grows leaves and keeps growing new branches.
44:38 this is a constant process in the . There's new synopsis and synoptic dendritic
44:44 that are being formed. There's new that's informing now as we're learning this
44:50 and these synopsis can change their can change their size and as that
44:56 and the communication between the axonal were by changes. They will also change
45:01 efficacy or the level of the ability communicate strong versus reading and such.
45:12 this is very important. Last slide I'm going to show you today,
45:17 talks about how if you have abnormal of dendritic spines that can cause mental
45:27 . So what you see here on left is a down drive from a
45:30 infant. And you can see that has thick and rigid shaft and it
45:35 a certain density of the british it's pretty uniform. How long is
45:40 british shaft? And on the right an example of the done drive from
45:45 mentally retarded infant and you can see these dendritic spines are abnormal. They're
45:53 too long. In some cases the too short and other cases their density
45:59 away off, there's no uniformity in density of these dendritic spines and the
46:05 form of retardation can be autism spectrum . So you have to have this
46:14 dendritic spine anatomy and precisely arrangement improving the development in order to process information
46:22 in order to developmentally normal social norman well. This is very important because
46:29 is an neuron, the picture of and every punk state. Every dog
46:35 you see here in green represents glutamate and glutamate synapses are excitatory synapse and
46:42 can see that these synapses are located precisely along dendrites of the contact the
46:48 spines, some very specific order and you're seeing the orange stain Orange
46:55 these are the Gaba receptors that doesn't synapses or gabbas enough. And so
47:02 neuron receives thousands of excitatory inputs and thousands of excitatory synapses and thousands of
47:10 inputs and has thousands of inhibitory. if this communication is imbalanced for
47:17 if there is no inhibition because the shot and spines are missing would inhibit
47:25 inputs coming in. Then the cell going to be overexcited and it's going
47:29 be abnormal and if the dendritic spines synaptic lihir containing glutamate receptors are
47:37 the process excited or information that means inhibition is going to dominate and the
47:42 is going to be sitting silent with completely inhibited also abnormal activity inside the
47:50 . And so it's very important. ultimate decision for this neuron Is to
47:55 inputs from hundreds thousands, sometimes 10 of exotica inhibitory neurons of other
48:02 Both excited to inhibit the neurons. fact excitatory cells, they're both excited
48:08 inhibitory neurons can talk to inhibitory cells the end, it's the Selda selma
48:14 integrates information from thousands of the synopsis is positive minuses, inhibitors synopsis and
48:21 whether it's excited enough, the producer action potential. And if it does
48:27 an actual potential, the actual potential going to reach the external terminal causing
48:32 neurotransmitter vesicles fusion the neurotransmitter release, affecting another interconnect themselves. So you
48:42 now understand and appreciate that this genetic and activity dependent code. If you
48:51 developing infant from certain sensor information, can reshape its brain, you can
48:57 this plasticity structure and autumn of the . And so when we come back
49:06 on monday, I will ask you start a new page and that page
49:12 going to be on autism spectrum and so we'll discuss in about 10
49:19 or so how autism spectrum disorders and we talk about autism spectrum disorders and
49:26 they're very different from the dementia that just discussed, such as Alzheimer's
49:34 But what we're talking about when we're about mental degradation or authors respective disorders
49:39 looking at this picture. You now that we're looking at the pathology,
49:45 is not a symptom when you're looking the pathological changes in the tissue,
49:49 is the pathologist and that the pathological that can lead to abnormal learning,
49:57 and mental reputation. So when we back, we will discuss this autism
50:04 disorders and one particular syndrome in greater . So, thank you very much
50:10 your attention. Today. I'm going pause the recording here and take any
50:15 that they
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