© Distribution of this video is restricted by its owner
Transcript ×
Auto highlight
Font-size
00:00 Yeah. So we're reviewing the syllabus Exam one. This is neuroscience.

00:06 is the meeting electric 10. We start talking about neural transmission as's

00:12 Your exams go and your grade a of each of these midterms will contribute

00:19 your final grade. The final exam also not cumulative. So it is

00:25 like midterm three exam. Um, some of you have expressed the desire

00:37 you would like to keep potentially just exams for an average of the final

00:45 . I'm dropping the third exam. is the lowest score. Um,

00:52 will consider that, of course, you may want to consider that usually

01:00 examine term Exam one is the highest grade, and typically Exam two and

01:09 is too, too few points below the average of midterm Wang. Because

01:15 one contains a lot off basic information introductory information and the complexity of material

01:24 in subsequent section Thio that we're starting in that section three later in the

01:33 I have requested with Casa One more and I'm waiting for them to respond

01:40 the previous years, which were different and not our typical year off 2020

01:48 the previous years, I have given a pop up quiz during class,

01:54 that pop up quiz counted as additional that students could add to their

02:02 Essentially, it served as a self for your grade. Your curving yourself

02:08 taking this quiz and seeing how many you can gain extra. So if

02:14 quizzes had anywhere between 5 to 8 , each question worth one point.

02:20 between 5 to 8 points. if you answer all quiz questions,

02:26 could potentially jump into different grade for of the midterm exams for the

02:34 the miracles course Now what? I enquiring with Casa. Of course,

02:39 cannot do a pop up quiz, it will have to be a different

02:44 that is your midterm to on the three. It will have to be

02:49 somewhere in the middle of this second that I am requesting Casa if I

02:56 give you a 10 minute quiz this is pretty extraordinary year, and

03:03 requires a separate event scheduling for This will not take place during

03:11 Well, uh, potentially have to place outside the class. But it

03:17 have to be at the much shorter window where everybody will just have one

03:26 two hours to log in to take 10 minute quiz. And if Gaza

03:31 me to do it during the class maybe we will allocate Onley half a

03:36 off the claws for everybody to join take that quiz for 10 minutes,

03:43 , likely will cover in our Follow that material will have the 10

03:51 quiz within this half A Now, that you can go on to casa

03:56 leave, zoom well down to Casa take the quiz during your regular

04:02 Our let me see the chat some questions and mentum was with which material

04:16 be on the quiz on the The if I if we do have

04:21 quiz, I will confirm with you week that we are able to do

04:26 with Casa. Once we have the material is gonna have to be

04:32 much material from the previous lecture. is really testing whether you're attending the

04:38 . Those quizzes originally were designed as quizzes for those that attempted class.

04:44 if you were not in the class day, there was no makeup

04:49 This was basically a privileged to those that attend the class because those that

04:55 attend the class, I do it those are folks that are not necessarily

05:00 interested in improving their grade. if you're attuned, you're attending the

05:06 and reviewing all of the materials in timely matter. As we study

05:11 you will be prepared for the But I will not specifically point to

05:15 area from the coming lecturers will be in that quiz. Uh huh.

05:22 you have to stay and keep up the materials, attend the lectures in

05:26 to score really well on the It's a different way of studying.

05:30 will not be a review session. you take this quiz. They will

05:34 be sample questions that were given. is just testing. Whether you're attending

05:39 class following the material boom, this your curve. You give it to

05:44 . Okay. So I will follow on how this will proceed with Casa

05:52 give you an update next week. . So today we're launching into talking

06:01 neural transmission. Uh, neural transmission synaptic transmission. The slide says that

06:11 in two weeks. Well, you have an exam in two weeks.

06:13 an older slide. My office used be an S r to science and

06:19 building, too. This tall What I call Soviet building.

06:25 and, uh, it was on second floor 2. 42 g,

06:32 offices and H B S B. is using biomedical Building one on the

06:39 floor. My email is the And so all of my contact information

06:43 the exam technical issues You can please me directly if I don't respond in

06:50 is origin. Please repeat your As I explained to you, if

06:54 still don't get a response, maybe a problem with me receiving or you

06:58 the email. So maybe chat me after the class. I will address

07:05 with you. I haven't heard in couple of days, but typically everybody

07:08 is back for me within the day their respective issues and much sooner in

07:17 where I see it's something that needs be addressed, that speedy, um

07:23 the speedy way, so Today we start talking about the connections between

07:31 The first course section, we understood neurons are neuronal anatomy and glial

07:41 And what you have thio think about all of the folks here that you

07:49 know on the slide your Monica we use Golgi stain. We describe

07:56 discreet individual neuronal units who reconstructed from stains these beautiful circuits who argued that

08:11 are discreet units and was a proponent neuron doctrine using his boss sustained Golgi

08:20 . Sir Charles Sherington is responsible for coining and describing this term of the

08:26 and what is happening in the synapse that is happening now again, the

08:32 toward the middle of the 20th What's interesting is in about the same

08:40 . Time is the third player that in a very famous scientists auto Lowy

08:46 makes the discovery off this chemical neural . So in the first part of

08:53 course, we described how these neurons an action potential at the acts on

08:58 segment these action potentials through solitary really, we, uh, ree

09:09 produce themselves each note over on beer that when this action potential which is

09:18 if the acts on initial segment reaches terminals and you can see that my

09:23 acts on the end of the accent not Miley native and then it's pleasant

09:27 multiple a ramifications where each one of external criminals becomes an individual synapse and

09:37 individual synapses we discussed pre synaptic Lee have mitochondria will have synaptic vesicles filled

09:43 neurotransmitters and plus synaptic Aly and across synaptic cleft. It would have receptor

09:51 to which these neurotransmitters bind and these channels and some of them are G

09:57 coupled receptors is we'll learn and there's whole effect, and that happens.

10:03 optically so this communication between pre synaptic , that zonal terminal plus synaptic cell

10:10 the synaptic transmission. And when we're about the grain, think about this

10:18 your brain contains billions of neurons. 100 billion neurons. Those neuron zones

10:35 through trillions of synapses, can have billion active neurons, billions of active

10:51 within the networks and these networks. active, and they're communicating to other

11:02 , engaging potentially billions of synapses and hemisphere or in other lobe that is

11:10 by a specific task or specific sensory . Incredible computational task. The brains

11:22 £3.5 containing billions of neurons and trillions synapses reacting underwater of milliseconds, synchronizing

11:33 regions of the brain to effectively execute functions. To accept effectively, process

11:40 sensor information. If you took and laid out this census, she,

11:50 , all of the membranes of each cell. In this case, you

11:57 out the membranes, a plasma membranes all of the neurons, all of

12:02 brain neurons, all of the plasma . And you laid it out.

12:06 unfolded. All of the Denver rides on the gendered expired so much and

12:10 laid it flat. That area from single brain would equate to four soccer

12:21 and size. We have many imaginations our cortex. We have many processes

12:33 from neurons and these when they laid , is what our minds are comprised

12:46 . This four soccer fields off very communication that is happening. This is

12:52 fabric of our minds, right? , synapses, neurotransmitters. So neurotransmitters

12:59 will learn today were discovered by at Lowy. And this is one of

13:07 favorite stories in this course, and is by what Allawi in the night

13:16 Easter Saturday, 1921. It's going be 100 years next year. 100

13:24 1921. I awoke, turned on light and jotted down a few notes

13:31 a tiny slip of paper. Then fell asleep again. It occurred to

13:37 at six o'clock in the morning that the night I had written down something

13:42 important. But I was unable to the scrawl that Sunday was the most

13:51 day in my whole scientific life. the next night, however, I

14:00 again at three o'clock, and I what it waas this time. I

14:06 not take any risk. I got immediately. Went to the laboratory,

14:11 the experiment on the frog's heart described , and at five o'clock, the

14:19 transmission of nervous impulse was conclusively This is a quotation from Workshop of

14:29 by Otello in 1953. So what the experiment that oughta Louis did?

14:39 is the dream that auto Louis Well, Dr Louis was working with

14:47 Hearts, woke up and did the and a frog heart would isolate a

14:53 heart. And as you isolate a heart, one of the most prominent

14:58 that is innovating. The heart is vagus nerve. It's cranial nerve.

15:05 . And you will learn about cranial . All 12 cranial nerves for with

15:09 end of this section. This is nerve, which is cranial nerve.

15:16 . It has the most extensive It comes from brain stem, most

15:23 innovations throughout the body of the viscera and very significant input onto the

15:32 So the experiments that after that we is he isolated two hearts, the

15:38 on the left he called the donor , and the one on the

15:42 At a vagus nerve, this blue attached it. This this this donor

15:48 , it's sitting in a vessel. this this jar in which is a

15:56 , has, ah, certain The second heart that he prepared.

16:01 call the recipient hard, and that does not have the vagus nerve attached

16:08 it. In this image experiment that did is auto. Lowy stimulated vagus

16:16 in the donor heart on the left he stimulated vagus nerve. So heart

16:24 a muscle cardiac muscle and it's contracting it's beating. So the faster is

16:30 . The faster is the heart When you stimulate vagus nerve, the

16:36 rate slows. Donald. So what did is he collected the fluid from

16:45 jar in which this donor heart was . He collected that fluid after he

16:51 the vagus nerve, and he transferred fluid into the adjacent jaar which contained

17:01 heart. Now this recipient heart, did not stimulate the vagus nerve,

17:08 instead collected the fluid from the dark and apply this new stimulated fluid onto

17:17 recipient heart. And when he added fluid to the recipient heart, the

17:25 trade slowed down. That demonstrated Thio Louis and Thio, all of the

17:34 around the world that the vagus nerve the nerves released some chemical that that

17:41 is found in the solution and the of that chemical causes the slowing down

17:47 the heart trade. And when you that chemical without stimulating the name Davis

17:53 onto their naive or recipient heart, get the equivalent affect. The heart

17:59 slows down. So there is something the fluid. It gets released by

18:02 vagus nerve in the donor heart, that fluid now becomes effectively an equivalent

18:09 the stimulation of the vagus nerve. it contains a camp, that chemical

18:15 a civil calling. So Seal Colleen discovered in this vagus nerve to cardiac

18:27 . Set up and a C Delco became the first known chemical or

18:36 So the take home message here is you fall asleep and you have a

18:47 . If you are having the heart , but you can be bothered,

18:54 , put it down on the You cannot be bothered. Thio.

18:59 it in a graph in a chart an experiment, it can be

19:08 The brain is also very interesting because brain will replay the patterns did you

19:15 during the day? And by replaying patterns, it's actually tuning the activity

19:24 networks, neuron, all networks and lot of the cells and communicating.

19:30 networks are undergoing plasticity, so synapses becoming potentially ated or they're becoming depressed

19:39 so, replaying the same patterns that your brain during the day. Same

19:47 so now being replayed at different frequencies night and they're very important because this

19:57 learning and memory. This is which you've learned during the day.

20:03 is forgetting things that are averse to physically and mentally through depression, long

20:10 depression of the synopsis, not the of the mind weakening of the

20:18 And so this is very important. lessons here are if you have that

20:25 moment, that clear, buoyant ah moment, try to realize it,

20:33 it's in a notebook or whether it's a chart or whether it's in a

20:39 or whether it's in a musical to your mind works, try Thio.

20:48 it. And if you wake up in the middle of the night,

20:52 may end up getting a noble price materializing realizing something that you have

20:59 This is in the case, Ought Allawi, who discovered the chemical

21:04 transmission. Yeah, the second thing that take home message is that we

21:10 playthings at night, so our brain that we talked about similar brain maps

21:15 get activated. Some of them will strengthened. Some of them will get

21:20 . If you're forgetting things, so have the replay of activity and so

21:26 we play of activity. A lot times, of course, is most

21:30 the time it's, uh, But if you remember, or if

21:36 are very strongly involved in a dream you can come out of that dream

21:41 still remember what you're dreaming, it might be useful thio for self

21:49 , Um, for for discoveries, . So this was the chemical synapse

21:54 the chemical neural transmission that was discovered the brain. And since then we

22:00 that there are two types of the between neurons and the second type of

22:05 synopsis, called Electrical so announced chemical you have release of neurotransmitter, and

22:13 neurotransmitter from the vesicles travels across the cleft 20 nanometer distance, and it

22:21 to the receptors, causing a poss effect, and in electrical synopsis or

22:30 electrical junctions. This is very It is different because you don't have

22:39 same distance. These are very special atomic call densities that form and bring

22:51 cell membranes very close to each An individual gap junction consists off individual

23:01 connections that form connects on, and connects on forums on the cell.

23:07 side applies. We call it pre , and the second connects on forums

23:12 cell to sidle plasma. We can it pasta Nap. Now, what

23:18 understood is that if we bring the membranes close together, that distance is

23:25 physically separating. The two neurons is 3.5 nanometers, but these trance member

23:32 protea ums these heavy channels half channels one side and another they use in

23:42 together, forming these gap junctions. gap junctions allow for the flow of

23:48 and small molecules and notice that it that the ions and small molecules can

23:55 in both directions. This is different when we discussed voltage gated sodium

24:00 both educated sodium channels where allowing for to come in all this gave the

24:06 channels were allowing for potassium to come of the south. In this

24:11 ions and small molecules can go in the cells back and forth. So

24:17 on such as potassium and calcium that discuss can pass very freely between these

24:23 junctions as well. A small molecules as cycling and P, which conserves

24:29 second messenger in the cells can enter leave the cells as the concentration of

24:36 ions or molecules, increases, it go down the concentration radiant because the

24:43 junctions and like voltage gated sodium channels voltage gated potassium channels that we

24:49 They're not gated by voltage. They're open. And so they allow the

24:55 for very fast flux of violence and molecules and bidirectional flux. And that's

25:01 important now. The original experiment and discovery of the Gap Junction was

25:10 uh, firstborn potter in the This experiment has shown here on the

25:17 , where at the very top there , an electrode is inserted in one

25:23 , and that top cell also has recording electrodes. So the electorate on

25:28 left will pass the current current pulse the pre synaptic cell, and that

25:33 you can see will flow down. of it will leak out. Some

25:37 it will flow down, using according the resistance capacitance circuit R C

25:44 and will cause a strong, deep in the pre synaptic self. But

25:51 any delay. There will also be immediate posson optic deep polarization of the

25:58 to only a fraction of that Only a fraction of the ions remember

26:05 size of the current is really the of the ions through the channel.

26:10 only a fraction of this current, a fraction of this deep, polarizing

26:15 will be found in cell number But there will not be any delay

26:21 happens in regular chemical synapses. In synaptic clap, the release of

26:27 that neurotransmitter has to travel through 20 of space to bind the receptors for

26:33 receptors to open. This whole process referred to as a synaptic delay,

26:41 that's an optic delays on the order a few milliseconds. So when the

26:47 potential arrives in the pre synaptic cell vesicles fuse, there's going to be

26:54 five or so milliseconds from the time record an action potential in the Saxon

27:01 to the time that you see a haptic response. And so the synaptic

27:06 because of the synaptic cleft because of space of neurotransmitters, have to traverse

27:12 order to buy into the parson OPIC . That is not the case with

27:19 gap junctions. There is no synoptic , Uh, but you can see

27:27 only a fraction. So there's no of the signal in the post synaptic

27:32 , only a fraction of the polarization the voltage. Only a fraction of

27:36 currents that air coming from Sal Juan be found in Cell two, but

27:40 will freely pass. And if you to dip polarized cell, too,

27:44 scarrans will flow in the reverse direction cell one if you with the reverses

27:51 . So what gap junctions allowed to is they allow for a very fast

27:58 between cells and cell networks. And happens is a lot of times each

28:07 of these lines you can interpret in video as a separate network signal.

28:15 you're looking at each one of these . Let's hypothetically assume is corresponding

28:24 a group of 10 neurons, and can see that the top group of

28:29 neurons is having a very slow oscillation . Okay, it's very slow oscillation

28:38 the middle group Of these 10 this is an average is adding a

28:42 oscillation. This is the third group having yet another oscillation, our voltage

28:50 in the network. But they're not and the reason why you would have

28:55 different rhythms is because you have different properties in the cells. Processing the

29:02 coming in different channels with their I curves within the snap works off the

29:09 and the synaptic delays that are happening these communicating neurons. What gap junctions

29:17 to do is they allow for these all three networks to synchronize within the

29:24 beat. So now you have a strong signal from the first cluster slightly

29:32 signal and implicate from the second cluster the weaker one from the third cluster

29:36 neurons. But all all of these are synchronized. All of these neurons

29:46 now synchronized in time and having gap having the ability for the ions to

29:56 across freely in a very fast way one of the advantages where the gap

30:03 allow for the cells to synchronize. when we talked about glial cells,

30:09 discussed that glial cells, especially the sides, they do special potassium buffering

30:17 there is local rises and potassium One Astra City process will slurp up

30:24 potassium, and what happens is that will distribute it through the processes of

30:29 one Astra side with Astra sides and legal south are interconnected through gap junctions

30:36 so that Sam potassium increases in potassium will now be able to freely cross

30:44 cells that contain gap junctions and Astra . In that way, through these

30:51 junctions will be ableto buffer, especially Increases in potassium concentration also spread the

31:00 of calcium, by which exercise communicate lot of that communication that is through

31:06 Gap Junction channels. Okay, so points here. It's synapses different from

31:14 Junction. You have synaptic cleft synaptic channels and the synapses are typically unit

31:26 . In the gap junctions this distance to 3.5 nanometers, and the heavy

31:31 connect to form. A continuous channel two cells, which allows for very

31:37 signaling of islands and small molecules without delay, allows for synchronization of cell

31:45 . And it's not only the glial that will have gap junctions, but

31:51 a few neuronal sometimes will also be through gap junctions through these electrical

31:59 so essentially neurons will have two types synapses the chemical synapses and the electrical

32:07 and the communication between neurons between networks neurons happen through both the chemical and

32:15 electric. Constant lapses. I think noticed maybe a question or two on

32:20 chat. How do cardio ourselves, keep the same amplitude when two polarizing

32:39 whole heart, they communicate through the junctions too? Well, that's a

32:50 good question. I mean, we're really talking about the hard, but

32:54 is one of the advantages in the , in this case, in the

32:59 muscle, not in the neuronal populations South and the cardiac muscle do have

33:05 junctions. And precisely. There's a example because this is where you have

33:12 contraction off the heart and the heart that synchronizes. So you have the

33:17 and a V notes and connect itself Gap junctions and engage networks off other

33:25 in the muscle, causing this Eso I hope that somewhat answers your

33:31 . It's not completely clear to Um, maybe I'm not understanding

33:37 but we are mostly going to focus gap junctions and communication between neurons,

33:43 you're correct to point out muscle cardiac muscles. Heart contains a lot

33:49 gap junctions now chemical synopsis. We know a lot about chemical synapses.

33:58 we zoom in on the pre synaptic terminal, we will see that it

34:01 again contains a lot of mitochondria, happy synaptic vesicles that have bunched up

34:07 close to the areas where they refused the pre synaptic plasma member in those

34:12 Serve referred to as the active zones you have higher densities of the your

34:17 . Vesicles some of them fused with plasma member and other sir primed and

34:22 to get fused and others are being before they're away and being transported closer

34:27 the external terminal Plasma member. So now the collapsed on them.

34:32 aside, you have receptors that are of the Boston optic densities, and

34:37 response of the most synaptic cell will depends on the receptors that are in

34:43 South rather than the neurotransmitter that is from the pre synaptic. So we'll

34:48 this example in a second synopsis. here is your home or classroom.

34:55 are down score of vesicles and how different from neurotransmitter vesicles. So this

35:01 here on the right, what you is we're seeing our electron microscope

35:05 You should be able to recognize that should be able to recognize the boundaries

35:09 the external terminal here. Zonal terminals off. The mitochondria need energy for

35:17 bicycle release. Recycling off the vesicles be filling of the vesicles. You

35:22 see that some of the vesicles air further away from the plasma membrane and

35:26 are gathered very close to the pre active zones and others you can even

35:31 event are using starting to fuse through plasma member and juxtaposed pasta.

35:37 Piccoli. You also see a Nah, pick cell and you can

35:41 on the other side of the pasta south the pasta napping densities. And

35:45 are the collections off the receptors that be bound by these neurotransmitters coming from

35:52 synaptic vesicles so synapses can be formed the dem drives of the South,

35:59 as one acts on contacting another dendrite those air called accident. Really,

36:05 can be formed on the Selma's off neurons, and those air referred toe

36:11 somatic from accent to Selma. But are also synapses that can be formed

36:17 one Axiron onto another accent, and are referred to access X tonic synapses

36:24 one accent onto another accent. So that you've learned so far, you

36:30 learning about synapses and the dendritic spines in the dendrite. And now I'm

36:35 you that they're actually points of contact communication on the accidents. Indeed.

36:41 there's also Denver dendritic synopsis, which don't understand very well. But we

36:45 that the gun rights communicate with each also through somewhat different but also specialized

36:51 off communication. Uh huh. So is the difference? And how can

36:57 three different types of synopsis influence activity another neuron in a If you were

37:04 exciting Terry solid, you were an solid. You were projecting onto this

37:08 drive. You need quite a view these dendritic synapses in order for the

37:14 to be de polarized enough, for , to produce an action potential,

37:18 that dendritic synapse should be very close the soma. The closer it is

37:23 the soma, the stronger impact that happen, the integrative properties of the

37:28 and the acts on initial segment. it will influence whether the cell will

37:33 an actual potential or not. In the synapses projecting onto the Selma,

37:41 actually have very strong influence on the properties of the south. If you're

37:47 to resell, you can excite the because you're located approximately very close to

37:53 zone that will be responsible for generating potential. That's so much acts of

37:58 segment. So you have very robust from the synapse. If it is

38:04 director of the SOMA robust influence on integrative properties of the self. Now

38:10 the third see diagram, you cannot the integrative properties off the neuron onto

38:19 your synapses notice that the sin So this acts on this contacting another

38:26 . So this this this ax on determine whether this other neuron will fire

38:34 potentials or will not bar will fire potentials or will not. We will

38:39 influence the integrative properties and decision making fire or not to fire. But

38:47 it will exert module A Torrey It will modulate the output of this

38:54 . So in a and B you influencing and you're affecting the integrative properties

39:00 these nerves and then see you modulating output off one neuron onto another

39:08 This is the actual sonic center. , we looked at these synapses.

39:15 certain anatomical features of these synopsis that us Thio just based on anatomy,

39:25 excited Torrey verses. Inhibitory synapses so tourist synopsis are typically as symmetric.

39:32 have as symmetrical, numbering differentiations by symmetrical. I mean that the pre

39:38 active zones are usually thinner and smaller compared to the pasta synaptic receptor densities

39:46 the Pasta Matic side and the vesicles very, very round in the exciting

39:51 cells in the inhibitory solace earmarked by the synapses air actually symmetrical. They're

39:59 , numbering differentiations, the same density size off densities of the membrane and

40:05 or the pre synaptic active zone in past synaptic density and also noticed that

40:12 vesicles has someone of a flatter shape . So vesicles are plasma membrane enclosed

40:20 . Alison Inside this vesicles you have . So exciting story, of

40:26 are glutamate. The glue dramaturgical synopsis the inhibitory cells. That symmetrical and

40:32 ship that's the cults are inhibitory Well, we said that we're going

40:42 talk mostly about neurons in the But it's very important that we come

40:47 and understand the rudimentary circuit that we studied, but in slightly different and

40:54 way. And actually, this is the last time we touch on

40:57 I'm actually going to talk about what call and play potential in the following

41:02 next week. But so you have motor neurons, our favorite multipolar motor

41:10 that live in the ventral aspects off spinal cord and project their different outputs

41:18 the muscle, in this case, muscle and release a single Colleen.

41:25 , you guys know so much. job. So when s until Colin

41:31 released on the muscle muscle contracts and increases the contraction of the skeletal

41:40 Wait, wait, wait, wait A Wait a second. You

41:44 us that if you have a Seattle , it will slow down the contraction

41:49 the muscle and slow down on hard . All more question. So settle

41:58 is inhibitory in the cardiac muscle, down activity off the heart and in

42:07 skeletal muscle biceps muscle, it's causing contraction. It's deep polarizing the

42:15 Why? Why is the Seattle call inhibitory to the cardiac muscle Alexis Editori

42:23 answer lies and the receptors that it . And the response is coming from

42:29 receptors, so look into it. is your home or question number

42:35 And look, let's look closer into anatomy of this external terminal again.

42:41 have the splits of these percent African terminals, each one of these terminals

42:47 an end plate motor and played region the muscle fibers. And if you

42:55 in again, you will see mitochondria we're all familiar with. You'll see

42:59 synaptic vesicles. The synaptic vesicles are with the Seattle coleene, and a

43:04 of them are sitting on these active , primed and ready to fuse.

43:08 when there is an action potential, synapses highly reliable, it's,

43:14 High Fidelity Synapse 121 and action potential results in a twitching a muscle unless

43:23 something wrong. Pathologically with the very powerful synapse. Activation of one

43:30 in the Motown played causes a deep of 70 million balls. How much

43:35 you need to de Pol? Arise South from resting member and potential in

43:39 to produce an action potential. Only 20 to 30 million moles so motor

43:45 played potential or and played potential is huge potential nerve to muscle potential of

43:54 70 million balls that always results in action potential in the muscle, So

44:01 to 1. So what happens is when the acts on, uh now

44:08 the action potential in action potential, rises the pre synaptic terminals. You

44:14 that there is influx of calcium. because of this deep polarization, influx

44:19 calcium, the neurotransmitter vesicles will fuse the plasma membrane. And as they

44:25 to the plasma membrane, they will released into the synaptic cloth. And

44:31 the synaptic cleft. These red dots corresponds to the Seattle Colin receptors.

44:39 so you can see that there is high densities of these acetylcholine receptors that

44:44 located proximal of these, uh, regions to the pre synaptic active results

44:53 ical release. And you can see these, uh, synapses on the

44:59 side they contain what we call All falls and these junction all falls

45:05 the surface area, and they also for the expression of high densities of

45:11 settle Colleen receptors. And so what happen initially is the release of a

45:17 Colin will cause the opening of acetylcholine . He's a ligand. Gated receptors

45:24 deep polarization through acetylcholine receptors will then on voltage gated sodium channels which are

45:32 deeper within that junction. All falls the voltage gated channels will then generate

45:39 action potential, which is different than muscle. The dynamics are different.

45:44 a longer action potential. We won't that much time. Thio look

45:48 It also has a significant calcium component the action potential in the CNS neurons

45:55 not. And so we actually have kind of ah, start understanding.

46:03 settle Colin is released that travels through clap monster receptors causes initial deep polarization

46:09 we'll be learning mawr and more and about the So if you are a

46:13 bit confused at this point about, does assembly potential happens? And how

46:18 this translate into generation of action potential come back to the following a

46:24 Okay, But just so this is important for us to learn today so

46:30 we understand and we understand that these very reliable, very high amplitude functioning

46:38 between the nerves and the muscles. if we're looking to see N s

46:44 we want to describe what we call our system, we have many different

46:51 , and we have neurotransmitter systems. what is a neurotransmitter system? Neurotransmitter

46:59 is the whole system that has a of components that have to exist.

47:03 synaptic Aly Apostle, optically pre synaptic . That neurotransmitter has to be produced

47:11 synthesized and found within the neuron. , that neurotransmitter should have synaptic vesicles

47:20 . That means that that neurotransmitter needs get loaded up into the synaptic

47:24 So you need to have proteins of that will transport the chemicals and in

47:31 them within the membranes off the you need re uptake. Transporters.

47:39 right, so reacting transporters. Synaptic vesicles, transporters and the ones

47:44 are going to transport the vesicles to plasma member and re optic transporters of

47:47 ones that are gonna, uh, the re uptake off off the vesicles

47:53 the vesicles doesn't get wasted. It refilled with neurotransmitters. It has to

47:58 degradation. Enzymes that once the New translator is released in the synaptic

48:03 It doesn't linger there around indefinitely. actually gets either diffused or it gets

48:11 into his constituents. Parts and usually parts reported back into the prison attic

48:18 and goes through the mechanism of re and bicycle transport following that exercise.

48:26 . Okay, so Boston optically you transmitter gated ion channels. Those are

48:30 channels that will bind these mini So these air ligand gated channels,

48:35 different. The Legans or the chemical going to open the channel, not

48:39 voltage change. Boston optically will have protein coupled receptors. G protein coupled

48:46 will also be the binding targets to dinner transmitters, but they're not

48:53 That means that transmitter gated ion channels allow for flow of ions through the

48:58 and actual channel, where G protein receptors are linked to G proteins and

49:04 G protein. So your translator, to G protein coupled with several active

49:09 protein which will turn, will activate protein gated ion channels Boston, AP

49:16 and, of course, Boston optically secondary messenger cascades that will then signal

49:21 information potentially all the way to the of this pot synaptic self and reacting

49:27 the levels of the activity. So criteria, when neuroma stimulated, do

49:34 that neurotransmitter that is synthesized. It be released when that chemical is

49:39 So let's say it's glued in It must cause a pasta Matic effect

49:43 you release them. Chemical doesn't cause possum attic effect. Then maybe it's

49:47 neurotransmitter. After Chemical is released, must be inactivated. It has to

49:54 on Boston optic receptor causing biological If it doesn't bind to the

50:00 it has to be now broken broken down and re up. Taken

50:06 into the present optic terminal. If chemical is applied on the Boston optic

50:11 and should have the same effect when is released buying neuron so it would

50:16 the same effect. If you isolated chemical here and they use non produces

50:21 skull Colin and you're isolated that that's tall colon, it should have an

50:25 . The fact is, if you to stimulate the Vegas now, so

50:30 air the neurotransmitter criteria do we have neurotransmitter systems, you know, our

50:37 do that qualify these criteria. So can see that there's pre synaptic

50:42 There is a synaptic degraded degradation. . There is possibility. Component.

50:47 is a system glutamate. It's a dramaturge. ICS system glutamate gets released

50:52 receptors. There, there there's gonna things that the great glutamate reacting

50:58 Gabba synapses, Gabba allergic synopsis. a gap allergic system that's still Colleen

51:04 allergic synopsis. Right? That's an thing to know for us. Is

51:09 impairment? Visit Seattle. Colleen is with which neurological disorder, which neurodegenerative

51:19 that we now you haven't impairment in Colleen. Anybody wants to take a

51:42 . Hello will be eventually. Parkinson's have an effect, but it's typically

51:51 by an impairment and dopamine systems and allergic impairment. We haven't discussed

51:58 so your hint is something that we discussed. Yes, Alzheimer's disease.

52:06 Alzheimer's disease what we talked about. talked about pathology. So go back

52:11 your announced now where you have you in Alzheimer's disease and you have the

52:15 of pathology that we discussed, which there, tangles inside the cells and

52:20 and what blacks outside the cells. we discussed the you know, the

52:26 short term memory loss anxiety. We discussed another pathology of shrunken gray

52:32 shrunken brains. Now this is a pathology, which sells air dying in

52:39 Alzheimer's disease. The earliest networks that deteriorated are the colon. Ergic networks

52:47 Colleen Networks. Uh huh. So that's That's an important note to put

52:54 to your Alzheimer's disease. Note. now we have all of these different

53:05 system times, and we have I acid in your translators that we're getting

53:13 know pretty well. This is gamma butyric acid or GABA glutamate glazing Gabba

53:20 a major inhibitory neurotransmitter in the Glutamate is a major excited to know

53:27 . Glide scene is a favorite neurotransmitter is contained and, uh, inhibitor

53:35 turnarounds of the spinal cord. There's to every rule glazing, and the

53:41 nervous system in the serene room actually as a cool factor. Too

53:47 So whilst in this final chord, is inhibitory in the serene room.

53:53 acts as a co factor in promoting and excited Torrey signaling interesting all depends

54:01 the receptors depends on the binding size of these molecules to the receptors just

54:07 an assault. Tell Colleen it can exact hitori, but can be

54:12 Correct. Nicotine Nicholas chapters. The muscle off the skeletal muscles is

54:20 going to cause the exciting Torrey effect the muscles. Other times, those

54:25 is up to you to find Okay, Now you have a group

54:30 the means that are very easy to . They're all ending in i n

54:38 . That's a little Colleen dopamine. any epinephrine? I nie histamine.

54:43 any norepinephrine i d and serotonin? the only one with exception. I

54:51 again. These are all very important systems in our brain. Acetylcholine is

54:57 important for no memory for, cognitive executive function dopamine and is involved

55:08 many different aspects. And it's correlated different behaviors. And different neurological disorders

55:15 been ephron and norepinephrine. Is that of the activation and the fight or

55:23 , um means in our brain. is related. Thio inflammatory reaction

55:29 and you'll learn later as we study about Sortino trick systems very widely expressed

55:35 the body. So when we talk neurotransmitter systems, it doesn't mean that

55:40 neurotransmitters, such as acetylcholine or serotonin only find in neuron. Serotonin in

55:48 means and other neurotransmitters can be expressed the periphery can be expressed in the

55:53 organs and peripheral cells again. um, peptides that we've mentioned.

56:00 you will not really have to know much about the baptizes color system kind

56:05 dine Orphan and Kath Elin's n acetyl in glutamate. Neuropeptide y's amount of

56:11 Substance speed. I would drop in hormones as active intestinal polyp type V

56:16 . P. Substance P. You know mediating pain signals so that a

56:22 we mentioned because we talked about certain of inter neurons and that you put

56:27 that have some out of Staten War calling sister kind. And so these

56:33 the major neurotransmitter systems. Sometimes what have to start thinking about is that

56:39 think of these amino acid neurotransmitters. glutamate has involved in very fast

56:46 and I see little coleene and opening mean and theft I Nero transmitters.

56:53 you need to have heightened levels of in order to start releasing or co

56:58 these neurotransmitters together with gabba or glutamate what you have to realize is that

57:06 one of these is dominated in a part of the brain. Therefore,

57:11 linked to slightly different function. each nor transmitter system can be linked

57:17 almost a specific behavior, so serotonin be link, for example, thio

57:23 behavior and appetite. Okay, so is how you have to start thinking

57:28 it and physiological on cellular level with molecules so look like and then on

57:33 holistic level, what kind of Where they expressing the brand, what

57:39 of behaviors they would be controlling For example. You have traumas and

57:45 disease because dopamine is very important and the motor commands and the structures of

57:51 brain straight. Um, that expressed a very important for the organization of

57:57 motor commands. So again, different different part of the brain, different

58:04 as it is related to the So let me positive for you to

58:09 notes on this one as well and particular. What I mean by that

58:13 that you have these classes of neurotransmitter and system neurotransmitter system types that we've

58:22 and this list is incomplete, so will actually add to this list.

58:31 happens? I added to this We have gas. Is that service

58:41 ? So you have Naturists oxide and monoxide that actually have the respective

58:47 Nitrous oxide receptor government oxide receptor. you have gas is gas neurotransmitters.

58:54 into that home or question that I , what's the difference between vesicles and

58:59 score dense core vesicles and neurotransmitter Right. And we're talking about storing

59:06 neurotransmitters inside the vesicles and packaging What we cannot do with the gas

59:11 so they're not packaged in the neurotransmitter us. There is a non sort

59:17 a nontraditional our transmitters that are very to always make this joke that next

59:23 somebody says I'm having a brain so you have too much natural socks

59:28 in your brain, our carbon Too much of the gas was

59:33 Going on in your brain can be smart Alex Alexander. And do

59:40 uh, that a nontraditional neurotransmitters that important that will mention you should know

59:46 the energy molecule 80 p. And and triphosphate actually serves as a

59:53 There are receptors to which a teepee . It's not just an energy

59:58 It's also a neurotransmitter. And the of that molecule at Denison is also

60:05 neurotransmitter, and it is very Actually. You know why? Because

60:14 overwhelming majority of us use a psychoactive that regulates the Dennison receptors. A

60:23 receptors shut down the signaling of so Donaldson receptors will essentially make the

60:31 less excitable. The synopsis. They're to be less excited if the dentist

60:38 activated and the Dennison is going to expressed at high levels at night time

60:44 then the dentist Similar Decrease in this . Normal synthesis levels in your brain

60:53 the morning time between you wake you sometimes feeling groggy and having difficulty

61:02 to kind of jump Start yourself for immediately engaged. And most of us

61:08 thio psychoactive substance that we know that called caffeine. And when we consume

61:18 and caffeine interacts with the Dennison and it blocks the Dennis Interceptor.

61:27 promotes the release of glutamate of the . So you glutamate is released.

61:37 have a psychoactive effect from caffeine, I'm not just talking about coffee,

61:45 drinks, energy drinks, caffeine This is all that we used to

61:53 glutamate signaling, and it's acting through Denison receptors. That interesting thing to

62:01 that we don't think that is a substance. But what is psychoactive?

62:06 that alters activity and psyche. If brain physiology out during the physiology of

62:14 brain is actually out there in the , if your brain is well,

62:18 interesting thing to know is caffeine is addictive, and this is actually quite

62:26 . An effective dose of caffeine. of us consume one, maybe

62:33 um, speaking Teoh guy regularly that about eight cups of coffee. It

62:38 pretty wired to me. I don't how he sleeps. This is the

62:43 does alright that z effective those that that it z accomplishing what you're It's

62:49 upper. You consumed an upper. by the way, these points of

62:54 for this addictive substance exist on every in this country. Whether it's called

63:01 or another type of cafe, you have three Starbucks on the intersection,

63:06 then you'll have dunking down and selling different type of caffeine on the fourth

63:11 . That's very typical because it is addictive, and the other thing is

63:15 . Does is this few cups of deadly does for caffeine is about 100

63:21 of the effective. Don't so, effective, does if one cup of

63:25 is makes you wired 100 cups of stand to kill you so caffeine can

63:32 toxic and especially synthetic cafe. An different form off caffeine, which can

63:40 quite quite strong. So it's very to keep these things in mind as

63:44 consume substances every day, you and we're seeing effects from these

63:50 but we don't think of them a . We don't talk about them a

63:55 . We don't even discuss that it's glutamate signaling. But now you know

64:01 you know better. Finally, we another very interesting class of neurotransmitters that

64:07 lipid soluble or their plasma member insoluble . The gas is so the lipid

64:14 neurotransmitters they cannot be stored and their vesicles because neurotransmitter vesicles have their own

64:21 membrane that forms the neurotransmitter vested. these are academic acid and and they're

64:32 and for their kanam annoys will actually a separate lecture attendant discourse. But

64:38 have these internal cannabinoids that are synthesized our bodies, the two dominant,

64:45 and best known as an anti mydd to a G, and you will

64:50 understand how their signal. Now our asset can be both the precursors under

64:56 and also a decorative byproduct of degradation the contaminants. Those molecules are

65:04 uh, synthesized on demand when there heightened levels of activity and released on

65:10 their membrane, or lipid soluble. , they will cross through the membranes

65:14 will buy into their own respective almost in the para crime like

65:20 in the sense that they're not stored the vesicles right across the road from

65:26 Boston optic densities. But rather they're through the plasma membranes leave. It's

65:31 lipid soluble molecules, and they traveled buy into their respective receptors. So

65:37 a way, there is a bidirectional in the chemical synapses as well.

65:42 of the cannabinoids will travel retrograde invited to the pre synaptic receptors rather

65:48 affecting the loss synaptic side and and Canavan alliance eyes a very important

65:55 It's expressed in the brain. It's throughout the body, different various organs

65:59 express different under cannabinoids, with virtually single cell in our body as an

66:06 noid system, which is really very him for a long time. There

66:11 this, uh, you may have off endorphins and dismiss that the runner's

66:20 runners run long distances. They get is called the runner's high, that

66:26 the feeling of bliss and by the , Ananda in Sanskrit means bliss.

66:32 Ananda mine is a bliss molecule, that makes you happy. Something that

66:37 steal mood, something that makes you makes you laugh. And it also

66:42 inflammation and appetite in your body, other things. So it's actually and

66:49 cannabinoids that our bodies release and the high is not because of them the

66:55 , because there's no endogenous morphine, is no more feeds like molecules that

67:00 synthesized and in our bodies that cannabinoids molecules and their cannabinoids are synthesized.

67:08 and the new and modern science understands the runners hide is good feeling of

67:16 . It happens typically when you run middle miles, so if you're a

67:20 , you know that, too. , mile is not very interesting.

67:23 you're somewhat of, ah, long runner. The random I was not

67:28 interesting. You run. It may for speed, you know, to

67:33 three miles is becoming a little bit interesting. Somewhere on the 2nd 3rd

67:38 , you may be getting that second . It's the middle mile. So

67:40 people run 10-K, which is about point, some are seven point some

67:48 miles this middle miles 2345 is actually a really nice you for a boost

67:56 the runners and after the run. , the whole physical activity that's stimulating

68:02 production of under cannabinoids. This resulting this, uh, this blissful happy

68:09 after the war cough. So in you didn't know, you could go

68:14 out, run a few miles and your own cannabinoids in your own

68:20 And if you wonder what other ways you can generate cannabinoids without injuring your

68:25 because that's when then the cannabinoid system really very active. Is during the

68:30 and inflammation other ways singing one of most effective ways Thio induce under contaminant

68:38 in your body This were singing or . We're having a workout, and

68:43 feeling of bliss. Next time you feel great after work out, think

68:48 you. And and, um, and to a G. So I'm

68:52 to stop the lecture here. And we come back, I will have

68:59 scores. I will have your Casas released. Uh, my next

69:06 You can look at the questions you ask me any questions specifically about the

69:12 . For now, I want you address technical issues you may have had

69:17 Casa. Have only a couple of to look over these because it's occupying

69:22 lot of their space, all of video recordings on their servers. So

69:26 address any technical issues. Example Get . You will see what you missed

69:31 the exam. The questions. You adjust them with me then and I'll

69:36 you know about the Casa quiz if going to do the quiz or if

69:39 have another way and try to accommodate toe help you with your grades.

69:46 . There's any outstanding questions. shoot me an email. Otherwise,

69:51 your weekend, and, uh, will see you next

-
+