© Distribution of this video is restricted by its owner
Transcript ×
Auto highlight
Font-size
00:00 Okay. So what we discussed the 2 3 lectures were resting number and

00:11 . And of course the action And when we talked about the action

00:17 , we learned that action potential is by two currents. The sodium conductance

00:24 is coming from outside of the south the inside of the cell, the

00:28 word, current positive charge moving inside the awkward current which is a potassium

00:37 from the south of the outside of south. We talked about how puffer

00:44 contain tetrodotoxin. The toxin is produced bacteria and that tetrodotoxin is an

00:53 It binds two potassium channel and blocks trump. Uh sorry sodium channel,

01:00 educated sodium channel in particular the vault sodium channel that is responsible for generating

01:06 action potentials. So in the presence tetrodotoxin you will not see these inward

01:13 is because the sodium current and sodium is going to be blocked. We

01:19 talked about tetra ethyl ammonium A. . A. Has a specific blocker

01:24 the potassium channels and the outward conductance in generating action country. And we

01:31 that these substances uh there's multiple substances lidocaine and we also mentioned cocaine that

01:40 be targeting multi educated sodium channels as . So there's many different things in

01:46 of course is the local anesthetic. when the action potential gets generated,

01:54 gets generated in the acts on initial . So in this scenario what you're

02:00 on the slide as this neuron here active and it sends a signal to

02:06 neuron. There's a synoptic transmission here will start discussing later today neurotransmitter is

02:12 and at the level of the downgrade are postion optic potentials. There is

02:16 great and synaptic potentials and they're either which means that our D polarizing to

02:22 cell and be polarizing plasma membrane or inhibitory. And they're hyper polarizing.

02:29 they are D polarizing enough at the of the soma, then the accident

02:35 segment right here which is located close the soma will generate the action

02:42 This action potential will travel down the which is insulated except for where you

02:50 the nodes of Ron veer and the there is exposed and nodes of ranveer

02:56 with voltage gated sodium and potassium each note of round year the action

03:02 is going to reproduce itself and arrive the external terminal having the same amplitude

03:13 it did. That the acts on segment was initially generated. So this

03:18 referred to assault a Tory conduction or action potential conduction down the axon.

03:27 so each one of these nodes of beers will have the machinery, the

03:35 potassium channel machinery to reproduce these spikes action potentials. Ra Monica. How

03:46 the person that not only made these drawings of neurons and neuronal circus.

03:53 if you recall in his drawings, showed that axons had arrows next to

04:00 and he postulated that gun rights received information are the side of the inputs

04:06 of like an antenna and the axon an output. And there was a

04:12 to the signal flow in his So he proposed his principle of dynamic

04:19 , meaning that there is a directionality the polarity to the flow of the

04:26 to the flow of the dynamics of information that is being carried through the

04:32 . And so he was absolutely The axons where the output. Although

04:40 did not know that physiologically, he derived it from the drawings that he

04:46 with the gold he stay. It also right that action potentials travel in

04:53 direction to the axon terminal. With exception of what has been discovered about

05:03 years ago in the form of what called the action potential that is back

05:08 action to come. In reality this area of the axon because it is

05:26 with very sensitive sodium channels that can polarize and produce this very fast spark

05:33 the form of the action potential, threshold or how much deep polarization the

05:39 initial segment has to see as compared how much deep polarisation has to be

05:44 in dendrites or Soma. It's actually in the sense that the synopsis that

05:51 contact the damn drives. They're far from excellent initial segment. So at

05:57 level of the downgrade downgrade may have be deep polarized, very, very

06:01 levels minus 30 million volts minus 35 bowls. Right? But if there

06:08 an input that is very close to accident initial segment it can actually influence

06:17 also have a very strong effect. , a small deep polarization in the

06:23 are close to the accident. Initial is very meaningful to these sodium channels

06:29 a small deep polarization that is far in the damn right. It's not

06:33 meaningful why? Because gun rights are insulated. And so these great and

06:40 potentials that are produced excitation and they will die down with distance.

06:46 electrical potential on that change will reduce distance. And that's why you need

06:51 or hundreds of synapses activated at the time in order for a cell to

06:57 an action potential. Because those synopsis you saw can be found on the

07:02 drives and the good experience on the . Some of them can also be

07:09 in the accidents. So, let's at how the action potential gets generated

07:18 how it travels in the forward And for that. Uh I have

07:28 in your special materials lecture materials and , which is about 12 years

07:43 But the mechanics and the channels behind are involved in generating what is happening

07:54 . Still hold true. So it called Hewlett the spikes out and who

08:01 the spice out room. Uh Which let the spikes out. That's really

08:10 question here. And you'll see, do you mean? Which channel?

08:14 sodium channel sodium channel is responsible for the action potential. And then I

08:21 it to divey plots that drew these lines everywhere. And I said look

08:25 these lines, they're all different types plots. One cell can have all

08:29 these lines as the dialect of that sour. Why can't it have all

08:34 these ivy applause. Because it has variety of different voltage gated and other

08:40 channels. And if you have voltage channels that have different lines, that

08:46 they process information differently. And that are also subtypes of voltage gated sodium

08:52 that there are subtypes of chicken potassium , calcium channels and so on.

08:58 so the way that action potential is at the accident. Initial segments can

09:06 represented by this cartoon. So there have an incoming deep polarization and you

09:11 see this green cloud here over the dendrite is here and this green cloud

09:18 sending the green arrow into the It's trying to excite the cell and

09:24 to de polarize the soul and trying de polarize the actual initial segment.

09:30 this neuron hypothetical model neuron is receiving lot of excitation on it's damned rights

09:37 dendritic spines, that this neuron is receiving a lot of inhibition. And

09:44 it happens in the neuronal circuitry and in the cortical circuitry in the brain

09:49 a lot of the inhibitory synapses and are formed on the selma or around

09:56 selma which we call perry somatic regions neurons And that is also important because

10:06 closer you are to the integrated region the cell which is the selma and

10:13 closer you are to the trigger region is excellent initial segment which triggers action

10:21 . The stronger impact you have, more control you have of what happens

10:27 the summer whether it's deep polarized hyper , whether an action potential gets fired

10:31 not. So when we talked about we looked at the hippocampal circuit we

10:38 there's a variety of these inhibit their . Um Some of them will project

10:41 selma some of them will project and drives. But in reality inhibitory cells

10:47 inhibitory inputs really dominate the paradigmatic regions neurons. There are fewer. There's

10:55 10-20% of inhibitory into neurons in the regions and the rest 80% 90% of

11:05 cells are excited through phenomenal selves. if you are on the 10% of

11:15 inhibition you want to you structure the and yourself with respect to the projection

11:21 and communicate information and in train and . As much of that information is

11:27 to the integrative and trigger points for south. If however this cloud of

11:36 which is the d polarizing input, excitatory synopsis breakthrough and reach the accident

11:49 segment and you have a deep polarization action initial segment. They're anatomically you

11:56 encounter two types of both is gated channels. And maybe 1.2. sodium

12:04 a V. Stands for voltage 1.2 a subtype And any of you 1.6

12:15 Maybe 1.2 are located closer to the . But m maybe 1.2 are what

12:24 call high threshold voltage gated channels. means that they have to have high

12:30 of deep polarization in order to open they give you 1.6 channels. They

12:37 further away from the SEA as compared 1.2. But they're low threshold both

12:44 sodium channels. That means that low of deep polarization or input is necessary

12:52 sufficient to open These NAV 1.6 So what happens is if this deep

13:05 reaches the accident initial segment, This charge will actually bypass the 1.2

13:14 It's not enough to open that 1.2 . But when it encounters and maybe

13:23 this charge is enough because they just a little bit the little threshold voltage

13:29 sodium channel. So low voltage low of changing voltage are okay to open

13:36 and they open. And as they there's a deep polarization they go through

13:43 positive feedback cycle in generating an explosion is the action potential and number

13:50 And this is the forward propagating action . This is the action potential that

14:00 that propagates from the excellent initial segment the way into the external terminal.

14:14 this is the forward propagating action potential it moves in that direction. But

14:20 what happens now? There's still deep input coming in. There's still some

14:27 charge left in this purple zone which to N A. V 1.2 And

14:33 nearby there was an explosion causing further polarization by M 81.6 channels the father

14:42 of sodium and more deep polarization. now locally here in the membrane The

14:49 the input excitation and deep polarization with deep polarization produced by the low threshold

14:57 1.6 channels can the two can some . And when they do that deep

15:04 that changes voltage is enough to open high threshold voltage gated sodium channels.

15:12 this back propagating action potential is called propagating because it is not going to

15:19 in the same direction down the Why? Because they're standing strong,

15:25 strong 100 million bowls change and positive that is happening right here. This

15:32 all happening within no second of So the only solution and the only

15:40 in which the this charge from N . B 1.2 can move is back

15:47 propagate back from the acts on initial into the selma and potentially into the

15:54 rights and injury spines. So the propagating action potential a lot of times

16:02 referred as orthodontic and of course the propagating action potential is referred as back

16:09 action potential. Back propagating spike. amplitude of the forward propagating action potential

16:16 what we've already learned on the order 100 million bushels. The amplitude of

16:22 dark propagating spike is small and just a few million volts. So

16:28 will say well how come? It's a greater potential than because it does

16:32 come from a synapse. It comes the neuron channels generating that small potential

16:39 sending it back toward the soma and the gun. Rights. So why

16:47 I care about this not propagating Well because of the rules by which

16:59 learn and some of these rules plasticity that will change the strength of the

17:06 and potentially the number of the So we already talked about dendritic spine

17:13 . We said that during early development is more spines that are grown and

17:17 can be strengthened or potentially ated or can be weakened, depressed are

17:24 You have this process. It's plastic . And really spine plasticity. So

17:30 the back propagating action potential, it's for them to expand plasticity. It

17:38 served in the way as an excited . D polarizing signal that tells the

17:45 that were active within one or two that we produced an action potential.

17:53 the pre synaptic neuron will say I I fired. I fired. And

17:57 the past synaptic neuron doesn't sound the propagating spike then these pre synaptic neuron

18:04 of firing, they don't know whether responding or not. So there is

18:08 linkage that strengthens the back propagating action , strengthens this linkage between the active

18:18 attic neuron saying fire active boston optic and saying I fired an active person

18:26 neuron is saying okay good I'm meaningful you because guess what if the pre

18:33 neuron fires fires, fires, fires and this accident initial segment doesn't produce

18:41 back propagating spike doesn't produce a spike all. These synopsis are meaningless Or

18:48 produces the spike 20 seconds later, is forever in the brain processing

18:54 It's not meaningful. And that's why response has to be also lengthen time

19:01 when the prison optic neurons activate on at the cellar this network and when

19:07 network responds and the closer in time input comes into closer in time and

19:15 in time you produce the action potential the back propagating spike within a few

19:21 to 20 to 40 milliseconds, the plasticity in the system you have,

19:26 more ability. This synopsis and communication the synopsis have the ability to

19:33 Uh huh. So this is what mean by spike farming dependent plasticity.

19:39 the spike timing from the neuron that fire fire fire is short between the

19:45 that says I fired then this plasticity strong and this timing is short.

19:53 if the incoming neurons says I'm firing , firing what what I'm firing,

20:02 , firing her fire. You're gonna up on that. This synopsis is

20:10 going to be meaningful, This communication it can actually weaken because the time

20:15 is too long and for the brain this time period is too long.

20:21 responds window with spike timing dependent plasticity either strengthening potential rating or depressing synapses

20:31 about 40 milliseconds plus minus 1 20 on each side. The ability for

20:40 networks process visual information is seven milliseconds the optimal plasticity in your visual

20:51 Fire response within seven milliseconds the networks to link together, neurons have to

20:57 together in order to process the ongoing visual information such as movies are tv

21:04 and so on. So we talked the propagation of deep polarization and the

21:12 and I have a challenge of the . Do you think dendrites prefer to

21:16 deep polarization and forward or backward how would you test this hypothesis?

21:23 ? S cage neurotransmitter and what is ? So again, if you go

21:30 your glass folder materials you will find an article that talks about caged

21:38 It's a very very cool technique. you may want to look it up

21:43 may have a question about that on quiz or what is engaging. And

21:48 can also go over a little bit the following lecture if anybody remembers

21:59 So orthodontic is moving from Selma. . Uh It's used mostly. You

22:21 you could it's not necessarily for testing the strength of the pathways as much

22:27 testing the strength of the synopsis. can say it's a path line but

22:32 not really looking at the conduction velocity axons that interconnect to networks. So

22:41 you're looking at is you're looking at close in time is the pre synaptic

22:45 firing? In the past, synaptic has responded if they're firing and responding

22:51 close in time that synapse strengthens if order is reversed that synapse weekends.

23:02 the time period gets longer between prison saying, fire and for synoptic saying

23:11 then that synopsis too long of a and it's not going to do either

23:20 nor strengthen or weaken. It's just of a signal that's out there that's

23:25 unrelated. Oh yeah. You know is one of the mechanisms or you

23:43 see this is one of the cellular for learning and memory. Despite

23:56 Spike timing plasticity in particular by timing . First testament is one of the

24:05 by which Meuron strengthened synopsis and weakened and by which they learn and when

24:14 strengthen synopsis and there's repeated activity and response. It can be likened to

24:21 studying new material that's really difficult and happens if you repeat it 34 times

24:28 somebody will just give you a trigger when you quit somebody just you can

24:33 the first Two words of a definition 20 words long and the person will

24:39 you an answer. But that will on the fourth time. And that's

24:44 equivalent of the synapses. Now repeating, repeating and strengthening. And

24:52 rules. Some of them are short learning rules, short term memory that

24:57 have, others are long term Uh Learning rules will come back to

25:01 a little bit later in the Talk about more about plasticity. The

25:05 way that the brain encodes strengthens the so weakens them using what we call

25:13 rate code or the frequency. So the timing this is spike timing the

25:21 code is this is high frequency stimulation represents high stimulus, strong stimulus or

25:29 infrequent stimulation which represents maybe a week or inconsequential stimulus. This is another

25:37 of learning. And in reality the takes advantage of both of those learning

25:45 , Their rate card, the timing and also the directionality of communication pre

25:52 and post pre. So I hope answers your question. That's really good

26:00 . And I think some of these will keep coming out during the course

26:05 I'll address them uh in a little more detail in a couple of

26:09 But if you're interested in what happens them. Rights. Look up this

26:16 about caged neurotransmitters because you can actually a neurotransmitters in the cage and lock

26:23 up. You can put chemicals in cage and lock them up and you

26:28 release them using lasers and you can in it just singled and riddick

26:33 That single synopsis, which is incredible . Okay so we have this propagation

26:40 drama. It is moving in the from the soma into accident to draw

26:45 . If you shocked the axon, will also move into the into the

26:50 . But that doesn't happen physiologically. Korea conduction refers to the regenerative action

26:58 it knows of ranveer and there are actions that are non violent nated and

27:04 non myelin ated and the signal will on overtime. Um And the reason

27:11 nose over and beer can regenerate this potentials is as is shown by the

27:16 and green and red. It's a high density of voltage gated sodium channels

27:22 voted to get potassium channels that are to produce action production. So,

27:30 channel diversity already talked about this but is an illustration of a channel

27:38 C. N. One channel It doesn't really matter what kind of

27:42 it is. Ih current doesn't doesn't us what type of channel it

27:48 The principle is what concerns us. is this HCM expressed in the

27:56 So first of all let's look at prom. It'll Soller favorite criminal sell

28:00 pickle vendor is have the most of . The cell has a strategy and

28:05 cellular early in places. Most of receptors in the optical generals. External

28:12 to sell. You will see that receptors. Okay these channels if CNN

28:20 density call them receptors well let's call ion channels, they're distributed evenly.

28:27 did they trade? Underwrite summer everywhere see red the channel is there.

28:34 we can pull basque itself only on external terminals, cerebellum basket self very

28:45 expression on the film and strong expression the external terminals and these cups

28:52 So first of all each cell has own sub cellular ionic channel distribution.

28:58 has its own strategy. If you to produce a lot of action potentials

29:03 an action potential you load Jackson initial with voltage gated sodium and both educated

29:10 channels. If you want to release affects on all terminal you load the

29:16 with voltage gated sodium charleston voltage gated channels which you learn is necessary for

29:22 release. It's a similar strategy. am channel distributions of cellular early After

29:29 different types of iron channels can be by one cell indifference of cellular

29:36 That's a lot of channels that's a of I. D. Plots that

29:41 exist. Coexist in one south and the diversity of these channels. This

29:46 going to account for the collect the behavior of neurons or the dialects that

29:53 described to you from from Very early and how neurons fire and produces action

30:00 . So have slightly different sub paths will express an 81.2 others will one

30:05 long. Others will number 1.6, their action potential dynamics are going to

30:11 different. The frequency at which they produce action potentials. The activation and

30:17 models are going to be different for subtypes of these channels. And that's

30:22 you get this incredible diversity and communication dialects among neurons that you're seeing.

30:32 , synaptic transmission, we're gonna start about synaptic transmission. We'll come back

30:38 review a little bit of back propagation time. But I encourage you to

30:42 at that article who let the spikes fully understand it. It's not the

30:48 and the people that are really responsible defining it. Thinking about it hypothesizing

30:57 and drawing, testing, measuring Good Cathal familiar goals is student drew these

31:08 networks and said there's snap the There's directionality, the principle of dynamic

31:16 , which he wasn't 100 right because that propagating action potential but he was

31:24 much right. The major signal and chemical communication happens down the axon and

31:32 terminal search all shankman who coined this of a synapse is a specialist location

31:39 communication between the cells. Even in 19 twenties, ra Monica ha fault

31:45 the synapses of plastic that the connections plastic. That means that new synopsis

31:53 form and certain synopsis can go away that they can strengthen. He postulated

32:00 of that 100 years ago. Ultra . We finally was the person that

32:06 discovered the chemical that is involved in synaptic transmission Examine two weeks. That's

32:14 true. Officer necessary to. That's true. It's from all slide the

32:19 is still the same if you need email me. Uh huh. Um

32:26 of 100 billions of neurons in the . That's what synaptic transmission is,

32:37 . Mhm. I think I can like a billion. I don't know

32:44 I can write 100 billion. How many Zeros is that?

32:55 Mhm. 12 Oh let's try so hundreds of billions of neurons in the

33:10 . 100 billion. They form Synopsis you're on can have 100,000 synopsis.

33:20 we're talking about trillions of synaptic trillions of sites in the cns or

33:30 communication, this electrochemical communication to take . If you were to lay out

33:36 membrane of the brain. All of neurons that you were unfolded them dries

33:43 then it expires all flat. It cover four soccer fields. The total

33:51 in the area of the brand. . Mhm. Or pretty much for

33:58 fields. Yeah this is what we the fabric of our minds. Think

34:06 it you lay it out flat. covers four football fields and then you

34:12 it up and put it in. scholar that has all of the

34:17 drives billions of south trillions of neuron synapses neurotransmitters from the maximum initial

34:25 produces this action potential. An action arise of external terminal. Now we

34:30 that there is a release of the . But to get there, this

34:36 one of the really cool stories that should uh never give up on your

34:43 and on your visions. In the of Easter Saturday 1920 100 years

34:52 bottle of champagne. I walk, down the light, enjoyed it.

35:00 a few miles from the tiny slip paper. Then I fell asleep again

35:06 it occurred to me at 6:00 AM during the night I had written down

35:12 most important but I was enabled to for this crawl that sunday was the

35:19 desperate day in my whole scientific life the next night however, I awoke

35:26 at 3:00 and I remembered what it this time. I did not take

35:32 risk. I got up immediately. to the laboratory, made the experiment

35:39 the frog's heart, described the below at five o'clock the chemical transmission of

35:47 impulse was conclusively proved quoted from OTA 1953 Ratings. Uh how cool is

36:00 ? So what did you do? he woke up and went to the

36:06 in the middle of the night, the vagus nerve Vagus nerve is one

36:15 the cranial nerves and in this class actually learn about the 12 cranial

36:20 And you'll certainly learn about the vagus because you're learning about it today.

36:24 cranial nerve tan it runs from the stone and it innovates extensively most extensively

36:33 the body and the viscera which has strong input including into the heart.

36:40 if you stimulate the vagus nerve in case on the frog heart the heart

36:47 will slow down. So he had heart because the donor heart sitting in

36:57 dish and he stimulates the vagus nerve he collects the fluid that is bathing

37:06 heart. Following the stimulation he takes fluid removes it from the donor heart

37:16 he applies it onto the recipient part heart is not being stimulated and does

37:24 have vagus nerve attached to it. wrote the vagus nerve off of it

37:28 he's not stimulating anything. Instead it's in the solution and he brings this

37:35 stimulated donor heart solution and drips on of the recipient heart. And the

37:42 is the same. The heart rate down. And so he definitively demonstrates

37:48 it's not the electricity that gets transferred the nerve and the heart or between

37:56 neuron to another neuron there is electricity gets transferred. We know that there's

38:02 junctions called gap junctions. But he that there is fluid and that once

38:09 stimulate the vagus nerve, that there's in that fluid. There's some substance

38:14 that fluid that if you apply it the virgin recipient in stimulated heart,

38:22 has the same effect. It's the in the chemical that has the

38:29 So one of my PhD postdoc mentors to say that sleep is for the

38:37 , I think you realize that when have your own kids at some point

38:42 then sleep is for the weak or too weak if you need to

38:49 The other thing is if you have vision, don't go back to

39:00 wake up and execute on it, out who cares? It's one night

39:06 am. Forget it. Sometimes you your best fish at night. Sometimes

39:12 take your best nails at night doesn't to be all the time. You

39:15 have to be a lunatic walking around the time, but an all nighter

39:20 or there can make you can help in, you know, not just

39:26 nighter, but something that you're working , but you have to resolve that

39:31 have to be confirmed experimentally and it wait. So this is quite an

39:41 story. What is the neurotransmitter that ? We discovered cecile Colin? It

39:52 and the city of Colin. This a neuromuscular junction. It's a junction

40:00 the nerve the vagus staff and the muscle which is the heart neuromuscular junction

40:11 it's a single Colin on a single , inhibits or slows down their heart

40:19 . So if you learned about the Colin in the skeletal muscles it actually

40:26 contraction speeds up the contraction of the . But in the heart it has

40:34 different effect that slows it down. as you will learn over the next

40:40 of lectures as we talk about synaptic , the response off the cell muscle

40:48 a neuron depends on the receptors that carries not on the chemical stimulus that

40:56 civil clothing for certain cells can be turning for other cells that can be

41:02 . Acetylcholine also has different subtypes of and some of those receptors will help

41:08 cells get more excited and others will them. Mm So we'll come back

41:14 talk about the pseudo Comey and cycle receptors. But sometimes later there was

41:23 a discovery that neurons indeed past the from one another. That there are

41:33 very specialist locations just like you have synopsis that have a synoptic left.

41:40 it's a specialist zone of 20 nm space. That's a part that's where

41:46 neurotransmitter goes and the receptors are on other side. Gap junctions or electrical

41:54 are also present in neurons and they very interesting because for gap junction to

42:04 two. How many channels. One one neuron cell one You're on one

42:12 of plasma membrane and neuron to Has come together and form a continuous channel

42:19 between the two selves. It was . Connex Solutions connection is a sub

42:26 that makes a single connects on and connect since make a gap junction or

42:31 electrical synapse electrical junction. Why is an electrical synapse and electrical junction?

42:38 if you were to inject current into top sell here and to place a

42:44 electrode. This is your injected Remember? It's a square wave like

42:50 that's electronic and the cell will respond its resistance capacity of properties. We'll

42:56 a strong response in this cell in you pass the current but in the

43:03 cell if you place another electrode immediately any delay, you'll also see a

43:12 current. But this this neuron that bottom is not being stimulated, it's

43:17 the top neuron is being stimulated. , gap junctions, there are certain

43:24 of the gap junctions. Gap past ions through them. So do

43:30 islands. Hyper polarizing islands. Gap also passed small chemicals and molecules through

43:38 . They even can pass the secondary like cycling a. Mp. Who

43:44 junctions. It is somewhat voltage gated there for the most part open all

43:51 time. It's just sit there a bit more open or less open.

43:57 would you want that signal to be so rapidly. And why is it

44:03 ? Why there's no delay because there no sin. Ops the two cells

44:06 touching each other. The car in is now immediately on the other side

44:10 the gap junction there's no synaptic There's no neurotransmitter binding release and travel

44:17 synaptic cleft which takes 5 to 10 for this synaptic process and the response

44:23 take place. This is almost almost immediate. That's very important because

44:30 many instances neurons and neuronal networks need respond and need to synchronize to that

44:39 in a very fast fashion. Therefore junctions electrical synapse allow for fast synchronization

44:49 the neurons through the gap junctions. if you excite one part of the

44:55 network it's connected to the gap junctions another side. The other side of

45:00 network who almost instantaneously get excited and in synchronized to be active at the

45:07 time. Mm So electrical synapses No synaptic delay. Great for synchronization

45:19 the south. But only a fraction this current gets transferred. So there's

45:25 a small amount of that town gets into adjacent south to the gap

45:32 And with the chemical neural transmission as will see there is a delay.

45:38 that's because when the oxen terminal produces terminal of the final action potential.

45:48 action potential will cause the deep polarization the plasma number and opening of the

45:53 gated calcium channels which is necessary for vesicles binding and the transmitter released And

46:00 neurotransmitter gets released and it will cross space of 20 nanometers before it bounces

46:06 synaptic response and then you will have Matic response. So there's a synoptic

46:12 in chemical synaptic transmission which you don't . And the gap junctions. But

46:18 chemical neural transmission you will amplify that . And in gap junctions only a

46:24 of that signal gets transferred. But any delay. There's another homework question

46:31 the year that I actually answer. it's not that much of a homework

46:36 but it's something that will show up the quiz or exam what a dance

46:41 vesicles are. They different from neurotransmitter . So first of all let's talk

46:46 neurotransmitter vesicles. And you have these here and you can see in the

46:53 you have loads of mitochondria. the lows of mitochondria right here and

47:01 you have these active zones, pre active zones and you can see that

47:07 sort of a stacking of these around bubbles. There's the neurotransmitter vesicles that

47:13 the chemical molecules and you can see they're mostly densely populated here and on

47:19 past synaptic side you see also passed density is there's a boston optic

47:24 This is an electron microscope image if look closer at these dots circles and

47:33 synapses. The rounded vesicles and the number and differentiations meaning that the boston

47:42 zone is so much thicker than the synaptic zone. They actually most of

47:48 time will identify with excited to ourselves electron microscopy serve you an electron microscope

47:55 vesicles and this estimate trickle number and . It's an excited tourists announced.

48:03 you see symmetrical number of differentiation You see that the pre synaptic and

48:08 fast synaptic sides are both both equal thickness so to speak in size.

48:15 you can see that these vesicles are flattened. Those are typically the inhibitory

48:21 inhibitor Anthony so excited her would be glutamate vesicles from the vesicles and the

48:27 flattened ones. The symmetrical number and will be that Gabber bicycles. And

48:37 we talked about the synopsis chemical synopsis form on the soma and mostly form

48:46 the damn dries. And if the on the so most are called access

48:51 . If they are formed on the are called accident riddick. Sometimes they're

48:57 formed on the axons and they're called . Oxymoronic. And then there are

49:03 cases to done rights can communicate to other through these chemicals analysis. So

49:11 part of most of the things that be studying is related to accident during

49:16 access synaptic and this actual external synapses gender the drinks synapses we won't really

49:23 time to talk about. Excuse Two improvement. Yeah. Mhm.

49:40 And so again a very good Um It is a microscopic awhile observation

49:47 the level of the I like to . Not certain why there's higher densities

49:55 the excited heard. Uh Plus synoptic are bigger. May have to do

50:02 the fact that and M. A. Receptors are quite large.

50:09 receptors that received glutamate fasten optical are large. It could be one of

50:15 reasons but I don't really have a answer why one is symmetrical. Why

50:20 is a symmetrical. But from anatomically is sort of a classical description of

50:26 excited her inhibitor synopsis. Mhm. So most of the excited their synopsis

50:41 contain when we come to coordinate neural and one or two electricity. There's

50:48 NBA channels. There's an emperor There's tiny channels and most of them

50:53 co express all three subtypes of these actually. So it's not that it's

50:59 than M. D. A. synapse but it's more specific to the

51:03 . There are synopsis per set person will have a combination of receptor

51:09 So again a very very good Um So let's talk about what what

51:18 different about when you're contacting at Right? You're basically sending the information

51:25 an antenna to done right and that is going to inform the soma.

51:30 going to integrate information, accent initial is going to produce an action potential

51:36 you are contacting the soma. You're the integrated region directly saying I got

51:43 talking I'm talking to you inhibiting I'm exciting you. Very tight control

51:48 the integration of what happens to the . A very tight control whether this

51:53 post synaptic cell will fire an action or not. If you excited stem

51:59 it's enough it will fire an action If you're excited so much enough it

52:02 fire an action production. But it's different situation where you have an accent

52:08 another accident. We call this arrangement module a Tory and in this case

52:13 you're doing, you're modulating the output this neuron onto the other south.

52:20 not modulating the integrative properties of this because your Axiron these axons contact dem

52:35 in soma. They are affecting the of the summer. This axon is

52:43 another accident. So what is it ? Is it affecting integration? No

52:50 affecting the output of the cell onto cell. So it's modulating the output

52:56 the sell. It could be that cell produces very high frequency of action

53:03 . This guy comes in as an guy. And all of a sudden

53:09 the cell only here did did did modulated the number of action potentials of

53:16 frequency that was produced by the Yes. Uh huh. But accidents

53:28 DeAndre relax into Selma are the two common ones. Yeah and accented dendritic

53:37 . Um Gun rights accident to Axiron also relatively common. I would say

53:43 done right and done right is relatively type of the synapse. A connection

53:57 . Yes. Yes. It's another commentary question that you will have these

54:07 arrangements. Whether it's an integration. fact a module a Tory effect on

54:12 output depending on the brain region on function and what you're trying to do

54:18 how you're trying to modulate that and fact that specific brain region and what

54:22 of cell you are, you're excited inhibitor itself. So yes.

54:28 Right. How did he says that's problem? Uh Yes. You know

54:45 you know what what my answer Everything is possible. And I say

54:51 because in every science, especially in science, there is rules and there

54:58 always exceptions to the rules And that not be a regular, normal physiological

55:04 . It could be a part of beginning of the physiological state. It

55:08 be a breakdown of some of the . It could be abnormal uh gap

55:15 information because the cells are pushed close physically because of the uh something encroaching

55:22 the territory like a tumor and stuff that. So yes, you

55:30 There are situations, there are models show that I don't know if there

55:35 probably few experiments and accent another accent how it can affect the other cells

55:41 also present. But in general a of things can happen. And I'm

55:49 believer that especially in the brain that pretty complex processing. There are rules

55:53 there's many different exceptions to these rules how the signal moves. And what

55:59 the brain is that when for example seller or brain network is experiencing a

56:07 . I don't channel selectivity is out door. Everything goes everywhere. Those

56:16 interactions with them in acid residues and for engaging out the door numbers are

56:23 . The charges crazy. You everything is open is shunting inhibition that

56:28 talk about where you that's excited to and inhibitory receptor channels can open and

56:36 to signal legs it out. So yeah, so it depends on the

56:41 of the brain but and most of things that that happened or that we

56:47 be learning about is in this realm mostly really on the gun rights and

56:52 symbols. But all of these are great questions. I really appreciate them

56:56 even if I don't have complete answers okay, our next stop was going

57:03 be neuromuscular junction and to understand your junction and we'll talk about the civil

57:09 but we will leave it for our lecture. So they had enough I

57:14 of the material today And again. you for being here. Thank you

57:20 being in zoom. I will see on monday. We'll continue covering synaptic

57:27 and start going into the neurotransmitter systems criteria. Start talking about a single

57:37 and quite a great detail but we'll touch on some other neurotransmitters and when

57:42 talk about neurotransmitter systems we'll come back make it relevant again to some of

57:47 pathologies and diseases that we started For example, when we talk about

57:52 Colin will come back and discuss it the context of Alzheimer's disease as

57:58 Alright, so have a great evening I'll see you next week.

-
+