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00:01 Okay. All right, you guys before we begin today, we're gonna

00:07 about the action potential. But before begin, I just want to kind

00:10 remind you of what the greatest potential . And I really hate the echo

00:14 this. You know? So like said, a lot of the stuff

00:19 we're dealing with is very conceptualized. mean you can't see an action

00:26 Can't see a greater potential. You stick a probe in to a cell

00:30 the inside and the outside and you measure it but you can't actually physically

00:33 it happen. Right? And this is not anatomy. This is

00:37 physiological process that cells take advantage And so when you think about a

00:42 potential, just remember we're looking at receiving cell, a cell that has

00:46 given a signal to open up a that allows ions to come in,

00:50 ions flow in and only flow a short distance away from where they entered

00:55 . Right? Remember they're the ones have found, oh, there's my

00:59 and they've run over to it. so this distance that they travel within

01:03 receiving cell, the one that's responding a signal causes a small deep polarization

01:08 small hyper polarization in that receiving All right. And this thing can

01:16 big or small, depending upon how the signal is. And you're sitting

01:20 going I could care less. Why I have to know this? And

01:24 reason for that is the reason you to know this is because the greater

01:28 gives rise to this here, the potential. Alright, so conceptually it's

01:35 , very similar. There's gonna be of channels, ions are gonna flow

01:39 . That's gonna cause a deep polarization is then going to move along the

01:43 of the cell to some distance, away. And we describe one type

01:47 cell where that could happen. We we have nerve cells in our bodies

01:51 originate like in our spinal cords that down to our little pinkie. And

01:57 we want to make our pinky we need to get that signal there

02:01 . We don't want to rely on that have to travel through the several

02:05 of our bloodstream to get down to point and say, oh yeah,

02:08 the way, it's time to Right, So you want a fast

02:13 that moves along the length of the and that's what the purpose of the

02:15 potential is. Now, when you at an action potential, they're always

02:19 to show you some sort of graph this. And when you look at

02:22 graph, most people look at the and say, okay, this is

02:24 weird picture. I don't understand So I'm gonna ignore it. All

02:27 . But when you look at a , the question you should be asking

02:31 is one, what am I looking ? What's the what are the axis

02:34 the graph? And on our graph can see up there on the why

02:39 it shows you the membrane potential and volts. And then on the X

02:43 it shows you time in milliseconds. so what we've really done is we've

02:47 out time so that we can look an actual potential action potential are very

02:51 quick when you look at them in time, they're basically lying, you

02:56 see what's actually going on. So is over a span of about four

03:01 here. Alright, that's the first . And then the second thing

03:03 what am I actually looking at on graph? And what they've done here

03:07 they've color coded everything which is very frustrating because it's really hard to see

03:11 red line that represents the change in volts in that cell. Now,

03:20 other thing that we need to understand we're looking at this graph is what

03:22 done is we've taken a probe and stuck it in the cell in a

03:26 specific location and we're asking what's going at that specific location over time.

03:34 , so when we look at an potential, we realized we got to

03:37 we're just focusing here, but the length of the cell is going up

03:42 either direction very very far away. what we're looking at is we're looking

03:46 this flow or this change in voltage a result of ions moving in and

03:51 of the cell specifically specifically at that . The easy way to visualize this

03:56 again, this is not easy to , is to think about the

04:00 You guys know what the wave right? She human sporting events,

04:04 ? Basically someone who's been drinking just kind of said, all right,

04:08 gonna start the wave and they whoa. And then they're trying to

04:12 the people and then they get all drunk friends to do the same

04:14 Whoa. And then the next you know, this thing is moving

04:17 the room or around the stadium, ? And if you could picture for

04:22 moment, one person in that stadium you're asking, what are that person's

04:28 doing? They're basically drawing this this little red line that you're seeing

04:33 . And just to prove it, going to do the wave in

04:37 Okay, What other class can you ? You've done the wave in And

04:41 already know this group over here. gonna say I'm too cool to do

04:44 . So, let's all watch Alright, let's we'll make sure that

04:47 do it. All right. So gonna start over here. I'm the

04:50 stimulus is basically saying this is the that starts everything off. So we

04:53 , whoa, you guys suck. try this again. 1,

04:59 3, Whoa. And look once goes, it keeps going Right?

05:04 you can pick one person. Let's on somebody right here and everybody watched

05:10 as the wave travels. Okay? you all know how the wave

05:15 So let's do the wave again But we're gonna watch him. So

05:18 it goes and look his hands go , they go down and if you

05:22 at that little red line, what do it's down and then it goes

05:25 and it goes back down and then back and reset itself. So what

05:29 doing when we're looking at a graph this is with regard to the action

05:33 . We're asking the question at the , what's going on? Okay?

05:39 we're gonna ask the question what is this line go up and go down

05:45 . That's what this whole point point the action potential is. Alright,

05:49 first off notice what I have here the very top. It's generated at

05:53 very specific location in the neuron. , so an action potential starts at

05:58 initial segment or what is called the hillock. Alright. We describe,

06:03 we describe the neuron, we said had the cell bodies, we have

06:06 dendrites growing area of the axon. that point of origin of the axon

06:10 the axon hillock. So this is the action potential starts and the purpose

06:14 the greater potentials is to create a enough signal to get this thing

06:20 Alright, so that's why it's important we understand that the greater potential has

06:26 magnitude to it that it travels a distance and the bigger it goes,

06:31 further it can travel. If you back and look at the slides,

06:34 think three or four in uh from lecture of where we are now.

06:38 , like if you go back three four slides, you'll see that little

06:41 where it's like you see here is and then it gets smaller and smaller

06:43 smaller as it travels further and further from the side of origin. All

06:48 . The action potential is not a potential. It's very different. What

06:53 have here is a very brief, rapid change. That is 100 million

06:58 change. What we say about it that it will really reverse what's going

07:04 inside the cell in terms of charge a very brief second, really

07:09 All right. So, again, very small portion of the membrane.

07:13 just looking at one point, You could do this along the whole

07:17 and you can see the actual potential like if we did it again,

07:20 said, everyone freeze some of you be here. Some of you will

07:22 here soon. Would be there someone coming down. We're looking at different

07:26 of that action potential depending upon where are. And so, what we're

07:31 is this movement of ion potential change this movement of ions going in and

07:36 of the cell along the entire All right, we say it's propagated

07:41 a non detrimental fashion, fancy word saying it never changes in size.

07:48 , so once you produce an action , it will always result in this

07:52 million volt change. It's just like your hands will always go up to

07:56 peak. They won't go up to higher peak. They won't go to

07:59 lower peak unless you're playing around and playing my game with me. But

08:03 this is where it goes. This not an action potential. This is

08:07 action potential. Alright. So what say is it follows a rule called

08:11 all or None law. Right? are no partial action potentials. There

08:15 no super action potentials. Action potentials what they are. You either do

08:20 or you don't. So, if can't create a stimulus strong enough to

08:26 that action potential, nothing happens. , we're looking at the axon hillock

08:31 the question, is there enough stimulus results in these internal graded potentials that

08:38 enough change in potential to trigger that potential? And if there isn't nothing

08:45 . And the neuron doesn't fire. if there is you got your action

08:50 and you're sending the signal along the of the cell that never gets

08:54 never shrinks. It goes the entire of the cell with the exact same

08:59 that started with. All right. that's the basics of an action

09:06 Now, let's see if we can of see how this happens.

09:11 So, remember when we talk about greater potential we had a channel and

09:14 we had to do was open the somehow and then ions will flow

09:18 So the same principles are gonna be here. It's just what type of

09:22 are gonna be involved. All So, the big players in this

09:28 are the voltage gated, sodium and channels. And notice here the channel

09:33 a specific thing that opens it Right? So, what that's telling

09:37 is that as ions move in that's to cause a confirmation. I'll change

09:43 these closed gates which are gonna cause gates to open, which allow ions

09:47 pass in. That's what voltage gated . So, they're dependent upon changes

09:51 voltage to cause the opening of And when I open channels in response

09:56 voltage, that means more ions come , which causes more changes in

09:59 yada yada yada. So, this how we get this action potential.

10:03 basically it's self propagating process. All now, the deep polarization.

10:10 if you look at our little action here, I'll first another thing I'm

10:14 gonna point out. So, the coding here is to help you visualize

10:19 . Alright? So, whenever you're at any sort of graph the question

10:22 should always ask yourself is where's change ? Because those are the important

10:26 Right. So, if you have graph and it's a flat line,

10:28 just like nothing ever changes. So tells me nothing interesting is happening.

10:32 if you're looking at a graph and of a sudden it changes direction,

10:35 happened where it changed directions. those are the things where you should

10:38 kind of focusing and going, what's on here? Why does it change

10:42 ? And what they try to do is they're trying to show you these

10:46 points where changes occurred. All So, it's kind of ask you

10:50 question is, can you picture and that this there's something small happening

10:55 All right. Now again, with artists can always trust the artist does

10:58 good job. But basically it's saying going on and there's a slight stimulation

11:03 causes a slight rise which ultimately causes a massive change where we get this

11:08 rise. Oh, and then look we're gonna change direction, we're gonna

11:10 the opposite direction. And look, gonna pass original starting point. We

11:14 going down at this point, we going up. They should have mark

11:18 point right there and then now we're to normal. So each of those

11:21 of represent points of change. And with regard to this, we see

11:26 deep polarization. We're moving from where were at rest and we start

11:32 Alright, and then we really start . That's that deep polarization. So

11:36 you see the deep polarization with regard an action potential, whether you're over

11:40 or whether you're over there, that's result of the opening of these voltage

11:43 sodium channels. Whenever you see the like this, that's a result of

11:51 closing of the voltage gated sodium channels the opening of a different type of

11:56 gated channel, which is the voltage potassium channel. So in essence,

11:59 we're saying is on the front we're gonna open up voltage gated sodium

12:03 , sodium is going to come into cell and then we're going to the

12:06 shut and then we're gonna the we're gonna allow potassium to go out

12:09 other direction to return kind of back normal. But then something weird kind

12:13 happens over here which will deal That's the nuts and bolts of

12:22 Now to understand why all that stuff is we've got to kind of look

12:27 deep at these channels. All Now, when you think of a

12:30 gated channel or just any sort of which has a gate, you think

12:33 has one gate to it. One . Right, Not true with the

12:38 gated sodium channel, it's a weird . It has two gates, It

12:42 what we call an activation gate and we call an inactivation gates. And

12:46 you can think of it like this I am the channel I have an

12:49 gate and I have an inactivation And so that means I exist in

12:54 states. My first state is with activation gate closed and my inactivation gate

13:00 . And so in this state I'm , right, nothing can pass through

13:06 . But if I Sorry, but I get stimulated that's going to open

13:10 activation gate. Now there's a path me. Alright? So my initial

13:14 is closed but capable of opening. with me on that. Yeah.

13:19 right, so now I'm in my state, I'm now in my open

13:23 , but the moment that I opened activation gate is the moment I begin

13:27 my inactivation gate. It's just a bit slower. So while this is

13:32 , there's a state where I'm capable of opening. Then I'm open

13:36 number two. But then this slowly and gets back to this third state

13:40 is closed but incapable of opening. what I have to do at this

13:44 is I have to reset the whole so I have to somehow magically get

13:48 over here and get that back over . All right within my body is

13:52 going to demonstrate that at all. , so really you have to pass

13:56 ST one This way, so I'm flipping you off state one right open

14:02 closed but capable of opening. Then go to state to open state three

14:07 closed but incapable of opening. I to go all the way back around

14:11 that first state. I can't go to that middle state. Alright,

14:15 I'm closed but capable of opening. , closed, incapable of opening.

14:20 to reset to go back to but capable of opening. All

14:24 And that's important because it allows our potential to develop as we've seen

14:30 Alright. Now, the other type vulture educated channel is that potassium voltage

14:36 channel is typical of most channels. has one gate, so it has

14:39 states open closed. Pretty simple. right. Now, the thing

14:44 is both of these channels are stimulated the same time. Alright. And

14:49 pointing this out now because it's going help you understand that little graph that

14:53 looking at over and over again when talk about the action potential.

14:56 when I stimulate one of these, I stimulate the cell, both channels

15:01 open are are stimulated at the exact time. All right. And what

15:06 gonna do is we're gonna walk through different stages stages. So here we

15:10 . We're at rest the book. a really good job of color coding

15:14 . So you can kind of see going on. Now. Remember these

15:17 exist along with all those leak channels we described yesterday or on Tuesday.

15:24 . So we have sodium leak We have potassium leak channels with chlorine

15:29 channels. These are all existing in context of the axon and on and

15:36 the cell in general. But we're of focusing in on the axon right

15:40 . Alright, so, what that is there's this natural movement of sodium

15:43 potassium. You have the sodium potassium pumps going no, no. You

15:47 back where I put you and then keep leaking out. No,

15:49 You go back where I put And that's why we have maintained that

15:52 potential at minus 70. That's what talked about on Tuesday. I'll remember

15:57 two heads are nodding. So maybe need to really come in with the

16:01 know, and because of the sodium . Absolutely. All right. So

16:09 leak channels are there? They're But these two voltage gated channels we

16:14 described are there but closed. remember we're kind of used this room

16:19 an example over here. This door a as an example of what we

16:24 described as a what the leak Alright, It's gate is open.

16:28 always open. You can pass in out that door back there is

16:34 That would be like a voltage gated because it's closed and something needs to

16:38 along and open it in order for to pass in and out of

16:41 Right. So there's this natural movement ions that are occurring that maintain that

16:45 potential to produce an action potential. gonna have to get the flow of

16:50 to change that. We're gonna have open up those voltage gated channels.

16:54 how do we do that? they tell you voltage gated, we're

16:57 to change the membrane potential. All Now there are very few leak channels

17:03 regard to the sodium leak channels. already described that. We talked about

17:07 the number of channels relative to the . So we said there was about

17:13 greater potassium leak channels on their sodium channels. Right? And that's what

17:17 rise to that membrane potential difference. that's why we're sitting down here at

17:22 -70. Right? We can measure movement and the difference between the two

17:28 of that membrane. All right. at the triggering event, the triggering

17:35 simply is the point that causes the of the voltage gated channels.

17:42 now, what we're doing here is trigger event? Remember I said it's

17:46 be triggering two things simultaneously. But going to focus only on one

17:50 Right now, the thing that we're on is the voltage gated sodium

17:55 This is when one of those uh the G. P. S.

17:58 . That grant post synaptic potential, we said with those were that's the

18:02 effect of all the graded potentials Right, if you get one that's

18:08 enough that causes deep polarization at the hillock that change in membrane potential is

18:15 to trigger the opening of some of voltage gated sodium channel. So you're

18:20 to see a slight bump or a rise Now, when you open voltage

18:25 sodium channel sodium flows into the By definition we said deep polarization is

18:31 result of sodium going into set into cell. Right? So if I

18:36 a slightly polarization with the greater potential open up a voltage gated channel that

18:40 more sodium to come in, what's to happen to the membrane potential?

18:45 going to he polarized. All So it's gonna start going up and

18:50 deep polarization is going to cause the of more voltage gated sodium channel,

18:54 allows more sodium to come in, causes more voltage gated channels to come

18:58 and so on and so on and on and so on. So,

19:01 of it just a slight deep what we're now getting is not just

19:05 additive effect, but a geometric It's like taking a snowball and rolling

19:10 down a steep hill. You you're going to pick up more and

19:14 and more snow. And so your isn't gonna be this little tiny

19:17 It's gonna be this massive thing that's build up and that's what you're seeing

19:22 . So, what you're seeing is slow build up, which is gonna

19:25 exponentially to the point where now all a legislative sodium channels that happened to

19:31 in that location are open and when happens, sodium begins rushing in the

19:37 as fast as it possibly can. I'm using a little hyperbole here that

19:41 talking a couple of ions but I you to envision it like, oh

19:45 I open up all the gates for then as much sodium that's available is

19:50 start rushing into the cell. And we really do is we're getting this

19:54 feedback loop to reach a state where those, all those channels are

19:59 We call that threshold, we measured about -55 million volts. Alright,

20:05 not gonna ask you what threshold is for every cell for neurons. That

20:08 to be about -55. Alright, what we've done now is if we've

20:14 up all the cells then we have choice but to de polarize very,

20:18 quickly. Alright, So at this now, the permeability of sodium,

20:23 other words, the number of channels to each other, sodium versus

20:28 The number of sodium channels that includes channels plus the voltage gated channels is

20:33 a thousandfold greater than the number of channels open. So you have no

20:39 but to deport that's what's going That's what that light green represents.

20:44 just it's overwhelming influx of sodium into cell. Now, all things being

20:52 . Remember what we said, voltage sodium channel has two gates. So

20:56 we've done is open up the gate then the other arm is slowly closing

21:00 . But it's that small period of where we're seeing this rapid climb climb

21:06 then we get up here to the . What do you think is happening

21:08 there at the top? All I think you're you she's got

21:13 All right. If I opened up channel and this one is closing no

21:18 sodium is coming in. And so happens is we don't keep rushing

21:22 We get that top because all those closed except for the leak channels.

21:28 if nothing else were to happen, what we'd expect is we sleep a

21:32 decline back to normal. But we see the normal climb back to

21:37 Right? We see it dropped back other direction very, very quickly.

21:42 that's because what we have is not that channel closing, but we now

21:49 the opening of the volt educated potassium . All right now to understand why

21:55 takes so long for the voltage gated channels to open up. Is I

21:58 you to think about your friend, dumb friends, You got your dumb

22:03 , the one you tell the joke . And they sit there and stare

22:06 you for a couple of seconds before start laughing because you have to think

22:09 it for a little bit. That's vault educated potassium channel, right?

22:14 a slow channel and so while you them to both open at the same

22:18 , the voltage gated potassium channels kind sitting there thinking now, what should

22:21 do now? Oh, I'm supposed open up. And so that by

22:25 time it opens up is the time the sodium channel has closed. And

22:30 why you get this massive reversal. , if you really want to understand

22:36 , you can kind of see why sodium channel, the vulture gets some

22:40 has two gates. It needs to enough time to have it open and

22:45 close. You don't want to just and closed. You want to force

22:48 to go through a process that takes little bit longer. So you're gonna

22:53 the opening for a little while and it's gonna shut itself up. Then

22:56 has to do some stuff before it itself back. And so what it's

23:00 , it's creating a natural delay to that we get a step up to

23:06 and then we're going to see a down to there. Okay, now

23:11 don't have to know that, but helps you kind of visualize it.

23:14 , I see it because if I two gates, I have to deal

23:17 both gates to to make my gate . So we're talking about re polarization

23:25 polarization occurs because the voltage gated sodium closes and second the voltage gated same

23:33 opens Where we were dominating for sodium . Now we flipped it back and

23:40 dinner again dominating by potassium permeability. not just that simple ratio of 25-1

23:46 . It's skewing it very, very , that we rapidly return back down

23:52 rest. The problem is is those are not very fast in terms of

24:00 and closing. So, it took while for it to open. It

24:03 takes a little while for it to . It takes a little while too

24:06 . You're gonna kind of overshoot, you? It's like if you have

24:10 breaks, right? And you're trying make that decision on that yellow red

24:15 , you know which one I'm talking ? The one that's kind of

24:17 And you're like going 60 miles an and you're like, I can make

24:20 . I can make it. no, no. I'm not going

24:22 hit those brakes and you kind of to stop, right? That's what's

24:27 on here. It's like, I'm make it I'm gonna make it,

24:30 , nope. And he overshoots the potential. All right. And so

24:36 what's gonna be the next step is are returning back towards rest. But

24:41 those potassium channels don't quite shut fast , is that you overshoot it.

24:50 , I'm just going to kind of up so that you can understand what

24:54 slide is. It's again taking this it's breaking it down via the voltage

24:59 sodium channels. So, you can at the sodium channel. What what's

25:02 voltage gated sodium channel. It's Now. I'm over here in that

25:06 zone. What's going on? I'm up slowly. I've opened up that

25:11 opening up the activation gate as I'm through here. I'm still open.

25:16 mean that open state. But now I'm doing is I'm moving that inactivation

25:21 into that closed position And here now that pink zone, that's where I

25:26 now going down. That voltage gated channel is now closed. So you

25:31 use this slide to kind of help visualize what's going on regard to that

25:36 and down motion. So here we in that hyper polarized state. Hyper

25:45 . Just remember what we said. starting off polarized when I move towards

25:50 . I'm deep polarizing. And this what I said. Remember I

25:53 even if we keep passing it we call it the polarization. And then

25:56 I returned back to where I that's re polarization. But if I

26:01 , if I become more negative, hyper polarization. So this little zone

26:05 in here is a hyper polarized state this is just a function of those

26:10 educated potassium channels remaining open too It allows them to overshoot and kind

26:17 become more hyper polarized than normal And they close eventually and then that voltage

26:23 then that sodium https goes wait a . Um I need you guys to

26:28 moving things back and forth again. it starts moving ions back to where

26:32 need to go. But because you leaked channels, potassium is allowed to

26:36 back out and return back to And so that's kind of what's going

26:40 here is that this is just that back to normal by the president of

26:45 leak channels as well as the sodium . All right now, all that

26:51 this time, remember we still have voltage gated sodium channels. They're still

26:54 around but they're stuck in that closed . And so what's going on during

26:58 period of time is that they're trying return back to that original configuration that

27:04 but capable of opening state. And what we have now is a very

27:09 pattern over here, voltage gated sodium and potassium channels are closed. But

27:14 leak channels are open Over here, begin opening up the voltage gated sodium

27:19 . We continue to open them, them to the point where they're all

27:23 here. The voltage gated sodium channels . But and the potassium voltage voltage

27:28 potassium channels open. Then we come down here. That's when those voltage

27:33 potassium channels are closed. And during period of time from here on

27:38 those voltage gated sodium channels are resetting . And then this slow change back

27:43 from here to there just represents the moving back through the leak channels to

27:48 back to a state of equilibrium in with the sodium potassium pump. And

27:54 we're back to normal again over there that's all that's going on now.

28:00 sounds scary but if you look at graph and ask the point where change

28:04 occurring and we're only dealing with two channels. It makes it a lot

28:08 to kind of look at it. you just have to ask the question

28:11 I. D. Polarization is sodium in? Re polarization is potassium moving

28:17 ? Hyper polarization is when potassium is out and this is just returning everything

28:23 to normal. So how are we with that scary or is okay?

28:28 OK. Okay. Some people are I don't know it's scary. Still

28:33 right. Part of this is if want to understand it, draw it

28:38 , draw your graph, This is , this is mila volts. Okay

28:43 doing nothing, slight change, massive . Return back to normal,

28:49 return back to normal back to rest ask why is it changing at each

28:57 ? Now remember the whole purpose of action potential is to create a electrical

29:04 that moves from one side of the all the way to the length of

29:07 other side of the cell. And so what that means is we're

29:11 to be using this which represents ions in and out that they're moving in

29:17 out. And so it's creating that of that wave that passes through the

29:28 . So the action potential is a signal. Just like what we saw

29:35 we started the wave. Did it go I mean after I said everyone's

29:39 to do this. Don't be too for school. Did it just

29:44 Let's see wave. Let's try Once it starts it keeps going.

29:50 if it's just one hand, It goes all right. And the

29:56 it goes is because of the states we just described. It always goes

30:01 to that plus 30 because the voltage sodium channels always all open in that

30:06 location. So, if you're looking this spot right here or this spot

30:11 here it doesn't matter at that particular . Every voltage gated sodium channel opened

30:17 and then they all closed. And over here when that signal got to

30:20 all the voltage gated sodium channels at location opened up and that's what allowed

30:25 to keep moving and propagating at that strength. Alright, So what we

30:31 think about is a sequential opening. like when you were moving your

30:36 what you did is you're watching over and you're going, when is it

30:39 turn? Okay, It's my turn hands begin to move up. You

30:43 sit there and go, well, gonna do something different. I'm gonna

30:46 . It's something silly, right? the pattern is going to be the

30:51 because all the players are the All right. And so it's responding

30:56 as this one is opening, the is leaking in and coming in the

31:00 area that's causing the deep polarization. causes all the votes educated sodium potassium

31:05 to start changing. And when that occurs here, it's going to affect

31:09 here. When that change occurs it's going to affect over here and

31:13 on and so on and so on so on. So that's always that

31:15 criminal movement. And it's just gonna sequential because everything is based on

31:22 right? When the voltage gated channels , there's a timing where it's

31:27 And then I'm going to slowly It's not waiting for a potential voltage

31:32 occur. It's that the signal is initial voltage. But everything else is

31:36 has to occur. And this has occur, then this has to occur

31:39 you're dealing with the voltage gated potassium , like when it opens in response

31:44 the voltage change. But the degree which it opens and the speed at

31:48 is open is dependent upon the structure the protein itself. So they open

31:54 close at specific rates. Which is we get that pattern that we

32:00 And so the whole length of the is gonna go and produce that action

32:06 . Just like the wave was moved . So no matter where you

32:09 you're gonna see that pass. And you remember, oh, looking at

32:14 that graph is over time at a location, the change in miller

32:19 The change in the membrane potential. hmm. Now all action potentials have

32:32 is called a refractory period or refractory . Simply by definition a period of

32:38 when something can't occur. Alright, with regard to an action potential,

32:43 refractory period refers to the period of when another action potential can occur at

32:48 same location. Now, again, get to pick on them because they're

32:55 the front. All right, I you to do what I want you

32:58 do. So, I'm gonna be stimulus you're going to an action potential

33:00 me. Okay, so just when do it, you do full action

33:03 boom. That's not an expert. that's being lazy. There we

33:08 Gotta go faster faster. You gotta my hands. He noticed. He

33:15 keep up with me. All So, you can imagine when you're

33:19 about chemical signals, each of those signals are resulting in the opening of

33:24 channel which allows ions to move which then have to travel through the

33:29 to get to the axon hillock. then once you get to the axon

33:32 , you're going to get that. so you can imagine if I have

33:35 signals that are close together. What's to happen is that this stimulus is

33:40 to initiate that action potential. But one over here while it's going to

33:45 the opening of voltage gated channels. I've already opened up all my volt

33:47 channels, can I open any more them? No. So a refractory

33:53 is dependent upon the availability of those are really the lack of availability of

33:59 channels. And so what we have we have two parts to a refractory

34:04 . We have a period of time called absolute, so it's called the

34:08 refractory period. We have a period time where yeah, maybe a stimulus

34:11 create an actual potential but we're going have to overcome a couple of

34:15 And so that's referred to as the refractory period. So the absolute refractory

34:21 here is going to be this period time where we've opened up all of

34:27 sodium gated or voltage gated sodium So no matter of stimulus can cause

34:33 to open up more voltage gated sodium if all your channels are open.

34:38 ? I mean, that's that you can't do it. So I can't

34:44 a stronger action potential because there's nothing me to do beyond what I've already

34:50 . So during that absolute period, what's going on now. This will

34:56 because I mean beyond just that little , right there continues. Because once

35:01 opened up that voltage gated sodium remember it has to go through those

35:05 states. That first state is it's . Second state, it's now

35:09 Right? So first let's closed. I'm open. So I'm now in

35:14 voltage. I'm starting the the absolute period. But then there's that period

35:18 time where I've reset myself. I'm mean, I'm closed but incapable of

35:24 . If I'm closed and incapable of , there's no amount of stimulus that's

35:27 to get me to open. I've to go all the way back to

35:29 initiation state. And so until that has been reset, I can't be

35:34 to open. All right. And what's going on here. Is that

35:40 I'm either fully active or I'm in but incapable of opening state, I

35:46 be stimulated. So, I'm in relative or sorry, that absolute refractory

35:50 . Now, what does that look for this little picture right here,

35:53 going to be this Greenstone and most this purple zone. All right,

36:01 relative refractory period is a function of things. All right here, I

36:07 start getting an action potential. In words, I can stimulate one,

36:11 really what it is is I have overcome two things first, there's gonna

36:16 some inactivated sodium gates. So the gated sodium channels that haven't reset

36:22 They're not capable of opening. They have a little bit of time.

36:26 there have been some that have already reset. And how do I know

36:28 already been reset. We'll remember this a this graph is a thing over

36:32 . And so over here, when beginning the process, I'm opening up

36:36 or two channels that then opens up couple more, which opens up a

36:39 more, which ends up opening all them. Right. So, you

36:42 imagine on the front end there are that are resetting earlier than everything.

36:48 ? So there's some that I've reset those can be opened. But then

36:52 are some that haven't been where you that can't be opened. So we're

36:56 for them to open. But if can start resetting, if I can

36:59 activating those first ones, I've got good start. So that would be

37:03 . The second thing I have to is I have these sodium or potassium

37:07 voltage gated potassium channels that are still the state of closing. They haven't

37:13 back to their original state. So they're open, that means my potassium

37:18 is higher than normal. That means have to overcome a cell that's trying

37:22 become more negative. So in other , down here, in this refractory

37:27 in this hyper polarized state, see , I am at -70 down

37:31 I'm just going to make up the of -75. So in order to

37:35 to threshold, we said that our around -55. So I have an

37:40 five million volts I have to overcome get back up to uh threshold.

37:46 if I'm down at -75, I to have something bigger and stronger to

37:50 me out of that hole. Would agree with that? Yeah. And

37:54 that's kind of what it's saying is , look, if I'm down in

37:56 hole, you're gonna need a bigger to get me out of the

38:01 And what I'm really doing, I'm those those potassium channels that are still

38:06 . I'm still overcoming sodium channels that still closed and have to be

38:11 But I can do it. It's gonna take a little bit more

38:15 All right. Now, the purpose the refractory period is to ensure that

38:25 signal is being sent. We need understand that an action potential represents the

38:32 between two cells in the nervous So, it's a coding event,

38:38 ? It's kind of like morse It's not morse code, but it's

38:41 of like that, right? You know morse code as dot dot dash

38:44 dash in different combinations. Right? so, what what the nervous tissue

38:50 doing is it's using those action potentials cause a release of chemicals. And

38:57 the way your brain understands what's going in the world around it is encoded

39:02 the number of action potentials that it's , right? So, I'm just

39:08 a dumb example so that you can of visualize this, but you can

39:11 about if I have someone touched that might be a couple of action

39:16 that are being sent to the brain this. Right? But if someone

39:20 me, there will be lots of potentials. And so duration and magnitude

39:27 encoded in the number of action So by forcing action potentials to have

39:32 single point, right? A single as opposed to what greater potentials

39:38 which are they can be long, can be really, really tall.

39:42 we're doing is we're creating a code the brain can then understand. Did

39:48 kind of makes sense? All So, with regard to the refractory

39:54 , the purpose of that refractory period to ensure that the action potential has

39:58 unique characteristic. That's what I'm trying get at. And so the refractory

40:04 prevents or really forces an action potential a single direction. Right? So

40:10 I'm opening up channels in this direction are closed behind me and that signal

40:16 go backwards. You can only go the direction that it started.

40:20 if I'm starting over here, then it's gonna start moving in this

40:25 . So you'll see sodium going in causes more channels to open up.

40:29 sodium comes in here. But in behind it, that's where all the

40:32 channels are closed and potassium channels are . And so by the time we

40:36 further and further away, the area was initially stimulated is too far away

40:40 be re stimulated. And so it that movement in that one direction.

40:46 actually potentials only move in the direction they're stimulated travel to. So there's

40:52 a question I asked on the I tell the people who are paying

40:56 . So this is where all people wake up now. That's a

41:00 He says, imagine if in a setting, if I took to action

41:05 one on this side of a one on this side of a neuron

41:08 I created them to travel towards each so they travel, doing exactly what

41:13 just described and then they get to other. What's going to happen?

41:17 they bounce off each other? Do die? Do they just pass each

41:22 ? What do you expect to happen on what you now know about the

41:26 period? Nothing happens, They died because if I'm going this direction,

41:32 refractory periods behind, if I'm going this direction, refractory periods here and

41:37 when they come remember refractory period only the period where an action potential can

41:44 . I can't go beyond the point I come into contact. That makes

41:49 sort of kind of in other there's no gates over here for this

41:55 potential to open? They're all stuck there close state and then moving in

42:00 direction all those gates are closed. the oxygen is traveling this direction.

42:04 open any gates are all closed and what the refractory period represents. All

42:12 now, different cells that use electrical will have different refractory periods. They

42:17 different lengths. They have different They're caused by different types of

42:24 You'll learn more about this when you into A. & p.

42:28 And they really talk about cardiac Have you noticed that your heart goes

42:33 periods of contraction relaxation? I hope . I mean, that's the

42:38 thump. Right, contract, contract. What creates it? That's

42:43 function of the refractory period of the muscle. They go contract and

42:50 contract, relax. Think about a muscle though. Can I contracted and

42:54 the contraction? Yeah. Do I my heart to have a sustained

43:00 No, that's bad. So, periods allow for these periodic stimulations to

43:11 . Alright. And create these patterns least for neurons to be able to

43:16 . And as I said, cardiac , you're going to see something a

43:18 bit different. All right. I you stuff is kind of conceptual kind

43:30 hard to visualize. So, how are action potentials? Well, there

43:35 fast and they're dependent upon two All right. First, there,

43:39 upon the diameter of a fiber. is the part where I ask those

43:43 files in here and the older I the fewer audiophiles there because you all

43:47 to stuff on your ipods and you little tiny buds in your ears,

43:52 ? But there was a time where who like to listen to music would

43:55 big speakers and they would have wires whatever the device was to that

44:02 Alright, so I'm gonna ask the for anyone who still does this or

44:05 this? The speaker from the amplifier the wire from the amplifier to the

44:12 . Do you want it to be or do you want it to be

44:15 thick? Why? Yes, they . Hi perfect answer. I'm gonna

44:23 it for you because it increases the of the signal. In other

44:29 when you think about a wire basically a bunch of electrons moving back and

44:33 to stimulate the speaker to go. creates all the sound that you then

44:37 . Okay, so if I have thicker wire I have greater conductivity.

44:42 other way you can look at this you can see it has less

44:47 Alright, so greater conductivity and If you ever wondered why all the

44:52 of these graduate programs in medicine and like that usually have you take at

44:56 one physics class so that you can something like that. This you

45:01 it deals with this resistance thing. P equals Ir you know, don't

45:08 about it. All right, but idea is alright, less resistance and

45:13 gonna be true when it deals with cell as well. Alright, the

45:18 the fatter. The cell in other fatter the axon. And this is

45:22 true for the dendrite. The less resistance you have, the easier it

45:27 to conduct an action potential. In words, the ions have room to

45:32 . That's really what it basically All right. And so, you

45:36 imagine if I want to get a from my brain down in my little

45:39 , I want a very very big wire, right? And if I

45:44 this for every single solitary axon in body, then all of a sudden

45:50 my finite spaces to finite. I need to create a bigger space

45:54 me. Right? So, I'd to be a bigger bigger dr

45:58 And I'm really trying hard. And because I'd become a bigger me,

46:04 have to have a bigger bigger And then those bigger cells would create

46:09 bigger me which create bigger cells. you see now we have a the

46:13 of just me growing out of Right? So that doesn't work.

46:20 helpful to have big fat fibers, but it's not possible to do

46:25 So, what happened is is that body came up with the second mechanism

46:31 help deal with this first problem, want fat axons, but we don't

46:36 the space for fat axons. So we're going to do is we're going

46:39 insulate the axons with my alan. my allen is simply just a cell

46:44 wrapped itself around another cell to create area of insulation. And what we're

46:48 do now is we're going to create where action potentials can occur in areas

46:54 action potentials can't occur. And so going to speed up the transmission of

46:59 signal because I don't have to cover full length of the cell any

47:03 I get to skip over parts. right. So that's what my on

47:08 own is. And these we have different types of cells in the central

47:12 system. Again, we haven't learned versus peripheral yet, but just bear

47:15 me, we have the alexander site the central nervous system, the neural

47:19 in the peripheral nervous system. And this is what a myelin sheath

47:24 All right. And so what we're at here is what we see in

47:26 peripheral nervous system. This is This is central nervous system.

47:30 location right now is just understanding that going to be slightly different. But

47:36 purpose here is that this support whether it's an olive garden site or

47:43 it's a Schwann cell or neuron lymphocyte cells with its original name, but

47:46 trying to get people's names out of . So neural inside is what we're

47:49 now. All right. And so we do is we take the cell

47:53 it wraps a portion of its body the cell over and over and over

47:57 to create this very thick layer of kind of fatty tissue or not

48:02 but fatty plasma membrane. And what does is it creates a zone where

48:07 neuron is no longer interacting with the environment. So you can see this

48:13 in the way with this stuff out here. But over there you can

48:17 I have my neuron, the action , it's around the or it's in

48:23 with the surrounding environment. And I the picture is not really easy.

48:27 you can see here here's in the nervous system. You can see a

48:30 has wrapped itself all the way around then you've got a little tiny space

48:33 there. Then you have another then a little space, another

48:35 little space on and so forth in central nervous system. The cell itself

48:39 wrapped around. It stands out So that's why it's called a dangerous

48:44 all ago, meaning many. And you can see here all these extensions

48:48 kind of go and then you can it's wrapped around. So we've got

48:51 area that's insulated area that's not insulated area that's not so on and

48:55 on. And so on. And so this insulation. The stuff

49:00 it's wrapped around is where you have contact with the surrounding fluid. The

49:06 cellular fluid. And remember that's where the ions are. So if the

49:11 of the cell can interact with the of the cell, no action potentials

49:14 gonna occur. There can only occur those areas where there are gaps.

49:22 little gap. So you're seeing So, they're just trying to show

49:27 that little gap is called the node Ranveer. All right. And that

49:32 of Ranbir that's where you're gonna see concentration of voltage gated channels. And

49:38 far enough apart from the distance from to here is far enough apart that

49:43 can still get stimulation from one point the other. But they're far enough

49:49 that you're you're you're stretching the action . All right. So here,

49:56 only contender site you've got these little . Again, there's your tender side

50:01 . They wrap around multiple. Multiple the neural imma site. It's a

50:05 cell. Single cell. Single So, structurally they're very, very

50:09 . So, they're short enough to for electrical activity. But far enough

50:14 to speed up transmission. And how it speed up transmission? It has

50:19 do with this propagation. All Now. Normally, what I would

50:23 about this time is I would challenge to a race James. You look

50:26 you want to race me. I I'm going to lose miserably.

50:32 come on up here. Mhm. right, James and I are gonna

50:37 You're gonna walk normal. We're just go, oh, I don't

50:39 Just over there. Someplace you're gonna normal. I'm gonna walk toe to

50:43 . All right. And we're gonna who gets over there someplace faster on

50:47 mark. Get set go all You must have cheated or something.

50:56 , we're gonna try it again. gonna go faster. You're just gonna

50:59 normal. Ready? Go? Mm . He's gonna always win.

51:09 Why you said James, thanks longer . What longer strides? Right

51:18 did we travel the same distance? , he actually have a little bit

51:22 , but he still beat me because got tired and lazy and it's just

51:26 I don't like losing. Actually, just want to tell the story.

51:29 time I asked the student come had her in three classes or four

51:32 , I can't remember. So she me pretty well. And so at

51:34 beginning of the race, she pushes like, really, I'm gonna let

51:40 win. I didn't make you do Tony hill stuff, but anyway,

51:44 , so it has to do with . And in fact, if you

51:48 run a race, people who have strides are able to cover longer distances

51:55 or equal distances faster. Alright. that's really what we're dealing with here

52:00 we're talking about the Myelin, the creates a zone where I can't do

52:05 . So the only place I can stuff is in those nodes of

52:08 And so the action potential, which normally go from here to here to

52:11 to here to here to here to , right, just like I was

52:14 total hell. I was walking to hill because there's a whole bunch of

52:17 to cover and I am required to the entire surface. But when I

52:23 a stride, in other words, Myelin, I get to step over

52:27 portion of the surface. And so means for your one little step,

52:32 get to travel further distance and in so, I'm gonna move faster along

52:37 entire length. All right. So two forms of propagation that we just

52:42 at, what I was doing that to heel stuff is what is referred

52:46 as contiguous or continuous conduction. Different use different words. And all.

52:52 just means is that there's no Myelin there's no Myelin, every point on

52:57 Axon has those voltage gated channels and the propagation of the action potential has

53:03 go all along the entire length. it's fairly slow, relatively speaking,

53:10 still talking faster than you can Right? Salvatori, conduction is what

53:17 was doing. It was just a step. He's stepping over a portion

53:21 the Myelin. Really what salvatori It comes from salvatore, which means

53:28 jump and literally means the action potential jumping from note of Ranveer, to

53:32 of ranveer, to note of Ranveer is able to skip over those little

53:38 areas. Just like we see it's stimulation there. To stimulation

53:41 To stimulation there. And so it faster. So this Myelin serves as

53:48 tool or the mechanism to speed up of an action potential. If I

53:54 make the axon fatter. Well, don't I just make it? So

53:58 action potential moves faster along the same axon and that's what this is

54:09 So just again, so that you visualize it here is continuous or

54:14 So, zone to zone two, two, zone, it's just moving

54:18 very stepwise. When you're doing you're going from here at the axon

54:26 . To uh to note of to note of Ranveer. Note of

54:29 noted. Ranveer noted Granville. so, to be 100% clear because

54:34 people do not visualize this, the is where there is no action

54:40 This area right here is being skipped because the myelin gets in the way

54:46 in those little zones in between. the note of Ranveer. All

54:54 just another pictures. Making the other bigger again. So 12 there so

55:00 you can see here, we can the island's moving in when the island's

55:03 , they're just far enough apart to the opening of the next channel.

55:07 channels open up and that causes enough and again, these won't open again

55:13 we're in the refractory period? That's we're moving or propagating in a single

55:20 . Now, why is this so . Well, we can make the

55:25 size axon And the actual potential travel about 50 times faster. Similarly,

55:33 we're localizing those signals to those nodes ranveer. That's the only place where

55:39 going to be consuming energy while we're sodium and potassium back out and

55:44 So the cells actually use less energy in the body, wherever you get

55:48 use less energy body gets really, happy about that stuff. Alright,

55:51 this is why this was advantageous as . We don't have to use as

55:55 energy to send signals faster. In , we use less energy. All

56:06 . So, I'm gonna start everything over there at the dendrites in the

56:12 . Or maybe we're over here soma the dendrites. Right? That's where

56:17 getting a signal that causes the opening channels. That creates a greater

56:22 Get a strong enough greater potential to the axon hillock to cause deep polarization

56:27 to threshold where you open up all channels and you're gonna get an action

56:31 . Action potential travels along the length the cell, gets down to those

56:35 terminals and at the axon terminals. signal is then used to cause the

56:42 of a chemical message. So, neurons primarily speak via chemical means action

56:49 are simply the way through which a sends a signal from one side of

56:54 to the other side of itself because long cells. All right. And

56:59 what we're looking at is down here the bottom end. We're down at

57:03 chemical synapse. Alright, So, synapse just refers to that area where

57:08 terminal is. And it's the interaction two cells. So, the cell

57:12 is sending the signal is called the synaptic cell. The cell that's receiving

57:17 signal is called the post synaptic Okay, That's kind of simple.

57:22 the synapse then, is the interaction the two? We refer? Sometimes

57:28 see it referred to as a synaptic . Alright. The space in between

57:32 cells now to really, truly visualize . How many of you guys have

57:35 sibling? Were they mean to Are you the older sibling or the

57:38 sibling? Oldest? Alright. Alright, this is to the older

57:45 . Remember when we got to torture younger siblings? Right? And we

57:49 to play that game in the car ? I'm not touching you. Did

57:53 ever play that game? And I'm touching you game. It's like when

57:55 come up to somebody like this go can't be mad. I'm not touching

57:59 . I'm not I'm not touching. can't get mad. And the younger

58:02 , do you remember that game? do you want to do? Do

58:05 want to just break their arms? , but they're bigger siblings. They're

58:08 gonna do that because if you do then you're getting pink belly.

58:14 All right. You can think of two cells playing the I'm not touching

58:18 game. Alright. There's a small between the post synaptic and the pre

58:22 cell. All right. So, neuro transmitter is the chemical that's the

58:29 that we refer to it as the that's being released at the synapse by

58:32 pre synaptic cell. It's the chemical . It's transmitting a signal from one

58:37 to the next. Hence the All right. And what's gonna happen

58:41 that chemical is going across across that ? It's gonna bind to a receptor

58:46 ligand gated channel. And when it that ligand gated channel, it's gonna

58:51 that channel and allow ions either move or move out and in doing so

58:55 the post synaptic cell, it produces grated potential which we called the

59:00 P. S. P. Or I. P. S.

59:03 And you see what we've done? come all the way back around the

59:06 . All right. So, that potential is where we started from

59:14 what's actually happening here? Well, a lot of stuff and you can

59:18 at a picture like this and get of panicky and freaked out, but

59:20 really basic. Alright. It says the action potential remembers the opening and

59:25 of voltage gated sodium channels and there's channels are opening their closing. And

59:30 signal is basically moving along the surface that cell and then it gets down

59:34 the axon terminal and then where there's more voltage gated sodium channels. So

59:38 there's no more voltage gated sodium do you have an action potential?

59:44 do you think if there are no gated sodium channels, can you have

59:47 action potential? No, Because the is simply the opening and closing of

59:52 channels to allow ions to move That's all it is. Instead,

59:55 we have down at the axon we have calcium channels, their voltage

60:00 , they're dependent upon electrical signals or signal is the action potential. So

60:05 we're doing is we're sending a signal to the end of that terminal to

60:08 , hey, we need you to up a calcium channel when we open

60:12 that calcium channel calcium floods into the . And you recall when we talked

60:17 vesicles way back when it's like, you mean I have to remember that

60:21 . Yes. When we talked about , we said, calcium comes in

60:25 signals to that vesicles to open up the surface to release its content into

60:30 extra cellular fluid. And that's what calcium does. The expedition comes in

60:35 calcium channels open the calcium floods in to the proper location on that vesicles

60:42 those proteins, parts those parts of snares and what it does, it

60:46 that neurotransmitter. The neurotransmitter then is and travels via? Simple diffusion.

60:52 ? Simple diffusion just simply says, go where there's less of me.

60:56 I just kind of flowed out into synapse and then so it floats out

61:00 the synapse and if it floats to of those receptors located on the post

61:05 cell then it opens up the It's pretty simple. Right? So

61:10 one potential arrives at the axon Step two opens up voltage gated calcium

61:15 . There are no voltage gated sodium so acts potential dies to just open

61:20 that one channel calcium floods in, the vesicles to open. If you

61:25 to put like magic happens, that's because we're not going to describe all

61:29 little steps in there, calcium open of us vestibule to open up neurotransmitters

61:34 that neurotransmitter then diffuses across the synaptic and binds to its specific receptor to

61:41 up an ion channel. Now synaptic is a term we use to describe

61:52 period of time it takes for that to get from that vehicle over to

61:57 channel. You can imagine in our models, we've always just used to

62:04 but you can imagine if you have multiple cell neuron chain that there's a

62:09 at each of those points. So cell one and cell to between cell

62:13 and sell three between cell three and four and so on and so on

62:16 so on. So if you add those up that can come up to

62:19 a bit of time. So the to get from here to there is

62:22 40.32 point five milliseconds. Which if think about it doesn't seem like a

62:26 time but if you have a lot them it can be kind of

62:30 Alright become pretty complex. So the complex your pathway is the greatest synaptic

62:37 . Now this has nothing to do it. But it helps you to

62:39 about. If someone asks you a and you sit there and go you

62:43 you could just think of that as delay as my neurons are trying to

62:47 things out that's not real but do memorize these things please. Okay it's

62:56 to go, oh there's a I got a memory of things in

62:58 picture. This is just to So when I release a neurotransmitter that

63:04 is a signal. I only want signal to do something for a very

63:08 brief time. So I do not that signal sitting in the synaptic cleft

63:12 kind of hanging out. I want gone. Alright. So what we

63:17 is that for every action potential we're to release a chemical message after we

63:21 a chemical message. We want to the message. So with termination there

63:26 four ways to terminate a message. one that everyone learns about is enzymatic

63:33 . And so what you can imagine that we have enzymes that sits in

63:36 synaptic cleft looking for that neurotransmitter, kind of like the world's most dangerous

63:42 of red rover, Red rover, rover, Red rover, Red

63:46 let acetylcholine come over and as acetylcholine released, you have acetylcholinesterase sitting out

63:52 , going to chew you up to , up to you up to you

63:54 it's destroying the stuff as fast as being released. So only a couple

63:58 messages get across the cleft. this is the only place where we

64:03 of an enzyme being president is in city of Kelowna is in the acetylcholine

64:08 . You don't need to know I'm not gonna ask you which one

64:10 which? Right? But so that's way chew things up so they so

64:16 don't exist anymore. The second thing is not shown in any of these

64:19 that that neurotransmitter can diffuse away. again, this is a chemical

64:24 so you don't want it floating So there are enzymes throughout the body

64:26 are they're looking for these freewheeling neurotransmitters to destroy them. Now when we

64:31 diffuse away you're not getting very we're talking a couple of millimeters

64:35 Alright, but if you're not in cleft, you're not capable of binding

64:38 receptor. So that's another way of third way and this is what is

64:43 common is that you can have the take them up. So there are

64:49 receptors that are there to bind to grab those neurotransmitters and move them back

64:55 the cell. Either one that released the one that's receiving so that it

64:58 gets it out of the cleft. then what you can do is you

65:01 break it and destroy it. Or can recycle it. And that's what

65:06 are all trying to show you with these little arrows pointing back in is

65:09 it's being taken up by that same that released it. The other one

65:14 is being shown right over here, that you can have other cells near

65:17 synaptic cleft. You're gonna have astro , even the post synaptic cell and

65:23 they can do is take it up then destroy um that neurotransmitter. So

65:28 not present. But the point in of this is to tell you that

65:33 we release that neuro transmitter we want out of the cleft as fast as

65:38 . It's only a quick message, ? It's just a signal says I

65:42 you to do this now so that get a quick response in the post

65:45 cell. You don't want it So we need to terminate the

65:55 This is another slide where people get , really upset because they think they

65:59 to start memorizing stuff why we look this slide first off and the next

66:03 is gonna be the same thing is at in your free time because this

66:08 not a good picture for you. at the shape of these molecules.

66:13 . And you can see that these have very common shapes as the way

66:18 they're grouped. All right. And what this shows you is that there

66:21 families or specific types of molecules that in a very similar capacity as a

66:28 molecule. So in this little what you're looking at here is up

66:33 . Those are these are all Alright, so those are chemical

66:38 There's about 100 different ones that have identified in the body so far.

66:42 probably even more. And what they're to do is they're going to fashion

66:46 the synaptic cleft in other words that synaptic or that pre synaptic cell is

66:49 to release this neurotransmitter. The neurotransmitter going to flow through that synaptic cleft

66:54 that post synaptic cell and they all so all of these different types of

66:58 to do the exact same thing. just this peregrine interaction between two

67:03 I'm cell number one is telling Cell two what to do and they can

67:07 excitatory, they can be inhibitory. they're primarily classified by structure, this

67:15 a big giant list. So you need another big giant list. I'm

67:18 to point out a couple of them you that you should know though.

67:21 , so for example, we have here. This is the very first

67:25 discovered. Everyone was very, very and said, oh we've got this

67:29 neurotransmitter. All the neurotransmitters are going look like this. None of them

67:33 like it. So it was here you go. Here's one.

67:36 all over the place and nothing else the body is like it.

67:40 That's very confusing. All right then you look at some of these molecules

67:45 say wait a second. This kind looks familiar to me. I've got

67:48 amine amino acids. So there's an group. Alright. And really what

67:54 two things are? They're just modifications amino acids you already know.

67:58 I thought amino acids make proteins. , they do. But they can

68:01 used for other things as well. that's one of the things is

68:06 We have things like the puritans. ATP wait a second. Doctor

68:11 I learned that ATP has to do energy in the self. Yes,

68:15 true. But it can also be as a neurotransmitter man. Try to

68:21 one thing and the next thing. know, they're screwing things up adding

68:24 on top of it. All gasses in our bodies. Some of

68:30 that don't smell so good hydrogen That's rotten eggs. That's a gas

68:36 our body uses as a signaling molecule monoxide. Wait a second. Isn't

68:41 monoxide. The stuff that that will me. It will bind my hemoglobin

68:45 I'll die because I can't carry Yes. But it's also a signaling

68:50 nitrogen or nitric oxide. There's another . These are gasses that are used

68:56 the body. A whole bunch of that we're not gonna go into a

69:00 of them. Even lipids. We about the A casa noise. These

69:03 signaling molecules that can serve as neurotransmitters if you look at the shapes of

69:08 . So here are the catacombs means is the type of mono means you

69:11 see that what they've done is they different uh configurations on the on the

69:18 the tails for example, but they're similar to one of them. They

69:22 started off as a single amino acid . So the ones you should know

69:29 these three Okay, acetylcholine. Why we need to know acetylcholine? It's

69:35 it has, it can be excitatory inhibitory. You're going to learn about

69:39 mostly in the context of muscles to your muscles move. It uses acetylcholine

69:46 the neurotransmitter to tell it what to . All right. Found everywhere.

69:51 nervous is peripheral nervous system contextually. need to know where you are to

69:55 whether the excitatory or inhibitory. We're gonna deal with that today. The

70:00 acids. We already talked about their blocks. These are the 3GS.

70:05 , there's another one um aspartame notice didn't highlight it alright, but the

70:10 Gs you should be able to recognize being different from another glutamate is an

70:16 neurotransmitter. It's also, you assets. Gabba is an inhibitory

70:23 google icing, an inhibitory neurotransmitter. we got the as potato which is

70:29 as well. But three GS make easier to visualize that. And lastly

70:34 biogenic amines. These are ones that probably already familiar with. But you

70:37 know you were familiar with. So called them the cata cola means you

70:41 ever heard of dopamine Dopamine? that was that was the easy

70:46 Have you guys ever heard of Yeah, you're probably more familiar with

70:50 demeanors and I got a puppy So I gotta take my all

70:55 That's what you're battling. Is that one? Serotonin may have heard of

71:01 one? So it also has a Ht these two, you know,

71:07 you probably don't know them by those . So epinephrine. Its real name

71:13 adrenaline. Its initial adrenaline. So know, epinephrine because you know adrenaline

71:19 then it has its cousin which is which is just a slight chemical

71:27 We're gonna be looking at the in quite a bit when we move on

71:33 the next couple of sections. All . But they're all related to each

71:38 because they have all these shapes, ? So here's the tire scenes,

71:42 dopamine and and um nor E and epinephrine down there. Um You can't

71:48 read these things anymore. That's That serotonin and their origins are simply

71:54 trip to fans that's tyrosine. They're modifications of amino acids. All

72:02 But this You should know those three should know. And probably those two

72:07 things that you're gonna become very familiar all the rest of them. Another

72:11 of them, who cares. Time to go. Alright. Last

72:19 slide. So, everything that we've about starting with the greatest potential on

72:24 the action potential all through that synaptic chemical synapse all deals with chemical

72:31 Even though we spent a whole bunch time talking about electrical signals. All

72:36 . Because most of the signaling that see a sneeze coming on. I

72:45 it was coming. Mm hmm. just one of the most wonderful time

72:50 year when the pollen comes out while chemical signal has ultimately is there to

72:59 that chemical. We have that electrical , 99% of the cells in our

73:05 are neural cells. Even probably even than that are using that sort of

73:10 . But there are a few types cells that are going to use this

73:14 signaling. And so, I just to remind you that while you're learning

73:19 the chemical synapse because that's primarily what going to deal with. There are

73:23 cells out there that don't do And so, what is an electrical

73:28 . Alright, Two cells are Notice there is no no space.

73:32 no synaptic cleft They're connected to each by gap junctions. And so what

73:36 gonna see when you have one of is that the ions are still going

73:40 be traveling but there's no chemical The signal is the presence of the

73:46 and the iron ion changes. So you're talking about cardiac muscle for

73:51 you can think of it as a of cardiac cells that are connected to

73:54 other. So when you initiate an potential here, it's the ion changes

73:59 take place that then are passed through gap junction and continued from cell to

74:04 to cell to cell to cell. , it's not a typical like

74:08 It's literally the ions moving back and using the same sorts of mechanisms we've

74:13 described when it came to the action is just slightly different, slightly different

74:18 that are gonna be involved. But how electrical synapses work. It's through

74:25 gap junctions. All right. Um pointed out that that can't be modulated

74:32 we won't deal with that right All right. That's going to sum

74:37 up. We have a test on . Right? I know. I

74:43 . I know. All right. everything we've covered up to this point

74:47 available on the Earth will be on exam. Obviously. Unit one not

74:50 everything in unit two on this So go out and kick some butt

74:55 I'll see you on thursday if you to show

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