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BIOL 3324 Human Physiology - BIOL3324_lecture06_0907
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00:06 All right y'all, let's uh let's up this unit. What do you
00:12 you all excited about a test on ? Mm. Just a reminder.
00:21 this will probably be the only time send out a reminder or making a
00:25 . We have an extra credit before test and an extra credit after the
00:29 . The extra credit before the test at 6 p.m. on Monday. It
00:35 at 9 a.m. on Tuesday, If you miss out on it because
00:40 903 on Tuesday morning. And that's you remember, I'm not reopening it
00:46 so put a reminder on your you know, be like my
00:50 This is the time a SOCA you know. All right.
00:55 so what we're going to do is going to try to continue where
00:59 we, we kind of left What we've been talking about is we
01:03 about how cells that are electrically oriented and ultimately muscles, how they use
01:13 movement of ions to create electrical signals their lengths in order for them to
01:19 from one side to the other. we haven't really gotten to even
01:23 you've kind of figured this out, sure by this point is all
01:26 So that electrical signal gets down to end of the cell. What does
01:29 do? Right. What we're trying talk about here is how do synapses
01:34 ? And that's really kind of the part of this lecture. And then
01:38 we're going to do is we're going just kind of, kind of dabble
01:40 in the nervous system for a moment about, oh, and this is
01:43 neurotransmitters are and yada, yada So we're really kind of taking what
01:47 learned about action potentials and graded And we're going to kind of bring
01:51 together so that we can understand that that's taking place between two neurons or
01:57 a neuron and a muscle. All . But before we get there,
02:01 have to throw this bad boy out because if I interrupted our conversation with
02:06 , it would be like, why you interrupting this? So it's easier
02:09 to put it up front and get out of the way. So a
02:12 is basically a point of communication between cells and one type of synapse is
02:18 to be the electrical synapse. And other is the chemical synapse, which
02:21 where we're spending all our time. electrical synapses are unique in that we
02:26 them only in some very specific For example, in the cardiac
02:31 that interaction there are some neurons that this. But this is, you
02:35 , few and far between. And are some smooth muscles that use this
02:38 of synapses. And here what we're is we're allowing ions to move between
02:44 . So there's a connection between the through these gap junctions that allow for
02:49 flow if you have some sort of to allow it to move from one
02:55 to the next, so that the potential moves from cell to cell to
02:59 directly. So when you think about heart beating and that spread of action
03:05 literally goes from cell to cell to to create the contraction that will ultimately
03:10 their heart to contract. All Now in saying this, there is
03:15 great deal of complexity to it that don't really want to dive into.
03:19 this is the level of complexity. want you to understand we have things
03:23 are called reciprocal synapses here in the is the closest picture that your book
03:29 of this. And you can see , I've got ions moving in this
03:32 . I've got ions moving in that . So basically, you have a
03:36 flow through uh so that we're basically ions in two directions at the same
03:42 . OK. So it would be we would consider reciprocal, right?
03:46 you hear the word reciprocal you give me, I give to you that's
03:51 , the other type of electrical synapse a term you'll hear over and over
03:55 . If you stay in biology, you move further up and go to
03:59 biology and molecular biology, you hear rectifying synapses or rectifying channels might be
04:05 term. And here it's one All right. And so up here
04:09 the top is the best way you see this sort of current. And
04:13 what's happening is is that these are gated channels that are opening and allowing
04:19 the increase of ions on one side flow in one direction downstream to the
04:25 one. And eventually, what would expect to happen if I'm flowing from
04:28 to the other? What's going to ? You'd expect equilibrium, right?
04:34 we prevent that from happening because we'll channels in the surface of the cell
04:39 that the ions flow back out. then, because you have channels open
04:43 the other side that allow them to in and you basically create a current
04:47 actually goes one direction through the cell then back out and then again through
04:53 kind of that pathway. So that's it one direction. So reciprocal both
04:59 , rectifying one direction. That's all going to talk about electrical signaling or
05:03 synapses until we get to the cardiac . Ok. And even then it's
05:08 more of a Oh yeah. Do remember the electrical synapses? Yeah.
05:12 then we just start going what we about what we're most interested in.
05:18 this the chemical synapse? All So when we think about synapses,
05:23 is what we see or what we and simply put what we have is
05:29 have two cells, a neuron and target cell downstream. So I think
05:34 this particular condition, we're probably uh didn't even say it just says postsynaptic
05:39 . All right. So what we is we have our, our
05:42 our sending neuron and we have a cell, we'll just call it receiving
05:46 just because I'll probably say that over over again. All right. So
05:50 cell that is sending is in front the synapse, the cell that's receiving
05:53 behind the synapse. So we have pre synaptic cell and a postsynaptic
05:57 All right. So one is always to be receiving side. One is
06:00 to be all the be the sending . They don't switch sides. It's
06:04 in one direction, always. All . The other thing I want to
06:08 out here is what we're doing is are sending an action potential, which
06:14 represented by the little lightning bolt of flashes because that's how artists do
06:19 And they're saying, hey, an potential has traveled down the AXON and
06:23 it's doing. It's arriving here at Axon terminal and it is causing the
06:29 of a chemical message at the end the terminal right out of that
06:35 So in the synapse, I'm releasing chemical signal. Now, so
06:38 you should not have learned anything new this is what we probably taught you
06:41 biology. One, it might have two. I don't know, probably
06:46 . All right. So this space called the synaptic cliff. This entire
06:53 is referred to as the synapse, relationship. Now, as we
06:59 this is a chemical synapse. So is no electrical activity coming here and
07:03 jumping over to the next cell. right. But you'll often hear that
07:09 or sorry neurons and that muscle cells electrical. And so it's very easy
07:14 say, oh, well, it's electrical synapse. No, it is
07:17 chemical synapse because the action potential is from one side of the cell to
07:21 other side of the cell to cause release of chemical, right. Other
07:28 in here, um like I it is unidirectional. So we're always
07:32 in this direction. And the reason that is because the sending material,
07:37 neurotransmitter is being released from that axon on the other side, that's where
07:43 have the receptors. So the receptors all going to be on the receiving
07:48 . So while this seems very, basic and stuff, understand that neurons
07:52 talking back and forth across the same , it's going in one direction,
07:56 always unidirectional. Now, we talked vesicles and I talked about how they
08:03 up and stuff. And I just to just remind you that what we're
08:07 is we're making neurotransmitter up here in SOMA that neurotransmitter is being packaged,
08:13 down along the length of the Axon it's finding its way to the Axon
08:18 and it's sitting there waiting 40 signal cause it to release. We're using
08:24 snare or those snares and the snaps be able to do this. So
08:29 is just again showing, did I this picture last time or did I
08:33 this my other class or you haven't this picture yet? OK. I
08:35 it to my other class, my level class, they kind of
08:38 some of them left and some of going to law school and then,
08:41 know, don't be scared by pictures this. The idea here simply put
08:46 that when you're dealing with a vesicle has something that you're secreting that associated
08:51 it are these docking proteins called All right. So the vesicle has
08:57 of these docking proteins. The target some docking proteins and they recognize each
09:02 . So it allows those two things come close together and you can see
09:06 what they do is they come into a position so they don't quite
09:11 but they're not quite separate either. they're just kind of in this state
09:15 like we're ready to go. So need a signal to tell them it's
09:20 to merge and release your content. so the the the chemical message that
09:25 that to happen is the release of . When calcium is present in that
09:31 , it causes the merging of the . So your, your vesicle fuses
09:36 then it opens up and then when calcium leaves, then all the docking
09:41 leave and they go find another And so that's how you get rid
09:44 it And so that you can recycle proteins over and over again. Now
09:50 question is how does this all Right? I want to make
09:54 Yeah, I didn't talk about I'm gonna go back. All
09:56 So we're coming back to this picture . All right. And so the
10:00 potential is traveling down the length of axon and it's opening sodium or voltage
10:05 sodium channels, which then result in opening of voltage gated potassium channels which
10:10 causes a cascade of events just like did. Remember we did this and
10:16 one did it and then we did . Oh man. See you guys
10:21 sleep. I got less sleep than of y'all last night. And I'm
10:24 here dancing like a monkey. You , let me have my little cup
10:29 you can play your organ grinder. right. So let's try one more
10:33 . So the Axion pencils travels down length of the axon and it gets
10:39 to the synaptic, the axon And what does it do?
10:44 we run out of voltage gated sodium and potassium channels and without them,
10:50 nothing to come in. Right. no more sodium coming in. So
10:53 can't cause it to go any But at the axon terminal, this
10:57 where we have voltage gated calcium All right. And so when that
11:03 potential arrives, it's not there to up a sodium channel, it's there
11:07 open up a calcium channel. Calcium flooding in. And when calcium floods
11:13 this happens. And so neurotransmitter is into the synaptic cleft. And when
11:22 arrives out in the synaptic cleft, neurotransmitter is now desperately looking for something
11:27 bind. And the thing that's supposed be binding is its receptor on the
11:33 cell. And so what we're doing is we're transferring a signal in a
11:38 way to the postsynaptic cell. So not particularly complex. It's just we
11:46 this magical calcium thing going on. . Bingo. The question was so
11:52 goes to electrical, to chemical, electrical. Yes. So if you
11:57 think of a neuron chain, so , we'll do a simple neuron chain
12:01 we're going to talk about. In next unit. We have a neuron
12:05 originates in your cortex, travels down spinal cord and terminates on another
12:11 which then goes out as a motor down to your big toe, which
12:15 described the other day So these are long cells, right? But if
12:18 want to wiggle your big toe, idea of wiggling, wiggling your big
12:21 begins here. So I say I'm to wiggle my big toe. So
12:26 do, you can't see it, I'm doing it right. So,
12:31 potential down to the axon terminal causes of calcium into the axon terminal,
12:36 know, allows it to come causes the vesicle to merge empty out
12:40 neurotransmitter empties out in the synaptic It binds to channels in the or
12:46 the synaptic cliff which opens up. this case, sodium channel sodium goes
12:52 into the postsynaptic cell which is a . In this particular case, something
12:59 happens because that's in about three minutes then that creates an action potential that
13:04 travels on down to your big which then does the same thing calcium
13:08 into the axon terminal. Synaptic You get the neurotransmitter back to synaptic
13:13 . This would be the neuromuscular junction uh neurotransmitter which is acetic colon.
13:19 this particular case, binds to its which causes channels on the muscle to
13:24 up, which causes an action potential start in a muscle which will lead
13:29 a contraction in the muscle. So muscle goes like this in your big
13:33 wiggle that seem hard. Well, you have a boring picture like
13:40 Yeah, it doesn't be 100% But let's kind of walk through some
13:44 these things, what's going on So part of the problem in trying
13:47 explain this is it's a chicken and egg thing which came first chicken or
13:50 egg. Who thinks chicken, who egg, chicken, egg,
14:04 some triple chicken egg? OK. want my answer to this? This
14:11 doesn't have to be right. You have to agree with me. The
14:13 came first because the chicken laid a egg. The thing that lead to
14:19 , the, the egg that the was in was in a proto
14:23 So it was a proto chicken egg then the chicken arose out of the
14:27 . The proto chicken egg. Does make sense? You're like, I
14:32 believe you. It's OK. You have to, we'll get to that
14:35 another, another lecture. Well, in our lectures. Um Maybe if
14:38 take Comparative Anatomy, we'll, we'll about that. All right. So
14:44 are delivered, vesicles arrive and are out. They're sitting and waiting for
14:48 calcium signal. And this is kind what it looks like. That's the
14:53 junction. So it's not just oh, there's a vesicle or
14:57 Do you see how they're lined up to go? They are just like
15:00 are, we are rocking, just me that signal. That's why I
15:05 this picture. So you kind of the sense this right here would be
15:10 synaptic cleft now, in a it goes by a special name.
15:13 called the motor in plate, but still a synaptic cleft. All
15:17 it just happens to be in a . Now, once that signal is
15:21 , all this neurotransmitter goes everywhere and neurotransmitter will activate these channels as long
15:28 the neurotransmitter is present. All you want neurotransmitter there the whole time
15:34 want your muscle to stay in a state. No, you want it
15:38 be a brief, quick signal to contract and then the muscle contracts.
15:42 you want to extend the contraction, wanna send multiple signals so that you
15:45 multiple contractions so that you get a contraction. So whenever you release a
15:51 , remember it is a brief quick, as quick as I can
15:54 rid of it signal. So you to have a mechanism to get rid
15:58 that signal, we call this So there are different ways. And
16:05 I was in your seats, there like two ways. Now, there's
16:07 than that. So I'm gonna kind approach this in the way that we
16:11 stuff and think how we know everything then it turns out. Nope,
16:15 , we don't know anything at So the first thing that we ever
16:18 kind of discovered was over here in . You do not need to memorize
16:21 different mechanisms. By the way, , these, this list is
16:25 which one does, which not OK. So the first thing we
16:30 is like, oh when we're looking the neuromuscular junction, when Aceto colon
16:33 released into that neuromuscular junction, there an enzyme that destroyed it. It
16:39 called Aceto colon aras. And we uh the way we terminate signals is
16:44 have enzymes in our clefts. So neuron must have an enzyme in its
16:50 to destroy the neurotransmitter that's been And then we started looking at other
16:54 . And what do we find Oh, yep. See, the
16:58 is the weird one. All Another way that we have so we
17:03 have enzymes in our clefts another And this is not the best
17:06 But um you can have a just kind of wander away from the
17:10 cleft. If it's not in the , it can't bind to its
17:14 can it? So that's a good to get rid of stuff. Just
17:17 it wander off and then we'll have enzyme deal with it someplace else in
17:20 body. Ok. So that's another . It's not a good way,
17:24 it's another way. Third way is can have other cells take things
17:31 So here you can see those are glial cells of some form, usually
17:36 because they like to wrap themselves around synaptic cliff. And so when you
17:41 neurotransmitter in there, these glial cells actually uptake that neurotransmitter and remove it
17:48 the cliff. So it's incapable of anything and then it will process it
17:52 by breaking it down and delivering the or just completely destroy it. And
17:57 have to go worry about making it again all over again. And then
18:00 way is you can actually have a itself, take it up. So
18:04 just released it. But you know , I got things over here that
18:07 come over and pick up the stuff just released and I'll recycle it.
18:11 these are different ways to remove neurotransmitter ensure that your signal is quick and
18:16 and over and done with. And can kind of see this in all
18:19 cases, right? You can look here is my Cetalol AA.
18:23 I'm also doing take up here, doing take up here, I'm doing
18:27 up. But so are these glial here's take up, here's take
18:31 here's take up, here's take All right. And we'll probably find
18:35 that this is not the final list that there are other mechanisms involved and
18:39 yada yada. But the key takeaway I get rid of neurotransmitter and there
18:45 a couple of different ways to do . So here we are, we're
18:52 that neuro, we're in that postsynaptic . I should stop here for a
18:58 so far. So good. Is easy to follow so far?
19:02 Right. So I'm, I'm in postsynaptic cell, I've just released acetylcholine
19:07 whatever the other neurotransmitter, that little just floated across synaptic cliff, it
19:12 to its channel. And depending upon that particular uh uh neurotransmitter is,
19:19 can be either excitatory or inhibitory. it's excitatory, it's going to bind
19:23 a channel that will allow for the of sodium or the e flux of
19:32 . So just make sure you understand E flux is. It's a term
19:35 just means moving outward. And if do that, what happens to the
19:38 is that the inside gets more All right. So I see a
19:45 . All right. And what I'm is a small depolarization inside the receiving
19:50 . If I see a small what do I call that? What
19:54 of potential is that action or It's a graded potential. All
20:00 So if I have more action potential results in more neurotransmitter being released,
20:07 more neurotransmitter combine more receptors. And that potential that I get in the
20:13 cell will be greater more. So we have here is we have a
20:20 of greater potential. We give it special name. It's called the excitatory
20:27 potential. And if you look at words that describe specifically excitatory, it's
20:33 depolarization. Where is it happening in post cell? And it's a graded
20:38 to hence the P the and then abbreviate it because saying all four of
20:42 words in a row is really long hard and tiring, especially on a
20:46 afternoon when you're exhausted. And so just say EPSP. All right,
20:52 ESP totally different area. Epsp. the opposite of that would be when
21:01 neurotransmitter causes the opening of a anionic or opens up potassium channels. So
21:08 potassium moves out. I said potassium in or out on this one.
21:13 yeah. So in other words, I'm doing is I'm gonna hyperpolarize the
21:18 . So it's inhibitory. I'm moving away from that threshold that we describe
21:24 it comes to an action potential. when that happens, the cell becomes
21:28 negative on the inside. And so , that uh graded potential that I'm
21:35 isn't going to cause any sort of moving further and further away from
21:41 All right. So this is the sp the the inhibitory postsynaptic potential.
21:47 note you can have one or the depending upon which type of neurotransmitter you're
21:52 or releasing into that uh synaptic So an action potential can be something
21:57 excites the next cell or it can the next cell. But what's happening
22:02 that next cell is a type of potential. Now, if these ep
22:08 are small, I'm gonna use EP for right now, then that means
22:13 a small, you know that small which then kind of ripples away right
22:18 the site of origin, right and it's very small, is it gonna
22:22 very far? No. But if big it will travel much further.
22:27 , if I have a bunch of EP SPS, how do I make
22:31 big signal? Well, how about I have a lot of them?
22:36 . Now I'm gonna use an example I've used for a long time.
22:40 haven't come up with a better one . So you can just know that
22:44 . It's a stupid one and I come up with better stupid ones.
22:48 right. But I want you to for a moment that you get on
22:52 social media uh environment of, of . So back in the day it
22:57 Facebook and you could have polls on . I don't know if you can
23:01 it on Instagram or any of the ones. But let's say you can
23:04 a poll and you're dating somebody, you don't have the guts to make
23:09 choice of whether or not you should or break up with this person.
23:13 you're gonna go contact all your followers 4000 of your best friends and you're
23:19 ask them the question. Should I or should I go? Right.
23:25 then all your followers are of gonna have a really valuable opinion,
23:29 ? And so some of them are tell you, no, no,
23:31 stay with this person. Some of are gonna uh uh you break up
23:34 this person and then what you're gonna is depend upon, you know,
23:40 strong of that signal, in other , how big the vote is,
23:46 ? Isn't that a great way to through life? Right? So if
23:53 take all the Epsp, so what looking at in this picture right here
23:56 what an actual neuron kind of looks you can see here. It's not
23:59 1 to 1 ratio. Is So the dark purple represents the cell
24:05 of one neuron. And all the purple is that lavender help me out
24:10 is that lavender. Ok. All lavender represent the axon terminals of all
24:17 neurons that are talking to this one . So there's a couple 100 if
24:22 a couple 1000 cells talking to this cell kind of like all your
24:27 you know, all the ones that have a really close relationship with and
24:31 yellow ones represent astrocytes just holding everything place. And so you can imagine
24:35 of these are sending signals that are excitatory. Some of them are sending
24:40 that are inhibitory. And what they're is they're telling that neuron you should
24:47 or no, you shouldn't fire. so processing the information is in
24:53 receiving excitatory signals and inhibitory signals resulting both PSPs and I PSPs. And
25:02 the sum of those S SPS and PSPs are going to create either something
25:08 or something smaller that will ultimately arrive the axon hili and what starts at
25:14 axon hili, the action potential. . So, the sum of all
25:24 EP SPS and the IP SPS collectively called the grand postsynaptic potential. The
25:32 P Yes, ma'am not. So, different neurons are gonna have
25:40 characteristics. We're gonna cover a very few. There are hundreds of
25:47 Some of them behave in excitatory some of them behave in inhibitory.
25:50 can be excitatory inhibitory depending upon which you're looking in and what you're looking
25:55 . So it's less important to learn they are and more of generally how
26:02 work. And then if you spend time studying, say dopamine, then
26:05 you should know exactly what it does now, this process of bringing things
26:14 is called summation. All right. there's different types we have here.
26:18 two basic definitions, temporal summation and summation. And they have specific
26:25 When you hear temporal, what does refer to time and spatial refers to
26:31 , nearness, so on and so . So we're gonna try to demonstrate
26:35 two types of things of what summation in a very simple way. So
26:38 over here on the left, you see that we're looking at a,
26:42 single stimulation. All right. So just gonna kind of point out.
26:47 we're, we're measuring up here to what sort of stimulation this cell is
26:52 right here, we're measuring at the he to see what sort of results
26:57 that stimulation. And then down here the axon, we're asking, is
27:01 an action potential or a series of potentials passing by? So you can
27:06 here, I've got this EPSP that producing, right? This EPSP is
27:12 , you see the depolarization, but it has to travel a certain
27:16 it's going to die over time. so by the time that signal gets
27:20 to the axon hili, it's still , but it's not particularly strong.
27:25 so it doesn't get to the point we open up all those voltage gated
27:29 . And so as a result, don't get an action potential. We
27:32 , we don't see or measure an potential traveling. All right. So
27:36 is a case where the, the of the EPSP is not strong enough
27:41 cause an action potential to be formed that postsynaptic cell. OK. And
27:48 the EPSP and the IP SP is the postsynaptic cell, it's not what
27:52 the sending cell is doing. It's result of receiving a signal.
27:57 And the second one, what we is you can see we have 123
28:03 uh axons, right? So different on that dendrite. And so here
28:07 saying, OK, this is spatial if I take two of these and
28:12 fire simultaneously. So I'm going to you here note both types of summation
28:19 a time component to them. All . But here what we're saying is
28:25 . So that's the spatial portion are at the same time. So we
28:30 small sp plus another small sp graded are additive. And so what you
28:37 is you get a larger postsynaptic potential can see here it's much higher than
28:42 one. And so when you look at the Axon Hili that much higher
28:47 into reaching a threshold. And when reach the threshold, what do I
28:51 ? I get an action potential? in this particular case, I'm over
28:55 long enough. So I get 12 potentials in the series. And so
29:00 I go and measure down here, I see those action potentials?
29:03 they're still there. So the two SPS together are great enough to cause
29:10 of the next cell. All So that would be spatial two things
29:15 the same time. And just to you that this is a summit,
29:19 we go. There's three, all of them are firing and look,
29:22 even get a bigger one. So get multiple action potentials because we're over
29:26 for a longer period of time, action potentials are then uh monitor or
29:31 monitored but are registering even further down line. So once you get the
29:34 potential member, it's an all or response. Once it starts, it
29:38 until the end. All right. spatial summation is taking multiple signals from
29:45 axons simultaneously to create a large enough so that I can get a response
29:52 that postsynaptic cell. Temporal summation is lot more difficult to visualize. I
30:01 . So let me, let me very quickly a visual for spatial
30:07 All right, if I clap, just call that an sp so it
30:13 a certain magnitude right now. Two us clap at the same time.
30:19 it a little bit louder? How three of us? 123? How
30:23 four of us? How about five us? Do you see how it
30:28 louder and louder each time? Just your head to say yes, of
30:32 . All right, we could do all day. All right. So
30:36 idea here is you can see at same time the more I add,
30:39 bigger it gets that's spatial in temor . This is harder to do that
30:43 visual. It's this one neuron is but the frequency at which it fires
30:51 . All right. So in other , what you can imagine is when
30:53 get a greater potential, remember their . So what happens? I get
30:58 and then we're gonna get repolarization back to rest. But if I can
31:02 the deep the rep polarization with another potential, another EPSP I can build
31:10 my first EPSP. And then if can get another one I can build
31:14 the next one. And as long I'm interrupting the down slope, I
31:18 keep rising up higher and higher and . And that's what this is trying
31:22 show you. It's like, if I were to look at this
31:26 right here, it should be the as this. And so it would
31:29 just kind of go downward right here that. But on its down
31:33 I interrupt with another stimulation. So go up again, same magnitude and
31:38 I start going down, but then interrupted again. And so while at
31:42 front end, I'm not getting my potential by now because I got three
31:47 in a row and I haven't relaxed or I shouldn't say relaxed, I
31:51 re polarized yet. I'm getting the potentials because I am now above
31:56 And so you'll see that action potential those action potentials because of that temporal
32:04 , an auditory or visual thing. can't do this well enough. All
32:08 . But if I do this, that one sound. But if I'm
32:17 get an opportunity for us to interrupt sound. And so the idea is
32:21 building and building and building till I threshold. So now I'm getting action
32:26 that kind of makes sense. All . So temporal summation and spatial summation
32:34 the way I'm going to finish my and they'll come right, temporal and
32:38 summation is the way that we take with varying magnitudes to create a strong
32:45 signal to activate or prevent activation in postsynaptic cell question. So, with
33:01 to that last one, what the is, why does it take
33:09 Sure. Uh that's probably an artist's . But what, what you could
33:15 here is generally speaking, an a or remember has that, that,
33:21 um refractory period. So you shouldn't any at all. It should literally
33:26 I fire and then I come down as long as I'm above that
33:30 then I will get the next one that period of time. So there's
33:34 be that period that's dependent upon that period. In this particular case,
33:38 think the artist just drew them further because reasons. All right, I
33:43 it's an artistic choice and you'll often these in, in physiology textbooks because
33:49 medical artist is not actually knowledgeable about he's drawing, he's just doing what
33:53 person told him to draw. Right. All right. So we're
34:05 use a bad example. But what , but what you're alluding to,
34:09 . So a sustained contraction in a is a function of hundreds of thousands
34:15 action potentials telling the muscle to contract, contract, contract,
34:20 And then so you get a sustained as opposed to like a series of
34:26 and it's really called a twitch. , the twitches are non visible they're
34:31 like that. OK? And so like that, but it's not that
34:37 . So it's a good way to about. It's like if I'm trying
34:39 contract this and let's just say this the activity in that cell, what
34:44 looking at is going, boom, , boom, boom, boom,
34:48 the signals are coming and they're becoming enough so that I can overcome the
34:53 to get the full contraction. All , like I said, it's,
34:58 not the best way to look at because of, of how a muscle
35:02 works. And we'll get to that the next unit. So if I
35:06 have summation, right? If I excitatory plus excitatory, then I can
35:12 have excitatory plus inhibitory. And you from the seventh grade math that when
35:18 started doing negatives, if I take positive and negative, it's the same
35:23 as subtraction, right? It's basically a negative number is the same thing
35:31 subtraction. So we call this All right. So it's the type
35:39 spatial summation. The difference is that signals are going to be.
35:44 one is inhibitory and one is excitatory some sort of strange combination there.
35:49 right. So what this is trying show you is it again, there's
35:53 lot of Presumptions in these photos. you got to remember that not every
35:58 potential has the same magnitude, You can have varying magnitudes, you
36:02 have an EP that is positive millivolts then you can have an IP SP
36:07 minus five millivolts or it might be 10 or it might be minus
36:11 So there's variation with regard to But principally you understand the concept A
36:17 negative B is the difference between those values. So if I have positive
36:23 millivolts and minus five, then my now is no or my GPS P
36:29 not 15, it's, it's right? And again, I'm just
36:35 numbers at you. And if I two things of the same value plus
36:38 and minus 10, then my, GPS P is going to have a
36:43 of zero, right? So that's cancellation is, is basically taking those
36:49 magnitudes and then duking it out and out where I level off. All
36:56 . And this one is showing you here, we're just presuming the same
36:59 . So they knock each other So I get no action potential.
37:03 down here, I'm not going to neurotransmitter because I got no action
37:08 So the downstream cells are not going be activated now where we're going to
37:17 these synapses can vary. All So in A and P, we're
37:22 dendrites in axons, axons terminate on and everybody's happy because that's an easy
37:28 to understand stuff. But as we forward, we understand that that's not
37:32 it's like the most common types of are going to be between an axon
37:38 the dendrites or some portion of the . So, one of the things
37:44 don't spend a lot of time talking are these little tiny spines that show
37:48 on the dendrites. And they're special onto which axons can terminate so that
37:54 create these unique synaptic clefts. So a, it's basically like a close
38:00 . It's like them holding hands. right. So I can have an
38:05 dendritic interaction. So that's axon Adri can uh terminate on a synapse.
38:12 I could be Axo spinous or I terminate where there is no spine and
38:18 is no dendrites. I'm someplace along shaft someplace. So that'd be just
38:23 shaft synapse. So dendrites typically are receiving end, but that's not the
38:27 place. One of the other more common places. I was gonna
38:32 you guys earlier if like, what's over under of falling on the
38:35 Glad I didn't ask my foot, caught. The other type is
38:43 And so here you can see I can terminate on the SOMA.
38:48 , just this is just a thinker . Let's see what you guys think
38:52 I have an Axon up here on dendrite and I have an Axion down
38:55 on the SOMA and they both produce same magnitude of Epp in the receiving
38:59 , which one is more likely to an action potential, which do you
39:05 the one on the dendrite and the on the SOMA when on the
39:08 Why it's closer? And so that ripple effect, you know,
39:13 wave that it's going to create has shorter distance to travel and that,
39:17 would be a good, a good . Right. That's probably,
39:21 doesn't necessarily guarantee it, but it's . And we have some weird
39:25 We can have axons down on axons right, right here. OK,
39:31 can have a or dendrites on It's not a picture of this.
39:36 . We have dendrites on the You'll see those in the nervous,
39:39 mean, in the central nervous system some cases where you're dealing with those
39:44 um uh neurons where there's no real . So they're just descriptive terms to
39:50 about their interactions. So, one the ways that a neuron increases or
39:59 its signal as we saw was through , right? So if I get
40:04 big signal, I can produce more potentials, right? So the strength
40:10 an action or of a signal inside neuron is dependent upon the number of
40:14 potentials it produces, right? And more action potentials I produce, the
40:20 I release in terms of neurotransmitter, ? So I get a bigger
40:24 Does that all make sense that track a simple way? So this is
40:28 we refer to as attenuating responses, responses in cells are the result of
40:35 action potentials, I code magnitude through number of action potentials that I
40:42 The thing is, is I don't attenuate signals, speed things up,
40:49 more signals only at the level of axon. I also do it at
40:54 level of the dendrite. All So diameter matters not only in the
41:01 in terms of how fast a signal go, but it also matters in
41:05 dendrite. And so this is what is trying to show you. Here
41:08 a really, really thin dendrite, a really fat dendrite. All
41:14 So here's the EPSP, we're producing same size EPSP, but because this
41:20 thinner, there's a less channel or for the signal, right? And
41:26 you don't get the signal down to SOMA. It's nice and fat.
41:31 you get a nice fat current and is enough to reach threshold. So
41:35 get an actual potential here. So neurons can regulate how well they respond
41:44 signals by changing the sizes of their . It's kind of cool. All
41:50 . So there is this this way regulation simply by changing how you receive
42:00 . Does that kind of make Yeah. No. Yeah.
42:04 you wanna hear. See Romano. . Oh By the way, I
42:09 make about 1000 movie references over the of the class. Corky Romano is
42:12 rare one. Corky Romano. There's scene where the actor I can't remember
42:17 name. He was in Saturday Night . He, he's working for the
42:20 , he's pretending he's an FBI man he's in the evidence room and he
42:24 a whole bag of cocaine dumped on and then he has to go speak
42:27 a bunch of kids about the use drugs. And so the whole time
42:31 in front of like this. You , you don't, you do,
42:33 don't, you do, You it's like a three minute stupid skit
42:36 him doing you do you don't, understand it? Don't understand,
42:48 Am I gonna have to come in with a squirt gun just trying to
42:54 out how to get you guys excited this stuff? All right, if
43:00 understand this, then we can kind expand on these ideas. All
43:04 So neurons are interacting with each right? They're forming multiple synapses with
43:10 other and they're found within these these of cells. So basically a network
43:16 neurons working together, they can be in nature or they can be divergent
43:21 nature. And what this means is we say focus is that the neurons
43:25 interacting with neurons near neighbors. And any sort of of of, you
43:31 , problem solving or whatever it is they're trying to do whatever the processing
43:35 they're doing is locally distributed. All . So for example, when I
43:42 information about sight coming in and I'm to determine color. That information goes
43:47 to the uh the optical regions of brain, the visual cortex. And
43:52 a specific region of the visual cortex go to. I hate to tell
43:56 this. Now, it's the weirdest ever but just bear with me.
43:59 regions of the brain that are responsible color processing are called blobs. And
44:07 very confusing. Once you start reading blobs, you're just like I give
44:11 and you're just like my A P . It's like law school is where
44:14 going. All right. But you your blobs. And so color processing
44:19 occurs in the blobs and then that is then passed on for other types
44:24 processing. OK? Or they converge other networks so that you can then
44:30 , oh this red apple got like , yada yada. All right.
44:36 it only does color. The other of processing is this divergent processing where
44:41 information is just sent everywhere. you understand that when you see something
44:48 it doesn't, your eyes are not , right? You don't have an
44:52 projected to the back of your brain your brain records it and you're
44:55 OK, it's watching a movie, ? You, you understand that I
44:59 instead what happens is is every aspect the things that you're seeing are sent
45:04 different areas. So for example, the brain, there's not one visual
45:10 uh region of the visual cortex, not two or three or four at
45:15 count, I think it was up like 20. All right. So
45:20 processing which we normally attribute to the lobe of the brain is really the
45:29 lobe and the temporal lobe and the lobe. Oh yeah. And the
45:33 lobe and information is broken down by and color and movement and shape and
45:40 sorts of other aspects and other information then distributed out to other processing centers
45:46 association areas in the brain. So you can understand that the thing you're
45:50 at is a hopping frog, So this would be an example of
45:56 divergent network information is sent everywhere. experiences of anything you have a meal
46:07 before you, right? You smell and that sense of smell goes
46:13 I'm gonna send it to the memory . Do I recognize the smell?
46:19 ? I'm gonna smell that and it , OK, this smell has different
46:24 in it. It's pleasant. So see it's being sent to different parts
46:27 the brain to get a response, ? So processing information can be done
46:37 a very localized area to do something or it's broadly sent out so that
46:43 have a greater, a greater breadth understanding of what it is that you're
46:50 . The other thing I'd add is the more neurons you have in a
46:55 , the more synaptic delay you have more it takes to process because each
47:00 takes time to process. Now. not very much. It's like we're
47:04 about 0.1 milliseconds, right? But you have 0.1 milliseconds to, to
47:11 an Epsp and you have 10 in chain, then that's 10 times 0.1
47:19 . That's a millisecond, right? you ever been walking across the street
47:25 out your phone like you always do all of a sudden you hear this
47:30 horn. So the first thing you to do is you have to unplug
47:34 brain for a second and you kind stop and you look and you see
47:38 bus barreling down on you have that happened? Something similar, right?
47:43 what do you do? Do you go oh I know how to respond
47:46 this or do you sit there and ? Huh? That's a bus,
47:56 ? My situation appears to be dire you always talk like somebody from the
48:01 century, right? Part of that your brain like I don't know what
48:08 do because I've got to process all info input. And so that delay
48:14 kind of there now. Is it all that? Is it really that
48:18 but it kind of gives you that , you mean if I have to
48:23 more and more processes? If I more neurons in this chain, it's
48:26 cause a problem. All right. I throw a baseball at your
48:29 What are you gonna do? I like that. You move your
48:33 . You don't even have to think some of you, you know,
48:35 too cool for school. You just . OK. A reflex has very
48:42 neurons in the pathway because it says will always do blank, right.
48:49 gonna talk about reflex again in the section, but you can have fun
48:51 it. You can go do your cross your leg thing and, and
48:54 the uh knee jerk reflex. See you can keep it from happening.
48:58 you hit that ligament. Just You guys know how to do the
49:01 jerk reflex, right? Doctor has it to you for years, basically
49:05 that wonderful little ligament right underneath the and you can just sit, you
49:08 just do it with like a little chop, just get a friend.
49:11 them start karate chopping your knee and just gonna sit there and just do
49:15 . All right. Why reflex always a reflex? All right. And
49:19 also a very, very short neuron . I promise you neurotransmitters. Hundreds
49:28 them. Should we memorize them Come on. Come on, let's
49:31 it. Let's not fun. All , neurotransmitter is simply the chemical signal
49:40 by a neuron. It's gonna be in nature, but they can act
49:46 an autocrine fashion. I mean, can talk back to myself.
49:50 you can all right, they're gonna at the synapse. So this is
49:56 message that we're releasing from that And as I mentioned, there are
50:01 of them. This is like the list of the families that we're familiar
50:06 , right? So Aceto Cole was first one discovered, we were very
50:10 in discovering acetycholine back in the early hundreds. And we're like, oh
50:14 , we got neurotransmitter, we figured out, we know how neurons talk
50:18 muscles. So I guarantee all we to do is look for things that
50:21 like Aceto Cole and we are going understand how the brain works and nothing
50:26 like Aceta Coli. All right, is nothing else like aceta coli.
50:31 right, turns out that a lot our neurotransmitters are just modifications of amino
50:37 . So we got the AOM means have the amino acids themselves.
50:40 by the way that A P that been spending your entire life learning is
50:43 molecule of energy can act as a . Great. What about gasses?
50:50 , we got gasses too, We're not talking about the stuff you
50:54 after a very, very, very meal, your body is filled with
50:58 acid filled with carbon monoxide filled with sulfide. Do any of these gasses
51:04 like gasses you want circulating through your . Hydrogen sulfide is what makes rotten
51:08 smell rotten, right? But it's neurotransmitter. It's called a uh it's
51:17 just forgot the name. It's a emitter. So they took neurotransmitter and
51:23 and jammed it together. Got These are more familiar and then the
51:29 themselves as IOS can serve as Now, with that in mind,
51:35 , I don't want you to sit and, like, write down
51:37 oh, these things, I just you to kind of get a
51:39 Are there a lot of different types classes of neurotransmitters? Yes. What
51:45 they have in common? They're released neurons and they cause signals. All
51:51 . What we're interested in are these right here. These three classes first
51:57 coin, as I mentioned, first discovered, um doesn't look like anything
52:02 . It is both excitatory or inhibitory upon which system you're looking at and
52:08 the situation or circumstances are. If want to see what Aceta Cole
52:12 it is up there in the blue Bono. The very first one,
52:16 can see a co A plus Cole together. That's where you get the
52:20 right now. Aceto Cole. This uh we're going to spend time talking
52:27 it over and over again. But just going to give you a really
52:29 one. Aceto Cole is found in neuromuscular junction. All right. So
52:33 neurons tell muscles what to do your contracts, it always, always,
52:39 contracts. So in the case of neuromuscular junction, Aceto colon is
52:44 always, always, always no exception the rule under no circumstances. Is
52:47 different? It's excitatory, but in systems, it can be excitatory or
52:55 . Another group, the amino we know what the amino acids
52:58 We've all had to learn something or about them and what we have here
53:03 we take these and either we have original amino acid or we do a
53:08 modification to them. So, the excitatory ones that you should know are
53:12 acids, you know, glutamate, heard of glutamate, right? And
53:15 heard of Sparta, haven't you? . Ok. So those are two
53:20 neurotransmitters, glutamate. You do a modification to it. You get
53:26 So Gaba, which is a modification glutamate is an inhibitory neurotransmitter. All
53:31 , or usually an inhibitory neurotransmitter. glycine is another amino acid which is
53:38 serving as an inhibitory neurotransmitter. I this was the easy one of these
53:43 is not like the others. I , we've got three GS in an
53:46 but you can see we've got two and A G and an A.
53:48 there's no easy pattern to remember other glutamate and asperate, they both end
53:55 AIDS. So that's the excitatory So you just have to kind of
54:00 them and internalize them. All the biogenic means these are amino or
54:05 are neurotransmitter you've already learned about or about, you just may not know
54:09 by name. All right. So have the CCO means what we've done
54:14 is basically take off the carboxyl So where are we looking? So
54:18 here we look at tyrosine, don't look at tyrosine, look at
54:22 . Um You can see we do modifications. So if you start up
54:25 at Thyro, we took off that group, we get down to
54:29 There's no carboxyl group, we do modification. Put a hydroxyl group.
54:33 is why you take organic chemistry, ? So you go oh OK.
54:36 know that word hydroxyl. OK. But you can see that's, it's
54:40 , you're just taking tyrosine and you're making modifications all the way, all
54:44 way down. All right. But are the catacholamines. You've heard of
54:48 , right? That's a, a word. Yeah. Have you heard
54:52 histamine? Right. When you think histamine, what do you think of
54:57 ? So you think of, don't the those that you get? And
55:01 when you got a of those, do you do? You take
55:06 OK. And then you can breathe . It's a vasodilator. That's why
55:11 , we, we do that. right. Sorry. Baso constrictor.
55:17 , I've confused myself. So I be careful. All right. Then
55:21 have the weird ones. The CTA means and so dopamine is Cine.
55:24 Serotonin, I should have mentioned you've of Serotonin, right? So that's
55:28 one. These are all happy fun . Uh with regard to the cats
55:35 . But then we have Ep and Epinephrine. Um, you may not
55:38 heard of Epinephrine, but you have of Adrenaline, haven't you?
55:43 you've heard of Adrenaline. Adrenaline and are the same thing. It's just
55:47 fancy word for one. And the behind it is that one. they
55:52 it and are able to manufacture but you can't give the manufactured name
55:56 the chemical or something like that. I think that's was why they changed
56:00 . And then Norine is epinephrine's close . So it's no adrenaline. All
56:05 . That's where those names come All right. And again, they
56:09 both excitatory inhibitory activities together. That be uh either or yes, when
56:16 comes to a neurotransmitter. And this why we take the Neuroscience class because
56:22 far more broad and, and goes a greater depth. A neurotransmitter can
56:28 what is referred to as a divergent or a convergent effect. All
56:32 So a divergent effect. And you see up here on the top it
56:35 , look here, I've got this and this neurotransmitter can bin to a
56:40 of different types of receptors. All , these are Agenor receptors that we're
56:46 in this list. And so what I do in this if I bind
56:49 the alpha one? Well, I cause a current are different types of
56:53 . I can open and close different of channels. I want to point
56:57 out here. So alpha one and two here, I'm closing a potassium
57:01 or reducing the flow of potassium through channel over here. What am I
57:07 ? I'm increasing it. So you see these are opposite effects. What
57:13 the opposite effect? Just the presence a particular channel, right? So
57:18 upon which receptor I have, I get different responses. This would be
57:23 example of divergent effects. A convergent says, hey, look, um
57:29 have all these different types of They combine their own specific types of
57:34 , but they all result in the response in that particular cell.
57:39 So here you can say, oh , I've got this cell and I
57:42 activate it through this or I can it through that or I can activate
57:45 through this or I can activate it that. So there's different ways to
57:49 the cell to get the same That would be a convergent, a
58:00 thing. But an important thing that can do because of those axonal ax
58:07 Axo axonal connections is that you can and facilitate specific interactions between two neurons
58:18 not affect the interactions with the other that the the presynaptic neuron is interacting
58:25 . See if we can understand I see the, I can see
58:28 fur brow in the background and said didn't say that. Well, I
58:33 this cell right here. That would the presynaptic cell. In our little
58:37 , the little white cells down those are postsynaptic cells. OK.
58:42 we're focusing here on that synaptic You can see I've stimulated this
58:48 So in reference to this synapse, is pre or post, pre.
58:53 this would be post. So all is is a frame of reference,
58:56 ? So here I've excited the cell produce an action potential. So this
59:02 synaptic cell is sitting that action potential its pathway or down its axon where
59:07 have two extra collaterals. So in case, I'm not activating one
59:13 I'm activating three different cells so So good you're with me,
59:18 If I have an axonal presynaptic um cell and that cell happens to be
59:29 , what it will do is if cell is stimulated, it will release
59:32 inhibitory neurotransmitter to block or inhibit the that, that uh signal here,
59:43 ? So in other words, what doing is saying, I don't want
59:46 to stimulate the cell downstream from I don't care about these other
59:52 I just care about this one. so this would be presynaptic inhibition.
59:57 cell has been stimulated, right? presynaptic cell has been stimulated, but
60:04 blocking the pre synaptic cleft or presynaptic to prevent a response. So I
60:12 get responses in the other ones, not in the one where I'm doing
60:16 inhibition. Let's flip it around. have no signal in that synaptic
60:23 So no action potential. So this is not being stimulated. That cell
60:27 not being stimulated. That cell is being stimulated. But instead of this
60:30 an inhibitory neuron, that's an excitatory and it's activated. So, am
60:36 going to see a response to this or no? What do you
60:41 You're nodding? Yes. Anyone want disagree with her. No one's brave
60:46 to disagree with you. But you're . So that would be facilitation.
60:52 would be presynaptic facilitation. OK. the relationship between neurons is not simply
61:01 to dendrite, axon to dendrite over over again, we can regulate neuronal
61:08 at different locations and affect specific So here, presynaptic inhibition is occurring
61:17 this cell and that one, but in the other two. Yeah.
61:28 , it's a separate one altogether. way you can think about it is
61:32 just going to use these, these here, these two are talking to
61:35 other. She's sending signals this right? But I'm sitting in between
61:40 and I'm saying no, the signal not allowed to go forward. So
61:43 would be the pre synaptic inhibition. the third cell interfering between the two
61:49 that are normally talking or they're not to each other at all. And
61:53 saying, go ahead and talk. would be the facilitation. Mhm
62:09 Yeah. So the question she's asking will facilitation always cause a response?
62:14 right. So let's ask that in biological terms. What do we
62:17 Will we always get a response? , it's, it's the always,
62:21 that qualifier right? There always is a good qualifier. We're likely to
62:26 a response. Right? So, you can think when I hear the
62:29 facilitation, I'm stimulating to get a . Whether I get one or not
62:34 dependent upon the strength of the Yada yada yada. So far we're
62:41 , is any of this stuff sound or hard or difficult, right?
62:47 isn't like trying to memorize all your . Here's an ugly, ugly word
62:59 . What do neuro modulators do? do you think they do? Just
63:03 the name? You can cheat and up there. But if you hear
63:06 neuromodulator, what do you think it modifies or modulates neurons? Yep.
63:12 then you're good to go. Neurotransmitters chemicals released from a cell. They're
63:18 from the cell neuro modulators modulate the . All right. So here we've
63:23 to deal with relationship. All So when I'm dealing with a pre
63:27 cell and a postsynaptic cell, there a ratio between the cells that are
63:34 amount of neurotransmitter being released and the of receptors available. All right.
63:42 let's just say for a moment, make our lives easy. We have
63:44 neurotransmitters and we have 10 receptors So happy. Every, every neurotransmitter has
63:54 receptor to bind tube. All What a neuromodulator does is it changes
63:59 relationship? And so there are different that we can change this relationship.
64:03 can cause more neurotransmitter to be In other words, if one vesicle
64:08 10 neurotransmitters, maybe instead of one being reopened, I now open
64:15 So I've doubled the amount of neurotransmitter that clip and in doing so,
64:19 am facilitating or up regulating the activity those two cells, aren't I?
64:28 . What's another way I could do ? What's another way I can up
64:32 the activity between the two more? heard the word receptors. So if
64:39 increase the number of receptors, so I still have 10 neurotransmitters and I
64:43 20 receptors, the probability of a finding a receptor quickly has increased two
64:48 , hasn't it? So, in of these cases, what I've done
64:51 I've facilitated the interaction. And so what a neuromodulator does. It will
64:57 increase, facilitate the interaction between those cells. Now, how can I
65:02 the interaction between two cells? I reduce, oh I heard, reduce
65:08 amount of neurotransmitter. I'm I'm right? Or I can reduce the
65:13 of receptor that's available. So that be um the type of inhibition that
65:18 might see. All right. So of the ways that your nervous system
65:24 its activity is, but through neuromodulation will either increase or decrease activity so
65:31 you increase and decrease relational activity between two cells. And since you have
65:36 of millions of these cells doing you can imagine facilitation and inhibition is
65:41 of the ways that we remodel our . How do you guys like
65:46 Sugar? Good, right. All . Let's make, let's chocolate,
65:51 and sugar together. Yeah. I , that's just, that's just like
65:55 winner recipe, right? And you what? That's what we do every
65:59 we do sugar, you reward your and your brain says give me more
66:02 that and neural modulation, it gives , right? And it's modifying how
66:09 brain responds to simple signals about fuel your body because my brain does not
66:15 that when I put in other I mean, maybe a little bit
66:18 fat but not protein. I put in my body. It's like,
66:20 , whatever, you know, it's like OK, that's kind of
66:24 . When I put sugar, it's like just keep shoving it in.
66:27 we could just put it through the directly, we'd be happier. And
66:32 basically what Cola are now. neuromodulation isn't done. Ionotropic,
66:40 They use metabolic pathways primarily. So methods. So, g protein coupled
66:46 is a very common way. Neuromodulation place now to give you a sense
66:52 scale here, I've got this little and it shows you look we have
66:57 , very fast sorts of interactions between . This would be like within the
67:01 of one millisecond. And then we things that last a little bit longer
67:05 then even longer and then ultimately modulation these long term changes that are taking
67:11 . So they're trying to give you sense of scale. All right.
67:15 when you're talking about fast, you're talking about some sort of, of
67:20 aer or something that's basically opening up channel really quickly so that you get
67:23 response very quickly. But as you along to the slow transmission and
67:29 what you're doing is you're acting through some sort of metabotropic pathway. And
67:36 those words don't mean anything to, just kind of look at them for
67:39 second, ionotropic means working with right? Tropic means regulating. So
67:45 ion regulation. And so over here the left, that's an ionotropic
67:51 right? I'm releasing a neurotransmitter, neurotransmitter. In this case, Aceto
67:55 binds to a channel, it opens the channel. Now you have an
68:00 of sodium into the cell. So get a very quick, very rapid
68:04 . So an sp for example, a rapid response odds and it's very
68:08 and it's very short lived. All . But then there is the metabotropic
68:13 of interactions. And so here um actually doing Aceto Cole again. But
68:17 could imagine this could be glutamate, example, glutamate has a metabotropic as
68:22 as an ionotropic. But here you see Aceto cole goes and binds to
68:25 G protein coupled receptor. Now, of that is to open up a
68:29 . But do you think if I a G protein coupled receptor, there
68:32 be something downstream of that? So I'm gonna get a longer lived
68:37 and it's gonna be a little bit as well. And I throw this
68:43 here just again to kind of do little bit of a comparison here,
68:48 ? You can see that there are ways that I can open up
68:53 right? So here is the YAP , right? Here's my neurotransmitter binds
68:57 ion comes through here. I have neurotransmitter bind a G protein couple
69:01 I can activate it directly through the protein. So here I am opening
69:06 the channel or I can open through signaling cascade like cycle K MP,
69:12 on PK A PK through some sort mechanism, the phosphorylation or the opening
69:18 another channel. So you can imagine terms of time, fastest,
69:23 fastest, slowest and then you have . So different mechanisms of activating through
69:38 different types of receptors and different I mentioned glutamate having both a metabotropic
69:47 an isotropic. And I want to you an example of this sort of
69:54 . All right. So glutamate by produces an sp the way that it
69:59 this, it can act through a receptor which we're ignoring. So just
70:03 not going to look at that What it does is it acts through
70:06 ample receptor receptor. All right, is a form of ionotropic and you
70:10 it down here. So here is binds the receptor ions come in and
70:15 starting to see cell depolarized. you can see here here's an MD
70:20 receptor. This MD MN MD A is also capable of binding glutamate.
70:27 when it does, nothing happens, have to make modifications to that receptor
70:32 order for it to happen. And happens through the activity of the ample
70:37 . So what happens is is when um I think it's potassium basically,
70:43 the cell depolarizes, it causes MD to remove or release magnesium from its
70:51 , right? And so when magnesium basically what you've unblocked it. And
70:55 now when glutamate binds to the N A receptor, we've created a second
71:01 through which it can act put into . Over here, I have one
71:09 , one channel small response. After slight modification, I now have two
71:15 , bigger response. What is Neuromodulation? Oh And by the
71:22 we have another one, Kate, can be found up here. Glutamate
71:27 actually bind up to that and it tells the cell itself, hey,
71:32 ahead and release more neurotransmitter. So by itself can regulate its own cell
71:41 cause more glutamate to be released. . Yeah. So the question
71:59 does neuromodulation cause changes or result or be translated into modifications and behavior?
72:05 answer is yes. Now that would much kind of further downstream. So
72:11 other words, it wouldn't be like immediate thing. But you can imagine
72:15 you keep repeating something over and over over again, then the cell is
72:21 to start saying, oh, this how I'm being stimulated. So I'm
72:25 to change the way I respond to . And that's going to be here
72:28 just a, in a second. want to show you what that,
72:33 it is collectively. What we refer this as is plasticity. All
72:38 So we have what we refer to neuroplasticity and that neuroplasticity is us changing
72:43 response to the signals that our body our nervous system receives. No,
72:52 necessarily. And I'm, I'm just that's biochemistry and that sounds scary to
72:59 . I'm, I'm afraid the answers of course or no, it's
73:04 I don't know the answer to Right. It's OK to say,
73:10 don't know, sometimes can do All right, let's look at neuroplasticity
73:15 , very briefly here. All with regard to neuroplasticity, what you're
73:20 is you are changing your responsiveness in to a particular stimuli. And so
73:26 little example of plasticity is what your used said. Look, we have
73:30 example of low frequency stimulation and high stimulation, you can see it marked
73:34 here. So you can see the potentials are like this and then down
73:41 a lot faster. So when I'm low frequency, I'm going to release
73:48 a small amount of neurotransmitter. All . But in the case of high
73:54 , I'm not only releasing the neurotransmitter I normally release, but what I'm
73:58 going to do is I'm going to releasing a second neurotransmitter to give a
74:02 bigger response at the synapse. All . So I respond differently when I'm
74:09 differently is how this neuron is If I change the type of stimulus
74:18 do, then the cell is going respond differently. The early experiments that
74:22 were doing in plasticity, what they using sea slugs, right? So
74:27 about those cute little slug like right? And what they do is
74:32 reason we use them is because they big fat neurons that you can work
74:36 . And you know, back in sixties and fifties when they're working on
74:39 , they don't have micro instruments, only have big ones. And so
74:42 are easy to get a hold of you can stick them for all sorts
74:45 stuff, right? But one of things they were doing with the sea
74:49 is they were stimulating by taking a tiny rod. And what do slugs
74:52 snails have? You have those big ice stocks. Right. And then
74:56 they did was they would take a rod and they would tap the ice
75:01 . So, here you are, a cute little slug cruising out into
75:04 little tiny aquarium and someone comes up baps you on your eye. And
75:09 do you do if you're a sea ? Right. And then after a
75:15 you're like, I didn't like Well, I think it's ok and
75:21 it comes again and the, and do you do? And over time
75:27 keep hitting that and it becomes less to you. And eventually what you're
75:32 is you're like, this is how live now as someone sitting there bapping
75:36 on my eye stock, right? is a form of, of plasticity
75:44 habituation. All right, you have habituated to all sorts of things,
75:50 ? You have modulated or changed behavior a function of a constant stimuli around
75:57 , right? This is normal. is what your body does and you
76:01 kind of see what happens here is series of action potential is just kind
76:04 always going on. And the cell , you know what, I'm not
76:09 respond to each one of these action anymore. You're gonna really have to
76:14 me on in order to make this . And so what happens is your
76:18 rate decreases over time is what it basically showing you up there. All
76:24 , don't here they're showing you different of changes. So there's what we
76:29 to as facilitation. We just saw very, very quick, we have
76:33 , which is a little bit longer then potentiation, which is even longer
76:36 that. And so in here, just trying to show facilitation versus
76:40 You can see how you get this term response after a massive uh change
76:46 the signal. Whereas facilitation was just , OK, I'm responding to the
76:50 signals. But then, you I'm stopping, depression is, is
76:54 to habituation, but it is more line or opposite of facilitation. So
77:01 kind of a form of inhibition. why do we care? You
77:10 I mean, ultimately, I just you a bunch of words and you're
77:12 , so what, why do I about these different things? Because really
77:18 is how your body responds and your system responds to changes so that it
77:25 then govern how you behave and govern you respond to different sorts of
77:33 The thing is is when you this is what's going on, it's
77:37 and depression, we're increasing activity between cells or we're decreasing or we might
77:46 doing both simultaneously where if I'm the , I may potentiate here and depress
77:52 here and then change that relationship. so thoughts, ideas, behaviors,
77:59 are a function of the potentiation of that occurs my second movie and I
78:07 get the name, right? The Carrey. One spotless sunshine of the
78:11 mind or whatever it is, you , the real, you guys know
78:14 one I'm talking about but I never the title right? OK. Something
78:20 that. Eternal sunshine of the spotless . There it is just write it
78:26 . These are the movies you have see because reasons, in essence,
78:29 this movie, what happens Jim Carey this girl break up and the girl
78:33 to forget that she was ever in breakup or that she ever dated
78:37 And so there's a company that can in and erase memories and the way
78:42 they portray this is that memories are in individual neurons. And so the
78:47 is is that the the thought the is trying to escape the process of
78:53 and somehow Jim Carey knows that he's trying to be forgotten or something like
78:58 . It's a really interesting concept, it's completely false because that's not what
79:02 is. Memory is. The interactions multiple cells and the number of neurons
79:08 are involved and the firing that's happening between them. So when you experience
79:14 , you create this this pattern and pattern is what is reproduced. When
79:18 remember an idea, I know that's of weird. So for example,
79:23 of Statue of Liberty the first time learned Statue of Liberty, right?
79:28 you can now visualize, you can statue of Liberty, you created a
79:33 of interactions. And so that that is what is being reproduced so that
79:38 can remember that idea. And it's of these processes here, Tuesday,
79:46 have a test. Now why you say to that is because it means
79:51 class is a quarter over. You thought about it like that,
79:56 And then we get to move on some more interesting stuff after this because
80:01 now leveled the playing field and we're on the same page. So,
80:04 class on Tuesday, I'll see you Thursday. Go, get A's,
80:09 the weekend. It's not all about . I know you think it
80:13 but you got to have some fun . This. Uh-huh. Um,
80:19 then our, the
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