Transcript for:
Understanding Muscle Relaxation and Physiology

All right, NingeNerds, if you guys are back for the fourth and final video, thank you guys for watching these. I really appreciate it. What we're going to try to finish up in this last video here is we're going to talk about the relaxation point, okay? How the muscle is relaxing. So thank you guys again for sticking in there with us and watching all these videos.

I hope they really make sense. Okay, so where do we leave off? We talked about specifically how the muscle contracted, right? Now let's talk about what happens whenever the muscle starts going into a relaxation state.

Now, where were we at on this graph up here? So on that graph, where were we at specifically at the peak point of contraction? So if you guys remember here, time on the x-axis in milliseconds, and then voltage in the form of millivolts on the y-axis.

We were up here at this top point right here, right, at positive 30 millivolts. And this was due to the voltage-gated sodium channels opening. And then the calcium. calcium was flooding in from the sarcoplasmic reticulum. Once we hit positive 30 millivolts, something really cool happens.

Let's look at these green channels for just a second. Okay, now these green channels are specifically called voltage gated potassium channels. Now like the sodium channels.

Certain literature will say that these have activation gates and inactivation gates. Okay? Now, in the same situation, the activation gate of this potassium channel is closed normally.

But, during this... actual contraction period but whenever you reach this peak potential that positive 30 millivolts so once you reach about positive 30 millivolts this activation gate of the potassium does what it opens right so if this potassium this activation gate opens whenever you reach peak potential or positive 30 millivolts, the peak point of the action potential. These activation gates of the potassium channels open.

Now, if that is the case, what is the concentration of the potassium inside of this actual muscle cell? It's in much, much higher concentration than it is outside of the muscle cell. So normally, if that's the situation, potassium will want to move. out of the cell.

And it's going to want to move out of the cell very, very fast and very quickly. You want to know why? Because it's what's called NERTS potential. And it loves to be able to move out until its equilibrium potential or NERTS potential is equal to his potential, which is almost about negative 90 millivolts, which is perfect because that's the resting membrane potential of this muscle cell. So potassium starts moving out, but here's another cool thing.

At positive 30 millivolts, it stimulates this gate. Again, what is this gate here called? It stimulates the activation gate. So this activation gate is stimulated to open by positive 30 millivolts, peak potential.

At the same time, it also stimulates this inactivation gate. And when this inactivation gate is stimulated, it starts slowly closing. And at what point does it completely close?

It completely closes whenever you reach... this resting membrane potential. We'll talk about that in just a second, but I want you guys to remember that this peak potential is also stimulating the inactivation gates. The activation gates open quickly. The inactivation gates close very slowly.

Okay, before we keep going into the activation gate, let's talk about what else is happening. But for a second here, I want you to realize if potassium ions are leaving the cell, that means positive ions are leaving the cell. If positive ions are leaving the cell, what starts happening to the inner side of the cell?

It starts losing positive charges. So eventually, some of these positive charges start dissipating, and the cell starts becoming a little bit more electronegative. If the cell starts becoming a little bit more electronegative, what will that show on the graph? Well, it looks like it's going down. And if it starts dropping and dropping and dropping...

This is called the repolarization phase. And this repolarization phase, due to this whole action potential event, is actually due to potassium ion efflux. But do you know that's not the only thing that's contributing to it? What was happening with this calcium during the contraction? Remember calcium was bound onto the troponin, specifically the troponin C, which moved this whole tropomyosin out.

Whenever we reach this peak potential, calcium says, Okay. I can't be out here anymore. The sarcoplasmic reticulum is whistling to tell me to come home. So I got to go home. So calcium tells troponin I got to go.

So calcium then leaves troponin. So look at this. Calcium leaves troponin. Okay, same thing over here, calcium will not bind to troponin and will leave troponin.

If it leaves troponin, then what is that going to do? That means, let's come back up to this little portrait here, if calcium is no longer binding, if calcium doesn't bind, then this troponin molecule will pull away from that troponin T. And then what will happen is the tropomyosin as a response will move. Where will it move?

it'll move back into its original position, its resting position, and that'll be blocking the myosin heads. And now the, I'm sorry, blocking the actin active sites so that the myosin heads can't bind in. So again, when calcium leaves, troponin actually, then actually prevents this tropomyosin from being prevented from blocking these active sites. So when calcium leaves, then troponin moves the tropomyosin back into its actual relaxed position, which blocks the actin active sites. and prevents myosin from binding in.

And it also will happen over here. And then look what will happen. This actual tropomyosin will block the active sites of the actin. And myosin can no longer bind because the cell has to rest.

Our muscle cells need to rest because if not, they're going to be pushed too hard. And that's good for certain situations like hypertrophy of the muscle. But whenever there's consistent hypertrophy of the muscle, the muscle starts to become very fatigued and eventually it can become weak.

And if that's progressive over time, it can cause muscle damage. So we need the muscles to relax. So now the calcium leaves. The question is, where does it go? Remember I told you the sarcoplasmic reticulum is like, hey, buddy, come home.

We need you guys to come home. So calcium is going to come over here. There's two special transporters on the sarcoplasmic reticulum membrane. One of them is really cool.

Let's draw the actual calcium over here again. So let's say here's our calcium ions. and they're getting called back home, right? This calcium is going to get pulled into this channel, right? It's going to get pulled into the sarcoplasmic reticulum.

But here's the thing. In which area is calcium more concentrated? Is it more concentrated here or out here? Generally, I told you that this is a storage of calcium. Lots of calcium in there.

And what prevents all this calcium from leaving excessively is calc sequestrant because he concentrates them. So the calcium concentration inside of this sarcoplasmic reticulum should be higher than the calcium concentration out here in the sarcoplasm. So that means it's going to have to go against its concentration gradient.

If something has to go against its concentration gradient, what does that require? It requires ATP. So in order for me to do this, this step right here requires ATP.

Now, here's another thing. This transporter not only transports calcium in, but guess what else it can do? It can transport potassium, sorry not potassium, protons out into the sarcoplasm.

That's one thing that can happen. Okay? So one thing that can happen is we're transporting calcium in and transporting protons out, okay? And utilizing ATP.

But that's not the only way we can do it. Another way we can do that is we can try to bring this calcium in, look at this calcium. He's going to try to come in through this channel. So there's many, many options for this guy. The calcium can also come in through this channel, into the sarcoplasmic reticulum.

But in order for that to happen, it has to go against its concentration gradient. So what happens? You know there's sodium ions?

And you know sodium ions are in very low concentration inside of the cell? Very low concentrations inside the cell. But they happen to be in a little bit more higher concentration.

inside of the sarcoplasmic reticulum. So what happens is sodium has the ability to move out and when it moves out it helps in assisting the calcium to come in. So this is an example of secondary active transport.

So this is secondary active transport. So this is called a sodium calcium exchanger and this is called a calcium ATPase pump. Okay, so what are these two proteins?

Calcium ATPase pump and sodium calcium exchanger. And it's pushing the calcium back into the sarcoplasmic reticulum. to prevent what?

Why don't we want calcium out here? Because if calcium is present, what does it do? It binds onto troponin, which changes the shape of the triple myosin and causes myosin to keep causing contraction. We don't want that.

We want the calcium to be out of here so that the muscle... muscle can relax but remember I told you that potassium is not the only thing contributing to that repolarization state you know what else can contribute to it these protein channels and you're gonna love this because guess what these protein channels are exactly the same as these ones so guess what if I want to bring so Sodium ions in. Okay, low sodium concentration inside of the cell, high sodium concentration outside the cell. So what would happen?

This sodium would want to move down his concentration gradient, which would help to get the calcium pushed. against his concentration gradient because there's low calcium inside of the cell and higher amounts of calcium outside the cell okay so calcium will go against this concentration gradient and again this is an example of secondary active transport Now the thing is, this one actually transports a little bit more sodium in. It's not significant, but about three sodium ions for every one calcium. So it's not the main one that's contributing to this actual repolarization state.

What is, though, a little bit, is there's another one. And it's the same concept, calcium. It's going to be moving out. But if I want to move the calcium out, I'm going to have some protons coming in. But again, both of these are going against their concentration.

gradients so this requires the use of ATP and if we convert ATP into ADP and organic phosphate this is an example of primary active transport But nonetheless, a little bit of positive ions are leaving here, so it can contribute a tiny, tiny little bit to this repolarization state. But I want you guys to remember, the main ion that is contributing to the repolarization state is potassium. Calcium, he is... leaving but he's not the main contributor he only contributes a tiny little bit to the repolarization state him getting pumped back into the sarcoplasmic reticulum and getting pumped out of the cell then I told you I was gonna explain what happens with this inactivation gate so let's do that now we said that this inactivation gate okay so this is the ball and chain the ball and chain model is supporting that this is the inactivation gate When we hit peak potential, positive 30 millivolts, this inactivation gate is stimulated. And I say that it starts slowly, slowly, slowly, slowly closing.

When does it finally close? This sucker right here finally closes whenever you reach. Resting membrane potential.

So when you reach resting memory potential that ball blocks the potassium channel and then the potassium cannot leak out. So if potassium can't leak out then what starts happening? The resting membrane potential kind of stays at that point there because we help to keep it at negative 90 by having the sodium potassium ATPase pumps and the potassium leaky channels to keep it at about negative 90 because we don't want it to overshoot.

Sometimes there is a problem with the potassium channel. can be a little bit of an overshoot. Not as common though.

It is a little bit more common in the actual neural tissue because potassium can leak out a little bit more, a little bit faster. And so that in neurons it can drop down a little bit to about negative 90 because their resting membrane potential is usually negative 70. But again at peak potential, action potential, the inactivation gates are stimulated and they start slowly closing and they finally close at resting membrane potentials to negative 90 millivolts and then the potassium cannot leak out of the cell. Once it's at that point, the cell will rest. And this takes a decent amount of time. Because you want the muscle to contract and you want to have a decent amount of time for it to rest and get prepared for another stimulus.

So that when another stimulus comes, what would happen? Eventually you would have acetylcholine release, in-plate potential, voltage-aided sodium channels open up. That will have the action potential and then potassium channels open. And then that will be your repolarization.

And it's the whole same. It'll just keep happening. And that's what's going to lead to the contraction of the actual skeletal muscles. Now, we covered the repolarization point. Now, I want you guys to think for a second.

If this calcium leaves and the troponin then is no longer pulling on the tropomyosin and the tropomyosin goes back into its relaxed state, blocks the myosin heads from being able to bind, what will happen to the actual sarcomere? Well, if you think about it, won't these thin filaments start going back and relaxing back to their normal point? Yes.

So shouldn't the H-zone go back to its normal spot? Yeah, it should reappear. The Z-discs, at one point they were really, really pulled closer to one another. Shouldn't the Z-discs return back to their normal point? Yes.

The A-band stayed the same, nothing happened with him. But what happened to the I-bands? Well, because we were pulling the Z-discs closer together, we were pulling the stent filaments closer together, the I-band also decreased in size. But whenever we relax it, the I-band should go back to normal position.

Alright guys, so it's really important to know the physiology of how the muscle is contracting and all of these action potentials and neurotransmission. But you know what's even more important? It's really important to understand the clinical correlations.

What can happen when certain systems like this break down? Because that's where good doctors and good PAs and good nurses and just good medical students in general come from. Okay?

So let's go ahead. I want to talk just briefly. I don't want to spend a whole bunch of time because this is... It's not a patho video, but we're going to specifically talk a little bit about a condition called myasthenia gravis.

And then I want to talk about another one that's very similar to it. It's clumped under like a type of myasthenia gravis. It's called Lambert-Eaton syndrome.

And then I want to talk about certain types of conditions like certain toxins. So I want to talk about certain toxins. And the toxins that I want to discuss with you, because it's all relevant, is the tetanus toxin.

I want to talk about the tetanus toxin. I want to talk about another one, which is called the botulinum toxin. I want to talk about adendrotoxin.

And then I'm going to talk another one about what's called the bungarotoxin. Okay, specifically the alpha type. And then we'll discuss at the end, we'll talk about another thing, I'll come back up here.

We'll talk about certain drugs, mainly that of succinylcholine. All right, because all of this is really relevant. We want to understand how pharmacologically, pathophysiology wise, how this can be affected. So let's start off first with myasthenia gravis.

Myasthenia gravis is considered to be an autoimmune disorder. And And what happens is, remember these nicotinic receptors? They have such a high affinity to bind onto these nicotinic receptors.

So to do this, some unknown cause, this actual myasthenia gravis is going to be having the actual immune system. producing antibodies against its own tissue. So it's an example of a hypersensitivity, right?

And if it's intrinsic to the tissue, intrinsic to the own tissue, that's a specific type of hypersensitivity. We'll talk about that in immunology. But look what happens here. Let's say here I have in green these antibodies. So here is this myasthenia gravis antibody, and it's acting against this actual nicotinic receptor, specifically where the acetylcholine binds.

So let's get rid of this acetylcholine now. If that's the case, if it binds on to this point, can the acetylcholine bind? No. So if acetylcholine can't bind, can we have any of this activity even occur?

No. We can't produce end plate potentials. Therefore, we can't produce action potentials.

Therefore, we can't release calcium. Therefore, contraction can't occur. That is not good.

So there's going to be an exhibiting paralysis, right? This is one of the dangerous situations is that if you can't stimulate this muscle, what's going to happen? over time to this person it's very progressive and so because of that if they don't have the acetylcholine binding onto these muscle cells the muscles become extremely extremely weak and that is one of the dangers of myasthenia gravis okay so again we're not going to go over all the symptoms and diagnosis we just want you guys to understand what is happening in myasthenia gravis is that it's an autoimmune disease where antibodies are produced against the own tissues specifically that of the nicotinic receptors of the actual scalp muscles so the type 1 and it binds there blocks acetylcholine from being able to bind and therefore the muscle cell cannot be stimulated and this will cause progressive weakness and eventually these people don't have the ability to walk and usually have that wheelchairs that they just have a lot of different terrible problems and it's unfortunate so that's myasthenia gravis now Lambert Eaton syndrome produces very similar symptomatic manifestations just a little bit different in the way that they're progressing we're not going to go into that again though but I want you guys to understand what it's doing. See this calcium channel right here? This calcium channel, this voltage sensitive calcium channel, what was it responsible for doing?

For coming in and causing what? Causing the synaptoproteins, the SNAP25, the synaptobrevin, the synaptotagmin, the syntaxin, all those proteins to fuse together. If this calcium doesn't come in, can the synaptic vesicle fuse with the cell membrane? No.

There's another condition, similar though. It's autoantibodies. You're having these antibodies and these antibodies are coming and blocking this channel. If this channel is actually having this antibody bound to it, right? So let's show that we have this antibody bound to it.

If that happens, can this calcium come in? No. And if calcium can't come in, can the actual synaptic vesicle fuse with the actual synaptic bulb membrane? No.

Can acetylcholine get released? No. And if acetylcholine is not present, isn't it similar to that of the myasthenia gravis? Yes.

And it causes similar manifestations, progressive weakness in the actual muscles. And that can become very, very scary because one of the skeletal muscles that is very important for us is our diaphragm. And the diaphragm is extremely important because it controls our actual breathing, specifically inspiration and a little bit of expiration, right? So because of that, if we have any damage to that, it can lead to respiratory failure, the ability not to breathe. as well as affecting a lot of the other muscles that control swallowing.

So it's very dangerous, very, very dangerous. Okay, so that covers Lambert-Eaton syndrome. Now, what's interesting is something else that's really important.

Okay, you know, we didn't talk about this. Shame on me. There's a specific enzyme, a special enzyme.

We didn't talk about what happens when acetylcholine is actually done binding to this receptor. What happens to this actual acetylcholine? Does it just disappear?

No. No. There's a special enzyme, and this enzyme is called acetylcholine esterases.

And what acetylcholine esterases do is they break down acetylcholine into its individual constituents. What were the individual constituents of acetylcholine if you guys remember? Remember acetylcholine?

It was specifically going to get broken down into its individual components which were acetate and... choline. Alright?

Now what's important about that? You don't want acetylcholine to just stay in this area forever and just continuously stimulate in the muscle cell. So we have to prevent that from happening. So how do we do that?

We have these acetylcholine esterase enzymes. They're normally in our muscle cell synapse. And what happens is acetylcholine esterases are constantly breaking down this acetylcholine into its individual constituents, acetate and choline. And then what will happen?

Well, remember we have choline channels. We can bring the choline in through these actual specials. special transport proteins. And then the acetate can actually be brought up through special mechanisms also. And we can refuse them together through the choline acetyltransferase enzyme, which we didn't really mention, but we know specifically it's right here, the choline acetyltransferase enzyme.

It's involved in this step right there. Okay, so that's important. Now, if you guys really are interested in this, you probably wonder, okay, what do they do to treat these people? And there's not a cure, but there is a little bit of a treatment to slow down the progressive weakness. And And what they can do is they can try to keep the acetylcholine as high and abundant as possible in this area.

What would you want to do then? Wouldn't you want to inhibit this enzyme? Yes. So there is drugs that they use to treat this acetylcholinesterase enzyme.

These drugs are specifically called phyzo, stigmine, and neostigmine. Okay, these drugs are specifically acetylcholinesterase inhibitors. So if you inhibit this acetylcholinesterase enzyme, what is it going to do now?

It's not going to be able to break down acetylcholine into choline and acetate. So what happens to the acetylcholine? It's more concentrated.

And eventually it can displace some of these actual antibodies and allow for the acetylcholine to bind so that we can still have muscle contraction. So that's one of the cool things. Another terrible thing, you know, people have come up with different ways of, you know. making society terrible you know there's what's called sarin sarin is actually a nerve gas and you know chemical warfare kind of stuff right there and what it can do is it can actually irreversibly bind to this acetylcholine esterase and if they're irreversibly blind so that acetylcholine esterase it can no longer break down the acetylcholine and this person usually dies very very quickly okay usually due to respiratory paralysis and other problems so yeah that's that's that enzyme okay so now that we covered that let's talk about something else we talked about Lambert eaton said and we've talked about myasthenia gravis and we talked about how you can try to treat it physostigmine and neostigmine which inhibits the acetylcholine esterase enzymes tries to slow down the progressive weakness and then terrible sarin nerve gas okay let's briefly talk about this drug succinyl succinylcholine and it's just trying to relate clinical aspects to it succinylcholine is actually a drug that they use with general anesthesia so whenever they're doing what's called a tracheal intubation so they're trying to intubate somebody Sometimes you want to relax those muscles that are responsible for controlling the actual trachea size and all the other structures around that area. So because of that, you don't want them to be contracting while you're trying to put a tube down their actual trachea, right?

So whenever you're trying to intubate someone, you want to relax. those muscles and so this drug here called succinylcholine does that you know how it does it it's really cool I really think this is amazing it's really cool so let's say here this is acetylcholine right now what I'm going to do is I'm going to have this succinylcholine And what succinylcholine does is it binds on and acts like an agonist basically to the acetylcholine. So it binds on to this actual receptor domain and stimulates this actual in-plate potential.

But here's the thing. It causes a very long and prolonged and drawn out action potentials or in-plate potentials. And if it continuously keeps generating more and more and more in-plate potentials, what happens is it eventually leads to these sodium channels.

Remember these. The sodium channels it eventually causes these sodium channels To start closing a little bit earlier than normal and so now sodium doesn't come into this actual muscle cell as much and Eventually what happens is muscle so if sodium isn't coming in as much then what happens? Then this muscle cell won't be able to generate an action potential And if it can't generate an action potential, it can't release calcium. If it can't release calcium, will the muscle contract? No.

And that leads to the passive relaxation of the muscle. So again, quickly, succinylcholine is binding onto the nicotinic receptors, and it's preventing a very prolonged and consistent and drawn out in play potential that eventually causes the inactivation gates to close earlier than normal and if it closes and it stays almost temporarily and it stays almost temporarily closed for a certain amount of time it will no longer allow for the sodium ions to come in and if sodium can't come in an action potential won't occur if an action potential doesn't occur you cannot release the calcium ions and the muscle will not contract okay so these are the big ones that I wanted to talk about now I want to talk very very quickly, not going to spend a lot of time on these, I want to talk very quickly about the tetanus toxin and the botulinum toxin. We're going to do it over here in this corner.

Okay, so remember I mentioned all these proteins. There was a reason why I mentioned all these proteins. I remember I told you guys that if I want you to remember at least specifically what proteins, at least remember Syntaxin and Synaptobrevin.

And there's a reason why. These proteins can be attacked. Snap 25 can be attacked also, too. But I want you guys to remember something.

You have this toxin here called the botulinum toxin. Now, me, I like to know where the heck these toxins come from. That's just how my mind thinks.

I like to know that the botulinum toxin comes from the body. botulinum toxin comes from certain types of anaerobic conditions. So if you guys like that canned food like the dentimore beef stew, hey that's great, but there's a chance that there's botulinum toxins in it, right?

Now that's not always the case, you know, enjoy your dentimore beef stew. But this botulinum toxin, what is it gonna do? It actually inhibits these proteins.

So it inhibits the contact of synaptobrevin and syntaxin. If synaptobrevin and syntaxin are not going to be joined together then what happens then you can't cause the actual fusion of the synaptic vesicle with this the actual synaptic bulb and then you cannot release acetylcholine if you cannot release acetylcholine what happens to the muscles they become paralyzed and that's what they use for Botox so you know what they use for Botox they use botulinum toxin so if you're a 50 year old trying to look like a 26 year old you get the Botox right however I don't think Botox works that great sometimes it can get too bad and you look like a 28 year old lizard but anyway botox right what is it doing it's specifically going to be acting like this botulinum toxin and inhibiting these synaptobrevin proteins and syntaxin proteins from fusing together preventing the release of acetylcholine same thing is true for the tetanus toxin however like i said we're not going to go into extreme detail here but tetanus toxin is also doing the same thing it's inhibiting the fusion of these proteins So therefore, acetylcholine can't be released. But it also does something else.

In our actual spinal cord, we have special, remember, oh, look here. Hmm. I forgot we had this.

All right. There's other neurons here. There's other neurons here.

And these neurons are. releasing what's called GABA, gamma-aminobutyric acid, which tries to inhibit these motor neurons and prevent these action potentials. But what the tetanus toxin can do is not only can prevent the release of acetylcholine, but the tetanus toxin inhibits these GABAergic neurons. If these GABAergic neurons can no longer release GABA onto these guys what happens?

They're gonna be hyper stimulated. But the problem is that we can't release the acetylcholine. What happens to these people?

Not only do they have paralysis but they have what's called a spastic paralysis. Now this doesn't happen in everybody but what can happen is there's a condition whenever the paralysis becomes so bad that the muscles contract very very strongly and simultaneously that sometimes depending upon the power of that contracture right there it can cause the actual some of the bones to fracture that's how intense the tetanus can actually be but some of you might have heard of lockjaw keeps it stuck into that position it's a spastic paralysis okay so we talked about the botulinum toxin and we talked about the tetanus toxin now I'm going to talk about these ones because I like snakes snakes are pretty cool and dendrotoxin and bungarow toxins are venom from the snakes so specifically the dendrotoxin comes from the black mamba. Okay, so the black mamba is a very venomous snake. And whenever it actually bites, it releases out this dendrotoxin.

What this dendrotoxin does is, is let's come, let's actually do it right, no, we'll do it over here. Over here you have these specialized channels. Okay, you see these green channels?

These green channels, you know whenever the actual neuron has to relax and prevent the release of acetylcholine, we have to bring the membrane potential back down to resting membrane potential in here too. So who controls that? Potassium, right?

Potassium leaves out through these channels, these voltage-gated potassium channels. Okay. This dendrotoxin though inhibits these channels. So if you give, if someone is actually bitten by this black mamba and the dendrotoxin is released, what can it do?

It can inhibit the release of potassium through these voltage-gated potassium channels. Now here's the question. How is that even related to all of this? If potassium can't leave, what happens to the inside of the cell membrane? It remains positive.

If it remains positive, what can keep leaking into this actual... synaptic bulb calcium and if calcium keeps leaking in what happens to this actual synaptic vesicles they start continuously fusing and releasing acetylcholine and this can cause the person to cause massive amounts of acetylcholine release we can cause a lot of problems one of those big things with the dendrotoxin is it can lead to what's called convulsions okay So you'd have to give them the antivenom as quickly as possible, right? Now, last one that we'll talk about and we'll finish it all up is the bungarotoxin, but specifically the alpha-bungarotoxin.

And the alpha-bungarotoxin is coming from the cobra, okay? The cobra bites. So the cobra... is a beast, okay?

And what the cobra can actually do, whenever it bites, it can release this bungarotoxin, the alpha-bungarotoxin. And if you remember how the myasthenia gravis was working and the succinylcholine was working, you know exactly how the alpha-bungarotoxin is working. What it does is, imagine here in blue, I take this bungarotoxin and I block off this channel, okay?

And if I block off this channel, can any of the sodium ions come in? Can any of the potassium ions go out try to trigger an in plate potential no and so that's one of the damaging things that can come from an actual Cobra bite is again you're not going to be able to generate in plate potentials you can't generate action potentials and the muscle can't contract so it causes a paralytic effect okay all right engineers we covered a heck of a lot of information throughout the series of these muscular contraction videos I hope it all made sense I really do hope you guys enjoyed it if you guys stuck in through all of these videos I appreciate it so much guys I hope you guys enjoyed it if you guys did please hit the like button subscribe, put some comments down in the comment section. Look forward to hearing from you.

All right, Nudge Nerds, until next time.