Neuromuscular Junction

hi everybody dr. Mikey in this video we're gonna take a quick look at the neuromuscular Junction now the neuromuscular Junction is basically the point in which a neuron speaks to a muscle to tell that muscle to contract if we want to be specific the neuron is going to be a motor neuron and the muscle is going to be skeletal muscle we know there's three different types of muscle right cardiac muscle of the heart and smooth muscle that lines the hollow organs here we've got skeletal muscle which is the muscle that's attached to the bones or the skeleton which allows for us to consciously move now what we need to do is this neuron needs to send a signal to this muscle and tell the muscle to contract now you can see that there is a space between the neuron and the muscle so something needs to cross this space we know that the signal from a neuron is an electrical signal and that the muscle won't accept an electrical signal it needs a chemical signal but it turns that chemical signal again into an electrical signal so what we have is an electrical chemical electrical signal that's happening so you all know well hopefully know a little bit about action potentials the way in neuron fires off and you know that there's an action potential being propagated across this membrane going down this neuron and what this action potential basically is is a whole bunch of voltage-gated sodium channels which are opening up in a response to a charge change so as that particular channel sodium channel opens up sodium which we know is specifically or most abundantly outside starts to diffuse in and because it's positive it makes the inside of this new membrane slightly positive which is actually the key to open up the next channel so what that means is a charge is responsible for opening a channel and this is called a voltage-gated channel and because it's for sodium it's called a voltage-gated sodium channel so the next voltage-gated gated sodium channel opens up in the next sodium makes that membrane positive opens up the next one and so forth and this domino effect of sodium moving in is basically the promulgation of a propagation of an action potential moving down the neuron now by the time it gets to the end of this neuron the charge change actually doesn't open a sodium channel the next channel it opens up is a calcium channel and calcium moves in to the neuron now here's the thing calcium is really good at telling neurons to release their neurotransmitters and the way it does it is because all of these neurotransmitters or neurons need to release a neurotransmitter that's the chemical that crosses the gap so what calcium does is calcium basically untethered these little bubbles that we call vesicles that are filled with neurotransmitters right there's going to be thousands of neurotransmitters in each of these vesicles and so what calcium does is it basically tells this vesicle to fuse with the membrane and when the because the vesicle is basically just a little membranous body and it fuses with this membrane and releases its components in this case neurotransmitters so what we've got so far is a sodium based action potential by the time it reaches the end of the neuron calcium comes in through a voltage-gated calcium channel calcium and tethers the vesicles that are filled with the neurotransmitter which we haven't said what it is yet the neurotransmitter is acetylcholine which we sometimes write as ACH like that and this vesicle binds with the terminal releases its contents and now we have the diffusion of a neurotransmitter specifically acetylcholine across this synapse all right couple of things what happens is when this neurotransmitter crosses the synapse it must bind to receptors specific for that neurotransmitter so if it's acetylcholine it must be acetylcholine specific receptors and there are two main types of acetylcholine receptors you have nicotinic and muscarinic now for skeletal muscle these are nicotinic receptors now Nikki tynix ounds like nicotine one of the components in cigarettes and this is how we determined that these are nicotinic receptors because nicotine activates them so this is one reason why I must kill effects when you smoke a cigarette so this acetylcholine will bind to acetylcholine specific receptors when it diffuses across this membrane and it causes this receptor to open up channels now these channels obviously open up so they gate is in a voltage their gate is a chemical and the chemical as acetylcholine so they're called ligand or chemically gated channels so settle choline binds flips the lid opens that channel up and what enters sodium sodium enters and we know again sodium is on the outside the cell and moves in so now I've got all this influx of sodium on the inner membrane of the muscle and what that means is it depolarizes which means it goes positive again just like the action potential were talking about before and this influx of sodium actually travels down the muscle cell and what you'll see is because when the muscle contracts we don't just want the membrane of a muscle to contract we want deep in the tissue of the muscle to contract because we've got all this contractile fibers are out there's myofibrils what are called sarcomeres they're the contractile unit of muscle we want it to contract and they're deep inside the muscle so we need channels that go deep inside the muscle these are called t tubules and so there's going to be all these sodium channels all the way across right all the way across even down these t tubules and the sodium is going to enter again it's gonna do that Domino like effect where sodium comes in now what happens is this as it the membrane depolarizes you've got this little area here called the Sarco plasmic reticulum which sounds like the endoplasmic reticulum and it's basically the endoplasmic reticulum of skeletal muscle sarcoplasmic reticulum and all you really need to know is it contains calcium now I did calcium in red up there I'll do calcium red here in skeletal muscle calcium is stored in the sarcoplasmic reticulum all right when the sodium comes in and depolarizes this triggers the sarcoplasmic reticulum to release calcium so now we've got all this calcium released now why do we want calcium released deep inside the muscle cell because calcium is the key that allows for muscle to contract in what way here we've got the two myofibrils that allow for contraction this whole thing here is what we call a sarcomere and we've got myosin which is what we call the thick filament and we've got actin here which is the thin filament now what we want are these little heads on mice and to bind to the actin and what it does is it binds to it and pulls it in so we get a shortening of these myofibrils the myosin head bonds to the actin and they walk their way along by pulling it like this like you're pulling a rope right and that's what it does short and shorter and that's how you the tower muscles contract it's shortening of these fibers what calcium does is there's actually a chain that's on this actin like a bike chain which locks the actin up and doesn't make it accessible to the mice and heads so the calcium comes in unlocks this chain and now the myosin heads can bind to the actin if ATP is present so ATP is also required so the two things you need for muscle contraction calcium and ATP so Teredo to reiterate this process what's happening is an action potential is moving down a neuron where sodium influx is occurring the sodium comes in when it hits the end it opens voltage-gated calcium channels they tell the vesicles to release acetylcholine thousands of acetylcholine molecules an actual fact it's probably about 10,000 per quanta right and there's probably a hundred thousand in the reserve pools that sit behind so there's heaps all this acetylcholine diffuses across binds to acetylcholine receptors specifically nicotine they open up these ligand-gated sodium channels sodium influxes depolarize the membrane causes the sarcoplasmic reticulum to release all of its stored calcium deep within the muscle cell calcium is the key that unlocks the chain that's wrapped around actin so that the myosin heads combined and with ATP the myosin will bind and pull on that chain and what we get is a shortening of the skeletal muscle cell there a couple of important points here this gap is 15 nanometers the synapse here is only 50 nanometers that's nothing right it's a very very narrow gap but in saying that when acetylcholine is released how long do you think it has in order to bind to its receptor to initiate sodium influx it has 1 milli second to do that one millisecond your question may be what happens after one millisecond there is a molecule which eats up acetylcholine in this synapse and this molecule is called acetyl choline esterase an acetylcholine esterase eats up acetylcholine molecules and forces them to be recycled back into the pre synaptic terminal of that neuron so it could be released again it has 1 milli second to do its function before it's gobbled up and thrown back in so a couple of things there are things called muscle relaxants right there's muscle relaxants they tell the muscles just to relax and there's two major types right there's a muscle Reluctant which comes in and pretends to be acetylcholine comes in pretends to be a set of choline binds to the receptor sodium comes in depolarizes the membrane calcium is released and the muscle converts but usually after 1 millisecond that acetyl kahlan's degraded but this drug right called succinylcholine right this drug lasts longer than acetylcholine so isn't degraded so that means this membrane remains polarized sodium stays in now the calcium has done its job right because the thority depolarized calcium's come in muscles contracted but this remains the polarized and doesn't reset like it normally would when acetylcholine jumps off sodium will be thrown back out and you reset the membrane you can't tell that muscle to contract without that depolarization but if that remains on Sonia remains in and it doesn't reset but the calcium gets thrown back in independent of that depolarization and the calcium jumps back in here so the muscle relaxes but can't be triggered again to contract because it's remained depolarized so that muscle becomes flaccid so with succinylcholine what you first get is muscle contractions called fasciculations immediately followed by paralysis and that's how these cynically Sassoon or choline I should say works often used as in anesthetics or operations now you've also got a touch so that's what what we call a depolarizing muscle relaxant but there's nondepolarizing muscle relaxants non depolarizing muscle relaxants that work as well which means they don't bind and cause this depolarization event what they do is they will bind to these acetylcholine receptors and inhibit acetylcholine from binding which just means that no depolarization occurs no calcium release occurs no contraction occurs all right so you've gotten you've got nondepolarizing muscle relaxants now in order to reverse these there is a particular drug that can be given and what this drug does is it gets rid of these pseudo choline esterase a--'s and that means the acetylcholine can now competitively bind against these nondepolarizing muscle relaxants and pop it off and then the acetylcholine combined and the muscle could contract okay so what we've gone through is a very quick run through a relatively quick run through of the neuromuscular Junction

Channel: Dr Matt & Dr Mike

Views: 5,245

Rating: 4.964602 out of 5

Keywords: neuromuscular, junction, acetylcholine, skeletal, muscle, ach, contraction

Id: ApaPlKPb4ek

Length: 13min 8sec (788 seconds)

Published: Sun May 03 2020