Health and medicine
- Myosin and actin
- How tropomyosin and troponin regulate muscle contraction
- Anatomy of a skeletal muscle cell
- Neuromuscular junction, motor end-plate
- Three types of muscle
- Type 1 and type 2 muscle fibers
- Skeletal structure and function
- Microscopic structure of bone - the Haversian system
Neuromuscular junction, motor end-plate
How do neurons talk directly to muscle cells? Learn about how a neuronal message is translated into a muscular action at the neuromuscular junction. By Raja Narayan. Created by Raja Narayan.
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- I thought that skeletal muscle did not have gap junctions. Only cardiac muscle?(36 votes)
- I'm glad that several others have picked up on this incorrect statement in the video....cardiac and some smooth muscles have gap junctions, but not skeletal (in general). Skeletal muscles (as organs) increase or decrease their contraction force by the nervous system adjusting the number of muscle fibers (cells) that are being activated at one time. This is called motor unit recruitment - each motor unit is made up of the muscle cells controlled by a single neuron. This is at least the second incorrect statement by this lecturer (Raja) - another is the incorrect notion that action potentials leave the axon at one node and then re-enter at the next node. Many students rely on these generally well done recordings to learn physiology - PLEASE get the facts correct....(57 votes)
- At about3:00"...to perform the worm...". What could that mean?(8 votes)
- He was referring to the dance move trying to be funny :)(2 votes)
- At5:00, nicotinic receivers are mentioned. Are those related to nicotine's addictive effects? It doesn't seem like nicotine or the lack thereof causes people to spasm, like a lack of calcium does...(5 votes)
- Nicotinic receptors are found throughout the body, not just in muscle. Nicotine-rich blood can reach the brain and stimulates neurotransmitter and hormonal release. Many studies have shown that this may occur in the "reward system" of the brain causing a sense of pleasure, leading to the addictiveness of nicotine. Nicotinic receptors are a type of cholinergic receptor. Acetylcholine (ACh) can bind these receptors and is the main ligand, however nicotine also can bind, hence the name. Moreover, another type of cholinergic recpetor is called muscarinic, because along with ACh it can bind muscarine.(16 votes)
- I know that in the video he said acetylcholine is a neurotransmitter, is it also a protein since it has to bind to the nAch receptor on the muscle membrane. My reasoning is that if it was a steroid it would diffuse through and would not require a receptor, or am I confusing hormones with neurotransmitters and am way off?(1 vote)
- No you are not way off, and that is a good way to think about it. If the compound is lipid-soluble or lipophilic, then it would most likely diffuse through the membrane and find its receptor intracellularly. Let’s think back to the beginning of its journey. Given that neurotransmitters are packaged into vesicles on the presynaptic side of the synapse, it would make sense that lipids or lipid-derived compounds would not be a category for neurotransmitters since such compounds would easily diffuse through the vesicles.
Neurotransmitters generally fall into the following categories: small-molecule, which include monoamine and amino acid, and peptide, which are larger in size. Monoamine neurotransmitters include serotonin, histamine, and the catecholamines (dopamine, epinephrine, norepinephrine). They are derived from aromatic amino acids, and the basic structure include an aromatic ring and an amine group. Amino acid neurotransmitters include glycine, GABA, glutamate, and aspartate. Peptide neurotransmitters include cholecystokinin and somatostatin. ACh, which is an ester of acetic acid (CH3COOH) and choline (+N(CH3)3CH3CH2OH), could be included under small-molecule.
Here is a link showing structures of neurotransmitters with the categories: http://www.ncbi.nlm.nih.gov/books/NBK10960/figure/A380/?report=objectonly
But yes, it is the hormones that are categorized as steroid, which are derived from the precursor cholesterol, and peptide, which are all chains of amino acids of varying lengths or glycoproteins. Sometimes they can be parsed into a third category monoamine, which as previously mentioned are derived from aromatic amino acids.(10 votes)
- At6:42, is it the change in membrane potential from both sodium and calcium influx that causes more calcium to be released from the SR?(6 votes)
- As this is working with muscles, would there be any adaptations over a period of time if you were to train? And would those adaptations differ if you trained aerobically in comparison to anaerobically?
Thank you(2 votes)
- Theres not a lot known about adaptations or morphing in neuromuscular junction in skeletal muscles during training. But, according to a study by Deschenes MR, training did produce hypertrophy in the neuromuscular junction and wider synapse clefts in the high intensity trained group in comparison to the low intensity trained. Training was not found to have altered densities of acetylcholine vesicles/receptors, nor did training affect change in synaptic coupling. However, nerve terminal branching seemed to have been affected as neuromuscular junctions from the high intensity training group shows lengthier and finer branching in comparison to the low intensity group.(4 votes)
- I have read that noradrenaline, as well as Ach can stimulate muscle contraction. Can you tell me on what occasions is noradrenaline used as a neurotransmitter? I know that noradrenaline is usually associated with the "fight-or-flight" response, could it be that it is used only when the brain tells the body there's danger? Also, it is thought that people under such circumstances can get greater performance from their body, for instance lift a heavy rock from their chest they couldn't have usually lifted. What is that due to?(3 votes)
- Noradrenaline as a neurotransmitter is released by a postganglionic neuron of the ANS and it can stimulate smooth muscles of the iris to increase the pupil size, when you are excited to see more for example. Also, you want to see more when there is danger to decide whether you need to fight or run away. At the same time, noradrenaline as a hormone can be released into blood by the adrenal medulla, an inner portion of the endocrine gland atop of the kidney. Its release is stimulated by preganglionic sympathetic fibers of the ANS, which is responsible for the fight-or-flight response associated with danger, excitement as well as embarrassment. Because the adrenal medulla releases the hormone noradrenaline into blood, it is carried throughout the body to target multiple organs and as such can have additive effect. At this point the release of Ach stimulated by motor cortex of the brain and targeting skeletal muscles helps you run away faster or fight harder.
Ach released by parasympathetic division however prepares you to relax and digest. It decreases the pupil size to dim the light when you prepare to go to bed, for example.(1 vote)
- I read this 5 times and i still don't understand, the rest makes sense but this.. "The mechanism of intracellular calcium being a trigger for release of even more calcium from the SR is the process that occurs in cardiac muscle, not skeletal muscle"(2 votes)
- http://dtch1d7nhw92g.cloudfront.net/content/ajpcell/308/9/C697/F1.large.jpg (skeletal muscle)
http://www.austincc.edu/apreview/NursingPics/CardiacPics/Picture12.jpg (cardiac muscle)
In cardiac muscle, calcium entering the cell or that is already present can induce more calcium release through the ryanodine receptor on the SR.
In skeletal muscle, the ryanodine receptor is connected to a DHPR protein also known as Cav1.1.
DHPR or Cav1.1 is a voltage-dependent calcium channel found in the transverse tubule of muscles. In skeletal muscle it associates with the ryanodine receptor RyR1 of the sarcoplasmic reticulum via a mechanical linkage. It senses the voltage change caused by the end-plate potential from nervous stimulation and propagated by sodium channels as action potentials to the T-tubules. It was previously thought that when the muscle depolarises, the calcium channel opens, allowing calcium in and activating RyR1 (as we would expect to occur in cardiac muscle), which mediates much greater calcium release from the sarcoplasmic reticulum. This is the first part of the process of excitation-contraction coupling, which ultimately causes the muscle to contract. Recent findings suggest that in skeletal muscle (but not cardiac muscle), calcium entry through Cav1.1 is not required; Cav1.1 undergoes a conformational change which allosterically activates RyR. - Wiki(2 votes)
- Does the sarcoplasmic reticulum have anything to do with the endoplasmic reticulum?(2 votes)
- Im sorry if this is a dumb question, im in 8th grade and we didn't really learn this in school, but where does the calcium and potassium come from in the synaptic cleft if only ACH passes through the cell(1 vote)
- It is not a dumb question, but I think a different area of Science would be a better place to start. My answer to you is that between cells we have extracellular fluids that contain calcium ions, potassium ions, sodium ions, bicarbonate ions and other molecules, it is called interstitial fluid. Inside cells, we also have these ions in different concentrations. https://en.wikipedia.org/wiki/Extracellular_fluid#Interstitial_fluid
I will look for a specific area that might help but here are some areas to look at:
Perhaps Biology would be better? This is Health and medicine at a college level.
Please look into a different area of science unless you really like a challenge. People like me began with courses that started with "what is a cell". :)(2 votes)
So when we're at a social gathering and we've determined that this is the most appropriate time to perform the worm, how does our brain tell our muscles to contract? Well, in this video, we'll talk about the place where neurons talk directly to muscles. That's the neuromuscular junction, the junction of where motor neurons talk to muscle cells. So that involves, first, the axon terminal. This is the end of an axon, which is the part of a neuron that casts a signal away. And it looks like this. It gets larger at the end right here. And then it tapers back off like that. Muscle cells sits adjacent to these axon terminals at the neuromuscular junction, and kind of look like a block, but not exactly. They have these in-foldings that I'm drawing right here, these in-pouchings. And why does nature cause in-pouchings to occur? What's the purpose of these guys? What function do they serve? Well, if you said that it serves to increase surface area, you're absolutely right. Because with the increased surface area, we're going to have extra space where we can have sodium channels present that will help us transmit a message into the muscle cell. And so it's not just present on the outside, but there are a bunch of sodium channels that are deep inside as well. And in addition to sodium channels, you definitely have calcium channels that are present as well. They are situated buried deep within your muscle cells, too, to make sure that the most deepest parts of your muscle cells will get an influx of calcium when it's the right time. And to foreshadow a point we'll discuss later, I'm going to draw another muscle cell right here, just kind of chilling out on its own. So now how does the axon send a message to the muscle cell? Well, if you recall, there's going to be a signal that's cast away from our motor neuron to this axon terminal. And that signal is in the form of an influx of sodium ions. So this is a depolarized membrane that propagates this signal to this axon terminal. But it's not just sodium that's influxing. You're also going to have some calcium that's running in as well. And the calcium here is actually going to play a major role. Because in our axon terminal, we have a bunch of vesicles that are sitting around in here. These are just little pockets that are waiting for something to happen. And in each of these pockets, we have a message that's waiting to be released into the space between our axon terminal and the muscle cell. This message is called a neurotransmitter, which is a very well-named scientific term. Because all this is is a molecule that the neuron uses to transmit a message. And so the neurotransmitter that we use in the neuromuscular junction is called acetyl-- like from chemistry, acetyl-- choline, acetylcholine. And oftentimes, you'll see it abbreviated as ACh. So when there's an influx of calcium into the axon terminal, what'll happen is that the calcium will actually bind to our vesicle. There are proteins that are on it that'll grab onto the calcium. And so when there's calcium attached to these proteins, the vesicle will be drawn to this axon terminal membrane and actually fuse with it to become one continuous membrane. As a result, we release the acetylcholine into this space we call the synaptic cleft. The synaptic cleft is just the space between our presynaptic membrane, the membrane of our axon terminal, as well as our postsynaptic membrane, which is just the membrane of our muscle cell. So this is our postsynaptic membrane. All right, and so we have a bunch of acetylcholine that's released into the synaptic cleft and is ready to send a message on. But let's take a minute here. What just happened here with the membrane? I mean, the vesicle literally became one with the membrane of the axon terminal. What would you call this, if you have to give it a name? Well, it looks like some compound within the cell exited the cell. So I'll say "exo." And it exited a cell, so a "cyte"-- exocytosis. Exocytosis, and that's the process of molecules, or substrates, leaving a cell by vesicles fusing with membranes. And so that's what we do when we want things to leave cells. The exact opposite process, where we have things enter cells by fusion of vesicles, is called endocytosis. And these are very important terms keep in mind. Great, so now we've got acetylcholine all over our synaptic cleft. What is it going to do here? Well, these sodium channels have receptors that sit on them that are called nicotinic acetylcholine receptors. And as the name suggests, acetylcholine can come and very snuggly sit here and send a message to this sodium channel that it's time to open and cause sodium to influx into our muscle cell. And that's going to happen across the membrane, causing a large amount of sodium to enter. And once we've depolarized the membrane enough, calcium will even start to enter. And so in this way, we'll have what's referred to as voltage-gated calcium release. All right, and so we have all this calcium that's entering the cell. Now what? Well, this is just one cell contracting. How does this make me able to do the worm, or to kick a ball, or to high five my best bro? Well, we can't just have calcium entering through the membrane. There's another reservoir within our muscle cells that releases calcium for our disposal. This reservoir-- kind of a large name, and I'll write it out right here-- is called the sarcoplasmic reticulum, R-E-T-I-C-U-L-U-M, sarcoplasmic reticulum. This guy holds a whole bunch of calcium. It's sitting in there waiting to be released, waiting to do something. So there are proteins that are attached to the membrane of the muscle cell. And they're just waiting for enough calcium to be present here so that one of these calcium cations could bind this protein complex and then effectively cause calcium to be released from the sarcoplasmic reticulum. This process is called calcium-induced calcium release. And so now we have a bunch of calcium in here, and this muscle cell will be contracting. But it's still just one muscle cell. What's the big deal? Well, this muscle cell is attached to its neighbor right here, actually. There are proteins that link muscle cells together. These proteins are called gap junctions. And they allow for cations to flow from one muscle cell into another. So these muscle cells aren't really separate at all. Actually, they're connected because of this gap junction and actually continuous. And there's a term that we use to drive home the fact that we can have our calcium cations move to this other muscle cell and to start a calcium-induced calcium release process here. And it's that our muscle cells are in a syncytium. What does that mean? Well, "cyte," just like we talked about her, just means a cell. And "syn" means that these muscle cells are in a synergy with each other. When one contracts, it causes its neighbor to contract as well, and that's how we scale up. Because when muscle cells start contracting as neighbors, you get the entire neighborhood contracting, because you can then scale up and imagine that not just muscle cells, but muscle fascicles will also be contracting, too, to produce a kick of a ball or the worm. So this signal that started from our axon terminal here that begins as just depolarization turns into an acetylcholine molecule that undergoes exocytosis to end up in the synaptic cleft, where it binds a nicotinic acetylcholine receptor to cause sodium to enter a muscle cell, and over time, calcium to enter a muscle cell, which would then cause calcium-induced calcium release, which can then go to an adjacent muscle cell to cause a synergy of muscle contraction that spans from muscle cell to muscle cell, from fascicle to fascicle. And that's what happens at the neuromuscular junction.