Explore the role of the sarcoplasmic reticulum in muscle cells, crucial for muscle contraction and relaxation. Learn how calcium ions are regulated, triggering muscle contraction when released into the cell's cytoplasm. Understand the interaction between troponin, tropomyosin, myosin, and actin, and how the nervous system controls these processes. Created by Sal Khan.
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- how about hypocalcemia (low calcium levels in the body)? its cardinal sign is having muscle spasms. how does that happen when low Ca++ levels actually means relaxation?(42 votes)
- When extracellular Ca2+ concentrations fall too low, the nervous system becomes more excitable as it become more permeable to sodium ion. When extracellular Ca2+ concentrations fall to ~50%, spontaneous action potentials occur, causing tetany due to an overactive Peripheral Nervous System. Seizures may also occur.
Hope that helps!
Ryan Grannell, 2nd Biochemistry(56 votes)
- Where do the Calcium ions in the Sarcoplasmic Reticulum come from?(8 votes)
- We have discussed in NCRT that ca++ ions enter the sarcoplasm when an action potential is generated in the neromuscular jun. and binds the sub-unit of troponin and remove the masking of active sites, and myosin binds the actin when an energy is produced aft ATP hydrolysis.but in your vedio you have said that ca++ enter into the sarcoplasmic reticulum when ATP hydrolysis takes place . can u please explain this ?(vedio-4:42-4:59)(6 votes)
- @12:05, when you say that Ca2+ is released out of the sarcoplasmic reticulum, and into the inside of the sarcolemma, wouldn't the +ve Na+s repel them? So not many Ca2+ can leave the SR.(6 votes)
- That's an excellent question. Mostly it happens because the Ca2+ concentration in the cytosol is very, very low at rest - on the order of nmol/L, typically. This means that the Ca2+ concentration gradient (and equilibrium potential) is usually particularly big, and that it doesn't take a lot of calcium to greatly increase a very low initial concentration. For the cells, putting the Ca2+ back into the SR is much harder than getting it back out, and means a lot of extra work for the sodium-calcium exchangers and the Na+/K+-ATPases to reestablish the initial concentration gradient.(6 votes)
- I have two questions. 1. How would you compare a vesicle to the Sarcoplasmic Reticulum?
2. How does a vesicle actually store things inside it? Does it have pumps to draw things inside it?(5 votes)
- 1. Not all membranes are the same! Vesicles and sarcoplasmic reticulum have different membrane protein compositions. Exocytotic vesicles / synaptic vesicles I think are clathrin coated so that they do not fuse with the synapse membrane until signaled. Sarcoplasmic reticulum has those Calcium pumps as stated to concentrate and store Ca++, and have that protein bridge that is under study.
2. Vesicles are packaged from the endoplasmic reticulum to Golgi apparatus to vesicle form. If there is a protein to be stored in a vesicle, that protein is actually synthesized/translated directly into the pre-vesicle by bound ribosomes on the ER ("rough" ER). Not sure about non-protein things, though.(4 votes)
- What is the proper function of the sacroplasmic reticulum in a muslce contraction?(2 votes)
- The sarcoplasmic reticulum releases calcium ions during muscle contraction and absorb them during relaxation.(6 votes)
- What role does the sarcoplasm reticulum have in sarcoidosis? I have sarcoidosis, with calcium present in my lungs.(4 votes)
- Muscle involvement in sarcoidosis is rare and usually asymptomatic.
Look at this one:
Sarcoidosis is a granulomatous disease of unknown etiology that involves multiple systems. It most commonly affects the lungs, lymph nodes, skin, and eyes but can also affect other organs and systems, including the musculoskeletal system.
Meaning that it is not known whether sarcoplasmic reticulum plays a role...
Do Actin, Myosin, troponin and tropomyosin remain inside the muscle cells?
I mean, if they remain in the cytoplasm of muscle cells, then why would contraction/relaxation of actin cause net movement of the muscle cell?
Consider, for example, kicking your friend sitting on a plane next to you, doesn't affect the plane.(3 votes)
- Actin, myosin, troponin and tropomyosin are all parts of the sarcomere. The sarcomere is the contracting unit that is repeated down the entire length of the muscle fiber or cell, If you take your hands and over lap your fingers slightly, then you are mimicking the relaxed sarcomere. If you inter-lace your fingers and push your fingers together, then you are mimicking the contracted sarcomere. When hundreds of sarcomeres contract and actin slides over myosin,(like your fingers) and they pull on the tendon attached to the bone and the leg kicks out. The only time these proteins leave the cell is when the cell is damaged and we analyze blood to identify that troponin is floating in the plasma. Perhaps a link to Crash Course biology would help.
- I have heard that low Na+ due to physical exertion and loss of Na+ from sweat can cause muscle cramps, how is this explained physiologically?(4 votes)
- Because the whole homeostasis is distorted and shifted. Once you create disbalance in one ion, you create disbalance in the whole body. Ions are connected and intertwined. Loss of Na is followed by loss of Ca and K as well.(1 vote)
We know from the last video that if we have a high calcium ion concentration inside of the muscle cell, those calcium ions will bond to the troponin proteins which will then change their shape in such a way that the tropomyosin will be moved out of the way and so then the myosin heads can crawl along the actin filaments and them we'll actually have muscle contractions. So high calcium concentration, or calcium ion concentration, we have contraction. Low calcium ion concentration, these troponin proteins go to their standard confirmation and they pull-- or you can say they move the tropomyosin back in the way of the myosin heads-- and we have no contraction. So the next obvious question is, how does the muscle regulate whether we have high calcium concentration and contraction or low calcium concentration and relaxation? Or even a better question is, how does the nervous system do it? How does the nervous system tell the muscle to contract, to make its calcium concentration high and contract or to make it low again and relax? And to understand that, let's do a little bit a review of what we learned on the videos on neurons. Let me draw the terminal junction of an axon right here. Instead of having a synapse with a dendrite of another neuron, it's going to have a synapse with an actual muscle cell. So this is its synapse with the actual muscle cell. This is a synapse with an actual muscle cell. Let me label everything just so you don't get confused. This is the axon. We could call it the terminal end of an axon. This is the synapse. Just a little terminology from the neuron videos-- this space was a synaptic cleft. This is the presynaptic neuron. This is-- I guess you could kind of view it-- the post-synaptic cell. It's not a neuron in this case. And then just so we have-- this is our membrane of muscle cell. And I'm going to do-- probably the next video or maybe a video after that, I'll actually show you the anatomy of a muscle cell. In this, it'll be a little abstract because we really want to understand how the calcium ion concentration is regulated. This is called a sarcolemma. So this is the membrane of the muscle cell. And this right here-- you could imagine it's just a fold into the membrane of the muscle cell. If I were to look at the surface of the muscle cell, then it would look like a little bit of a hole or an indentation that goes into the cell, but here we did a cross section so you can imagine it folding in, but if you poked it in with a needle or something, this is what you would get. You would get a fold in the membrane. And this right here is called a T-tubule. And the T just stands for transverse. It's going transverse to the surface of the membrane. And over here-- and this is the really important thing in this video, or the really important organelle in this video. You have this organelle inside of the muscle cell called the sarcoplasmic reticulum. And it actually is very similar to an endoplasmic reticulum in somewhat of what it is or maybe how it's related to an endoplasmic reiticulum-- but here its main function is storage. While an endoplasmic reticulum, it's involved in protein development and it has ribosomes attached to it, but this is purely a storage organelle. What the sarcoplasmic reticulum does it has calcium ion pumps on its membrane and what these do is they're ATP ases, which means that they use ATP to fuel the pump. So you have ATP come in, ATP attaches to it, and maybe a calcium ion will attach to it, and when the ATP hydrolyzes into ADP plus a phosphate group, that changes the confirmation of this protein and it pumps the calcium ion in. So the calcium ions get pumped in. So the net effect of all of these calcium ion pumps on the membrane of the sarcoplasmic reticulum is in a resting muscle, we'll have a very high concentration of calcium ions on the inside. Now, I think you could probably guess where this is going. When the muscle needs to contract, these calcium ions get dumped out into the cytoplasm of the cell. And then they're able to bond to the troponin right here, and do everything we talked about in the last video. So what we care about is, just how does it know when to dump its calcium ions into the rest of the cell? This is the inside of the cell. And so this area is what the actin filaments and the myosin heads and all of the rest, and the troponin, and the tropomyosin-- they're all exposed to the environment that is over here. So you can imagine-- I could just draw it here just to make it clear. I'm drawing it very abstract. We'll see more of the structure in a future video. This is a very abstract drawing, but I think this'll give you a sense of what's going on. So let's say this neuron-- and we'll call this a motor neuron-- it's signaling for a muscle contraction. So first of all, we know how signals travel across neurons, especially across axons with an action potential. We could have a sodium channel right here. It's voltage gated so you have a little bit of a positive voltage there. That tells this voltage gated sodium channel to open up. So it opens up and allows even more of the sodium to flow in. That makes it a little bit more positive here. So then that triggers the next voltage gated channel to open up-- and so it keeps traveling down the membrane of the axon-- and eventually, when you get enough of a positive threshold, voltage gated calcium channels open up. This is all a review of what we learned in the neuron videos. So eventually, when it gets positive enough close to these calcium ion channels, they allow the calcium ions to flow in. And the calcium ions flow in and they bond to those special proteins near the synaptic membrane or the presynaptic membrane right there. These are calcium ions. They bond to proteins that were docking vesicles. Remember, vesicles were just these membranes around neurotransmitters. When the calcium binds to those proteins, it allows exocytosis to occur. It allows the membrane of the vesicles to merge with the membrane of the actual neuron and the contents get dumped out. This is all review from the neuron videos. I explained it in much more detail in those videos, but you have-- all of these neurotransmitters get dumped out. And we were talking about the synapse between a neuron and a muscle cell. The neurotransmitter here is acetylcholine. But just like what would happen at a dendrite, the acetylcholine binds to receptors on the sarcolemma or the membrane of the muscle cell and that opens sodium channels on the muscle cell. So the muscle cell also has a a voltage gradient across its membrane, just like a neuron does. So when this guy gets some acetylcholene, it allows sodium to flow inside the muscle cell. So you have a plus there and that causes an action potential in the muscle cell. So then you have a little bit of a positive charge. If it gets high enough to a threshold level, it'll trigger this voltage gated channel right here, which will allow more sodium to flow in. So it'll become a little bit positive over here. Of course, it also has potassium to reverse it. It's just like what's going on in a neuron. So eventually this action potential-- you have a sodium channel over here. It gets a little bit positive. When it gets enough positive, then it opens up and allows even more sodium to flow in. So you have this action potential. and then that action potential-- so you have a sodium channel over here-- it goes down this T-tubule. So the information from the neuron-- you could imagine the action potential then turns into kind of a chemical signal which triggers another action potential that goes down the T-tubule. And this is the interesting part-- and actually this is an area of open research right now and I'll give you some leads if you want to read more about this research-- is that you have a protein complex that essentially bridges the sarcoplasmic reticulum to the T-tubule. And I'll just draw it as a big box right here. So you have this protein complex right there. And I'll actually show it-- people believe-- I'll sort some words out here. It involves the proteins triadin, junctin, calsequestrin, and ryanodine. But they're somehow involved in a protein complex here that bridges between the T-tubule the sarcoplasmic reticulum, but the big picture is what happens when this action potential travels down here-- so we get positive enough right around here, this complex of proteins triggers the release of calcium. And they think that the ryanodine is actually the part that actually releases the calcium, but we could just say that it-- maybe it's triggered right here. When the action potential travels down-- let me switch to another color. I'm using this purple too much. When the action potential gets far enough-- I'll use red right here-- when the action potential gets far enough-- so this environment gets a little positive with all those sodium ions flowing in, this mystery box-- and you could do web searches for these proteins. People are still trying to understand exactly how this mystery box works-- it triggers an opening for all of these calcium ions to escape the sarcoplasmic reticulum. So then all these calcium ions get dumped into the outside of the sarcoplasmic reticulum into-- just the inside of the cell, into the cytoplasm of the cell. Now when that happens, what's doing to happen? Well, the high calcium concentration, the calcium ions bond to the troponin, just like what we said at the beginning of the video. The calcium ions bond to the troponin, move the tropomyosin out of the way, and then the myosin using ATP like we learned two videos ago can start crawling up the actin-- and at the same time, once the signal disappears, this thing shuts down and then these calcium ion pumps will reduce the calcium ion concentration again. And then our contraction will stop and the muscle will get relaxed again. So the whole big thing here is that we have this container of calcium ions that, when the muscles relax, is essentially taking the calcium ions out of the inside of the cell so the muscle is relaxed so that you can't have your myosin climb up the actin. But then when it gets the signal, it dumps it back in and then we actually have a muscle contraction because the tropomyosin gets moved out of the way by the troponin., So I don't know. That's pretty fascinating. It's actually even fascinating that this is still not completely well understood. This is an active-- if you want to become a biological researcher, this could be an interesting thing to try to understand. One, it's interesting just from a scientific point of view of how this actually functions, but there's actually-- there's maybe potential diseases that are byproducts of malfunctioning proteins right here. Maybe you can somehow make these things perform better or worse, or who knows. So there actually are positive impacts that you could have if you actually figured out what exactly is going on here when the action potential shows up to open up this calcium channel. So now we have the big picture. We know how a motor neuron can stimulate a contraction of a cell by allowing the sarcoplasmic reticulum to allow calcium ions to travel across this membrane in the cytoplasm of the cell. And I was doing a little bit of reading before this video. These pumps are very efficient. So once the signal goes away and this door is closed right here, this this sarcoplasmic reticulum can get back the ion concentration in about 30 milliseconds. So that's why we're so good at stopping contractions, why I can punch and then pull back my arm and then have it relax all within split-seconds because we can stop the contraction in 30 milliseconds, which is less than 1/30 of a second. So anyway, I'll see in the next video, where we'll study the actual anatomy of a muscle cell in a little bit more detail.