- Integumentary system questions
- Meet the skin! (Overview)
- What is skin? (Epidermis)
- What lies beneath the epidermis? (Dermis and Hypodermis)
- Where do our nails and hair come from?
- What's in sweat? (Holocrine, Apocrine, Merocrine Glands)
- LeBron Asks: Why does sweating cool you down?
- Overview of Sensation and Meissner's Corpuscle
- Pacinian's Corpuscle and Merkel's Disk
- Ruffini's Ending and Hair Follicle Receptor
- Pain and temperature
- Thermoregulation mechanisms
Explore our senses of pain & temperature. By Ron. Created by Ronald Sahyouni.
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- At5:14there is a correction stating "Ron said "A beta fibers" but meant " A delta fibers."" However later Ron refers to the medium size fiber as A delta fibers - which is which?(49 votes)
- I believe the correction is wrong, Ron saying A-beta as the fast fibers is correct!
- What happens in people who can't feel pain, like people with congenital analgesia?(15 votes)
- Since pain is protective in function, people with congenital analgesia are likely to get injured without them even realizing it, further causing damage to that part of the body by not allowing it to rest/treating it. People may even purposely injure themselves(often children who don't understand what they're doing) because it does not cause any suffering to them, so they have no initiative to stop. They need to be regularly examined for signs of injury.(24 votes)
- Aren't our cells always dying? So why aren't TRPV1 receptors always sending pain signal to our brains?(14 votes)
- Old cells in our body die by a mechanism called apoptosis. In short, it is "programmed cell death". This means that a specific sequence of events occurs inside the dying cell to properly destroy all components. Further, once dead, this cell is immediately recognized by phagocytes which engulf it and thereby prevent inflammation. None of the dead components are allowed to interact with surrounding cells.
But when a needle pricks our skin, some cells die accidentally and thus in an unprogrammed way. This causes the affected cells to swell and burst. The contents of the cells are discharged into the surroundings and are detected by neighbouring receptors. It takes some time for the phagocytes and macrophages to remove the debris. Meanwhile, TRPV1 receptors are stimulated.(37 votes)
- The video talks about how pain and temperature are connected via the TrpVI receptor, but is there any connection to dryness and wetness as well? Sometimes when I touch something cold, my brain processes that as wet. Is that because wetness is also incorporated into nociception?(8 votes)
- So why is it that some use Capsaicin as a natural form of pain relief (you can find this product at health food stores and possibly a pharmacy). Although this cannot be true, it seems as if the Capsaicin would just activate more nocioceptors, therefore exacerbating the pain not relieving it.(5 votes)
- Yes, it's true Capsaicin is used to relieve pain however it's used topically like as in cream and some patches. Capsaicin alleviates the pain by desensitizing certain sensory receptors that carry the signal to the brain and also decreases the production of Substance p which is a neurotransmitter necessary for perception of pain.(7 votes)
- If I pinch my skin, why do I feel pain ?
Following the video :
- No cell is being destroyed (is it true ?)
- No temperature effect
I would say that I'm not supposed to feel any pain.
Nevertheless, I just tried it, and it does hurt ^^ !(4 votes)
- The neurons in the skin have receptors, dendrites, that are stimulated. They send action potentials, APs, to the brain and neurons in the brain interpret those APs as pain. Some neurons are dedicated to touch, temperature or pain, however, too much stimulation of any neuron will be interpreted as pain by the brain. Think about noise, too much causes us to say that was painful. Yes, you are supposed to feel pain, it keeps us alive. No cell is destroyed from a pinch.(5 votes)
- Is there a video that explains how mammals use negative feedback loops to maintain optimal internal temperatures? Basically, how do we regulate temperature?(4 votes)
- Do people with pain conditions such as fibromyalgia have more of the fast A-Beta Fibers than people without pain conditions?(5 votes)
- what happens with chronic pain when there is no longer any outside stimulus but pain still persists?(4 votes)
- Central and peripheral sensitization.., threshold of the Ab, Ad and C receptors change in the peripheral tissue like (RCPS)such the area becomes more sensitive to normal stimuli (peripheral sensitization) that results in changes taking blace in several areas of the brain (central sensitiation)(1 vote)
- Are pain and temperature receptors different somehow? (I.e. different forms of TrpV1?) If not, how do we tell the difference between pain and temperature?(2 votes)
- It depends on what type of nociceptor we're talking about. Ron generalized to the extreme on this video lol, we actually have a few different types of TRP channels for different types of nociception. We actually have an enormous family of TRP channels involved in a whole bunch of different processes! To give you a bit of an idea, TRPM8 is the predominant channel involved in the detection of noxious cold stimuli, and may be modified by other types of TRP channels. As for noxious mechanical stimuli, I don't think researchers are actually quite sure what protein receptor is responsible for transduction.(4 votes)
So two senses that are extremely important for our survival are our sense of pain and our sense of temperature. And, of course, we have more scientific terms for pain and temperature. So pain is known as nociception, and temperature, our ability to sense temperature, is known as thermoception. So how is it that we're able to sense pain and temperature? Well, just like all of our other senses, we rely on a very specialized type of receptor found in various cells throughout our body. And in this case, in order for us to sense temperature, we rely on a receptor known as the TrpV1 receptor. And interestingly enough, this TrpV1 receptor is also sensitive to pain. And we're going to go into how this receptor is able to recognize when there's some kind of painful stimulus in the environment. So over here, I have a little representation of what the TrpV1 receptor looks like. And this is not-- you don't need to know this, you don't need to memorize this. This is just to give you an idea of what it looks like. It's a very complex structure, and it's actually located within the cell membrane. So you have cells that are sensitive to temperature and pain located throughout your entire body. And within the membrane of each one of these cells are thousands of these little receptors. And how this receptor works is whenever there's a change in temperature-- so let's imagine that you place your hand on the stove, so there's a little fire. I know you can't see that. So let's imagine that there's a little fire under here. The heat actually causes a conformational change in this protein. And basically what a conformational change is, is just a change in the physical structure of the protein. So you can imagine that we-- the protein was a little box. And you apply heat to it. Maybe we'll make it look like a rectangle. So this is the general idea behind a conformational change. So when heat is applied and also when pain applied via a particular molecule, you have a conformational change in the TrpV1 protein. So let's look at a diagram of a hand and go into this in a little bit more detail. OK, so here we have a hand. And as I mentioned before, we have cells located throughout the hand. And these cells are sensitive to temperature and to pain. And within these cells, there are TrpV1 receptors. So let's imagine that each one of these cells sends a little projection to a nerve that eventually reaches the brain. So these cells, whenever they are stimulated by either a change of temperature or the presence of some sort of painful stimulus-- so we keep saying a painful stimulus. So what can that be? So let's imagine that something pokes your hand. So let's imagine that we have a sharp object, and it pokes your hand. What happens is, the cell, when it gets poked, thousands of cells get broken up. So the cell gets broken up. And when it gets broken up, it releases all kinds of different molecules. And these molecules will travel around. So let's imagine it releases this little green molecule. It will travel around, and it will bind to one of the little TrpV1 receptors. And when it binds to a TrpV1 receptor, it causes the same conformational change that a change in temperature causes. And so that conformational change actually activates the cell, and the cell will send a signal to the brain. So this nerve over here actually contains three different types of fibers. So there are fast, medium, and slow fibers. And let's go into why we have three different fibers. So fast fibers are really, really fat in diameter. So we have these really big, fat fibers, and they have a lot myelin. So they are covered in myelin. And what myelin is, it's an insulator that basically allows the cell to conduct an action potential very quickly. So as an action potential or as a signal travels down the cell, if we have a lot of myelin surrounding the cell, the signal is able to travel really quickly. And another way that a signal is able to travel quickly is if the cell has a really big diameter. So a big diameter lowers the resistance. So you have less resistance and you have greater conductance because of the myelin. And these two things produce a very fast-- a cell that is able to produce-- send a signal pretty quickly. So these types of fibers are known as A-beta fibers. And these fibers are able to send a signal really quickly to your brain saying, hey, there's some sort of change in temperature. It's really hot, or there is something that's painful, and allows you to withdraw your hand from that painful or really hot stimulus. We also have medium fibers. And basically these medium fibers are a little bit smaller in diameter. So they might be about this big. And they have a little bit less myelin. And since they have a little bit smaller diameter and a little bit less myelin, they don't conduct a signal as quickly as these fast fibers. So these medium diameter fibers are known as A-delta fibers. So these A-delta fibers are also found in this big nerve that goes to your brain. And there's one more type of fiber. So there's a slow fiber. And this slow fiber-- I'll draw it out over here-- is really small in diameter, and it's unmyelinated. And so this sends a signal very, very slowly. It does get your brain, but it takes a lot longer for the signal to get your brain. So one way that we could conceptualize these three different fibers is if you think about touching a hot stove. Your hand quickly moves away from the hot stove. So this is this really big A-beta fiber activating to get your hand off the hot stove. Then you feel this really quick sensation of pain immediately after you touch the hot stove. So that's this A-delta fiber sending a painful stimulus to your brain. And for minutes to maybe even hours after you've removed your hand from the hot stove, you feel this lingering sense of pain. You feel this burning sensation. And so those are these C fibers that really small in diameter and unmyelinated. So we went into how temperature can induce a conformational change in this TrpV1 receptor and how that conformational change can cause a cell to send a signal to the brain. So let's go to how pain can do the same thing. So whenever you eat a jalapeno, you might have notice that you get this-- you start sweating. Everything feels like it's burning. And you basically have the same physiological response that you would if it was really hot outside. And that again is because this temperature receptor is the same receptor as a pain receptor. So when you eat a jalapeno-- I'm drawing a little jalapeno. When you bite into the jalapeno, again, you break the cells apart. And the cells contain a molecule known as capsaicin. So I'll write that down over here-- capsaicin. And this capsaicin molecule exits the jalapeno cell and travels around until it binds to a TrpV1 receptor in your tongue. So this is a TrpV1 receptor in the hand, but let's imagine that it's in the tongue. And it triggers the same response that a change in temperature would. And so your body reacts to this capsaicin molecule in the same way that it would react to a change in temperature. So if it was really hot outside, you would start sweating. You'd feel this burning sensation. And so that is why when you eat a really hot chili pepper you have that type of response. So in summary, we have our ability to sense pain, which is known as nociception, and our ability to sense temperature, known as thermoception. And these two senses rely on this TrpV1 receptor that is found within various sensory cells located throughout our body. And the TrpV1 receptor is activated by changes in temperature and by molecules, such as capsaicin, or by molecules found within dying cells. And it can activate this TrpV1 receptor and send a signal to your brain, letting your brain know that, hey, there are painful stimulus, or there's a change in temperature, and allows you to react to that stimulus.