Why we hurt from hot and cold?

At first glance, the hot metal of the kettle and ice cube have nothing in common. But these two objects can cause pain. Strong heat and extreme cold have on the human skin is extremely unpleasant effects is that we know from childhood. But what we learned recently is that the brain perceives these almost the same temperature extremes. We often think that the skin and nerves which it contains, is directly responsible for the sense of touch, however, what biologists call "somatosensory system" actually includes a wider range of feelings.

Among them, of course, is touching in itself, that is, the recognition of mechanical stimuli of the skin, but also proprioception, i.e. the ability to sense the orientation and position of the body, and nociception, which is responsible for the body's ability to detect noxious stimuli. Feeling pain is the body's response to nociception.

Whatever the stimulus of pain — mechanical, chemical or thermal — nociception motivates us to get rid of it. Put your hand in the fire and you will feel a burning sensation that will force your body to pull the hand out of the fire as quickly as possible. It's not the most pleasant feeling — the pain — but it proves that your body is trying to keep you safe. Lose the ability to feel pain and will be very bad.

"the Main principle," says a neuroscientist at Duke University York Grundle, "is that sensory neurons that are found everywhere in your body, have a set of channels that are directly activated by cold or hot temperatures." Studying genetically modified mice for the last fifteen years, scientists have been able to prove that these channels are proteins embedded in the walls of neurons, is directly involved in the perception of temperature.

The best studied channel TRPV1 responds to strong heat. TRPV1 is normally not activated until the stimulus reaches a temperature of 42 degrees, which is of mice and men are generally seen as painfully hot. Once your skin reaches this threshold, the channel aktiviziruyutsya, activates all of the nerve and into the brain transmitted a simple signal: Oh!

"With the cold, in principle, subject to the same mechanisms," says Grundle, except that it appears the protein TRPM8, which is activated just when it gets cold, definitely not too cold.

Still TRPA1, which is perhaps the least studied class of these proteins. While the researchers found that it is activated in response to extremely cold stimuli, it is unclear whether it takes part in the process of detection of these stimuli.

Together, these three protein — TRPV1, TRPM8 and TRPA1 — allow the skin to determine the temperature range and the body to react accordingly. And since it's the nociceptors, the work of these proteins is to help you avoid certain temperatures, and not to look for them. Mice with defective versions of the receptor TRPM8, for example, never avoided the cold temperatures. This means that mouse — and maybe we are not actively seeking pleasant temperatures. Instead, they actively avoid extraordinary heat and cold, preferring warm, calm environment.

Although scientists have determined the thermal boundary at which these TRP receptors become active, it does not mean that they can not modulate. In the end, a warm shower can be unbearably hot if you burnt the sun. "It has been shown that this is because the inflammation of the skin makes the sensitive channel TRPV1," said Grundle, "lowering the threshold at which these nerves transmit pain sensations to the brain."

But the temperature is not the only thing that activates these receptors; plants too. You may not be surprised that TRPV1, which is activated emergency heat, is also activated by capsaicin that gives chili pepper its pungency. While TRPM8 responds to cooling strength of menthol in mint leaves. TRPA1 is also called the "wasabi receptor" because it is activated by pungent components of mustard plants.

In plants the chemical substances that activate receptors are usually activated by temperature? A molecular biologist at the University of Washington Ajay duck explains that capsaicin does nothing with TRPV1 in fish, birds or rabbits, but activates the same receptor in humans and rodents. "Maybe the plants developed capsaicin to any animals they do not eat, be left alone", but the plants were edible to other creatures. It is possible that similar mechanisms led to the evolution of menthol and mustard.

In Other words, these curious relations between plants and temperatures may reflect deep evolutionary history of plants rather than animals. Maybe the plants have found a way to crack the possibility of detecting the temperature in our bodies, and then forged components, activating pain receptors.

So the fact that we are sweating it out, eating adjika with horseradish, not connected with any property inherent in the pepper, but only with the fact that capsaicin and heat activate the skin nerves the same way.

Using a receptor configured to noxious stimuli, these plants have found a sneaky way to avoid the fate of being pornname... until we found a way to enjoy the painful burning spicy food and pour all the mustard. So next time when you notice that you just ripped a powerful chili pepper, take a moment and think that what is happening is the result of millions of years of evolutionary battle between plants and animals. A battle in which we, like, win (but not sure).