At first glance, the hot metal of a teapot and an ice cube have nothing in common. But these two objects can be painful. Strong heat and strong cold have an extremely unpleasant effect on human skin - we have known this since childhood. But what we have learned more recently is that the brain perceives these temperature extremes in almost the same way. We often think that it is the skin - and the nerves that it contains - that are directly responsible for the sense of touch, but what biologists call the "somatosensory system" actually includes a wider range of senses.
Among them, of course, there is touch itself, that is, the recognition of mechanical stimuli of the skin, but also proprioception, that is, the ability to sense the orientation and position of the body, and nociception, which is responsible for the body's ability to identify harmful stimuli. Feeling pain is the body's response to nociception.
Whether the pain stimulus is mechanical, chemical or thermal, nociception encourages us to get rid of it. Stick your hand into the fire and you will feel a burning sensation that will make your body pull your hand out of the fire as quickly as possible. This is not the most pleasant feeling - pain - but it proves that your body is trying to keep you safe. If you lose the ability to feel pain, it will be very bad.
"The basic principle," says a neuroscientist at Duke University York Grundle, "is that sensory neurons that are found throughout your body have a set of channels that are directly activated by cold or hot temperatures." By studying genetically modified mice over the past fifteen years, scientists have been able to prove that these channels - proteins embedded in the walls of neurons - are directly involved in the perception of temperature.
The best-studied channel TRPV1 responds to intense heat. TRPV1 is usually not activated until the stimulus reaches 42 degrees, which humans and mice generally view as excruciatingly hot. As soon as your skin reaches this threshold, the channel is activated, activates the entire nerve and a simple signal is transmitted to the brain: oh!
"With cold, in principle, the same mechanisms apply," explains Grundle, except that there is a protein called TRPM8, which is activated when it just gets cold, not necessarily very cold.
There remains TRPA1, which is perhaps the least studied class of these proteins. While researchers have found that it is activated in response to extremely cold stimuli, it is unclear if it is involved in the very process of detecting these stimuli.
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Together, these three proteins - TRPV1, TRPM8 and TRPA1 - allow the skin to detect temperatures in a range and the body to respond accordingly. And because they are nociceptors, the job of these proteins is to help you avoid certain temperatures, not seek them out. Mice with defective versions of the TRPM8 receptor, for example, no longer shunned cold temperatures. This means that mice - and perhaps we - are not actively looking for pleasant temperatures. Instead, they actively avoid extreme heat and cold, preferring a warm, calm environment.
Although scientists have identified the thermal boundaries at which these TRP receptors become active, this does not mean that they cannot be modulated. After all, a warm shower can be unbearably hot if you're not sunburned. "This has been shown to be due to skin inflammation sensitizing the TRPV1 channel," Grandl says, "lowering the threshold at which these nerves transmit pain to the brain."
But temperature isn't the only thing that activates these receptors; plants too. It may not surprise you that TRPV1, which is activated by extreme heat, is also activated by capsaicin, which gives the hot pepper its spice. And TRPM8 responds to the cooling power of menthol, which is found in mint leaves. TRPA1 is also called the "wasabi receptor" due to the fact that it is activated by the pungent components of mustard plants.
How did plants develop chemicals that activate receptors, usually activated by temperature? University of Washington molecular biologist Ajay Dhaka explains that capsaicin does nothing with TRPV1 in fish, birds, or rabbits, but activates the same receptor in humans and rodents. "The plants may have developed capsaicin so that some animals would not eat them, left alone," but the plants were edible for other creatures. It is possible that similar mechanisms led to the evolution of menthol and mustard.
In other words, this curious relationship between plants and temperatures may reflect the deep evolutionary history of plants rather than animals. Plants may have found a way to hack the temperature detection capabilities of our bodies, and then tampered with components that activate pain receptors.
Therefore, the fact that we are sweating, eating adjika with horseradish, is not associated with any property inherent in pepper, but only with the fact that capsaicin and heat activate the nerves of the skin in the same way.
Using a receptor tuned to noxious stimuli, these plants found a sneaky way of avoiding the fate of being devoured … until we found a way to enjoy the painfully scalding spicy food and pour mustard on everything. So the next time you notice yourself being literally ripped apart by a powerful chili, take a moment and consider that what is happening is the result of millions of years of evolutionary battle between plants and animals. Battles in which we seem to be winning (but this is not certain).
ILYA KHEL
