Eat a chili and the temperature in your mouth barely moves, because there is no source of heat anywhere in it. The sensation is still close to a burn. So what exactly is being switched on?
Curiosity counts. Here is the answer.
The temperature barely moves. Capsaicin binds to a channel in sensory cells that also opens to heat at the point where it starts to injure tissue, around 43 degrees Celsius. The brain gets exactly the signal of a mild burn. The sensation is real and the physical cause is not there.
In 1997 researchers isolated a receptor called . It is an ion channel, and it opens to two different things: , the compound that makes a pepper hot, and heat at the level where it starts to damage tissue. The brain receives the same message it would get from a mild burn, with no flame and no scalding drink involved.
The detail that organizes everything is a simple measurement: the temperature in your mouth barely changes when you eat a pepper. There is no real heat, so the question is not about energy. It is about a signal.
What emerged in 1997 is that capsaicin binds to a channel in sensory cells and opens it. The same channel also opens from heat, at around 43 degrees Celsius, which is exactly the threshold where heat begins to damage tissue.
So this is an alarm and not a thermometer, and what capsaicin does is trip it directly. The brain receives precisely the signal a mild burn would send, which is why the sensation is entirely accurate even though it has no physical cause.
The proof came by a blind and convincing route. Researchers used , feeding genes into cells indifferent to capsaicin a batch at a time and watching for any that began to respond. The cells that lit up gave away the gene. From there opened a whole field of translating heat, cold and pressure into nerve signals, and that work took a Nobel Prize. It is worth saying that the receptor does not explain the whole experience: concentration, the state of the tissue and habit all matter.
wat. Chili feels hot because capsaicin presses the same nerve button that warns the body about heat painful enough to do damage.
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It turned an everyday food sensation into a window onto pain, inflammation and temperature, and opened up the wider family of TRP channels.
How do we know?
Expression cloning: DNA from sensory nerve cells was introduced into laboratory cells in batches, and the cells were tested for calcium entry and an electrical response to capsaicin and to heat.
What is still unknown
The receptor does not account for the whole experience of heat. Concentration, the state of the tissue, eating habits and other receptors all shape it.
Learn something?
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