The Nobel Prize in the fields of Physiology and Medicine have been awarded to a pair of researchers who have accelerated our scientific understanding of how human beings can sense touch and temperature.
In an official release, The Nobel Assembly jointly awarded the prize to Dr David Julius PhD and Ardem Patapoutian PhD, who together found two novel classes of sensor molecules in the nerve endings of our skin that respond to different types of stimuli.
It is a principle that is taken for granted in everyday life, and even in pharmaceutical distribution when drugs are distributed via patches or injections that can be felt on the skin, that we can sense heat, cold, different types of textures and pressure on our skin.
However, we did not really have a strong basis for understanding why these sensations happened, but instead simply took for granted that they did.
In some respects, our understanding of the nervous system traced its way back to the work of the philosopher Descartes, who foresaw the notion of a nervous system as threads that connected different parts of the body with the brain.
This would later be formalised by Joseph Erlanger And Herbert Gasser into a discovery of nerve fibres that could each react to specific stimuli, winning the 1944 Nobel Prize for their achievement.
Despite further neurological advances working out the level of sophistication and nuance our nerve fibres could provide in feeling subtle differences in textures or levels of temperature, that unsolved question of how these stimuli were perceived in the first place was left largely unanswered.
For Dr Julius, the answer began in the mid-1990s with the compound capsaicin, the active ingredient in chilli peppers that makes our skin feel like it is burning when it comes into contact.
Dr Julius looked into exactly why capsaicin feels hot when it isn’t and the answer came through finding the single gene that made cells sensitive to the chilli compound.
Further experimentation with this gene led to Dr Julius and his team finding out about a new protein with a capsaicin receptor, later known as TRPV1.
However, when he tested the protein’s response to heat, it also activated, suggesting that capsaicin’s painful effect on the skin was caused by heat-sensitive pain, rather than other forms of pain response.
The discovery of TRPV1 opened the floodgates for finding other temperature-sensitive receptors, and both Dr Julius and Dr Pataputian both used the compound menthol to find TRPV1’s opposite, TRPM8.
With the discovery of temperature-sensitive receptors well underway, Dr Patapoutian wanted to go further and find the receptors that were sensitive to mechanical stimuli, such as touch, texture and pressure.
It first started by poking individual cells with a micropipette until one of them gave off an electrical signal that could be detected. After they found an ion channel they believed to be responsible, Dr Patapoutian and his team turned off the genes one by one to find the gene responsible.
This led to the discovery of Piezo1 and Piezo2, both of which were important to the perception of touch.
However, Piezo2 turned out to be an essential part of not only touch, but also sensing body position, motion, and also other processes such as respiration and managing blood pressure.