With temperatures soaring across the UK, our ability to detect and avoid places that are too warm is vital for regulating our body temperature. However, until now, little was known about the molecular mechanisms responsible for detecting warmth in the sensory neurons of our skin.

A new  King’s College London study, published in Nature, reveals that a gene called TRPM2 initiates a ‘warm’ signal in mice that drives them to seek cooler environments. When this gene is removed, the mice are unable to distinguish between cool and warm temperatures.

Dr Chun-Hsiang Tan  and  Professor Peter McNaughton both from the  IoPPN  identified an ion channel called TRPM2, which had not previously been linked to the sensation of warmth. Having isolated this channel, they removed the TRPM2 gene in a group of mice and compared their behaviour to normal mice when walking across warmed surfaces at 33°C or 38°C. The researchers found that normal mice preferred a cooler temperature of 33°C and avoided the warmer temperature of 38°C, while the mice in which the TRPM2 gene had been deleted were unable to distinguish between the two.

Dr Chun-Hsiang Tan said: ‘The removal of TRPM2 in these mice eliminated their ability to detect non-painful warmth, yet the capacity to detect painful levels of heat using other known receptors was unaffected. This reveals how we are able to detect environments that are too warm at a sensory level.’

Professor Peter McNaughton, said: ‘The temperatures we examined are certainly comparable to those you might find on a London bus or tube carriage in the height of summer. At 38°C a busy tube carriage would be quite suffocating, so sensory neurons in our skin allow us to detect that the environment is too warm and drive us to take action – whether that be removing an article of clothing or alighting the tube and seeking a cooler environment.’

Read the full story on the  King’s website.
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