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 today 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.
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 today 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.
Some 'TRP' (Transient Receptor Potential) proteins were already known to be activated by painful levels of heat. These proteins can conduct positively charged ions across the cell membrane, and so can change the internal voltage of a nerve cell. This change in voltage in turn triggers nerve activity, and so signals the painful sensation of heat, such as from touching a hot kettle. However, previous research had not revealed ion channels which may be activated by milder levels of non-painful warmth.
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Image via NOAA
