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Leuven researchers uncover ion channel trio that mediates painful heat sensing

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Gary Johnson
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Having three redundant molecular heat-sensing mechanisms provides a powerful fail-safe mechanism that protects against burn injuries.

Although the sensory neurons involved in acute pain signaling in mammals were described more than a century ago, the molecular mechanisms whereby these neurons detect harmful signals have remained largely unresolved.

A research team jointly led by prof. Thomas Voets (VIB - KU Leuven) and prof. Joris Vriens (KU Leuven) used genetic knockout models to pinpoint which molecular partners are involved.

"We already knew several potential molecular heat sensors, but none of them, when deactivated, resulted in severe loss of acute noxious heat sensing," explains Ine Vandewauw, postdoctoral scientist in the lab of Thomas Voets.

The researchers started by eliminating two different heat-activated TRP ion channels, including one known to be also activated by capsaicin, the active component of chili peppers.

But this only resulted in very mild deficits in heat sensing.

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