Researchers at the VIB-KU Leuven Center for Brain & Disease Research uncover how the upregulation of an ion channel called TRPM3 causes hypersensitivity in inflamed tissue. The new findings, published by professor Thomas Voets and his team in eLife, suggest new therapeutic avenues to help patients suffering from chronic pain.
Two mutations identified in individuals with developmental and epileptic brain disease can be traced back to the same ion channel. Researchers have now elucidated how both independent mutations affect the channel’s function: by making it overly active and highly sensitive to stimulation. The findings are an important step towards unraveling what causes the patients’ symptoms.
After years of ongoing experiments and an extended review process, the teams of Thomas Voets (VIB-KU Leuven Center for Brain & Disease Research) and Joris Vriens (KU Leuven) have successfully published a boundary-pushing paper on mammalian heat-sensing channels in the high-impact journal Nature. The researchers are credited with a hot discovery: the presence of three redundant ion channels in neurons, forming a fail-safe heat-sensing mechanism for extra burn protection. It took plenty of commitment – and sometimes 80 behavioral mouse experiments per day – but all the hard work has paid off for Thomas and team members Ine Vandewauw, Katrien De Clercq and Marie Mulier.
Researchers at VIB & KU Leuven have uncovered a trio of complementary ion channels in sensory neurons that mediate detection of acute, harmful heat. Having three redundant molecular heat-sensing mechanisms provides a powerful fail-safe mechanism that protects against burn injuries. The seminal findings have been published today in Nature.