NEW DELHI, Oct 27: A study has uncovered a new way by which a cell in human body senses temperature, which researchers said could play a role in how the body differentiates between warmth from harmful heat.
Upon detecting heat in the environment, a sensor called ‘TRPM3’ located in the cell membrane — the cell’s outermost protective — allows charged particles to enter, the team from Northwestern University in the US said.
The flow of charged particles in the cell generates nerve signals that the brain interprets as ‘heat’ or ‘pain’, they explained.
Because TRPM3 is also involved in pain, inflammation and epilepsy, the findings published in the journal Nature Structural and Molecular Biology may help develop non-addictive treatments for chronic pain, the researchers added.
Epilepsy is caused by a disrupted electrical signalling in the brain, resulting in recurrent seizures.
“When TRPM3 becomes overactive, it can cause pain,” lead researcher Wei Lü, professor of molecular biosciences at Northwestern University, said.
“By learning how this sensor detects heat and how to control its activity, we may discover new pain-relief strategies that are safer and less likely to cause addiction,” Lu said.
Tuning the activity of TRPM3, which is found in both the brain and sensory nerve cells in the skin, could help manage chronic pain or neurological disorders, the researchers said.
The study used cryo-electron microscopy — a technique that takes thousands of pictures of proteins in a flash — to create three dimensional images of TRPM3’s behaviour at an almost atomic detail.
Because heat does not have a physical shape or does not bind to proteins in a cell, the researchers used a heat-mimicking chemical to capture the TRPM3 in its active state.
The ‘inactive’ state of the sensor was observed when an epilepsy drug was bound to the protein. Comparing the two sets of images revealed that parts of TRPM3 move when the protein is active.
The team found that TRPM3 functions as a molecular switch made of four parts — when the inner regions of the parts are tightly connected, the sensor remains inactive, they said.
However, exposure to heat or chemicals disrupts these connections, triggering the protein to become active.
“Both heat and chemical activators push the same internal switch to activate the channel. In contrast, the epilepsy drug jams that same switch, preventing it from changing shape,” co-lead researcher Juan Du, professor of molecular biosciences at Northwestern University, said.
Du added that temperature is among the ever-present environmental factor impacting how one senses the world.
“It also affects how our bodies heal and how diseases progress. Understanding how temperature is detected at the molecular level can help us design better treatments for pain and inflammation,” Du said. (PTI)
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