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Scripps research team sheds light on long-sought cold sensation gene

t the tips of sensory neurons, which innervate the skin. When opened, ions flowing through TRPM8 lead to the activation of the sensory neuron, which in turn sends a signal to the brain. The Patapoutian teams results support the idea that activation of TRPM8 by temperature triggers cold sensation. "TRPM8 acts as a gate," says Dhaka, "At warm temperature it remains closed, but opens when exposed to cool temperature."

The TRPM8-deficient mice did not lose their ability to feel pain in response to extreme cold, as evidenced by responses similar to wild type mice when exposed to -1 C cold plates. This suggests that other genes are responsible for this facet of cold sensation.

Though cold can be unpleasant or painful under certain circumstances, it can also deaden pain, as illustrated by icing an injury to relieve pain. To test this side of cold sensation, the researchers injected the mice with small amounts of a pain-causing chemical, formalin, and then exposed the affected paw area to a cold plate.

Cold temperature clearly reduced the acute pain felt by control mice as shown by a reduction in the response to formalin injection when compared to the amount of time control mice spent flicking and licking their paws when placed on a room temperature plate. In contrast, TRPM8-deficient mice did not receive any acute pain relief from the cold plate suggesting that cold activation of TRPM8 can mediate some of the analgesic effects of cold.

Just how the same sensation can be interpreted as unpleasant under certain circumstances and pleasant in others is still not clear, but is a question the group plans to investigate. "It would be really interesting to find out how the brain takes essentially the same signal and, depending on context, interprets it differently, says Dhaka.


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Contact: Marisela Chevez
mchevez@scripps.edu
858-784-2171
Scripps Research Institute
2-May-2007


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