Scientists have found a biochemical pathway that may explain why sunburn and other injuries hurt when exposed to heat, according a report in the latest issue of Proceedings of the national Academy of sciences . The discovery could one day lead to treatments that blunt the heat sensitivity of an injured person.
Peter McNaughton and Paolo Cesare King's College in London nociceptors of isolated rat sensory neurons that collect painful stimuli. After quickly heated nerve cells at 49 degrees Celsius, they detected an increase in the electric current flowing through the cell membrane, suggesting that the current plays an essential role in the perception of pain. When they exposed these cells to injured another burst of heat, they should see an increased electrical response of the sensitized neuron. But the answer was unchanged. The team concluded that the culture was missing a key factor that sensitizes the injured tissues to heat.
This, the scientists quickly found, is bradykinin, a protein produced in the damaged tissue that is known to stimulate the pain receptors. When they added bradykinin to the mix, the current has almost doubled. Subsequent experiments teased that the increased current from the activation of bradykinin of protein kinase C. This enzyme, they found, triggers membrane current at lower temperatures in the damaged tissues, which lowers the threshold of pain sensation.
The results suggest that doctors might be able to remove the pain in patients sensitive to heat treating them with drugs that inhibit protein kinase C, said Jon Levine, a neuroscientist at the University of California, San Francisco. But he warned that clinical fruits are far away. An immediate advantage, Levine said, is that the study provides a model for studying how other types of painful stimuli can work. "This opens the door not closing," he said.
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