Scientists have discovered a biochemical pathway that may explain why sunburns and other injuries ache when exposed to heat, says a report in the latest issue of The Proceedings of the National Academy of Sciences. The finding may someday lead to treatments that blunt an injured person's heat sensitivity.
Peter McNaughton and Paolo Cesare of King's College in London isolated rat nociceptors, sensory neurons that perceive painful stimuli. After rapidly heating the nerve cells to 49 degrees Celsius, they detected a rise in electrical current flowing through the cell membrane, suggesting that the current plays an integral role in perceiving pain. When they exposed these injured cells to another burst of heat, they expected to see a heightened electrical response from the sensitized neuron. But the response was unchanged. The team concluded that the culture was missing a key factor that sensitizes injured tissue to heat.
That factor, the scientists soon found, is bradykinin, a protein produced in damaged tissue that's known to stimulate pain receptors. When they added bradykinin to the mix, the current nearly doubled. Subsequent experiments teased out that the increase in current came from bradykinin's activation of protein kinase C. This enzyme, they found, triggers the membrane current at lower temperatures in damaged tissue, thereby decreasing the threshold for pain sensation.
The findings suggest that physicians might be able to suppress pain in patients sensitive to heat by treating them with drugs that inhibit protein kinase C, says Jon Levine, a neuroscientist at the University of California, San Francisco. But he cautions that clinical fruits are far off. One immediate benefit, Levine says, is that the study provides a model for investigating how other types of pain stimuli may operate. "This is opening the door, not closing it," he says.