But the researchers didn't stop there. Looking at electrical data from nerve firings in these rats, they discovered that the TRPM8 neurons, when activated, released a neurotransmitter, glutamate, into the spinal cord. And they found that glutamate released from cooling neurons turned around and inhibited signals from pain neurons. "What's clever about this system and what nobody understood is...the TRPM8 sensory nerves are acting as a sort of control gate so the painful inputs don't reach the brain," says Fleetwood-Walker.

Observers say the findings are promising, albeit preliminary. "It is very unlikely that any one pathway or any one treatment is going to work on all types of pain, so instead we chip away at pain a little at a time," says John T. Farrar, a chronic pain researcher at the University of Pennsylvania Medical Center in Philadelphia. "The animal model used in this study represents only one possible mechanism by which pain can occur in humans. However, it is clearly worth exploring -- and perhaps we will get lucky with this one."

The Edinburgh team plans to start human tests next year, experimenting with topical solutions of icilin on patients with nerve-related pain where treatments with morphine have been unsuccessful. The group is also looking for even more effective compounds than icilin as possible active ingredients for use in a topical cream that could one day provide cooling relief for people suffering from chronic pain.