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news.In experiments with mice, researchers have found that eliminating what appears to be a "master genetic switch" for the development of pain-sensing neurons knocks out the animals' response to neuropathic pain.
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Neuropathic pain is abnormal pain that outlasts the injury and is associated with nerve and/or central nervous system changes. The animals rendered deficient in the gene, called Runx1, also showed lack of response to discomfort caused by heat and cold and inflammation.
The researchers said that their findings, reported in the journal Neuron, could have implications for the design of improved pain therapies.
In their experiments the researchers studied the Runx1 gene, one of a group of proteins that are key players involved in transmitting external sensory information, like pain and the perception of movement, to the spinal cord.
When they knocked out the gene, they found that the normal development of pain sensing nerve cells was impaired. The animals had lost ion channels known to be involved in reacting to painful heat or cold, as well as those involved in pain due to damaged tissue. The researchers also found that the Runx1-deficient animals showed deficient wiring of certain types of pain neurons.
“The identification of a core transcriptional control program for many of the ion channels and receptors known to transduce noxious stimuli has intriguing implications for the design of more effective pain therapies,” wrote the researchers.