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." Such 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 February 2, 2006, issue of Neuron, could have implications for the design of improved pain therapies.
In their experiments, Qiufu Ma and colleagues studied the Runx1 gene because past research had shown it to code for a protein "transcription factor," which is a master regulator of multiple genes. Runx1 is 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. In two other related papers in the same issue, Silvia Arber and colleagues and Tom Jessell and colleagues examine related aspects of the biological importance underlying the Runx transcription factors.
Runx1 was known to be expressed only in sensory nerve cells called "nociceptive" cells, involved in sensing pain. Such pain-sensing cells function by translating painful stimuli into nerve signals via specialized pores called "ion channels" in the neurons, as well as specialized receptors. The researchers studies of Runx1 in these cells revealed that during embryonic development, the gene is characteristically expressed in pain-receptor cells involved in neuropathic pain. When they knocked out the gene, they found that the normal development of such specialized 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.
Heidi Hardman | EurekAlert!
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