Atlanta, Ga. (OCT. 15, 2006) -- Researchers at Johnson & Johnson Pharmaceutical Research & Development (J&JPRD) today announced that they have discovered a new molecular mechanism that may underlie neuropathic pain. The clearer understanding of the root-cause of chronic neuropathic pain, and the preclinical validation of new targets for pharmaceutical therapies shown in this research, together present an opportunity for the development of new ways to treat the severe pain associated with such common conditions or diseases as sciatica, diabetic neuropathy and shingles.
This research was presented at Neuroscience 2006, the annual meeting of the Society for Neuroscience.
Neuropathic pain, or the spontaneous pain and abnormal sensitivity following a nerve injury, typically results from a traumatic injury, an infection or disease, or surgery, and can persist long after the initial injury has healed. Millions of people worldwide suffer some form of neuropathic pain, and the current treatment options are limited or inadequate for many people. The research presented today suggests that the persistent pain may be caused by specific types of ion channels, called "pacemaker channels," which initiate a constant and rhythmic transmission of pain signals to the brain, rhythmically similar to those generated by pacemaker cells that regulate one's heart rate.
"What we have shown in our early preclinical research is that we can inhibit the inappropriate neuronal activity and resulting sensitivity that follows nerve injury," said Alan Wickenden, Ph.D., Research Fellow in the Pain and Related Disorders Team at J&JPRD. "Trauma to nerves and the tissues that surround them seems to trigger a complicated cascade of events that results in an increase in the activity of these pacemaker ion channels and the resulting transmission of pain signals to the brain. We are encouraged by early evaluations of certain chemical structures that seem to disrupt this rhy
Contact: Ernie Knewitz
Johnson & Johnson Pharmaceutical Research & Development, L.L.C.