Washington, DC - In a study that could lead to new treatments for chronic pain, scientists have relieved pain in rats by dispatching molecular "smart bombs" to selectively destroy certain nerve cells in the spinal cord. Because this approach targets just those nerve cells, or neurons, that send pain messages to the brain, it shouldn't cause the side effects of drugs such as morphine or the complications of surgery. The study appears in the 19 November issue of Science.
Thus far, the scientists' method kills the pain-signaling neurons, so its uses may be limited to stopping the extreme pain of terminally ill patients. However, designing a less drastic variation that would temporarily silence the neurons should now be "a very do-able thing," according to Patrick Mantyh, of the University of Minnesota and the Veterans Affairs Medical Center in Minneapolis, who led the research team.
The team of scientists also includes Michael L. Nichols, Brian J. Allen, Scott D. Rogers, Joseph R. Ghilardi, Prisca Honore, Nancy M. Luger, and Matthew P. Finke, from the University of Minnesota and the Veterans Affairs Medical Center in Minneapolis; Jun Li and Donald A. Simone, from the University of Minnesota, in Minneapolis; and Douglas A. Lappi, from Advanced Targeting Systems, in San Diego.
Chronic pain is an extremely common affliction that occurs in a variety of forms, from the specific pain of a migraine headache to the mysterious all-over body pain of fibromyalgia. In all of its incarnations, chronic pain seems to be the result of faulty signaling by a small group of neurons in the spinal cord. These signals can either make patients hypersensitive to stimuli that are minimally painful (such as a pinprick), or they can cause patients to feel pain in response to stimuli that are not painful at all (a warm shower, for example).
The group of neurons responsible for these inappropriate responses transmit electrical signals to each other with the help of a c
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Contact: Heather Singmaster
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American Association for the Advancement of Science
18-Nov-1999