Pain is an extremely disabling condition leading to an annual cost of $65 billion lost in work productivity and 4 billion work days. It also accounts for 40 million visits per year to physicians for "new" pain and $3 billion in sales each year of over-the-counter analgesics. Scientists studying animal models with support from the National Institutes of Health have found that a chemical, called neurokinin A, may be responsible for the body's response to moderate-to-intense pain. This finding, reported in the March 26, 1998, issue of Nature(1), may eventually lead to new treatments for pain.

Under the leadership of Allan I. Basbaum, Ph.D., neuroscientists at the University of California at San Francisco (UCSF) and the University of Minnesota have found that mice with a mutation in a gene that encodes for two chemicals, peptides called substance P and neurokinin A, have a reduced response to increased pain stimuli.

The experiment suggests that these peptides play a role in the body's pain responses and are essential components in the production of moderate-to-severe pain.

"After seeing this change, we now believe that substance P and neurokinin A must work in combination to account for pain responses in the body," said Dr. Basbaum, Chair of the Department of Anatomy and Physiology and the Division of Neuroscience at UCSF.

The scientists interrupted the gene encoding for preprotachykinin, whose peptide products include substance P, long believed to play an important role in pain response, and neurokinin A. They observed that the colony of mutant animals maintained the same response to mild pain as their non-mutant mouse counterparts. The mutant mice, however, exhibited a reduced response when subjected to stimuli producing moderate-to-intense pain. Scientists believe that neurokinin A, along with substance P, is released directly in response to intensified pain stimuli.

The study authors received funding from several institutes at th
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Contact: Stephanie Clipper
301/496-5751
NIH/National Institute of Neurological Disorders and Stroke
25-Mar-1998