BREAKING DOWN THE PAIN BARRIER
Most limbs are packed with sensory nerve endings that detect touch, heat and acute pain — sensations that are transmitted rapidly and accurately to the brain by the nerves. Drugs — such as the widely used, but ill-understood, non-steroidal anti-inflammatories or NSAIDs (a group that includes aspirin) — that silence these peripheral sensory nerves relieve acute pain well.
But two studies reported this week in Nature (Vol. 410, No. 6827, pp471-475; News & Views, 22 Mar 2001) shed light on how new-generation NSAIDs might be better used when local inflammation blocks nerve impulses or when pain arises from systemic infection.
Clifford J. Woolf of Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, and colleagues and Anders Blomqvist of the University of Linköping, Sweden, and colleagues show that local inflammation can cause pain in nearby non-inflamed areas via the action of secreted mediators which upregulate the production of the enzyme cyclooxygenase II (COX2) in the central nervous sytem. COX2 is targetted by NSAIDs and is a central regulator of inflammatory pain. This implies that NSAID better able to penetrate the blood-brain barrier would make better pain killers.
Tamas Bartfai of the Scripps Research Institute, La Jolla, California, discusses the background and ramifications of this work in an accompanying News and Views article.
Clifford J. Woolf
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(C) Nature press release.
Message posted by: Trevor M. D'Souza