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Inflammation: Pain in the brain
When tissue is injured, it sends out signaling molecules that cause inflammation in the vicinity of the damaged tissue. Nonsteroidal anti-inflammatory drugs (NSAIDs) work by blocking an enzyme, cyclooxygenase (cox), that is produced in response to these local signals. Cox makes a pain-inducing mediator that acts on nerve cells. In rat studies, the researchers find that it's not a nerve signal but a signal transported in the bloodstream that triggers the central nervous system to produce molecules such as interleukin-1b and release them into the cerebrospinal fluid. These molecules are too large to have been carried into the brain from the bloodstream, although a smaller molecule may enter the brain this way to initiate the process. Interleukin-1b causes nerve cells to start to produce cox, thereby initiating pain signals within the nervous system. Injecting NSAIDs directly into the cerebrospinal fluid inhibits cox there and makes the inflammation less painful, the researchers find. This class of painkillers had heretofore been thought to work exclusively outside of the brain. The new work suggests drugs might be more effective if specifically designed to penetrate better into the brain.
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