A recent discovery by researchers could help explain the current failings in the drug development process for painkillers. A team, led by Dr Nikita Gamper of the University's Faculty of Biological Sciences, have found a previously unknown mechanism through which pain is signalled by nerve cells.
They investigated the difference between persistent pain, such as toothache, and pain that results from the increased sensitivity of nerves in injured or diseased tissue (for example when we touch inflamed skin), known as hyperalgesia and discovered that these two types of pain are generated by the same nerves, but result from different underlying mechanisms.
The project, funded jointly by the Wellcome Trust and the Medical Research Council, investigated the painful effects of two substances that cause local inflammation: bradykinin and substance P.
Both substances bind to specific receptors on nerve cells, generating signals to the central nervous system. Because the receptors are from the same family, it has always been presumed they stimulate the same signalling pathway.
However, the team found that each receptor produces different signals; the one associated with bradykinin causing both hyperalgesia and persistent pain, whereas the one associated with substance P only caused hyperalgesia.
"Pain originates from a series of electrical signals sent by nerve cells in to the central nervous system and ultimately the brain. Despite much progress, we still don't know enough about the mechanisms by which these pain signals are generated. However, this research has shown that whilst the sensation of pain can be similar between various conditions, the underlying molecular mechanisms may in fact be very different," Dr Gamper said.
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"What's exciting about these findings is that substance P may actually suppress the activation of the pain sensing nerves themselves," noted Dr Gamper.
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The study was published online this week in Proceedings of the National Academy of Sciences (PNAS).
Source-ANI