Washington: A new discovery by University of Leeds researchers could explain the current failings in the drug development process for painkillers and may offer opportunities for a new approach.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.
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