One step closer to chronic pain relief

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AARHUS
Sortilin, which is a protein expressed on the surface of nerve cells, plays a crucial role in pain development in laboratory mice and in all likelihood in humans as well. This is the main conclusion of the study ‘Sortilin gates neurotensin and BDNF signaling to control peripheral neuropathic pain’. The results are based on a decade of basic research, and even though studies on mice have only been done so far, the study provides hope for the development of a medicine that can help people with pain induced by nerve injury called neuropathic pain by medical professionals. This pain may be triggered by an acute injury or a chronic disease such as e.g. diabetes in the pain pathways and is characterized by different sensations including burning, pricking, stinging, tingling, freezing or stabbing in a chronic and disabling way. The patients have in common that they could fill a shopping basket with pain killers ranging from local anesthetic ointments to morphine without ever really getting any good results as the primary author of the article, Assistant Professor Mette Richner, puts it. She is employed at the Department of Biomedicine and the DANDRITE research center, both part of Aarhus University, Denmark. Mette Richner explains that chronic pain is triggered by overactive nerve cells, i.e. nerve cells where the regulation of their activity is not working properly. For this reason, it is necessary to gain knowledge of the changes happening at the molecular level to be able to ‘nudge things into place again’. And it’s here, at the molecular level, that we’ve now added a crucial piece to a larger puzzle, says Mette Richner, who explains that sortilin and now things get a little convoluted appears to ‘put the brakes on the brake’ which, at the molecular level, stops the body’s pain development. Once nerve damage has occurred, and the nerve cells go into overdrive, molecules are released which start a domino effect that ultimately triggers pain. The domino effect can be inhibited by a particular molecule in the spinal cord called neurotensin, and our studies show that the neurotensin is ‘captured’ by sortilin, so that the brake is itself inhibited, explains Mette Richner, who began on the project as a PhD student in Professor Anders Nykjaer’s group and subsequently completed it as a postdoc in Associate Professor’s Christian B. Vegter’s research group. Both are the last authors of the study. The research group’s hope is that the pharmaceutical industry will continue to investigate whether it is possible to block sortilin locally in the spinal cord, so that the neurotensin can move freely and get the brake to function, thereby inhibiting the pain. — VoM

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