Inhibiting the function of a protein called sortilin — an important regulator of nerve damage-induced pain in mice — may represent a potentially effective strategy for treating chronic pain in humans, including those with multiple sclerosis, a study in mice suggests.
The researchers say more work is needed to determine if it is possible to block sortilin locally in the spinal cord.
These findings were reported in a study, “Sortilin gates neurotensin and BDNF signaling to control peripheral neuropathic pain,” published in the journal Science Advances.
Neuropathic pain is a specific type of pain that is triggered by damage to nerve cells and fibers. This damage-induced pain can be caused by an injury or by chronic diseases, including diabetes and multiple sclerosis.
Damage to nerve cells can make these cells become “uninhibited,” sending pain signals in the absence of an actual painful stimulus. The pain sensation itself can come in many forms, such as burning, pricking, stinging, tingling, freezing, or as a stabbing feeling, and is often chronic and disabling. In MS, it typically occurs in the legs as a persistent and burning pain.
“Once nerve damage has occurred, and the nerve cells go into overdrive, molecules are released which start a domino effect that ultimately triggers pain,” Mette Richner, PhD, professor at Aarhus University and lead author of the study, said in a press release.
Evidence shows that a natural molecule called neurotensin has analgesic, or painkilling, effects in experimental models, acting as a “brake” for the pain signals. Now, researchers have demonstrated that sortilin protein, which is also known as neurotensin receptor 3 (NTSR3), can regulate neurotensin analgesic signals.
In other words, neurotensin acts as a “brake” for the pain signals, and sortilin drives these pain signals by inhibiting neurotensin — essentially acting as a “brake for the brake,” the researchers said. At the molecular level, this stops the body’s pain development.
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