Researchers modify drug to enter cells and treat pain PNASNews
, illustrates how pain signaling occurs inside cells rather than at the surface, highlighting the need for drugs that can reachG protein-coupled receptors are a large family of proteins that regulate many processes in the body and are the target of one third of clinically used drugs. A subset of these receptors plays an important role in pain, including the neurokinin-1 receptor, which is activated by a pain-transmitting neuropeptide called substance P.
Several FDA-approved drugs that target the NK1 receptor are used to prevent nausea and vomiting associated with chemotherapy or surgery. Scientists previously hoped that the NK1 receptor would be a promising target for treating pain—butin the 1990s and early 2000s. One reason why drugs targeting the NK1 receptor may not have been effective against pain is that most drugs block receptors at the surface of cells. However, researchers at the NYU Pain Research Center have shown that GCPRs signal pain not from the surface of cells, but from compartments inside the cell called endosomes.
"Sustained signaling in endosomes is necessary for the hyperexcitability of pain-sensing neurons involved in," said Nigel Bunnett, professor and chair of the Department of Molecular Pathobiology at NYU College of Dentistry and the study's senior author."As a result, treating pain may require the development of drugs that penetrate cells, are retained in endosomes, and disrupt signaling inside the cell.
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