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Researchers from the Nuffield Department of Clinical Neurosciences at the University of Oxford, along with colleagues at Cambridge University and Barts and the London School of Medicine and Dentistry, have shown the potential of a new gene therapy approach to silence human sensory neurons (nerve cells) as a means of treating persistent pain. Many current drugs for chronic pain are highly addictive, which makes it important to discover new alternatives.

Illustration of a nerve cell © Andrej Vodolazhskyi/ Shutterstock

Chemogenetics is a process where molecules that control the excitation (stimulation) of neurons are engineered so they only become active in the presence of a non-toxic drug. This process has already shown promise as a means of suppressing such excitability in research involving animals. Jimena Perez-Sanchez, a postdoctoral research scientist at the Nuffield Department of Clinical Neurosciences and joint author of the study with Steven Middleton, and her colleagues have now shown that there is a chemogenetic approach that is suitable for human applications.

First, the team expressed the gene PSAM4-GlyR, a chemogenetic system based on the human protein receptors nicotinic acetylcholine and glycine, in mouse sensory neurons. They activated PSAM4-GlyR with the clinically approved drug varenicline, which inhibited sensory neurons and also reduced the pain hypersensitivity normally associated with arthritis or nerve injury in mice.

Read the full story on the University of Oxford's website.