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UC Davis Researchers Find Key Mechanism That Causes Neuropathic Pain

Scientists at the University of California, Davis (UC Davis) have identified a key mechanism in neuropathic pain. The discovery could eventually benefit millions of patients with chronic pain from trauma, diabetes, shingles, multiple sclerosis, or other conditions that cause nerve damage.

A biological process called endoplasmic reticulum stress, or ER stress, is the significant driver of neuropathic pain, said lead researchers Bora Inceoglu, Ph.D., of the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center and Ahmed Bettaieb, Ph.D., of the UC Davis Department of Nutrition. The research article is published in the journal Proceedings of the National Academy of Sciences.

The research is supported by the Superfund Research Program, as well as other National Institutes of Health grants from the National Institute of Environmental Health Sciences and the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

"This is a fundamental discovery that opens new ways to control chronic pain," said UC Davis SRP Center Director and co-author Bruce Hammock, Ph.D., distinguished professor at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center.

Inceoglu, working in Hammock's laboratory, showed that neuropathic pain could be initiated by compounds that cause ER stress and reversed by agents that block it.

The work sheds new light on at least one biological process that mediates neuropathic pain, Inceoglu said. With this knowledge, researchers can now test ER-stress blocking drugs in the clinic and carry out fundamental research on how different types of pain grouped under the name "neuropathic" differ from each other and respond to new drugs.

To learn more about the research findings, see the UC Davis News Webpage.

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