Magazine article Science News

Molecular Switch: Protein May Influence Chronic-Pain Disorder

Magazine article Science News

Molecular Switch: Protein May Influence Chronic-Pain Disorder

Article excerpt

A cell-surface protein found in the nervous system plays a central role in a chronic-pain condition known as neuropathy, a new study in rodents suggests.

In a normal reaction to injury or disease, pain signals activate immune cells in the central nervous system. These cells signal other cells and proteins, triggering inflammation and other healing processes.

Typically, this pain-inducing signaling subsides once healing is well under way. But in neuropathic pain the signaling persists. In this way, the nervous system generates its own pain.

Neuropathic pain can afflict people with diabetes, herpes, AIDS, amputated limbs, and other conditions. Its precise mechanism in the nervous system remains poorly understood and long-lasting treatments can have side effects.

To address those issues, Joyce A. DeLeo of Dartmouth Medical School in Lebanon, N.H., and her colleagues conducted a series of experiments on mice and rats to clarify the role in neuropathic pain of a cell-surface protein dubbed TLR4, short for toll-like receptor 4. TLR4 is displayed prominently by microglia, the primary immune cells residing in the central nervous system.

The scientists induced a form of neuropathic pain in the rodents by severing a nerve near the spinal cord, an injury that throws the animals' nervous systems into disorder and causes the same kind of hypersensitivity to temperature and touch experienced by people with neuropathy.

DeLeo and her colleagues first compared groups of mice--some normal and some genetically engineered to lack TLR4 or to make a defective version of it. …

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