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Taste Researchers Make Bittersweet Discovery

A single receptor provides response to garlic, mustard

THURSDAY, March 23, 2006 (HealthDay News) -- The pleasure and pain diners get from sharp tastes such as garlic, mustard or the sushi condiment wasabi rely on one newly identified pain receptor, researchers report.

This new information about the receptor -- called TRPA1 -- may help in the development of new anti-inflammatory and pain medications, the researchers said.

"By understanding what triggers TRP channel receptors, we can learn something new about how pain is sensed," lead researcher David Julius, of the University of California, San Francisco, said in a prepared statement.

The finding appears in the March 24 issue of Cell.

The study also concluded that TRPA1 underlies the body's response to a number of environmental irritants, including acrolein, which is responsible for the toxic and inflammatory effects caused by tear gas, vehicle exhaust, tobacco smoke, and the byproducts of some chemotherapy drugs.

Neurons taken from mice that lacked TRPA1 were completely insensitive to garlic and mustard oil, the UCSF team reported. In addition, mice that lacked TRPA1 did not flinch or try to lick their paws after mustard oil was applied to them -- something that normal mice would do. The paws of the TRPA1-deficient mice also swelled less and became less sensitive to pain in response to mustard oil exposure.

"By characterizing cellular and behavioral deficits in mice lacking functional TRPA1 channels, we have now demonstrated that the TRPA1 channel constitutes the sole site of mustard oil and garlic action on the nerve cells that elicit tissue damage, discomfort and pain," the study authors wrote.

"We've also found that the receptor plays an important role in the response to environmental irritants found in air pollution, smoke, and as a byproduct of some chemotherapy drugs," the study authors added.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about pain research.

SOURCE: Cell Press, news release, March 23, 2006
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