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Back To Vidyya Novel New Pain Research At SmithKline Beecham

Hot Pepper Plants And "Knock-Out Mice" Aid The Process

The current issue of Nature reports that scientists at SmithKline Beecham have demonstrated that a cell-surface protein that senses the pungent ingredient in chili peppers also plays a role in the sensation of pain and may be a useful target for pain-relieving drugs.

The protein is a cell-surface receptor found predominantly on sensory neurons. The receptor has been known for several years to respond to heat as well as to capsaicin, the component of chili peppers that induces a burning sensation. Yet because this understanding was based on experiments limited to cells grown in the laboratory, the role of the receptor in actual pain sensation in animals had yet to be determined.

Scientists have taken the next experimental step by studying not only cultured cells but "knock-out" mice that had been genetically altered to inactivate the capsaicin receptor, also called the vanilloid receptor-1 (VR1).

As reported in Nature, the investigators used electrophysiological tests to examine the effects of various stimuli on isolated cells in culture. The study found no specific responses to capsaicin or heat in the cells from altered mice, in contrast to the expected responses observed in cells from normal mice. More relevant to drug discovery, behavioral studies found that the altered mice lacked altogether the enhanced sensitivity to heat that normal mice show when tissue is inflamed.

"The most intriguing finding is that the mice lost the hypersensitivity to heat which is associated with inflammation," said Dr. Frank S. Walsh, Vice President and Director, Neuroscience Research, SB. "This suggests that targeting VR1 may be useful in treating pain resulting from tissue injury, such as pain associated with surgery, infection, ulcers, and cancer or its treatment."

Except in responding to certain stimuli, the mice exhibited apparently normal behavior, as might be expected given the prevalence of VR1 in sensory neurones as contrasted with other cell types. This observation gives an early suggestion that a drug modifying VR1 may have few side effects.

Another finding of the study indicated there remains much to be learned about the molecular basis of pain. Although the altered mice were markedly less sensitive than normal mice to heat in inflamed tissue, all the mice exhibited much the same sensitivity to moderate heat when inflammation was not present. The implication is that other receptors play a role in sensing heat. Years of investigation remain before this work might lead to a novel painkiller. However, the findings are very interesting and give scientists a new direction to investigate.

Nature offers another example of the usefulness of "knockout mice" in research intended to yield new therapies. In such studies, the gene encoding a protein of interest, in this instance the gene encoding VR1, is inactivated. The likely role of the protein can then be determined by the effect of its absence.

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Editor: Susan K. Boyer, RN
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