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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2006-10-27T00:00:00-04:00" class="date-display-single">October 27, 2006</span></p><div class='syndicate'><h1>Gene Affects Pain Sensitivity</h1><div class="media-float-right"><div class="ds-1col file file-image file-image-jpeg view-mode-floated_media clearfix">
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</div><p>Researchers have identified a gene that affects both a person’s sensitivity to short-term (acute) pain and their risk of developing chronic pain after a kind of back surgery.</p>
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<p>A team led by Dr. Clifford J. Woolf of Massachusetts General Hospital and Harvard Medical School in Boston identified the gene, called <em>GCH1</em>, which codes for an enzyme called GTP cyclohydrolase. Dr. Mitchell B. Max of NIH’s National Institute of Dental and Craniofacial Research was part of the research team; the work was also funded by NIH’s National Institute on Alcoholism Abuse and Alcoholism, NIH’s National Institute of Neurological Disorders and Stroke and other organizations.</p>
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<p>The researchers explain in the October 22, 2006, advance online publication of <em>Nature Medicine</em> that they identified <em>GCH1</em> by looking for genes that underwent significant changes in activity after sciatic nerve injury. <em>GCH1</em> is one of several genes that code for enzymes needed to produce a chemical called tetrahydrobiopterin (BH4). BH4 is involved in producing dopamine and several other nerve-signaling chemicals.</p>
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<p>The investigators tested the effects of GTP cyclohydrolase and BH4 in several animal models of pain. They found that rats with pain caused by nerve damage had greatly increased levels of <em>GCH1</em> gene activity and BH4, and that injecting a GTP cyclohydrolase inhibitor called DAHP alleviated hypersensitivity to pain in animal models. Injecting BH4 greatly increased pain sensitivity.</p>
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<p>The researchers looked for <em>GCH1</em> gene variations in people and found that a specific variant of the gene protected against development of chronic pain in people who had participated in a study of a surgery for back pain. About 28% of the people in the study had at least one copy of the pain-protective variant of the gene. People with two copies of the protective version of <em>GCH1</em> had the lowest risk of developing chronic pain, those with one copy had an intermediate risk and those with no copies had the highest risk.</p>
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<p>The researchers went on to show that the gene variant appeared to reduce acute pain in normal volunteers. Those with two copies of the protective gene variant were less sensitive to temporary pain induced by pressure and other stimuli than those with one or no copies.</p>
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<p>"This is a completely new pathway that contributes to the development of pain," Dr. Woolf says. "The study shows that we inherit the extent to which we feel pain, both under normal conditions and after damage to the nervous system."</p>
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<p>The GTP cyclohydrolase inhibitor used in this study, DAHP, is not very strong and is unlikely to be useful as a human drug, Woolf says. Researchers are now looking for other substances that might work as GTP cyclohydrolase inhibitor drugs in humans.</p>
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<p>Dr. Woolf and his colleagues are also planning studies to learn how <em>GCH1</em> regulates pain. They hope to identify other gene variants that affect pain sensitivity and the risk of chronic pain. This gene accounts for some of the inherited differences in pain, but other genes likely also play a role.</p>
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</div><h2 class="label-above">Related Links</h2><ul class="spaced print-urls"><li><a href="http://health.nih.gov/result.asp?disease_id=493&terms=pain" target="_top">Pain</a></li></ul>
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<p><strong>Editor:</strong> Harrison Wein, Ph.D.</p>
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<p><strong>Assistant Editors:</strong> Vicki Contie and Brian Doctrow, Ph.D.</p>
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<p><strong><em>NIH Research Matters </em></strong>is a weekly update of NIH research highlights reviewed by NIH’s experts. It's published by the <a href="/institutes-nih/nih-office-director/office-communications-public-liaison">Office of Communications and Public Liaison</a> in the <a href="/institutes-nih/nih-office-director">NIH Office of the Director</a>.</p>
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<p>ISSN 2375-9593</p>
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