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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="healthcare" lang="en"><front><journal-meta><journal-id journal-id-type="publisher">IJCRR</journal-id><journal-id journal-id-type="nlm-ta">I Journ Cur Res Re</journal-id><journal-title-group><journal-title>International Journal of Current Research and Review</journal-title><abbrev-journal-title abbrev-type="pubmed">I Journ Cur Res Re</abbrev-journal-title></journal-title-group><issn pub-type="ppub">2231-2196</issn><issn pub-type="opub">0975-5241</issn><publisher><publisher-name>Radiance Research Academy</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1983</article-id><article-id pub-id-type="doi"/><article-id pub-id-type="doi-url"/><article-categories><subj-group subj-group-type="heading"><subject>Healthcare</subject></subj-group></article-categories><title-group><article-title>ANTINOCICEPTIVE EFFECTS OF DIAZOXIDE IN RODENT MODEL OF CHRONIC PAIN INDUCED BY&#13;
CHRONIC CONSTRICTION NERVE INJURY&#13;
</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>B.</surname><given-names>Deshmukh A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>K.</surname><given-names>Patel J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>R.</surname><given-names>Prajapati A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>S.</surname><given-names>Patel K.</given-names></name></contrib><contrib contrib-type="author"><name><surname>J.</surname><given-names>Jadav R.</given-names></name></contrib></contrib-group><volume/><issue/><fpage>34</fpage><lpage>43</lpage><permissions><copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement><copyright-year>2009</copyright-year><license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p></license></permissions><abstract><p>Aim: Previous studies show that neuropathic pain is refractory against conventional analgesics and thus novel medicaments are desired for the treatment. Activated K+ channels are associated with reducing inappropriate or excessive neuronal activity. The aim of this study was to__ampersandsignnbsp;investigate the possible analgesic effects of potassium channel opening on neuropathic pain. Therefore, the present study was designed to investigate whether potassium channel activator can generate qualitative analgesic effects on the acute pain induced by thermal and mechanical stimulation. Methods: The effect of diazoxide at the dose of 200 mg/kg on acute thermal and mechanical nociception were assessed by sensory testing like spontaneous pain, mechanical hyperalgesia, tactile as well as cold allodynia in chronic constriction injury (CCI) induced pain in rat. Results: After CCI surgery, the rats developed neuropathic pain syndrome. Behavioral studies demonstrated that rats with the CCI experienced spontaneous pain, dynamic allodynia and mechanical hyperalgesia which were significantly different from the sham group. Treatment with diazoxide decreased significantly the withdrawal durations in all sensory tests. Conclusion: The present study indicates that activity of K+ channel may contribute significantly to the development of central sensitization-mediated pain and suggests that K+&#13;
openers may be an important molecular target for the treatment of chronic pain of neuropathic origin.__ampersandsignnbsp;&#13;
</p></abstract><kwd-group><kwd>Neuropathic pain</kwd><kwd> Diazoxide</kwd><kwd> Potassium channels</kwd><kwd> Chronic constriction injury</kwd><kwd> sensory test</kwd></kwd-group></article-meta></front></article>
