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In the present study, the respective roles of peripheral and spinal<jats:styled-content style=\"fixed-case\">5\u2010HT<jats:sub>7<\/jats:sub><\/jats:styled-content>receptors in the modulation of mechanical hypersensitivity were investigated under two different experimental pain conditions. In a first set of experiments, the selective<jats:styled-content style=\"fixed-case\">5\u2010HT<jats:sub>7<\/jats:sub><\/jats:styled-content>receptor agonist,<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431, was systemically, intrathecally or peripherally (intraplantarly) administered to rats sensitized by intraplantar injection of capsaicin. Oral administration of<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431 (1.25\u201310\u2009mg\/kg) was found to exert a clear\u2010cut dose\u2010dependent reduction of capsaicin\u2010induced mechanical hypersensitivity. Interestingly, intrathecal administration of<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431 (100\u2009<jats:styled-content style=\"fixed-case\">\u03bcg<\/jats:styled-content>) also inhibited mechanical hypersensitivity secondary to capsaicin injection. In contrast, a dose\u2010dependent enhancement of capsaicin\u2010induced mechanical hypersensitivity was observed after local intraplantar injection of<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431 (0.01\u20131\u2009<jats:styled-content style=\"fixed-case\">\u03bcg<\/jats:styled-content>). In a second set of experiments,<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431 was systemically or intrathecally administered to rats submitted to neuropathic pain (spared nerve injury model). Significant inhibition of nerve injury\u2010induced mechanical hypersensitivity was found after intraperitoneal (10\u2009<jats:styled-content style=\"fixed-case\">mg\/kg<\/jats:styled-content>) as well as intrathecal (100\u2009<jats:styled-content style=\"fixed-case\">\u03bcg<\/jats:styled-content>) administration of<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u201057431 in this chronic pain model. These studies provide evidence that, under sensitizing neurogenic\/neuropathic conditions, activation of<jats:styled-content style=\"fixed-case\">5\u2010HT<jats:sub>7<\/jats:sub><\/jats:styled-content>receptors exerts antinociceptive effects at the level of the spinal cord and pronociceptive effects at the periphery. The antinociceptive effect mediated by central<jats:styled-content style=\"fixed-case\">5\u2010HT<jats:sub>7<\/jats:sub><\/jats:styled-content>receptors seems to predominate over the pronociceptive effect at the periphery when a selective<jats:styled-content style=\"fixed-case\">5\u2010HT<jats:sub>7<\/jats:sub><\/jats:styled-content>receptor agonist is systemically administered.<\/jats:p>","DOI":"10.1016\/j.ejpain.2011.07.004","type":"journal-article","created":{"date-parts":[[2011,8,17]],"date-time":"2011-08-17T04:45:30Z","timestamp":1313556330000},"page":"72-81","source":"Crossref","is-referenced-by-count":43,"title":["Role of peripheral versus spinal<scp>5\u2010HT<sub>7<\/sub><\/scp>receptors in the modulation of pain undersensitizing conditions"],"prefix":"10.1002","volume":"16","author":[{"given":"A.","family":"Brenchat","sequence":"first","affiliation":[{"name":"Department of Pharmacology Drug Discovery and Preclinical Development ESTEVE. Av. 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