{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:47:19Z","timestamp":1772120839414,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,1,13]],"date-time":"2012-01-13T00:00:00Z","timestamp":1326412800000},"content-version":"vor","delay-in-days":165,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2011,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Experimental animal pain models involving peripheral nerve lesions have expanded the understanding of the pathological changes caused by nerve damage. However models for the pathogenesis of chronic pain patients lacking obvious nerve injuries have not been developed to the same extent. Guided by clinical observations, we focused on the initiating noxious event, the context when applying nociceptive stimulation targeting long\u2010lasting pain elicited by muscle insult. The administration of a nociceptive agent (6% hypertonic saline: HS; 5\u2010time repeated\u2010injection: HS5) after pretreatment with an immuno\u2010inflammatory agent (lipopolysaccharide: LPS, 2\u03bcg\/kg) into one gastrocnemius muscle produced markedly long\u2010persisting biphasic sustained mechanical hypersensitivity on the plantar surface of\n                    <jats:italic>both<\/jats:italic>\n                    hindpaws. In the acute phase, the blockade of afferent inputs from the injected\u2010site was effective in returning the contralateral enhanced\u2010responses to baseline levels. In contrast, similar blockade during the chronic phase did not affect the contralateral enhanced\u2010responses, indicating that the hypersensitivity in the two phases was probably induced by different mechanisms. However, increasing the dose of LPS (20\u03bcg\/kg) before applying HS5 eliminated the development of mechanical hypersensitivity in the chronic phase, while the hypersensitivity in the acute phase was significantly more severe than with low\u2010dose LPS\u2010pretreatment. In this model, the development of hypersensitivity could be modulated by manipulating LPS\u2010doses prior to noxious stimulation. This novel chronic pain model based on a preceding \u2018priming\u2019 myalgic stimulus provides an intriguing means for studying the pathogenesis of chronic pain.\n                  <\/jats:p>","DOI":"10.1016\/j.ejpain.2011.01.001","type":"journal-article","created":{"date-parts":[[2011,2,9]],"date-time":"2011-02-09T04:56:47Z","timestamp":1297227407000},"page":"724-731","source":"Crossref","is-referenced-by-count":5,"title":["Low rather than high dose lipopolysaccharide \u2018priming\u2019 of muscle provides an animal model of persistent elevated mechanical sensitivity for the study of chronic 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