Erin D Milligan PhD , Steven F Maier PhD , Linda R Watkins PhD
{"title":"Review: neuronal-glial interactions in central sensitization","authors":"Erin D Milligan PhD , Steven F Maier PhD , Linda R Watkins PhD","doi":"10.1016/S1537-5897(03)00044-2","DOIUrl":null,"url":null,"abstract":"<div><p>Pain facilitation has conventionally been viewed as being created and maintained solely by neurons, whereas glia (microglia and astrocytes) were not considered to be involved. Current views of glial function include a dynamic role within the spinal cord dorsal horns to create and maintain enhanced pain. This review summarizes how spinal cord glia are now implicated in diverse exaggerated pain states by proinflammatory cytokines and other potential mediators of glia-neuron communication. Glial activation is shown to be necessary and sufficient to create pain facilitation in laboratory animals. The implications for potential clinical therapeutic treatment is discussed.</p></div>","PeriodicalId":101158,"journal":{"name":"Seminars in Pain Medicine","volume":"1 3","pages":"Pages 171-183"},"PeriodicalIF":0.0000,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1537-5897(03)00044-2","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Seminars in Pain Medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1537589703000442","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 10
Abstract
Pain facilitation has conventionally been viewed as being created and maintained solely by neurons, whereas glia (microglia and astrocytes) were not considered to be involved. Current views of glial function include a dynamic role within the spinal cord dorsal horns to create and maintain enhanced pain. This review summarizes how spinal cord glia are now implicated in diverse exaggerated pain states by proinflammatory cytokines and other potential mediators of glia-neuron communication. Glial activation is shown to be necessary and sufficient to create pain facilitation in laboratory animals. The implications for potential clinical therapeutic treatment is discussed.