title: Neuron-glial communication mediated by TNF-α and glial activation in dorsal root ganglia in visceral inflammatory hypersensitivity.
abstract: Communication between neurons and glia in the dorsal root ganglia (DRG) and the central nervous system is critical for nociception. Both glial activation and proinflammatory cytokine induction underlie this communication. We investigated whether satellite glial cell (SGC) and tumor necrosis factor-α (TNF-α) activation in DRG participates in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat model of visceral hyperalgesia. In TNBS-treated rats, TNF-α expression increased in DRG and was colocalized to SGCs enveloping a given neuron. These SGCs were activated as visualized under electron microscopy: they had more elongated processes projecting into the connective tissue space and more gap junctions. When nerves attached to DRG (L6-S1) were stimulated with a series of electrical stimulations, TNF-α were released from DRG in TNBS-treated animals compared with controls. Using a current clamp, we noted that exogenous TNF-α (2.5 ng/ml) increased DRG neuron activity, and visceral pain behavioral responses were reversed by intrathecal administration of anti-TNF-α (10 μg·kg(-1)·day(-1)). Based on our findings, TNF-α and SGC activation in neuron-glial communication are critical in inflammatory visceral hyperalgesia.
authors.affiliation: Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; and.
authors.forename: Dan-dan
authors.initials: DD
authors.lastname: Song
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.forename: Dong
authors.initials: D
authors.lastname: Tang
authors.forename: Li-ya
authors.initials: LY
authors.lastname: Huang
authors.forename: Yao-zong
authors.initials: YZ
authors.lastname: Yuan
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D001522:Behavior, Animal; D002450:Cell Communication / Q000187:drug effects; D022081:Cell Surface Extensions / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D003106:Colon / Q000294:innervation*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005727:Ganglia, Spinal / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D017629:Gap Junctions / Q000276:immunology / Q000378:metabolism; D006930:Hyperalgesia / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism*; D008297:Male; D009457:Neuroglia / Q000276:immunology / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D017288:Pain Threshold / Q000187:drug effects; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000276:immunology / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D000911:Antibodies, Monoclonal; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D014302:Trinitrobenzenesulfonic Acid
keywords: satellite glial cells; tumor necrosis factor-α