title: Dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor trafficking in inflammatory pain.
abstract: Activation of synaptic N-methyl-D-aspartic acid receptor and its intracellular downstream signals in dorsal horn neurons of spinal cord contribute to central sensitization, a mechanism that underlies the development and maintenance of pain hypersensitivity in persistent pain. However, the molecular process of this event is not understood completely. Recently, new studies suggest that peripheral inflammatory insults drive changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit trafficking via N-methyl-D-aspartic acid receptor-triggered activation of protein kinases in dorsal horn and raise the possibility that such changes might contribute to central sensitization in persistent pain. This review presents current evidence regarding the changes that occur in the trafficking of dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunits GluR1 and GluR2 under persistent inflammatory pain conditions and discusses the potential mechanisms by which such changes participate in the development and maintenance of inflammatory pain.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ytao1@jhmi.edu
authors.forename: Yuan-Xiang
authors.initials: YX
authors.lastname: Tao
mesh_terms: D000818:Animals; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology*; D010146:Pain / Q000378:metabolism* / Q000473:pathology*; D020671:Posterior Horn Cells / Q000378:metabolism* / Q000502:physiology; D021381:Protein Transport / Q000502:physiology; D018091:Receptors, AMPA / Q000032:analysis / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate
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