Reactive oxygen species (ROS) modulate AMPA receptor phosphorylation and cell-surface localization in concert with pain-related behavior.

摘要: Sensitization of dorsal horn neurons (DHNs) in the spinal cord is dependent on pain-related synaptic plasticity and causes persistent pain. The DHN sensitization mediated by a signal transduction pathway initiated activation N-methyl-d-aspartate receptors (NMDA-Rs). Recent studies have shown that elevated levels reactive oxygen species (ROS) phosphorylation-dependent trafficking GluA2 subunit α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA-Rs) are part signaling for sensitization. However, relationship between ROS AMPA-R phosphorylation not known. Thus, this study investigated effects scavengers cell-surface localization GluA1 GluA2. Intrathecal NMDA- intradermal capsaicin-induced hyperalgesic mice were used since both pain models share NMDA-R activation-dependent cord. Our behavioral, biochemical, immunohistochemical analyses demonstrated that: 1) vivo increased AMPA-Rs at (S818, S831, S845) (S880) subunits; 2) but decreased GluA2; 3) reduction PBN (N-tert-butyl-α-phenylnitrone) or TEMPOL (4-hydroxy-2, 2, 6, 6-tetramethylpiperidin-1-oxyl) reversed these changes AMPA-Rs, as well behavior. Given to cell surface synapse regulated GluA2, our suggests ROS-dependent necessary thus, We further suggest will ameliorate molecular