Minocycline prevents impaired glial glutamate uptake in the spinal sensory synapses of neuropathic rats

摘要: Activation of glutamate receptors and glial cells in the spinal dorsal horn are two fundamental processes involved pathogenesis various pain conditions, including neuropathic induced by injury to peripheral or central nervous systems. Numerous studies have demonstrated that minocycline treatment attenuates allodynic hyperalgesic behaviors tissue inflammation nerve injury. However, synaptic mechanisms which prevents hyperalgesia not fully understood. We recently reported deficient uptake transporters (GTs) is key for enhanced activation N-methyl-d-aspartate (NMDA) sensory synapses rats receiving partial sciatic ligation (pSNL). In this study, we investigated how affects NMDA with pSNL whole cell recordings currents laminea I II neurons from slices. The effects treatments on expression GTs astrocyte marker fibrillary acidic protein (GFAP) were analyzed immunohistochemistry. normalized activated both weak strong input temporally associated attenuated mechanical allodynia intraperitoneal injection minocycline. Minocycline ameliorated downregulation GT astrocytes horn. further revealed preventing at synapse crucial preserving treated Our suggest may be a potential target development analgesics.