GroupⅠmGluR-mediated inhibition of Kir channels contributes to retinal Müller cell gliosis in a

• 作 者: MinJi[1]YanyingMiao[2]Ling-DanDong[2]JieChen[2]Xiao-FenMo[1]Xing-HuaiSun[1]ZhongfengWang[2]
• 机 构: Institutes of Brain Science,Eye & ENT Hospital,State Key Laboratory of Medical Neurobiology,Fudan Un
• 出 处: The 3rd Ion Channel Conference: Ion channels-Structure, Func
• 发表日期: 2011年期

　　Müller cell gliosis is a universal response in many retinal pathological conditions,including glaucoma.Accompanying the enhanced expression of glial fibrillary acidic protein (GFAP),the Kir K+ channel is downregulated in most, if not all, retinal diseases.The mechanisms underlying Müller cell gliosis and the downregulation of K+ currents are poorly understood.Here, we show that Müller cell Kir currents were reduced significantly and GFAP expression was increased in a rat chronic ocular hypertension (COH) model.The group I mGluR agonist DHPG mimicked the COH-induced suppression of Kir currents, and this was selectively blocked by the mGluR5 antagonist MPEP.The intracellular Ca2+-dependent PLC/IP3-ryanodine/PKC signaling pathway mediated the DHPG effect.COH-induced changes in Müller cells were eliminated by injecting MPEP and were mimicked by an intravitreal injection of DHPG.Thus, mGluR5-mediated suppression of Kir currents contributed to retinal Müller cell gliosis in a rat COH model.