【摘 要】
：
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+ chann
【机 构】
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Institutes of Brain Science and Eye & ENT Hospital, State Key Laboratory of Medical Neurobiology; Fu
【出 处】
：
中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
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.
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