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视网膜脱离期间神经胶质细胞介导的视网膜变性扩散:基于兔实验研究的假说

Glial cell-mediated spread of retinal degeneration during detachment: a hypothesis based upon studies in rabbits.

作者信息

Francke Mike, Faude Frank, Pannicke Thomas, Uckermann Ortrud, Weick Michael, Wolburg Hartwig, Wiedemann Peter, Reichenbach Andreas, Uhlmann Susann, Bringmann Andreas

机构信息

Paul Flechsig Institute of Brain Research, University of Leipzig, D-04109 Leipzig, Germany.

出版信息

Vision Res. 2005 Aug;45(17):2256-67. doi: 10.1016/j.visres.2004.08.028. Epub 2005 Apr 12.

Abstract

In human subjects with peripheral retinal detachments, visual deficits are not restricted to the detached retina but are also present in the non-detached tissue. Based upon studies on a rabbit model of rhegmatogenous retinal detachment, we propose a glial cell-mediated mechanism of spread of retinal degeneration into non-detached retinal areas which may also have importance for the understanding of alterations in the human retina. Both detached and attached portions of the rabbit retina display photoreceptor cell degeneration and cystic degeneration of the innermost layers. An inverse mode of photoreceptor cell degeneration in the attached tissue suggests a disturbed support of the photoreceptor cells by Müller cells which show various indications of gliosis (increased expression of intermediate filaments, cell hypertrophy, decreased plasma membrane K(+) conductance, increased Ca(2+) responsiveness to purinergic stimulation) in both detached and attached tissues. We propose that gliotic alterations of Müller cells contribute to the degeneration of the attached retina, via disturbance of glial homeostasis mechanisms. A down-regulation of the K(+) conductance of Müller cells may prevent effective retinal K(+) and water clearance, and may favor photoreceptor cell degeneration and edema development.

摘要

在患有周边视网膜脱离的人类受试者中,视觉缺陷不仅局限于脱离的视网膜,在未脱离的组织中也存在。基于对孔源性视网膜脱离兔模型的研究,我们提出一种神经胶质细胞介导的视网膜变性扩散至未脱离视网膜区域的机制,这对于理解人类视网膜的改变可能也具有重要意义。兔视网膜的脱离部分和附着部分均显示出光感受器细胞变性以及最内层的囊性变性。附着组织中光感受器细胞变性的相反模式表明,Müller细胞对光感受器细胞的支持受到干扰,在脱离和附着组织中,Müller细胞均表现出多种胶质增生迹象(中间丝表达增加、细胞肥大、质膜钾离子电导降低、对嘌呤能刺激的钙离子反应性增加)。我们认为,Müller细胞的胶质增生性改变通过干扰胶质稳态机制,导致附着视网膜的变性。Müller细胞钾离子电导的下调可能会阻止视网膜有效清除钾离子和水分,并可能促进光感受器细胞变性和水肿形成。

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