Bringmann A, Francke M, Pannicke T, Biedermann B, Faude F, Enzmann V, Wiedemann P, Reichelt W, Reichenbach A
Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, FRG.
Invest Ophthalmol Vis Sci. 1999 Dec;40(13):3316-23.
To determine differences of K+ channel activity between Müller glial cells obtained from retinas of healthy human donors and of patients with retinal detachment and proliferative vitreoretinopathy.
Müller cells were enzymatically isolated from retinas of healthy donors and from excised retinal pieces of patients. The whole-cell and the cell-attached configurations of the patch-clamp technique were used to characterize the current densities of different K+ channel types and the activity of single Ca2+ -activated K+ channels of big conductance (BK).
Cells from patients displayed a less negative mean membrane potential (-52.8 mV) than cells from healthy donors (-80.6 mV). However, the membrane potentials in cells from patients scattered largely between -6 and -99 mV. The inwardly rectifying K+ permeability in cells from patients was strongly reduced (0.3 pA/pF) when compared with cells from healthy donors (6.0 pA/pF). At the resting membrane potential, single BK channels displayed a higher mean activity (open probability, Po, and channel current amplitude) in cells from patients (Po, 0.30) than in cells from healthy donors (Po: 0.03). The variations of BK current amplitudes were correlated with the variations of the membrane potential.
The dominant expression of inwardly rectifying channels in cells from healthy donors is thought to support important glial cell functions such as the spatial buffering of extracellular K+. The downregulation of these channels and the less negative mean membrane potential in cells from patients should impair spatial buffering currents and neurotransmitter clearance. The increased activity of BK channels may support the proliferative activity of gliotic cells via feedback regulation of Ca2+ entry and membrane potential.
确定从健康人类供体视网膜以及视网膜脱离和增殖性玻璃体视网膜病变患者视网膜中获取的 Müller 胶质细胞之间钾离子通道活性的差异。
通过酶解法从健康供体视网膜和患者切除的视网膜组织块中分离 Müller 细胞。采用膜片钳技术的全细胞模式和细胞贴附模式来表征不同类型钾离子通道的电流密度以及大电导钙激活钾离子通道（BK）的单通道活性。
患者来源的细胞平均膜电位（-52.8 mV）比健康供体来源的细胞（-80.6 mV）更负性减小。然而，患者来源细胞的膜电位在 -6 mV 至 -99 mV 之间有很大的离散度。与健康供体来源的细胞（6.0 pA/pF）相比，患者来源细胞的内向整流钾离子通透性显著降低（0.3 pA/pF）。在静息膜电位下，患者来源细胞中单个 BK 通道的平均活性（开放概率，Po，以及通道电流幅度）高于健康供体来源的细胞（Po：0.30 对比 Po：0.03）。BK 电流幅度的变化与膜电位的变化相关。
健康供体来源细胞中内向整流通道的优势表达被认为有助于支持重要的胶质细胞功能，如细胞外钾离子的空间缓冲。这些通道的下调以及患者来源细胞中平均膜电位更负性减小应会损害空间缓冲电流和神经递质清除。BK 通道活性的增加可能通过对钙离子内流和膜电位的反馈调节来支持胶质化细胞的增殖活性。
