Serum-induced changes in the physiology of mammalian retinal glial cells: role of lysophosphatidic acid
Serum-induced changes in the physiology of mammalian retinal glial cells: role of lysophosphatidic acid
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DOI：
10.1111/j.1469-7793.1998.445bw.x
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发表时间：
1998-01-15
影响因子：
5.5
通讯作者：
Puro, DG
中科院分区：
文献类型：
--
作者：
Kusaka, S;Kapousta-Bruneau, N;Puro, DG
1.随着血管-CNS屏障的破坏，血清进入神经系统。虽然这是一种常见的病理生理学事件，但血清对神经系统功能的影响的知识有限。在这项研究中，我们研究了血清对视网膜主要神经胶质细胞Muller细胞离子通道活性的影响。新鲜分离的牛和人视网膜Muller细胞的膜片钳技术的穿孔膜片配置进行了研究。在其他实验中，记录离体大鼠视网膜的视网膜电图（ERG）。穿孔贴片记录显示，血清诱导钙渗透性，非特异性阳离子（NSC）电流。在诱导该电流后约40 s，还检测到向外整流的K+电流。对胭脂虫毒素和玛格毒素的敏感性表明，这种K+电流是由于K（v）1.3通道的激活。K（v）1.3电流的这种增加依赖于细胞外钙离子。NSC和K（v）1.3电流分别在100%和95%的取样Muller细胞中被血清激活。此外，在少数（21%）的细胞，内向整流K+电流略有抑制。离子通道的这些变化。活性与Muller细胞的去极化有关.我们假设NSC通道的激活将减少通过Muller细胞的K+虹吸。与这一想法一致，来自离体视网膜的ERG显示出血清诱导的慢P-III组分的减少，慢P-III组分是由Muller细胞响应光诱发的细胞外K+浓度变化而产生的。溶血磷脂酸（LPB），血清的一个组成部分，对Muller细胞的作用，定性类似于血清诱导。我们的观察表明，暴露于血清改变了哺乳动物视网膜的Muller神经胶质细胞中多种类型的离子通道的活性。当血-视网膜屏障被破坏时，LPA可能是调节Muller细胞生理学的血清衍生分子之一。
1. With a breakdown of the vascular-CNS barrier, serum enters the nervous system. Although this is a frequent pathophysiological event, knowledge of the effects of serum on the function of the nervous system is Limited. In this study, we examined the effects of serum on the activity of ion channels in Muller cells: the principal glia of the retina.2. Freshly dissociated Muller cells from the bovine and human retina were studied with the perforated-patch configuration of the patch clamp technique. In other experiments, electroretinograms (ERGs) were recorded from isolated rat retinas.3. Perforated-patch recordings revealed that serum induced a calcium-permeable, non-specific cation (NSC) current. Approximately 40 s after induction of this current, an outwardly rectifying K+ current was also detected. Sensitivity to charybdotoxin and margatoxin indicated that this K+ current was due to the activation of K(v)1.3 channels. This increase in the K(v)1.3 current was dependent on extracellular calcium.4. The NSC and K(v)1.3 currents were activated by serum in 100% and 95% of the sampled Muller cells, respectively. Also, in a minority (21%) of the cells, the inwardly rectifying K+ current was inhibited slightly. These changes in ion channel. activity were associated with depolarization of the Muller cells.5. We hypothesized that activation of NSC channels would reduce the siphoning of K+ via the Muller cells. Consistent with this idea, ERGs from isolated retinas showed serum-induced reductions in the slow P-III component, which is generated by Muller cells responding to light-evoked changes in the extracellular K+ concentration.6. Lysophosphatidic acid (LPB), a component of serum, had effects on Muller cells that were qualitatively similar to those induced by serum.7. Our observations demonstrate that exposure to serum alters the activity of multiple types of ion channels in Muller glial cells of the mammalian retina. When there is a breakdown of the blood-retina barrier, LPA may be one of the serum-derived molecules which regulates the physiology of Muller cells.