Meucci O, Fatatis A, Holzwarth J A, Miller R J
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637, USA.
J Neurosci. 1996 Jan 15;16(2):519-30. doi: 10.1523/JNEUROSCI.16-02-00519.1996.
We examined the properties of glutamate agonist-induced Ca2+ fluxes in cultured CG-4 and O-2A progenitor cells from rat cortex. Kainate-induced Ca2+ fluxes in these cells were found to be attributable to the activation of AMPA receptors. Thus, these fluxes were enhanced by cyclothiazide but not by concanavalin A and were blocked completely by GYKI-53655. We simultaneously examined kainate-induced Ca2+ entry and Na+ currents in these cells under voltage-clamp conditions. Both of these parameters were blocked by Joro spider toxin (JSTx) in undifferentiated cells. However, neither JSTx nor Argiotoxin 636 effectively blocked either parameter in cells differentiated into type II astrocytes. This change in toxin sensitivity occurred slowly over a period of several days. Similar results were obtained in Ca(2+)-imaging studies. When cells were differentiated into oligodendrocytes, they showed an intermediate sensitivity to block by JSTx as assessed using imaging and voltage-clamp studies. Analysis of the expression of AMPA-receptor subunits showed an increase in the concentration of glutamate receptor-2 (GluR2) in CG-4 cells as they differentiated into type II astrocytes and oligodendrocytes. These results demonstrate that the AMPA receptors in cells of the O-2A lineage flux appreciable amounts of Ca2+ but may contain variable amounts of edited GluR2 subunits.
我们研究了谷氨酸激动剂诱导的大鼠皮质培养CG-4细胞和少突胶质前体细胞系（O-2A）中Ca2+通量的特性。发现这些细胞中由海人酸诱导的Ca2+通量归因于AMPA受体的激活。因此，这些通量可被环噻嗪增强，但不能被伴刀豆球蛋白A增强，并且可被GYKI-53655完全阻断。我们在电压钳制条件下同时检测了这些细胞中海人酸诱导的Ca2+内流和Na+电流。在未分化细胞中，这两个参数均被乔罗蜘蛛毒素（JSTx）阻断。然而，在分化为II型星形胶质细胞的细胞中，JSTx和银环蛇毒素636均不能有效阻断这两个参数中的任何一个。毒素敏感性的这种变化在几天的时间内缓慢发生。在Ca(2+)成像研究中也获得了类似的结果。当细胞分化为少突胶质细胞时，通过成像和电压钳制研究评估，它们对JSTx阻断表现出中等敏感性。对AMPA受体亚基表达的分析表明，CG-4细胞在分化为II型星形胶质细胞和少突胶质细胞时，谷氨酸受体2（GluR2）的浓度增加。这些结果表明，O-2A谱系细胞中的AMPA受体可使相当数量的Ca2+通过，但可能含有不同数量的编辑型GluR2亚基。
