THE ROLE OF POTASSIUM CHANNELS IN SCHWANN-CELL PROLIFERATION IN WALLERIAN DEGENERATION OF EXPLANT RABBIT SCIATIC-NERVES
THE ROLE OF POTASSIUM CHANNELS IN SCHWANN-CELL PROLIFERATION IN WALLERIAN DEGENERATION OF EXPLANT RABBIT SCIATIC-NERVES
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DOI：
10.1113/jphysiol.1989.sp017455
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发表时间：
1989-01-01
影响因子：
5.5
通讯作者：
WILSON, GF
中科院分区：
文献类型：
--
作者：
CHIU, SY;WILSON, GF
1.对培养0 - 10天的成年家兔坐骨神经外植体段中有髓轴突的雪旺细胞进行全细胞离子电流的膜片钳研究和增殖的生物化学研究。2.通过[3 H]胸苷掺入和电子显微镜放射自显影测定，神经外植体后雪旺细胞增殖增加。增殖进行平行于逐渐超极化的静息电位和有髓轴突的雪旺细胞中的K+电流的增加。3.通过在各种K+通道阻断剂存在下孵育外植体神经来研究K+通道与增殖之间的关系。奎宁，TEA和4-氨基吡啶（4-AP），阻断了雪旺细胞中的K+电流，也被发现以剂量依赖性方式和相似的浓度阻断雪旺细胞增殖。电子显微镜检查显示，TEA不会延迟髓鞘和轴突的分解，而髓鞘和轴突的分解被认为是许旺细胞增殖的有丝分裂原的来源。4.用去极化培养液孵育外植神经，研究静息电位与增殖的关系。去极化一价阳离子（K+和Rb+）导致雪旺细胞增殖的显着抑制。然而，Cs+和NH 4+，这并没有在膜片钳研究中去神经鞘细胞，也抑制增殖。短杆菌肽和藜芦定也抑制增殖。5.结果表明，K+通道的表达是重要的功能，在华勒变性的雪旺细胞增殖。K+通道与细胞增殖之间的一个可能联系可能是通过雪旺细胞增殖时发生的静息膜电位超极化。
1. Patch clamp studies of whole‐cell ionic currents and biochemical studies of proliferation were carried out on Schwann cells of myelinated axons in explant segments of sciatic nerves of adult rabbit maintained in culture for 0‐10 days. 2. Schwann cell proliferation, as assayed by [3H]thymidine incorporation and by electron microscopic autoradiography, showed an increase following nerve explant. Proliferation proceeded in parallel with a gradual hyperpolarization of the resting potential and an increase in K+ currents in Schwann cells of myelinated axons. 3. The relation between K+ channels and proliferation was studied by incubating explant nerves in the presence of various K+ channel blockers. Quinine, TEA and 4‐aminopyridine (4‐AP), which blocked K+ currents in Schwann cells, were found also to block Schwann cell proliferation in a dose‐dependent fashion and over similar concentrations. Electron microscopy showed that TEA did not retard myelin and axonal break‐down which is thought to be the source of mitogens for Schwann cell proliferation. 4. The relation between resting potential and proliferation was studied by incubating explant nerves in depolarizing culture media. Depolarizing monovalent cations (K+ and Rb+) led to a marked inhibition of Schwann cell proliferation. However, Cs+ and NH4+, which did not depolarize Schwann cells in patch clamp studies, also inhibited proliferation. Gramicidin and veratridine also inhibited proliferation. 5. The results suggest that the expression of K+ channels is functionally important for Schwann cell proliferation in Wallerian degeneration. A possible link between K+ channel and proliferation might be via a hyperpolarization of the resting membrane potential which occurs when Schwann cells proliferate.