昆虫胶质细胞中去极化诱导的钙瞬变的发展依赖于传入轴突的存在。

C. Lohr, E. Tucker, L. Oland, L. Tolbert
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引用次数: 13

摘要

研究了去极化诱导的细胞内Ca(2+)浓度([Ca(2+)](i))的变化,这些变化是在不同胚胎后发育阶段从Manduca sexta的触角叶急性分离的神经胶质细胞中测量的。将外部K(+)浓度从4增加到25 mM,可引起胶质细胞膜的去极化。在5期中期和早期,不到20%的细胞对25 mM K(+)(1分钟)有反应,[Ca(2+)](i)短暂增加约40 nM。1天后,在5期晚期,68%的细胞对25 mM K(+)有反应,[Ca(2+)](i)瞬态振幅平均为592 nM。在晚期,所有细胞都对25 mM K(+)有反应,伴有[Ca(2+)](i)瞬态,振幅与晚期5无显著差异。从触角叶分离的第6期神经胶质细胞中,即从长期剥夺嗅觉受体轴突的触角叶分离的神经胶质细胞中,只有30%的细胞对[Ca(2+)](i)瞬变有反应。这些[Ca(2+)](i)瞬变的振幅平均为93 nM,明显小于正常6期胶质细胞的振幅。[Ca(2+)](i)瞬态在无Ca(2+)的egta缓冲盐水中,以及在Ca(2+)通道阻滞剂镉和维拉帕米的存在下大大减少。结果表明,细胞膜的去极化诱导Ca(2+)通过电压激活的Ca(2+)通道流入天线叶胶质细胞。去极化诱导的Ca(2+)瞬态在5期中期和6期之间发展迅速,并且依赖于来自天线嗅觉受体细胞的传入轴突的存在。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Development of depolarization-induced calcium transients in insect glial cells is dependent on the presence of afferent axons.
Changes in the intracellular Ca(2+) concentration ([Ca(2+)](i)) induced by depolarization have been measured in glial cells acutely isolated from antennal lobes of the moth Manduca sexta at different postembryonic developmental stages. Depolarization of the glial cell membrane was elicited by increasing the external K(+) concentration from 4 to 25 mM. At midstage 5 and earlier stages, less than 20% of the cells responded to 25 mM K(+) (1 min) with a transient increase in [Ca(2+)](i) of approximately 40 nM. One day later, at late stage 5, 68% of the cells responded to 25 mM K(+), the amplitude of the [Ca(2+)](i) transients averaging 592 nM. At later stages, all cells responded to 25 mM K(+) with [Ca(2+)](i) transients with amplitudes not significantly different from those at late stage 5. In stage 6 glial cells isolated from deafferented antennal lobes, i.e., from antennal lobes chronically deprived of olfactory receptor axons, only 30% of the cells responded with [Ca(2+)](i) transients. The amplitudes of these [Ca(2+)](i) transients averaged 93 nM and were significantly smaller than those in normal stage 6 glial cells. [Ca(2+)](i) transients were greatly reduced in Ca(2+)-free, EGTA-buffered saline, and in the presence of the Ca(2+) channel blockers cadmium and verapamil. The results suggest that depolarization of the cell membrane induces Ca(2+) influx through voltage-activated Ca(2+) channels into antennal lobe glial cells. The development of the depolarization-induced Ca(2+) transients is rapid between midstage 5 and stage 6, and depends on the presence of afferent axons from the olfactory receptor cells in the antenna.
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