Hochstrate P, Piel C, Schlue W R
Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Brain Res. 1995 Oct 23;696(1-2):231-41. doi: 10.1016/0006-8993(95)00883-r.
The effects of extracellular K+ on the intracellular free Ca2+ concentration ([Ca2+]i) of neuropile glial cells and Retzius neurones in intact segmental ganglia of the leech Hirudo medicinalis were investigated by using iontophoretically injected fura-2. In both cell types, an elevation of the extracellular K+ concentration ([K+]o) caused an increase in [Ca2+]i, which was blocked by Co2+, Ni2+ and menthol, whereas nicardipine, flunarizine, omega-conotoxin GVIA and omega-agatoxin IVA were ineffective. In Ca(2+)-free solution, the K(+)-induced [Ca2+]i increase was largely suppressed in neuropile glial cells and completely abolished in Retzius neurones. The results indicate that the K(+)-induced [Ca2+]i increase was mainly due to Ca2+ influx through voltage-dependent Ca2+ channels. The Ca2+ channels of the two cell types were activated at different membrane potentials but at the same [K+]o. In both cell types, the recovery from a K(+)-induced [Ca2+]i increase was unaltered in Na(+)-free solution, indicating that active Ca2+ transport across the plasma membrane is mediated by Na(+)-independent mechanisms.
通过离子电泳注入fura-2，研究了细胞外K⁺对药用水蛭完整节段神经节中神经毡胶质细胞和Retzius神经元细胞内游离Ca²⁺浓度（[Ca²⁺]i）的影响。在这两种细胞类型中，细胞外K⁺浓度（[K⁺]o）升高均导致[Ca²⁺]i增加，这被Co²⁺、Ni²⁺和薄荷醇阻断，而尼卡地平、氟桂利嗪、ω-芋螺毒素GVIA和ω-阿加毒素IVA无效。在无Ca²⁺溶液中，K⁺诱导的[Ca²⁺]i增加在神经毡胶质细胞中被大幅抑制，在Retzius神经元中则完全消除。结果表明，K⁺诱导的[Ca²⁺]i增加主要是由于Ca²⁺通过电压依赖性Ca²⁺通道内流。两种细胞类型的Ca²⁺通道在不同膜电位下被激活，但在相同的[K⁺]o下。在这两种细胞类型中，在无Na⁺溶液中，K⁺诱导的[Ca²⁺]i增加后的恢复未改变，表明跨质膜的主动Ca²⁺转运由不依赖Na⁺的机制介导。
