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Potassium-Efflux Channels in Extensor and Flexor Cells of the Motor Organ of Samanea saman Are Not Identical. Effects of Cytosolic Calcium1

机译:大鼠伸肌和屈肌细胞钾流出通道。 Samanea saman的运动器官不完全相同。的影响 胞质钙1

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摘要

Leaflet movements in the mimosa-family tree Samanea saman stem from coordinated volume changes of cells in the leaf motor organs in the adaxial and abaxial motor cells (“flexors” and “extensors”). Shrinking, initiated by dissimilar light signals in extensors and in flexors, depends in both cell types on K+ efflux via depolarization-dependent potassium (KD) channels. To compare between flexor and extensor KD channels and to test for a possible interaction of these channels with the Ca2+-mobilizing phosphoinositide cascade evoked in these motor cells by the “shrinking signals,” we probed the channels with varying (5 nm–3 mm) cytosolic free-Ca2+ concentration ([Ca2+]cyt) in patch-clamped inside-out excised membrane patches. Ca2+ was not required for KD channel activation. [Ca2+]cyt of 600 nm decreased the mean number of open KD channels in flexors, as monitored at −30 mV. Detailed analysis revealed that in flexors millimolar [Ca2+]cyt decreased the maximum number of open channels, but simultaneously increased KD channel opening probability by negatively shifting the half-maximum-activation voltage by 40 to 50 mV. Thus, the promoting and the inhibitory effects at millimolar [Ca2+]cyt practically cancelled-out. In contrast to flexors, none of the gating parameters of the extensor KD channels were affected by [Ca2+]cyt. Irrespective of [Ca2+]cyt, the steady-state gating of extensor KD channels was slightly but significantly more voltage sensitive than that of flexors. The unitary conductances of flexor and extensor KD channels were similar and decreased by approximately 20% at millimolar [Ca2+]cyt. It is intriguing that the extensor KD channels were significantly less K+ selective than those in flexors.
机译:含羞草科Samanaa saman的小叶运动源于上,下运动细胞(“屈肌”和“伸肌”)中叶运动器官中细胞的协调体积变化。收缩是由伸肌和屈肌中不同的光信号引起的,在两种细胞类型中,依赖于通过去极化依赖性钾(KD)通道的K +外排。为了在屈肌和伸肌KD通道之间进行比较,并测试这些通道与这些“收缩信号”在这些运动细胞中诱发的Ca2 +迁移的磷酸肌醇级联反应的可能相互作用,我们探查了变化的通道(5 nm–3 mm)膜片固定的内外切膜碎片中的胞质游离Ca2 +浓度([Ca2 +] cyt)。 CaD不需要激活KD通道。 600 nm的[Ca2 +] cyt降低了屈肌中开放KD通道的平均数量,在-30 mV处进行了监测。详细的分析显示,屈肌中[Ca2 +] cyt减少了最大打开通道数,但同时通过将最大激活电压的一半负移40到50 mV,从而增加了KD通道打开的可能性。因此,毫摩尔[Ca2 +] cyt的促进和抑制作用实际上被抵消了。与屈肌相反,伸肌KD通道的门控参数均不受[Ca2 +] cyt的影响。与[Ca2 +] cyt无关,伸肌KD通道的稳态门控对屈肌的电压敏感性略高,但明显更高。屈肌和伸肌KD通道的单位电导相似,在毫摩尔[Ca2 +] cyt下降低约20%。有趣的是,伸肌KD通道的K +选择性远低于屈肌中的K +通道。

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