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成年大鼠视网膜神经节细胞中无内向整流钾通道(Kir)时的内向整流电流(Ih)

Ih without Kir in adult rat retinal ganglion cells.

作者信息

Lee Sherwin C, Ishida Andrew T

机构信息

Section of Neurobiology, Physiology and Behavior, University of California, Davis, CA 95616-8519, USA.

出版信息

J Neurophysiol. 2007 May;97(5):3790-9. doi: 10.1152/jn.01241.2006.

DOI:10.1152/jn.01241.2006
PMID:17488978
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3241988/
Abstract

Antisera directed against hyperpolarization-activated mixed-cation ("I(h)") and K(+) ("K(ir)") channels bind to some somata in the ganglion cell layer of rat and rabbit retina. Additionally, the termination of hyperpolarizing current injections can trigger spikes in some cat retinal ganglion cells, suggesting a rebound depolarization arising from activation of I(h). However, patch-clamp studies showed that rat ganglion cells lack inward rectification or present an inwardly rectifying K(+) current. We therefore tested whether hyperpolarization activates I(h) in dissociated, adult rat retinal ganglion cell somata. We report here that, although we found no inward rectification in some cells, and a K(ir)-like current in a few cells, hyperpolarization activated I(h) in roughly 75% of the cells we recorded from in voltage clamp. We show that this current is blocked by Cs(+) or ZD7288 and only slightly reduced by Ba(2+), that the current amplitude and reversal potential are sensitive to extracellular Na(+) and K(+), and that we found no evidence of K(ir) in cells presenting I(h). In current clamp, injecting hyperpolarizing current induced a slowly relaxing membrane hyperpolarization that rebounded to a few action potentials when the hyperpolarizing current was stopped; both the membrane potential relaxation and rebound spikes were blocked by ZD7288. These results provide the first measurement of I(h) in mammalian retinal ganglion cells and indicate that the ion channels of rat retinal ganglion cells may vary in ways not expected from previous voltage and current recordings.

摘要

针对超极化激活的混合阳离子通道(“I(h)”)和钾离子通道(“K(ir)”)的抗血清可与大鼠和兔视网膜神经节细胞层中的一些胞体结合。此外,在一些猫的视网膜神经节细胞中,超极化电流注入的终止可触发动作电位,这表明I(h)激活引起了反弹去极化。然而,膜片钳研究表明,大鼠神经节细胞缺乏内向整流或仅存在内向整流钾电流。因此,我们测试了超极化是否能激活成年大鼠离体视网膜神经节细胞胞体中的I(h)。我们在此报告,虽然我们在一些细胞中未发现内向整流,在少数细胞中发现了类似K(ir)的电流,但在电压钳记录的约75%的细胞中,超极化激活了I(h)。我们发现该电流可被Cs(+)或ZD7288阻断,仅被Ba(2+)轻微降低,电流幅度和反转电位对细胞外Na(+)和K(+)敏感,并且在呈现I(h)的细胞中未发现K(ir)的证据。在电流钳中,注入超极化电流会诱导缓慢松弛的膜超极化,当超极化电流停止时会反弹至几个动作电位;膜电位松弛和反弹动作电位均被ZD7288阻断。这些结果首次测量了哺乳动物视网膜神经节细胞中的I(h),并表明大鼠视网膜神经节细胞的离子通道可能以先前电压和电流记录未预期的方式变化。

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