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钙离子对静息膜电位的影响。

The Effect of Calcium Ions on Resting Membrane Potential.

作者信息

Elliott Elizabeth R, Cooper Robin L

机构信息

Department of Biology, University of Kentucky, Lexington, KY 40506, USA.

出版信息

Biology (Basel). 2024 Sep 23;13(9):750. doi: 10.3390/biology13090750.

DOI:10.3390/biology13090750
PMID:39336177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11428845/
Abstract

Regulating membrane potential is key to cellular function. For many animal cells, resting membrane potential is predominantly driven by a family of K2P (two-pore domain) potassium channels. These channels are commonly referred to as leak channels, as their presence results in the membrane being permeable to K ions. These channels, along with various pumps and exchangers, keep the cell resting membrane potential (Rp) relatively close to potassium's equilibrium potential (E); however, in many cells, the resting membrane potential is more depolarized than the E due to a small Na ion leak. Raising [Ca] (extracellular Ca concentration) can result in hyperpolarization of the membrane potential from the resting state. The mechanism for this hyperpolarization likely lies in the blockage of a Na leak channel (NALCN) and/or voltage-gated Na channels. The effects may also be connected to calcium-activated potassium channels. Using , we here illustrate that changing [Ca] from 0.5 to 3 mM hyperpolarizes the muscle. Replacing NaCl with LiCl or choline chloride still led to hyperpolarization when increasing [Ca]. Replacing CaCl with BaCl results in depolarization. K2P channel overexpression in the larval muscle greatly reduces the effects of [Ca] on cell membrane potential, likely because potential is heavily driven by the E in these muscles. These experiments provide an understanding of the mechanisms behind neuronal hypo-excitability during hypercalcemia, as well as the effects of altered expression of K2P channels on membrane potential.

摘要

调节膜电位是细胞功能的关键。对于许多动物细胞来说，静息膜电位主要由一类K2P（双孔结构域）钾通道驱动。这些通道通常被称为泄漏通道，因为它们的存在导致膜对钾离子具有通透性。这些通道与各种泵和交换器一起，使细胞静息膜电位（Rp）相对接近钾的平衡电位（E）；然而，在许多细胞中，由于少量钠离子泄漏，静息膜电位比E更去极化。提高[Ca]（细胞外钙浓度）可导致膜电位从静息状态超极化。这种超极化的机制可能在于钠泄漏通道（NALCN）和/或电压门控钠通道的阻断。其效应也可能与钙激活钾通道有关。通过实验，我们在此表明将[Ca]从0.5 mM改变至3 mM会使肌肉超极化。当增加[Ca]时，用LiCl或氯化胆碱替代NaCl仍会导致超极化。用BaCl替代CaCl会导致去极化。幼虫肌肉中K2P通道的过表达极大地降低了[Ca]对细胞膜电位的影响，这可能是因为这些肌肉中的电位主要由E驱动。这些实验有助于理解高钙血症期间神经元兴奋性降低背后的机制，以及K2P通道表达改变对膜电位的影响。

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