Abstract：
GABA (gamma-aminobutyric acid) receptors represent the major inhibitory receptors in the nervous system and their inhibitory effects are mediated by the influx of chloride ions that tends to hyperpolarize the resting membrane potential. However, GABA receptors can depolarize the resting membrane potential and thus can also show excitatory effects in neurons. The major mechanism behind this depolarization is mainly attributed to the accumulation of chloride ions in the intracellular compartment. This accumulation leads to increase in the intracellular chloride concentration and depolarize the Nernst potential of chloride ions. When the membrane potential is relatively hyperpolarized, this will result in a chloride efflux instead of influx trying to reach their depolarized equilibrium potential. Here, we propose different mechanism based on a major consequence of quantum mechanics, which is quantum tunneling. The quantum tunneling model of ions is applied on GABA receptors and their corresponding chloride ions to show how chloride ions can depolarize the resting membrane potential. The quantum model states that intracellular chloride ions have higher quantum tunneling probability than extracellular chloride ions. This is attributed to the discrepancy in the kinetic energy between them. At physiological parameters, the quantum tunneling is negligible to the degree that chloride ions cannot depolarize the membrane potential. Under certain conditions such as early neuronal development, gain-of-function mutations, stroke and trauma that can lower the energy barrier of the closed gate of GABA receptors, the quantum tunneling is enhanced so that the chloride ions can depolarize the resting membrane potential. The major unique feature of the quantum tunneling mechanism is that the net efflux of chloride ions is attained without the need for intracellular accumulation of chloride ions as long as the energy barrier of the gate is reduced but still higher than the kinetic energy of the chloride ion as a condition for quantum tunneling to take place.
摘要：
GABA（γ-氨基丁酸）受体代表神经系统中的主要抑制性受体，其抑制作用是由氯离子的流入介导的，氯离子的流入倾向于使静息膜电位超极化。然而,GABA受体可以使静息膜电位去极化，因此也可以在神经元中表现出兴奋作用。这种去极化背后的主要机制主要归因于氯离子在细胞内区室中的积累。这种积累导致细胞内氯化物浓度增加，并使氯离子的能斯特电位去极化。当膜电位相对超极化时，这将导致氯化物流出，而不是试图达到去极化平衡电位的流入。这里,我们基于量子力学的一个主要结果提出了不同的机制，这是量子隧穿。将离子的量子隧穿模型应用于GABA受体及其相应的氯离子，以显示氯离子如何使静息膜电位去极化。量子模型指出，细胞内氯离子比细胞外氯离子具有更高的量子隧穿概率。这归因于它们之间动能的差异。在生理参数上，量子隧穿可以忽略不计，以至于氯离子不能使膜电位去极化。在某些条件下，如早期神经元发育，功能增益突变，中风和创伤可以降低GABA受体关闭门的能量屏障，增强了量子隧穿，使氯离子可以去极化静止的膜电位。量子隧穿机制的主要独特特征是，只要门的能垒降低但仍高于氯离子的动能，就无需在细胞内积累氯离子，即可获得氯离子的净流出。量子隧穿发生的条件。
