Department of Anesthesia and Intensive Care Unit, The Hashemite University, Zarqa 13115, Jordan.
School of Medicine, The University of Jordan, Amman 11942, Jordan.
Cells. 2022 Mar 28;11(7):1145. doi: 10.3390/cells11071145.
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.
GABA(γ-氨基丁酸)受体是神经系统中主要的抑制性受体,其抑制作用是通过氯离子内流引起的,氯离子内流倾向于超极化静息膜电位。然而,GABA 受体可以去极化静息膜电位,因此也可以在神经元中表现出兴奋作用。这种去极化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离子浓度增加,从而去极化氯离子的 Nernst 电位。当膜电位相对超极化时,氯离子会流出而不是流入,试图达到去极化平衡电位。在这里,我们提出了一种基于量子力学主要后果的不同机制,即量子隧穿。将离子的量子隧穿模型应用于 GABA 受体及其相应的氯离子上,以显示氯离子如何去极化静息膜电位。量子模型表明,细胞内氯离子的量子隧穿概率高于细胞外氯离子。这归因于它们之间动能的差异。在生理参数下,量子隧穿对氯离子不能去极化膜电位的程度可以忽略不计。在某些条件下,如早期神经元发育、功能获得性突变、中风和创伤,这些条件可以降低 GABA 受体关闭门的能量壁垒,从而增强量子隧穿,使氯离子能够去极化静息膜电位。量子隧穿机制的主要独特特征是,只要门的能量壁垒降低,但仍高于氯离子的动能,作为量子隧穿发生的条件,就可以获得氯离子的净流出,而不需要细胞内氯离子的积累。