Al-Rawashdeh Baeth M, Qaswal Abdallah Barjas, Suleiman Aiman, Zayed Fuad Mohammed, Al-Rawashdeh S M, Tawalbeh Mohamed, Khreesha Lubna, Alzubaidi Ayham, Al-Zubidi Enas, Ghala Zuhir, Almasri Ahmad, Yasein Mohammed, Ojjoh Khaled, Alraiqib Ahmad, Iswaid Mohammad, Emar Murad, Haimour Shahed, Saifan Ala', Mahameed Zaid
Department of Special Surgery, Jordan University Hospital, School of Medicine, The University of Jordan, Amman 11942, Jordan.
School of Medicine, The University of Jordan, Amman 11942, Jordan.
Brain Sci. 2022 Mar 23;12(4):426. doi: 10.3390/brainsci12040426.
Tinnitus is a well-known pathological entity in clinical practice. However, the pathophysiological mechanisms behind tinnitus seem to be elusive and cannot provide a comprehensive understanding of its pathogenesis and clinical manifestations. Hence, in the present study, we explore the mathematical model of ions' quantum tunneling to propose an original pathophysiological mechanism for the sensation of tinnitus. The present model focuses on two major aspects: The first aspect is the ability of ions, including sodium, potassium, and calcium, to depolarize the membrane potential of inner hair cells and the neurons of the auditory pathway. This membrane depolarization is induced via the quantum tunneling of ions through closed voltage-gated channels. The state of membrane depolarization can be a state of hyper-excitability or hypo-excitability, depending on the degree of depolarization. Both of these states aid in understanding the pathophysiology of tinnitus. The second aspect is the quantum tunneling signals between the demyelinated neurons of the auditory pathway. These signals are mediated via the quantum tunneling of potassium ions, which exit to the extracellular fluid during an action potential event. These quantum signals can be viewed as a "quantum synapse" between neurons. The formation of quantum synapses results in hyper-excitability among the demyelinated neurons of the auditory pathway. Both of these aspects augment and amplify the electrical signals in the auditory pathway and result in a loss of the spatiotemporal fidelity of sound signals going to the brain centers. The brain interprets this hyper-excitability and loss of spatiotemporal fidelity as tinnitus. Herein, we show mathematically that the quantum tunneling of ions can depolarize the membrane potential of the inner hair cells and neurons of the auditory pathway. Moreover, we calculate the probability of action potential induction in the neurons of the auditory pathway generated by the quantum tunneling signals of potassium ions.
耳鸣在临床实践中是一种广为人知的病理实体。然而,耳鸣背后的病理生理机制似乎难以捉摸,无法全面解释其发病机制和临床表现。因此,在本研究中,我们探索离子量子隧穿的数学模型,以提出一种关于耳鸣感觉的原始病理生理机制。本模型主要关注两个方面:第一个方面是包括钠、钾和钙在内的离子使内毛细胞和听觉通路神经元的膜电位去极化的能力。这种膜去极化是通过离子通过关闭的电压门控通道的量子隧穿诱导的。膜去极化状态可以是高兴奋性状态或低兴奋性状态,这取决于去极化的程度。这两种状态都有助于理解耳鸣的病理生理学。第二个方面是听觉通路脱髓鞘神经元之间的量子隧穿信号。这些信号是通过钾离子的量子隧穿介导的,钾离子在动作电位事件期间释放到细胞外液中。这些量子信号可以被视为神经元之间的“量子突触”。量子突触的形成导致听觉通路脱髓鞘神经元的高兴奋性。这两个方面都会增强和放大听觉通路中的电信号,并导致传向脑中枢的声音信号的时空保真度丧失。大脑将这种高兴奋性和时空保真度丧失解释为耳鸣。在此,我们通过数学证明离子的量子隧穿可以使内毛细胞和听觉通路神经元的膜电位去极化。此外,我们计算了由钾离子的量子隧穿信号在听觉通路神经元中诱导动作电位的概率。