Department of Biosciences and Bioengineering, Indian Institute of Technology Bombay, Mumbai, Maharashtra, India.
School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, England, United Kingdom.
PLoS One. 2018 Jul 26;13(7):e0200712. doi: 10.1371/journal.pone.0200712. eCollection 2018.
Urinary incontinence is associated with enhanced spontaneous phasic contractions of the detrusor smooth muscle (DSM). Although a complete understanding of the etiology of these spontaneous contractions is not yet established, it is suggested that the spontaneously evoked action potentials (sAPs) in DSM cells initiate and modulate the contractions. In order to further our understanding of the ionic mechanisms underlying sAP generation, we present here a biophysically detailed computational model of a single DSM cell. First, we constructed mathematical models for nine ion channels found in DSM cells based on published experimental data: two voltage gated Ca2+ ion channels, an hyperpolarization-activated ion channel, two voltage-gated K+ ion channels, three Ca2+-activated K+ ion channels and a non-specific background leak ion channel. The ion channels' kinetics were characterized in terms of maximal conductances and differential equations based on voltage or calcium-dependent activation and inactivation. All ion channel models were validated by comparing the simulated currents and current-voltage relations with those reported in experimental work. Incorporating these channels, our DSM model is capable of reproducing experimentally recorded spike-type sAPs of varying configurations, ranging from sAPs displaying after-hyperpolarizations to sAPs displaying after-depolarizations. The contributions of the principal ion channels to spike generation and configuration were also investigated as a means of mimicking the effects of selected pharmacological agents on DSM cell excitability. Additionally, the features of propagation of an AP along a length of electrically continuous smooth muscle tissue were investigated. To date, a biophysically detailed computational model does not exist for DSM cells. Our model, constrained heavily by physiological data, provides a powerful tool to investigate the ionic mechanisms underlying the genesis of DSM electrical activity, which can further shed light on certain aspects of urinary bladder function and dysfunction.
尿失禁与逼尿肌平滑肌(DSM)的自发性相位收缩增强有关。尽管尚未完全了解这些自发性收缩的病因,但有人认为 DSM 细胞中自发诱发的动作电位(sAPs)引发并调节收缩。为了进一步了解 sAP 产生的离子机制,我们在此介绍了单个 DSM 细胞的生物物理详细计算模型。首先,我们根据已发表的实验数据,为 DSM 细胞中发现的九个离子通道构建了数学模型:两个电压门控 Ca2+ 离子通道、一个超极化激活离子通道、两个电压门控 K+ 离子通道、三个 Ca2+ 激活 K+ 离子通道和一个非特异性背景泄漏离子通道。根据电压或钙依赖性激活和失活,用最大电导率和微分方程来描述离子通道的动力学。所有离子通道模型均通过将模拟电流和电流-电压关系与实验工作中报道的电流和电流-电压关系进行比较来验证。将这些通道整合到我们的 DSM 模型中,我们的模型能够再现具有不同形态的实验记录的尖峰型 sAP,从显示后超极化的 sAP 到显示后去极化的 sAP。还研究了主要离子通道对尖峰产生和形态的贡献,作为模拟选定药物对 DSM 细胞兴奋性影响的一种手段。此外,还研究了 AP 沿连续电平滑肌组织传播的特征。迄今为止,DSM 细胞的生物物理详细计算模型尚不存在。我们的模型受到生理数据的严格限制,为研究 DSM 电活动产生的离子机制提供了有力工具,这可以进一步揭示膀胱功能和功能障碍的某些方面。