软体动物神经元放电机制中钙依赖性异常的计算机模拟研究。

F Pongrácz, M Szente
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引用次数: 0

摘要

提出了计算机建模技术,以协助无脊椎动物神经元膜的生理研究。研究了无脊椎动物神经元膜单片放电机制与最大钙离子电导的关系。计算是基于对霍奇金-赫胥黎数据的修正,通过在Ca++电流和早期瞬态钾电流的动力学参数的实验点之间的直线近似完成的。假设电导变化的时间过程与Ca++电流的m2h成正比。模型涉及三种不同的钾电流,即瞬态钾电流、延迟钾电流和依赖Ca++的钾电流。本文采用在数字计算机上运行的修正欧拉法对动力学方程进行了数值积分。Ca++电导对电穗展宽、高原发育和超极化后电穗有显著影响。在小的Ca++电导范围内,可以由短(超阈值)电流脉冲触发无限自发活动,这可以被认为是起搏器活动的模型。在较大的电导范围内,钙离子电导促进了钾离子阻断或钾离子平衡降低所导致的高原发育。研究了描述Ca++依赖的K+通道电流的耦合系数对电压敏感性的影响,并与电压无关的情况进行了比较。耦合系数似乎是一个关键因素,在扩大范围的钙离子电导负责心脏起搏器的活动。当Ca++电导值较大时,耦合系数的减小导致从持续爆发到爆发后超极化中断爆发活动的转变。该模型研究了4-氨基吡啶对快速外向电流的阻断作用,考虑到氨基吡啶是一种惊厥剂,该模型具有实际意义。我们认为用基于离体神经元膜动力学的模型来研究氨基吡啶的惊厥效应是合理的。该模型可能有助于理解在哺乳动物神经元癫痫放电期间异常网络活动的离子背景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Computer simulation for studying calcium dependent abnormalities in firing mechanism of molluscan neurones.

Computer modelling technique is proposed to assist in physiological research on invertebrate neuronal membranes. The firing mechanism of a single patch of invertebrate neuronal membrane has been studied in dependence on maximum Ca++ conductance. The calculations are based on modification of Hodgkin-Huxley's data completed by a straight line approximation between experimental points of the kinetic parameters of Ca++ current and early transient potassium current. The time course of conductance changes is assumed to be proportional to m2h for Ca++ current. Three distinct potassium currents are involved into the model, viz. transient potassium current, delayed potassium current and Ca++-dependent potassium current. The modified Euler method run on a digital computer has been used for numerical integration of kinetic equations. Significant effects of Ca++ conductance on spike broadening, plateau development and spike afterhyperpolarization are represented. In the range of small Ca++ conductance an infinite spontaneous activity can be triggered by a short (suprathreshold) current pulse which may be considered a model of pacemaker activity. Plateau development resulting from potassium blocking or decreasing potassium equilibrium is facilitated by Ca++ conductance in the range of greater Ca++ conductance. The effects of voltage sensitivity of the coupling coefficient describing the current of Ca++-dependent K+ channels were studied and compared to the voltage independent case. The coupling coefficient seems to be a crucial factor in broadening the range of Ca++ conductance responsible for pacemaker activity. For greater values of Ca++ conductance, a decrease of the coupling coefficient leads to a transition from prolonged bursting to interruption of burst activity by burst-afterhyperpolarization. The blocking effect of 4-aminopyridine on fast outward current has been studied by the model which has a practical significance considering that aminopyridine is known as a convulsive agent. We suppose that it is reasonable to study the convulsive effects of aminopyridine by the model based on the kinetics of the isolated neuronal membrane. The model may help in understanding the ionic background underlying abnormal network activity during epileptic discharges of mammalian neurones.

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