Pongrácz F, Szente M
Acta Physiol Acad Sci Hung. 1982;60(4):189-203.
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.
提出了计算机建模技术以辅助对无脊椎动物神经元膜进行生理学研究。已根据最大Ca++电导研究了单个无脊椎动物神经元膜片的放电机制。计算基于对霍奇金-赫胥黎数据的修正，该修正通过Ca++电流和早期瞬时钾电流动力学参数实验点之间的直线近似完成。假设Ca++电流的电导变化时间过程与m2h成正比。模型涉及三种不同的钾电流，即瞬时钾电流、延迟钾电流和Ca++依赖性钾电流。在数字计算机上运行的改进欧拉方法已用于动力学方程的数值积分。展示了Ca++电导对峰电位展宽、平台期发展和峰电位后超极化的显著影响。在小Ca++电导范围内，短（阈上）电流脉冲可触发无限的自发活动，这可被视为起搏器活动的模型。在较大Ca++电导范围内，Ca++电导促进了因钾阻断或钾平衡降低导致的平台期发展。研究了描述Ca++依赖性K+通道电流的耦合系数的电压敏感性效应，并与电压无关的情况进行了比较。耦合系数似乎是拓宽负责起搏器活动的Ca++电导范围的关键因素。对于较大的Ca++电导值，耦合系数的降低导致从长时间爆发转变为通过爆发后超极化中断爆发活动。该模型研究了4-氨基吡啶对快速外向电流的阻断作用，鉴于氨基吡啶是一种惊厥剂，这具有实际意义。我们认为，基于分离的神经元膜动力学的模型来研究氨基吡啶的惊厥作用是合理的。该模型可能有助于理解哺乳动物神经元癫痫放电期间异常网络活动背后的离子背景。
