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海兔神经元R15爆发活动的模拟:离子电流、钙平衡及调制性递质的作用

Simulation of the bursting activity of neuron R15 in Aplysia: role of ionic currents, calcium balance, and modulatory transmitters.

作者信息

Canavier C C, Clark J W, Byrne J H

机构信息

Department of Electrical and Computer Engineering, Rice University, Houston 77251-1892.

出版信息

J Neurophysiol. 1991 Dec;66(6):2107-24. doi: 10.1152/jn.1991.66.6.2107.

DOI:10.1152/jn.1991.66.6.2107
PMID:1725879
Abstract
  1. An equivalent circuit model of the R15 bursting neuron in Aplysia has been combined with a fluid compartment model, resulting in a model that incorporates descriptions of most of the membrane ion channels that are known to exist in the somata of R15, as well as providing a Ca2+ balance on the cell. 2. A voltage-activated, calcium-inactivated Ca2+ current (denoted the slow inward current ISI) was sufficient to produce bursting activity without invoking any other calcium-dependent currents (such as a nonspecific cation current, INS, or a calcium-activated K+ current, IK,Ca). Furthermore, many characteristics of a typical R15 burst could be simulated, such as a parabolic variation in interspike interval, the depolarizing afterpotential (DAP), and the progressive decrease in the undershoots of spikes during a burst. 3. The dynamic activity of R15 was analyzed by separately characterizing two different temporal domains; the fast dynamics associated with action potentials and the slow dynamics associated with low-amplitude oscillations lasting tens of seconds ("slow waves"). The slow dynamics were isolated by setting the Na+ conductance (gNa) to zero and then studied by the use of a system of equations reduced to two variables: intracellular concentration of Ca2+ and membrane potential. The fixed point of the system was located at the intersection of the nullclines for these two variables. A stability analysis of the fixed point was then used to determine whether a given set of parameters would produce slow-wave activity. 4. If the reduced model predicted slow-wave oscillations for a given set of parameters with gNa set to zero, then bursting activity was observed for the same set of parameters in the full model with gNa reset to its control value. However, for certain sets of parameters with gNa at its usual value, the full model exhibited bursting activity because of a slow oscillation produced by the activation of INS by action potentials. This oscillation resulted from an interaction between the fast and slow dynamics that the reduced model alone could not predict and was not observed when gNa was subsequently set to zero. If gNS was also set to zero, this discrepancy disappeared.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 海兔R15爆发性神经元的等效电路模型已与流体隔室模型相结合,得到了一个模型,该模型纳入了已知存在于R15体细胞中的大多数膜离子通道的描述,并实现了细胞内的Ca2+平衡。2. 一种电压激活、钙失活的Ca2+电流(称为慢内向电流ISI)足以产生爆发活动,而无需调用任何其他钙依赖性电流(如非特异性阳离子电流INS或钙激活K+电流IK,Ca)。此外,典型R15爆发的许多特征都可以被模拟出来,比如峰间期的抛物线变化、去极化后电位(DAP)以及爆发期间峰电位负后电位的逐渐减小。3. 通过分别表征两个不同的时间域来分析R15的动态活动;与动作电位相关的快速动态和与持续数十秒的低幅振荡( “慢波” )相关的缓慢动态。通过将Na+电导(gNa)设为零来分离缓慢动态,然后使用简化为两个变量的方程组进行研究:细胞内Ca2+浓度和膜电位。系统的固定点位于这两个变量零倾线的交点处。然后通过对固定点的稳定性分析来确定给定的一组参数是否会产生慢波活动。4. 如果简化模型在gNa设为零时对给定的一组参数预测出慢波振荡,那么在gNa重置为其控制值的完整模型中,相同的一组参数会观察到爆发活动。然而,对于某些gNa处于其正常值的参数组,完整模型由于动作电位激活INS产生的慢振荡而表现出爆发活动。这种振荡是由快速和缓慢动态之间的相互作用导致的,仅简化模型无法预测,并且当gNa随后设为零时未观察到。如果gNS也设为零,这种差异就会消失。(摘要截断于400字)

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Simulation of the bursting activity of neuron R15 in Aplysia: role of ionic currents, calcium balance, and modulatory transmitters.海兔神经元R15爆发活动的模拟:离子电流、钙平衡及调制性递质的作用
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J Neurosci. 1988 Apr;8(4):1162-71. doi: 10.1523/JNEUROSCI.08-04-01162.1988.

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