Pinsky P F, Rinzel J
Mathematical Research Branch, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA.
J Comput Neurosci. 1994 Jun;1(1-2):39-60. doi: 10.1007/BF00962717.
We have developed a two-compartment, eight-variable model of a CA3 pyramidal cell as a reduction of a complex 19-compartment cable model [Traub et al, 1991]. Our reduced model segregates the fast currents for sodium spiking into a proximal, soma-like, compartment and the slower calcium and calcium-mediated currents into a dendrite-like compartment. In each model periodic bursting gives way to repetitive soma spiking as somatic injected current increases. Steady dendritic stimulation can produce periodic bursting of significantly higher frequency (8-20 Hz) than can steady somatic input (< 8 Hz). Bursting in our model occurs only for an intermediate range of electronic coupling conductance. It depends on the segregation of channel types and on the coupling current that flows back-and-forth between compartments. When the soma and dendrite are tightly coupled electrically, our model reduces to a single compartment and does not burst. Network simulations with our model using excitatory AMPA and NMDA synapses (without inhibition) give results similar to those obtained with the complex cable model [Traub et al, 1991; Traub et al, 1992]. Brief stimulation of a single cell in a resting network produces multiple synchronized population bursts, with fast AMPA synapses providing the dominant synchronizing mechanism. The number of bursts increases with the level of maximal NMDA conductance. For high enough maximal NMDA conductance synchronized bursting repeats indefinitely. We find that two factors can cause the cells to desynchronize when AMPA synapses are blocked: heterogeneity of properties amongst cells and intrinsically chaotic burst dynamics. But even when cells are identical, they may synchronize only approximately rather than exactly. Since our model has a limited number of parameters and variables, we have studied its cellular and network dynamics computationally with relative ease and over wide parameter ranges. Thereby, we identify some qualitative features that parallel or are distinguished from those of other neuronal systems; e.g., we discuss how bursting here differs from that in some classical models.
我们构建了一个CA3锥体细胞的双房室、八变量模型，作为对复杂的19房室电缆模型的简化 [特劳布等人，1991年]。我们的简化模型将用于钠峰电位的快速电流分离到一个近端的、类似胞体的房室中，而将较慢的钙电流和钙介导电流分离到一个类似树突的房室中。在每个模型中，随着体细胞注入电流的增加，周期性爆发会转变为重复性的体细胞峰电位。稳定的树突刺激能够产生频率（8 - 20赫兹）显著高于稳定的体细胞输入（< 8赫兹）的周期性爆发。我们模型中的爆发仅发生在电子耦合电导的中间范围内。它取决于通道类型的分离以及在房室之间来回流动的耦合电流。当胞体和树突在电学上紧密耦合时，我们的模型简化为一个单房室模型，不会产生爆发。使用兴奋性AMPA和NMDA突触（无抑制）对我们的模型进行网络模拟，得到的结果与使用复杂电缆模型 [特劳布等人，1991年；特劳布等人，1992年] 所获得的结果相似。对静息网络中的单个细胞进行短暂刺激会产生多个同步的群体爆发，快速的AMPA突触提供主要的同步机制。爆发的数量随着最大NMDA电导水平的增加而增加。对于足够高的最大NMDA电导，同步爆发会无限重复。我们发现，当AMPA突触被阻断时，有两个因素会导致细胞去同步：细胞之间特性的异质性和内在的混沌爆发动力学。但即使细胞是相同的，它们也可能只是近似同步而不是完全同步。由于我们的模型具有有限数量的参数和变量，我们相对轻松地在广泛的参数范围内通过计算研究了其细胞和网络动力学。由此，我们确定了一些与其他神经元系统平行或不同的定性特征；例如，我们讨论了这里的爆发与一些经典模型中的爆发有何不同。
