Intrinsic and network rhythmogenesis in a reduced Traub model for CA3 neurons.
Intrinsic and network rhythmogenesis in a reduced Traub model for CA3 neurons.
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DOI：
10.1007/bf00962717
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发表时间：
1994-06-01
影响因子：
1.2
通讯作者：
Rinzel, J
中科院分区：
文献类型：
--
作者：
Pinsky, P F;Rinzel, J
我们开发了一个CA 3锥体细胞的双室、八变量模型，作为复杂的19室电缆模型的简化[Traub et al，1991]。我们的简化模型将钠尖峰的快速电流分离到近端的胞体样隔室中，而将较慢的钙和钙介导的电流分离到树突样隔室中。在每个模型中，随着体细胞注入电流的增加，周期性爆发让位于重复性索马尖峰。稳定的树突刺激可以产生比稳定的躯体输入（<8Hz）显著更高频率（8-20 Hz）的周期性爆发。在我们的模型中，爆发只发生在电子耦合电导的中间范围。它取决于通道类型的隔离和在隔室之间来回流动的耦合电流。当索马和树突紧密电耦合时，我们的模型简化为一个单室，并且不会破裂。使用我们的模型，使用兴奋性AMPA和NMDA突触（无抑制）进行网络模拟，得到的结果与使用复杂电缆模型获得的结果相似[Traub et al，1991; Traub et al，1992]。短暂刺激静息网络中的单个细胞产生多个同步群体爆发，快速AMPA突触提供主导同步机制。爆发的数量随着最大NMDA电导的水平而增加。对于足够高的最大NMDA电导同步爆发重复无限期。我们发现，当AMPA突触被阻断时，有两个因素会导致细胞失同步：细胞之间特性的异质性和本质上混乱的爆发动力学。但是，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，我们已经研究了它的细胞和网络动力学计算相对容易和广泛的参数范围。因此，我们确定了一些与其他神经元系统平行或区别于其他神经元系统的定性特征;例如，我们讨论了这里的破裂与一些经典模型中的破裂有何不同。
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.