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首页> 外文期刊>Journal of Neurophysiology >Computer simulations of morphologically reconstructed CA3 hippocampal neurons.
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Computer simulations of morphologically reconstructed CA3 hippocampal neurons.

机译：形态重建的CA3海马神经元的计算机模拟。

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摘要

1. We tested several hypotheses with respect to the mechanisms and processes that control the firing characteristics and determine the spatial and temporal dynamics of intracellular Ca2+ in CA3 hippocampal neurons. In particular, we were interested to know 1) whether bursting and nonbursting behavior of CA3 neurons could be accounted for in a morphologically realistic model using a number of the known ionic conductances; 2) whether such a model is robust across different cell morphologies; 3) whether some particular nonuniform distribution of Ca2+ channels is required for bursting; and 4) whether such a model can reproduce the magnitude and spatial distribution of intracellular Ca2+ transients determined from fluorescence imaging studies and can predict reasonable intracellular Ca2+ concentration ([Ca2+]i) distribution for CA3 neurons. 2. For this purpose we have developed a highly detailed model of the distribution and densities of membrane ion channels in hippocampal CA3 bursting and nonbursting pyramidal neurons. This model reproduces both the experimentally observed firing modes and the dynamics of intracellular Ca2+. 3. The kinetics of the membrane ionic conductances are based on available experimental data. This model incorporates a single Na+ channel, three Ca2+ channels (CaN, CaL, and CaT), three Ca(2+)-independent K+ channels (KDR, KA, and KM), two Ca(2+)-dependent K+ channels (KC and KAHP), and intracellular Ca(2+)-related processes such as buffering, pumping, and radial diffusion. 4. To test the robustness of the model, we applied it to six different morphologically accurate reconstructions of CA3 hippocampal pyramidal neurons. In every neuron, Ca2+ channels, Ca(2+)-related processes, and Ca(2+)-dependent K+ channels were uniformly distributed over the entire cell. Ca(2+)-independent K+ channels were placed on the soma and the proximal apical dendrites. For each reconstructed cell we were able to reproduce bursting and nonbursting firing characteristics as well as Ca2+ transients and distributions for both somatic and synaptic stimulations. 5. Our simulation results suggest that CA3 pyramidal cell bursting behavior does not require any special distribution of Ca(2+)-dependent channels and mechanisms. Furthermore, a simple increase in the Ca(2+)-independent K+ conductances is sufficient to change the firing mode of our CA3 neurons from bursting to nonbursting. 6. The model also displays [Ca2+]i transients and distributions that are consistent with fluorescent imaging data. Peak [Ca2+]i distribution for synaptic stimulation of the nonbursting model is broader when compared with somatic stimulation. Somatic stimulation of the bursting model shows a broader distribution in [Ca2+]i when compared with the nonbursting model.(ABSTRACT TRUNCATED AT 400 WORDS)
机译：1.我们就控制着火特征并确定海马CA3海马神经元中细胞内Ca2 +的时空动态的机制和过程测试了几种假设。特别是，我们有兴趣知道1）CA3神经元的爆发和非爆发行为是否可以使用许多已知的离子电导在形态学上逼真的模型中解释; 2）这样的模型在不同细胞形态上是否健壮; 3）爆发是否需要某些特定的Ca2 +通道非均匀分布; （4）这样的模型是否可以再现由荧光成像研究确定的细胞内Ca2 +瞬变的大小和空间分布，并且可以预测CA3神经元的合理细胞内Ca2 +浓度（[Ca2 +] i）分布。 2.为此，我们开发了高度详细的海马CA3突触和非突触锥体神经元膜离子通道分布和密度模型。该模型重现了实验观察到的激发模式和细胞内Ca2 +的动力学。 3.膜离子电导的动力学基于现有的实验数据。该模型合并了单个Na +通道，三个Ca2 +通道（CaN，CaL和CaT），三个Ca（2+）无关的K +通道（KDR，KA和KM），两个Ca（2+）依赖性K +通道（ KC和KAHP），以及胞内Ca（2+）相关的​​过程，例如缓冲，泵送和径向扩散。 4.为了测试该模型的稳健性，我们将其应用于CA3海马锥体神经元的六种不同形态上准确的重建。在每个神经元中，Ca2 +通道，Ca（2+）相关过程和Ca（2+）依赖性K +通道均匀分布在整个细胞中。 Ca（2 +）-独立的K +通道被放置在躯体和近端顶端树突上。对于每个重建的细胞，我们都能够针对躯体和突触刺激复制爆发和非爆发的射击特征以及Ca2 +瞬变和分布。 5.我们的模拟结果表明，CA3锥体细胞的爆发行为不需要任何特殊的Ca（2+）依赖性通道和机制分布。此外，Ca（2+）独立的K +电导率的简单增加足以将我们的CA3神经元的放电模式从爆发转变为非爆发。 6.该模型还显示与荧光成像数据一致的[Ca2 +] i瞬变和分布。与体细胞刺激相比，用于突触模型的突触刺激的峰[Ca2 +] i分布更宽。与非爆发模型相比，爆发模型的体细胞刺激显示[Ca2 +] i分布更广。（摘要截断为400字）

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