A model of gamma‐frequency network oscillations induced in the rat CA3 region by carbachol in vitro
A model of gamma‐frequency network oscillations induced in the rat CA3 region by carbachol in vitro
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DOI：
10.1046/j.1460-9568.2000.00300.x
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发表时间：
2000-11
影响因子：
3.4
通讯作者：
R. Traub;A. Bibbig;A. Fisahn;F. LeBeau;M. Whittington;E. Buhl
中科院分区：
文献类型：
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作者：
R. Traub;A. Bibbig;A. Fisahn;F. LeBeau;M. Whittington;E. Buhl
Carbachol （> 20 μm）和kainate （100 nm）在体外CA3区以≈40 Hz的频率诱导神经元群同步振荡，其特点是：(1)振荡持续数小时；（ii）在5-20 Hz的频率下，kainate放电的中间神经元的放电与场电位最大值紧密锁定（记录于s. radiatum）；（iii）相比之下，氨基甲酸乙酯和氨基甲酸乙酯中的锥体细胞以低至2 Hz的频率放电，并且它们的放电不太紧密地锁定于场电位；（iv）振荡需要GABAA受体、AMPA受体和间隙连接。利用一个由3072个锥体细胞和384个中间神经元组成的网络（每个神经元都是多室的，包含一段无髓鞘轴突），我们采用计算机模拟来检查网络振荡可能发生的条件，这些振荡可能具有实验确定的特性。我们发现，当间隙连接位于锥体细胞轴突之间时，这种网络振荡可以产生，这是基于体外海马体中自发高频（> 100 Hz）网络振荡的研究提出的。在模型中，锥体细胞的体细胞放电不是振荡的必要条件。该模型的关键组成部分是：(i)锥体细胞轴突的神经丛，它们通过间隙连接随机而稀疏地相互连接；（ii）谷氨酸突触连接到中间神经元；（iii）中间神经元之间、锥体细胞轴突和体细胞上的突触抑制；（iv）锥体细胞轴突产生足够高的自发动作电位率。该模型解释了网络振荡对GABAA和AMPA受体以及间隙连接的依赖。除了存在轴突-轴突间隙连接外，该模型还预测，在持续的伽马振荡期间，锥体细胞的许多动作电位是在轴突中启动的。
Carbachol (> 20 μm) and kainate (100 nm) induce, in the in vitro CA3 region, synchronized neuronal population oscillations at ≈ 40 Hz having distinctive features: (i) the oscillations persist for hours; (ii) interneurons in kainate fire at 5–20 Hz and their firing is tightly locked to field potential maxima (recorded in s. radiatum); (iii) in contrast, pyramidal cells, in both carbachol and kainate, fire at frequencies as low as 2 Hz, and their firing is less tightly locked to field potentials; (iv) the oscillations require GABAA receptors, AMPA receptors and gap junctions. Using a network of 3072 pyramidal cells and 384 interneurons (each multicompartmental and containing a segment of unmyelinated axon), we employed computer simulations to examine conditions under which network oscillations might occur with the experimentally determined properties. We found that such network oscillations could be generated, robustly, when gap junctions were located between pyramidal cell axons, as suggested to occur based on studies of spontaneous high‐frequency (> 100 Hz) network oscillations in the in vitro hippocampus. In the model, pyramidal cell somatic firing was not essential for the oscillations. Critical components of the model are (i) the plexus of pyramidal cell axons, randomly and sparsely interconnected by gap junctions; (ii) glutamate synapses onto interneurons; (iii) synaptic inhibition between interneurons and onto pyramidal cell axons and somata; (iv) a sufficiently high rate of spontaneous action potentials generated in pyramidal cell axons. This model explains the dependence of network oscillations on GABAA and AMPA receptors, as well as on gap junctions. Besides the existence of axon–axon gap junctions, the model predicts that many of the pyramidal cell action potentials, during sustained gamma oscillations, are initiated in axons.