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首页> 外文期刊>Journal of Neurophysiology >Role of mossy fiber sprouting and mossy cell loss in hyperexcitability: a network model of the dentate gyrus incorporating cell types and axonal topography.
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Role of mossy fiber sprouting and mossy cell loss in hyperexcitability: a network model of the dentate gyrus incorporating cell types and axonal topography.

机译：苔藓纤维发芽和苔藓细胞损失在过度兴奋性中的作用：包含细胞类型和轴突形貌的齿状回的网络模型。

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Mossy cell loss and mossy fiber sprouting are two characteristic consequences of repeated seizures and head trauma. However, their precise contributions to the hyperexcitable state are not well understood. Because it is difficult, and frequently impossible, to independently examine using experimental techniques whether it is the loss of mossy cells or the sprouting of mossy fibers that leads to dentate hyperexcitability, we built a biophysically realistic and anatomically representative computational model of the dentate gyrus to examine this question. The 527-cell model, containing granule, mossy, basket, and hilar cells with axonal projections to the perforant-path termination zone, showed that even weak mossy fiber sprouting (10-15% of the strong sprouting observed in the pilocarpine model of epilepsy) resulted in the spread of seizure-like activity to the adjacent model hippocampal laminae after focal stimulation of the perforant path. The simulations also indicated that the spatially restricted, lamellar distribution of the sprouted mossy fiber contacts reported in in vivo studies was an important factor in sustaining seizure-like activity in the network. In contrast to the robust hyperexcitability-inducing effects of mossy fiber sprouting, removal of mossy cells resulted in decreased granule cell responses to perforant-path activation in agreement with recent experimental data. These results indicate the crucial role of mossy fiber sprouting even in situations where there is only relatively weak mossy fiber sprouting as is the case after moderate concussive experimental head injury.
机译：苔藓细胞丢失和苔藓纤维发芽是反复发作和头部创伤的两个特征性后果。但是，它们对过度兴奋状态的确切贡献尚不十分清楚。由于很难（通常是不可能）使用实验技术独立检查是由于生苔细胞的丢失或生苔纤维的发芽而导致牙齿过度兴奋，所以我们建立了齿状回的生物物理现实和解剖学上具有代表性的计算模型，检查这个问题。 527细胞模型包含颗粒，生苔，篮状和肺门细胞，其轴突投射到穿孔路径终止区，显示苔藓纤维发芽甚微（在毛果芸香碱癫痫模型中观察到强发芽的10-15％） ）在穿孔路径聚焦刺激后导致癫痫样活动扩散到相邻的模型海马薄片。模拟还表明，在体内研究中报道的发芽的苔藓纤维接触的空间受限的层状分布是维持网络中癫痫样活动的重要因素。与长满苔藓的纤维发芽的强烈的过度兴奋诱导作用相反，与最近的实验数据一致，除去长满苔藓的细胞会导致颗粒细胞对穿孔途径激活的反应减少。这些结果表明，即使在仅较弱的苔藓纤维发芽的情况下（如中度脑震荡实验性头部受伤后的情况），苔藓纤维发芽的关键作用。

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