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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The pentylenetetrazole-kindling model of epilepsy in SAMP8 mice: glial-neuronal metabolic interactions.
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The pentylenetetrazole-kindling model of epilepsy in SAMP8 mice: glial-neuronal metabolic interactions.

机译：SAMP8小鼠癫痫的戊四氮点燃模型：神经胶质-神经元代谢相互作用。

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摘要

Recently, a new experimental model of epilepsy was introduced by the authors [Neurochem. Int. 40 (2002) 413]. This model combines pentylenetetrazole (PTZ)-kindling in senescence-accelerated mice P8 (SAMP8), a genetic model of aging. Since imbalance of glutamate and GABA is a major cause of seizures, the study of glial-neuronal interactions is of primary importance. Nuclear magnetic resonance spectroscopy (NMRS) is an excellent tool for metabolic studies. Thus, we examined whether NMRS when combined with administration of [1-13C]glucose and [1,2-13C]acetate might give valuable insights into neurotransmitter metabolism in this new model of epilepsy and aging. The 2- and 8-month-old SAMP8 were kindled with PTZ alone, received PTZ and phenobarbital (PB), or served as controls. In older animals, PTZ-kindling decreased labeling in glutamate C-4 from [1-13C]glucose, whereas, in the younger mice, labeling in glutamine C-4 was decreased both from [1-13C]glucose and [1,2-13C]acetate. It could be concluded that PTZ-kindling affected astrocytes in younger and glutamatergic neurons in older animals. In the presence of PTZ, phenobarbital decreased labeling of most metabolites in all cell types, except GABAergic neurons, from both labeled precursors in the younger animals. However, in older animals only GABAergic neurons were affected by phenobarbital as indicated by an increase in GABA labeling.
机译：最近，作者介绍了一种新的癫痫实验模型[Neurochem。诠释40（2002）413]。该模型结合了衰老的遗传模型衰老加速小鼠P8（SAMP8）中的戊四氮（PTZ）点燃。由于谷氨酸和GABA的失衡是癫痫发作的主要原因，因此胶质神经元相互作用的研究至关重要。核磁共振波谱（NMRS）是进行代谢研究的绝佳工具。因此，我们检查了NMRS与[1-13C]葡萄糖和[1,2-13C]乙酸盐联合使用时，是否可以在这种新型的癫痫和衰老模型中对神经递质代谢提供有价值的见解。将2个月和8个月大的SAMP8单独与PTZ一起点燃，接受PTZ和苯巴比妥（PB）或作为对照。在年长的动物中，PTZ点燃会降低[1-13C]葡萄糖对谷氨酸C-4的标记，而在年幼的小鼠中，[1-13C]葡萄糖和[1,2]会降低谷氨酰胺C-4的标记。 -13C]乙酸盐。可以得出结论，PTZ点燃会影响年轻动物的星形胶质细胞和年长动物的谷氨酸能神经元。在存在PTZ的情况下，苯巴比妥降低了年轻动物中两种标记前体中除GABA能神经元以外所有细胞类型中大多数代谢物的标记。但是，在年长的动物中，只有GABA能神经元受苯巴比妥影响，如GABA标记的增加所示。

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