Patterns of increased glucose use following extracellular infusion of glutamate: an autoradiographic study.
Patterns of increased glucose use following extracellular infusion of glutamate: an autoradiographic study.
复制标题
细胞外输注谷氨酸后葡萄糖消耗增加的模式：放射自显影研究。
DOI：
10.1089/neu.1996.13.245
复制
发表时间：
1996
影响因子：
4.2
通讯作者：
R. Bullock
中科院分区：
文献类型：
--
作者：
H. Fujisawa;H. Landolt;R. Bullock
在几种模型中，全脑和局灶性缺血后，局部葡萄糖利用率在某些脑区表现出明显的一过性增加。在许多这些模型中，在相同的脑区域中已经显示出细胞外谷氨酸的同时瞬时增加。为了检验代谢增加是谷氨酸兴奋性毒性作用的重要组成部分这一假设，我们将不同浓度（0.01，0.1，0.5，1 M）的谷氨酸灌注到细胞外间隙中，并在输注90分钟后进行2-脱氧葡萄糖放射自显影。此外，我们注入14 C标记的谷氨酸，研究其扩散特性在脑内使用放射自显影方法。谷氨酸在0.5和1 M浓度引起大的一致的区域的脑损伤与急性梗死的所有组织学特征，虽然缺血不发生在这个模型中。在组织学损伤和正常脑之间的边界处，葡萄糖利用率显著增加（对照组为115 +/- 20 vs. 56 +/- 13 mumol/100 g/min，p < 0.01），表明未被谷氨酸破坏的活细胞对葡萄糖代谢的增加有反应。[14C]谷氨酸以剂量依赖性方式扩散到大脑中，其扩散模式与组织学病变和葡萄糖吸收增加区的扩散模式密切对应。我们推测，在该模型中，葡萄糖使用的增加不是由缺血引起的，而是由于对谷氨酸的代谢反应，并且可能是由于试图恢复离子稳态或修复细胞损伤。
An apparent transient increase in local glucose utilization has been demonstrated in certain brain areas after global and focal ischemia in several models. A coincident transient increase in extracellular glutamate has been shown in the same brain regions in many of these models. To test the hypothesis that an increase in metabolism is an important component of the excitotoxic effect of glutamate, we perfused glutamate at different concentrations (0.01, 0.1, 0.5, 1 M) into the extracellular space, and performed 2-deoxyglucose autoradiography after 90 min of infusion. Furthermore, we infused 14C-labeled glutamate to investigate its diffusion characteristics within the brain using autoradiographic methods. Glutamate at 0.5 and 1 M concentration caused large consistent areas of brain damage with all the histological features of acute infarction, although ischemia does not occur in this model. Glucose utilization was significantly increased (115 +/- 20 vs. 56 +/- 13 mumol/100 g/min in controls p < 0.01) in a sharply demarcated concentric zone, at the boundary between histologically damaged and normal brain, suggesting that viable cells not yet destroyed by glutamate respond by increased glucose metabolism. [14C] Glutamate diffused into the brain in a dose-dependent manner, and the pattern of its diffusion corresponded closely to that of the histological lesion and the zone of increased glucose uptake. We speculate that the increase in glucose use, which is not caused by ischemia in this model, is due to a metabolic response to glutamate and may be due to attempts to restore ionic homeostasis or repair cell damage.
影响因子：
4.1
作者：
BOUMA, GJ;MUIZELAAR, JP;YOUNG, HF
通讯作者：
YOUNG, HF