Glutaric aciduria type I:: Pathomechanisms of neurodegeneration
Glutaric aciduria type I:: Pathomechanisms of neurodegeneration
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DOI：
10.1023/a:1005595921323
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发表时间：
1999-06-01
影响因子：
4.2
通讯作者：
Röper, R
中科院分区：
文献类型：
--
作者：
Ullrich, K;Flott-Rahmel, B;Röper, R
在大鼠脑的器官型皮质纹状体和海马切片培养物中，3-羟基谷氨酸而不是谷氨酸和戊烯二酸通过激活NMDA受体诱导神经变性。电生理学研究（非洲爪蟾卵母细胞表达谷氨酸受体;大鼠混合皮层培养）显示3-羟基谷氨酸与谷氨酸受体没有直接相互作用。我们推测，3-羟基葡萄糖酸诱导轻度能量剥夺，干扰电压依赖性Mg 2+阻断NMDA受体。
In organotypic corticostriatal and hippocampal slice cultures from rat brain, 3-hydroxyglutaric acid but not glutaric and glutaconic acids induced neurodegeneration by activation of NMDA receptors. Electrophysiological investigations (Xenopus laevis oocytes expressing glutamate receptors; rat mixed cortex culture) revealed no direct interaction of 3-hydroxyglutaric acid with glutamate receptors. We speculate that 3-hydroxyglutaric acid induces a mild energy deprivation that interferes with the voltage-dependent Mg2+-block of NMDA receptors.