McBean G J, Roberts P J
J Neurochem. 1985 Jan;44(1):247-54. doi: 10.1111/j.1471-4159.1985.tb07137.x.
Destruction of the glutamatergic corticostriatal pathway potentiates the neurotoxic action of 1 mumol L-glutamate injected into the rat striatum, whereas the toxic effects of 10 nmol kainate are markedly attenuated. Injection of 170 nmol of the glutamate uptake inhibitor, DL-threo-3-hydroxyaspartate, into the intact striatum also causes neuronal degeneration, which is accompanied by a reduction in markers for cholinergic and GABAergic neurones. Prior removal of the corticostriatal pathway destroys the ability of DL-threo-3-hydroxyaspartate to cause lesions in the striatum. These results indicate that removal, or blockade, of uptake sites for glutamate increase the vulnerability of striatal neurones to the toxic effects of synaptically released glutamate.
谷氨酸能皮质纹状体通路的破坏增强了注入大鼠纹状体的1微摩尔L - 谷氨酸的神经毒性作用，而10纳摩尔红藻氨酸的毒性作用则明显减弱。向完整的纹状体注射170纳摩尔的谷氨酸摄取抑制剂DL - 苏式 - 3 - 羟基天冬氨酸也会导致神经元变性，同时伴有胆碱能和GABA能神经元标志物的减少。事先切断皮质纹状体通路会破坏DL - 苏式 - 3 - 羟基天冬氨酸在纹状体中造成损伤的能力。这些结果表明，谷氨酸摄取位点的去除或阻断会增加纹状体神经元对突触释放的谷氨酸毒性作用的易感性。
