代谢型谷氨酸受体的激活可保护神经细胞免受氧化应激的影响。
The activation of metabotropic glutamate receptors protects nerve cells from oxidative stress.
作者信息
Sagara Y, Schubert D
机构信息
Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
出版信息
J Neurosci. 1998 Sep 1;18(17):6662-71. doi: 10.1523/JNEUROSCI.18-17-06662.1998.
Abstract
Metabotropic glutamate receptors (mGluRs) have been implicated in a variety of cellular responses to glutamic acid. The work described in this manuscript extends the role of mGluRs to include protection from oxidative stress-induced programmed cell death. Glutamate analogs regulate inositol-1,4,5 triphosphate mass accumulation in accordance with their ability to protect cells from oxidative glutamate toxicity, and protection appears to take place at the level of glutathione metabolism. Short-term exposure of cells to low concentrations of glutamate desensitizes cells to a subsequent challenge from glutamate. Glutamate exposure upregulates the expression of mGluR5 in hippocampal HT-22 cells and mGluR1 in cortical primary cultures. Finally, group I mGluR agonists also protect cells from death programs initiated by glucose starvation and cystine deprivation.
摘要
代谢型谷氨酸受体（mGluRs）参与了谷氨酸引发的多种细胞反应。本手稿中所描述的研究工作将mGluRs的作用扩展至包括抵御氧化应激诱导的程序性细胞死亡。谷氨酸类似物根据其保护细胞免受氧化型谷氨酸毒性影响的能力来调节肌醇-1,4,5-三磷酸的质量积累，并且这种保护作用似乎发生在谷胱甘肽代谢水平。细胞短期暴露于低浓度谷氨酸会使其对随后的谷氨酸刺激产生脱敏作用。谷氨酸暴露会上调海马HT-22细胞中mGluR5的表达以及皮质原代培养物中mGluR1的表达。最后，I组mGluR激动剂也能保护细胞免受由葡萄糖饥饿和胱氨酸剥夺引发的死亡程序的影响。
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