华中科技大学学报(医学英德文版)
華中科技大學學報(醫學英德文版)
화중과기대학학보(의학영덕문판)
JOURNAL OF TONGJI MEDICAL UNIVERSITY
2001年
1期
62-64,74
,共4页
陈劲草%雷霆%Ritz M-F%Mendelowitsch
陳勁草%雷霆%Ritz M-F%Mendelowitsch
진경초%뢰정%Ritz M-F%Mendelowitsch
An in vivo model of glutamate excitotoxicity in which glutamate is applied to the cortex of rats through a microdialysis probe has been used to investigate the neuroprotective processes initiated by 17β-estradiol. Rats were pre-treated with 17β-estradiol i.v. before local application of glutamate. The experimental results showed that pre-treatment with 17β-estradiol significantly reduced the size of the glutamate-induced lesion. In the microdialysates, the peak of lactate observed immediately after glutamate application was significantly higher and longer lasting after 17β-estradiol pre-treatment. The level of extracellular glucose was markedly decreased concomitantly to the increase in lactate, but no difference could be observed with and without 17β-estradiol pre-treatment. These suggest a new neuroprotective mechanism of 17β-estradiol by activating glutamate-induced lactate production. This effect on lactate production and lesion reduction is estrogen receptor dependent and is abolished totally by estrogen antagonist tamoxifen. It was also demonstrated here that high lactate subserves estrogen neuroprotection during glutamate toxicity.