Effect of 17 beta-estradiol on the brain damage and metabolic changes in rats

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 17 beta-estradiol. Rats were pre-treated with 17 beta-estradiol i.v. before local application of glut...

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Bibliographic Details
Published in:Current medical science 2001, Vol.21 (1), p.62-64
Main Authors: Chen, J, Lei, T, Ritz, M F, Mendelowitsch, A
Format: Article
Language:English
Subjects:
Animals
Brain Diseases - chemically induced
Brain Diseases - metabolism
Estradiol - pharmacology
Glutamic Acid
Male
Microdialysis
Neuroprotective Agents - pharmacology
Rats
Rats, Wistar
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Summary: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 17 beta-estradiol. Rats were pre-treated with 17 beta-estradiol i.v. before local application of glutamate. The experimental results showed that pre-treatment with 17 beta-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 17 beta-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 17 beta-estradiol pre-treatment. These suggest a new neuroprotective mechanism of 17 beta-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.
ISSN:0257-716X
2096-5230
2523-899X
DOI:10.1007/bf02888040