Effect of estrogen on glutamate-induced neuronal cell death and calcium influx.
Published: 2005
Language: eng
Number of pages: 162
Description: High concentrations of glutamate can cause neuronal cell death and this involves changes in the regulation of cellular calcium (Ca 2+) through the N-methyl-D-aspartate (NMDA) receptor and subsequent activation of nitric oxide synthase (NOS). Estrogen has been shown to protect against glutamate-induced cell death possibly by a reduction in the excitotoxic Ca2+ influx. In the present study, the effect of 17beta-estradiol (17beta-E2) and a more potent antioxidant estrogen, Delta8,17beta-estradiol (Delta8,17beta-E2) on cell viability and intracellular Ca 2+ ([Ca2+]i) on glutamate-induced cell death was studied. Estrogens, 17beta-E2 and Delta8,17beta-E 2, significantly protected against glutamate-induced excitotoxicity with 17beta-E2 being more potent than Delta8,17beta-E 2. The neuroprotective effect of estrogens in cortical cells occurs through a mechanism that does not involve a reduction of [Ca2+] i. This is to our knowledge a first such observation. Whether decreases in NOS related products, such as peroxynitrite, is one mechanism by which estrogens provide neuroprotection against glutamate-induced excitotoxicity, remains to be investigated.
Notes: Source: Masters Abstracts International, Volume: 44-02, page: 0765.

Thesis (M.Sc.)--University of Toronto, 2005.

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