Protection of cortical cells by equine estrogens against glutamate-induced excitotoxicity is mediated through a calcium independent mechanism |
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| Authors: | Joel?Perrella Email author" target="_blank">Bhagu?R?BhavnaniEmail author |
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| Institution: | (1) Department of Obstetrics and Gynecology, University of Toronto, Toronto, Canada;(2) Institute of Medical Sciences, University of Toronto, Toronto, Canada;(3) Department of Obstetrics and Gynecology, St. Michael's Hospital, Toronto, Canada |
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| Abstract: | Background High concentrations of glutamate can accumulate in the brain and may be involved in the pathogenesis of neurodegenerative
disorders such as Alzheimer's disease. This form of neurotoxicity involves changes in the regulation of cellular calcium (Ca2+) and generation of free radicals such as peroxynitrite (ONOO-). Estrogen may protect against glutamate-induced cell death by reducing the excitotoxic Ca2+ influx associated with glutamate excitotoxicity. In this study, the inhibition of N-methyl-D-aspartate (NMDA) receptor and
nitric oxide synthase (NOS) along with the effect of 17β-estradiol (17β-E2) and a more potent antioxidant Δ8, 17β-estradiol (Δ8, 17β-E2) on cell viability and intracellular Ca2+ (Ca2+]i), following treatment of rat cortical cells with glutamate, was investigated. |
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