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• W1998941799 abstract "Increasing lines of evidence indicate that estrogen acts as a neuroprotective agent through a nongenomic mechanism. We tested the hypothesis that 17β-estradiol could rapidly attenuate glutamate-induced calcium (Ca2+) overload in rat primary hippocampal neurons via a membrane receptor-dependent mechanism. The bulk cytosolic intracellular Ca2+ level was measured in neurons with fluorescent Ca2+ probe fluo3. Preexposure of primary cultured hippocampal neurons to 17β-estradiol for 3 min attenuated intracellular Ca2+ increase induced by glutamate in a concentration-dependent manner. The action of 17β-estradiol was reversible after washout. Administration of membrane-impermeable 17β-estradiol conjugated to bovine serum albumin (E2–BSA) produced the same effect, suggesting possible involvement of cell membrane receptors. ICI 182,780, a specific estrogen receptor (ER) antagonist, blocked the neuronal response to 17β-estradiol and estradiol BSA, indicating a role of specific ERs. The present study demonstrates that 17β-estradiol acutely reduces glutamate-stimulated intracellular Ca2+ increase via ERs probably on the cell surface of the hippocampal neurons." @default.
• W1998941799 created "2016-06-24" @default.
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• W1998941799 date "2004-11-01" @default.
• W1998941799 modified "2023-10-17" @default.
• W1998941799 title "Estradiol acutely attenuates glutamate-induced calcium overload in primarily cultured rat hippocampal neurons through a membrane receptor-dependent mechanism" @default.
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• W1998941799 doi "https://doi.org/10.1016/j.brainres.2004.08.038" @default.
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