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Protective action of 17 β ‐estradiol and tamoxifen on glutamate toxicity in glial cells
Author(s) -
Shy Hogan,
Malaiyandi Latha,
Timiras Paola S.
Publication year - 2000
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(99)00097-0
Subject(s) - tamoxifen , glutamate receptor , estrogen , endocrinology , medicine , biology , antiestrogen , toxicity , pharmacology , breast cancer , cancer , receptor
Estrogens influence differentiation, growth and function of neurons, but less is known of their effects on glia. In our experiments reported here, the ovarian steroid, 17 β ‐estradiol, and the “designer”, non‐steroidal estrogen, tamoxifen, effectively protected C‐6 glioma 2B clone cells from the cytotoxicity of the excitatory neurotransmitter, glutamate. Exposure of these cells to 10–20 mM glutamate induced 61–78% cell death. Pre‐treatment of the cells with 0.01 mM estradiol or with 2 μM tamoxifen significantly reduced the glutamate‐induced cell death, estradiol being the most effective in this regard. Estradiol‐ or tamoxifen‐treated cells that had survived glutamate damage appeared more mature than controls. Thus, estrogens often used in therapy (estradiol as replacement after menopause and tamoxifen for treatment/prevention of breast cancer) may significantly protect glial cells against glutamate toxicity and stimulate cell differentiation.