17beta-Estradiol protects against NMDA-induced excitotoxicity by direct inhibition of NMDA receptors.
Several lines of evidence suggest that 17beta-estradiol (betaE2) has neuroprotective properties. The risk and severity of dementia are decreased in women who have received estrogen therapy, and betaE2 protects neurons in vitro against death from a variety of stressors. Neuroprotection by betaE2 has been suggested to be due to free radical scavenging. We demonstrate an additional neuroprotective mechanism whereby betaE2 protects against NMDA-induced neuronal death by directly inhibiting the NMDA receptor.
Weaver
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CE
Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, MA 02118-2394, USA.
Park-Chung
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M
Gibbs
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Farb
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DH
D000818:Animals; D002478:Cells, Cultured; D002642:Chick Embryo; D004958:Estradiol / Q000494:pharmacology*; D018690:Excitatory Amino Acid Agonists; D006624:Hippocampus / Q000166:cytology; D016202:N-Methylaspartate; D009474:Neurons / Q000737:chemistry / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009498:Neurotoxins / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*
D018690:Excitatory Amino Acid Agonists; D018696:Neuroprotective Agents; D009498:Neurotoxins; D016194:Receptors, N-Methyl-D-Aspartate; D004958:Estradiol; D016202:N-Methylaspartate