{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:42:08Z","timestamp":1773290528129,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,7,27]],"date-time":"2005-07-27T00:00:00Z","timestamp":1122422400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Medical measures that bear no known danger for the adult brain may trigger active neuronal death in the developing brain. Pharmacological blockade of <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>D<\/jats:sc>\u2010aspartate or activation of GABA<jats:sub>A<\/jats:sub> receptors, blockade of voltage\u2010dependent sodium channels, and oxygen induce widespread apoptotic neurodegeneration during the period of rapid brain growth in rodents. Because such measures are often necessary in critically ill infants and toddlers, search for adjunctive neuroprotective strategies is warranted. We report that 17\u03b2\u2010estradiol ameliorates neurotoxicity of drugs that block <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>D<\/jats:sc>\u2010aspartate receptors, activate GABA<jats:sub>A<\/jats:sub> receptors, or block voltage\u2010gated sodium channels and reduces neurotoxicity of oxygen in the infant rat brain. This neuroprotective effect is reversed by tamoxifen and cannot be reproduced by 17\u03b1\u2010estradiol. 17\u03b2\u2010Estradiol did not affect GABA<jats:sub>A<\/jats:sub> or <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>D<\/jats:sc>\u2010aspartate currents in hippocampal neuronal cultures, indicating that direct modulation of neurotransmitter receptor\/channel properties by this compound cannot explain neuroprotective effect. 17\u03b2\u2010Estradiol did, however, increase levels of phosphorylated extracellular signal\u2010regulated kinase 1\/2 and AKT, suggesting that activation of these prosurvival proteins may represent one mechanism for its neuroprotective action. 17\u03b2\u2010Estradiol and related compounds may be neuroprotective agents suitable for use in critically ill infants and toddlers. Its supplementation may particularly help to improve neurocognitive outcome in preterm infants who are prematurely deprived of maternal estrogen. 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