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The Journal of Neuroscience, March 1, 2000, 20(5):1694-1700

Estrogen-Induced Activation of the Mitogen-Activated Protein Kinase Cascade in the Cerebral Cortex of Estrogen Receptor-alpha Knock-Out Mice

Meharvan Singh1, György Sétáló Jr1, 3, Xiaoping Guan1, Donald E. Frail4, and C. Dominique Toran-Allerand1, 2

Departments of 1 Anatomy and Cell Biology, and Centers for Neurobiology and Behavior and Reproductive Sciences, and 2 Neurology, Columbia University College of Physicians and Surgeons, New York, New York 10032, 3 Department of Biology, University Medical School of Pécs, Pécs H-7643, Hungary, and 4 Womens Health Research Institute, Wyeth-Ayerst Research, Radnor, Pennsylvania 19087

We have shown previously in the developing cerebral cortex that estrogen elicits the rapid and sustained activation of multiple signaling proteins within the mitogen-activated protein (MAP) kinase cascade, including B-Raf and extracellular signal-regulated kinase (ERK). Using estrogen receptor (ER)-alpha gene-disrupted (ERKO) mice, we addressed the role of ER-alpha in mediating this action of estrogen in the brain. 17beta -Estradiol increased B-Raf activity and MEK (MAP kinase/ERK kinase)-dependent ERK phosphorylation in cerebral cortical explants derived from both ERKO and their wild-type littermates. The ERK response was stronger in ERKO-derived cultures but, unlike that of wild-type cultures, was not blocked by the estrogen receptor antagonist ICI 182,780. Surprisingly, both the ER-alpha selective ligand 16alpha -iodo-17beta -estradiol and the ER-beta selective ligand genistein failed to elicit ERK phosphorylation, suggesting that a different mechanism or receptor may mediate estrogen-induced ERK phosphorylation in the cerebral cortex. Interestingly, the transcriptionally inactive stereoisomer 17alpha -estradiol did elicit a strong induction of ERK phosphorylation, which, together with the inability of the ER-alpha - and ER-beta -selective ligands to elicit ERK phosphorylation, and of ICI 182,780 to block the actions of estradiol in ERKO cultures, supports the hypothesis that a novel, estradiol-sensitive and ICI-insensitive estrogen receptor may mediate 17beta -estradiol-induced activation of ERK in the brain.

Key words: estradiol; estrogen receptor; ERK; ERKO; signal transduction; brain; cerebral cortex

Copyright © 2000 Society for Neuroscience  0270-6474/00/2051694-07$05.00/0


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