期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：2
页码：703-708
DOI：10.1073/pnas.242735799
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The present study stems from our previous observations that the brains of adult estrogen receptor {beta} knockout (ER{beta}-/-) mice show regional neuronal hypocellularity especially in the cerebral cortex. We now show that ER{beta} is necessary for late embryonic development of the brain and is involved in both neuronal migration and apoptosis. At embryonic day (E)18.5, ER{beta}-/- mouse brains were smaller than those of the wild-type (WT) littermates, and there were fewer neurons in the cortex. There were no differences in size or cellularity at E14.5. When proliferating cells were labeled with 5'-bromodeoxyuridine (BrdUrd) on E12.5, a time when cortical neurogenesis in mice begins, and examined on E14.5, there was no difference between WT and ER{beta}-/- mice in the number of labeled cells in the cortex. However, when BrdUrd was administered between E14.5 and E16.5, a time when postmitotic neurons migrate to layers of the cortex, there were fewer BrdUrd-labeled cells in the superficial cortical layers by E18.5 and postnatal day 14 in mice lacking ER{beta}. At E18.5, there were more apoptotic cells in the ventricular zone of mice lacking ER{beta}. In addition, the processes of the cortical radial glia, which are essential for guiding the migrating neurons, were fragmented. These findings suggest that by influencing migration and neuronal survival, ER{beta} has an important role in brain development.
