title: Culture condition and embryonic stage dependent silence of glucocorticoid receptor expression in hippocampal neurons.
abstract: Glucocorticoid (GC) plays a key role in controlling numerous cellular processes during embryogenesis and fetal development. The actions of glucocorticoids are mediated by interaction with their receptors. We previously reported that hippocampal neurons from embryonic day 18 (E18) rats showed silence of glucocorticoid receptor (GR) expression when cultured in serum-free condition. In this study, using western blot, immunofluorescence staining and real-time RT-PCR, we found that while this silence occurred in hippocampal neurons isolated from E16 and E18 rats, it did not happen in those from E20 and neonatal (P0) rats. And when cultured under serum-containing condition, none of them showed GR silence anymore. Corticosterone could not rescue the expression of GR in E16 and E18 neurons in serum-free condition, whereas adding of serum could induce the re-expression of the silenced GR. The absence of GR silence in P0 neurons was not due to the perturbation during parturition. Moreover, the unique expression profile of GR in protein and mRNA level was well reflected in the changes of GR function. These results suggested that under in vitro condition, serum was critical for the maintaining of GR expression in hippocampal neurons of early embryonic stages but less important in later developmental stages. Thus, our data implied that at different developmental stages, the expression of GR in hippocampal neurons might have different susceptibilities to environment changes and there might be a critical time window for the switching of such characteristics during development.
authors.affiliation: Institute of Neuroscience, Department of Neurobiology, Second Military Medical University, 800 XiangYin Road, Shanghai 200433, PR China.
authors.forename: Lin
authors.initials: L
authors.lastname: Xiao
authors.forename: Yizhang
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D006690:Bisbenzimidazole / Q000378:metabolism; D018929:Cell Culture Techniques; D002478:Cells, Cultured; D003345:Corticosterone / Q000494:pharmacology; D016895:Culture Media, Serum-Free; D003907:Dexamethasone / Q000494:pharmacology; D004622:Embryo, Mammalian / Q000166:cytology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005456:Fluorescent Dyes / Q000378:metabolism; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005865:Gestational Age; D005938:Glucocorticoids / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology; D007700:Kinetics; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D011247:Pregnancy; D011506:Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000235:genetics* / Q000378:metabolism*; D012235:Rhodamines / Q000378:metabolism
chemical_list: D015415:Biomarkers; D016895:Culture Media, Serum-Free; D005456:Fluorescent Dyes; D005938:Glucocorticoids; C489787:MAP2 protein, rat; D008869:Microtubule-Associated Proteins; D011506:Proteins; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D012235:Rhodamines; C009434:tetramethylrhodamine isothiocyanate; D003907:Dexamethasone; D006690:Bisbenzimidazole; D003345:Corticosterone