Expression of glucocorticoid and mineralocorticoid receptors in hippocampus of rats exposed to various modes of hypobaric hypoxia: Putative role in hypoxic preconditioning

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• 作者：Elena Rybnikova^b ; ^{rybnikova1@rambler.ru} ; Tatiana Glushchenko^a ; Anna Churilova^a ; Svetlana Pivina^b ; Michail Samoilov^a ; ^{samoilov@pavlov.infran.ru}
• 关键词：Brain ; Hypoxia ; Preconditioning ; Neuronal injury and tolerance ; Glucocorticoid receptor ; Mineralocorticoid receptor
• 刊名：Brain Research
• 出版年：2011
• 出版时间：24 March 2011
• 年：2011
• 卷：1381
• 期：Complete
• 页码：66-77
• 全文大小：1643 K

文摘

Effects of mild (preconditioning) and severe injurious hypobaric hypoxia (SH), as well as of their combination on hippocampal expression of glucocorticoid (GR) and mineralocorticoid (MR) receptors and HPA axis activity have been examined in rats. As revealed by quantitative immunocytochemistry, three-trial exposure to mild hypoxia produced robust GR and MR overexpression located mainly in the neuronal nuclei in the dentate gyrus (DG) but only MR overexpression was observed in the CA1. SH induced sharp reduction of MR levels and enhanced GR expression in the CA1, suggesting that the unbalance of GR and MR observed might be at the bottom of the extensive neuronal loss seen in this area in response to SH. Contrastingly, SH in tolerant (preconditioned) rats failed to imbalance GR and MR expression in CA1 and up-regulated GR levels in DG. Radioimmunoassay of serum corticosterone showed that both preconditioning hypoxia itself and SH in tolerant rats produced moderate activation of HPA axis followed by its proper inactivation. In the non-preconditioned rats, HPA axis response to SH was impaired. Taken together, these novel results suggest that modifications of the hippocampal expression of GR and MR produced by preconditioning may contribute to the molecular and neuroendocrine mechanisms of tolerance to severe hypoxic stress.