Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10306685 | Psychoneuroendocrinology | 2013 | 13 Pages |
Abstract
Glucocorticoid hormones and their receptors have been identified to be involved in emotional and cognitive disorders in early stressed subjects during adulthood. However, the impact of other steroid hormones and receptors has been considered less. Especially, functional roles of estrogen and estrogen receptors in male subjects are largely unknown. Therefore, we measured hippocampal concentrations of 17β-estradiol, corticosterone and testosterone, as well as the gene expression of estrogen receptor α and β (ERα, β), androgen receptor (AR), glucocorticoid (GR) and mineralocorticoid (MR) receptors after stress in adulthood in maternally separated (MS+; at postnatal days 14-16 for 6 h each day) and control (MSâ) male rats. In vivo hippocampal long-term potentiation (LTP) serves as a cellular model of learning and memory formation. Population spike- (PSA) and the fEPSP-LTP within the dentate gyrus (DG) were reinforced by elevated-platform-stress (EP-stress) in MSâ but not in MS+ rats. MRâ and ERβ-mRNA were upregulated 1 h after EP-stress in MSâ but not in MS+ rats as compared to non-stressed littermates. Infusion of an MR antagonist before LTP induction blocked early- and late-PSA- and -fEPSP-LTP, whereas blockade of ERβ impaired only the late PSA-LTP. Application of a DNA methyltransferase (DNMT) inhibitor partly restored the LTP-reinforcement in MS+ rats, accompanied by a retrieval of ERβâ but not MR-mRNA upregulation. Basal ERβ gene promoter methylation was similar between groups, whereas MS+ and MSâ rats showed different methylation patterns across CpG sites after EP-stress. These findings indicate a key role of ERβ in early-stress mediated emotionality and emotion-induced late-LTP in adult male rats via DNA methylation mechanisms.
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Authors
Han Wang, Katrin Meyer, Volker Korz,