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Fig. 2 | BMC Neuroscience

Fig. 2

From: Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

Fig. 2

Epigenetic Mechanisms of Memory Alteration Following Chronic Psychological Stress. Simplified and schematic model of epigenetic mechanisms for slow (> 1 h) genomic effects induced by nuclear receptors. During chronic stress, increased nuclear levels of GRs-cortisol complex promote DNA methylation. Methylated DNA sites prevent CREB binding, and vice versa (depicted in double arrows as “synergetic inhibition”). At the same time, CREB activity largely correlates to histone acetylation which is essential for memory consolidation. CH3, methyl group; CH3CO, acetylation; CREB, cAMP response element-binding protein; GR, glucocorticoid receptor; GRE, glucocorticoid response elements; H, histone; PO32, phosphorylation

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