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Epigenetics, Oestradiol and Hippocampal Memory Consolidation
Author(s) -
Frick K. M.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12106
Subject(s) - epigenetics , histone , memory consolidation , dna methylation , biology , neuroscience , hippocampal formation , histone methylation , epigenetic regulation of neurogenesis , hippocampus , psychology , endocrinology , histone methyltransferase , genetics , dna , gene expression , gene
Epigenetic alterations of histone proteins and DNA are essential for hippocampal synaptic plasticity and cognitive function, and contribute to the aetiology of psychiatric disorders and neurodegenerative diseases. Hippocampal memory formation depends on histone alterations and DNA methylation, and increasing evidence suggests that the regulation of these epigenetic processes by modulatory factors, such as environmental enrichment, stress and hormones, substantially influences memory function. Recent work from our laboratory suggests that the ability of the sex‐steroid hormone 17β‐oestradiol (E 2 ) to enhance novel object recognition memory consolidation in young adult female mice is dependent on histone H3 acetylation and DNA methylation in the dorsal hippocampus. Our data also suggest that enzymes mediating DNA methylation and histone acetylation work in concert to regulate the effects of E 2 on memory consolidation. These findings shed light on the epigenetic mechanisms that influence hormonal modulation of cognitive function, and may have important implications for understanding how hormones influence cognition in adulthood and ageing. The present review provides a brief overview of the literature on epigenetics and memory, describes in detail our findings demonstrating that epigenetic alterations regulate E 2 ‐induced memory enhancement in female mice, and discusses future directions for research on the epigenetic regulation of E 2 ‐induced memory enhancement.

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