Early life stress‐induced histone acetylations correlate with activation of the synaptic plasticity genes Arc and Egr1 in the mouse hippocampus

Xie, Lan; Korkmaz, Kemal; Braun, Katharina; Bock, Jörg

doi:10.1111/jnc.12210

Cited by 85 publications

(66 citation statements)

References 50 publications

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“…Several findings suggest an important role of Zif268 in experience-dependent epigenetic mechanisms that underlie memory. For example, regulation of histone methylation at the Zif268 promoter can facilitate contextual fear memory [38], histone H4 acetylation at the Zif268 promoter correlates with Zif268 expression in the hippocampus [39] and histone acetylation critically modulates object recognition memory consolidation [40]. Furthermore, exploration of objects was recently shown to trigger rapid phosphorylation, acetylation and methylation of histones at the Zif268 promoter in the hippocampus and the prefrontal cortex [41].…”

Section: Discussionmentioning

confidence: 99%

Zif268 / Egr1 gain of function facilitates hippocampal synaptic plasticity and long-term spatial recognition memory

Penke

Morice

Veyrac

et al. 2014

Phil. Trans. R. Soc. B

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It is well established that Zif268/Egr1 , a member of the Egr family of transcription factors, is critical for the consolidation of several forms of memory; however, it is as yet uncertain whether increasing expression of Zif268 in neurons can facilitate memory formation. Here, we used an inducible transgenic mouse model to specifically induce Zif268 overexpression in forebrain neurons and examined the effect on recognition memory and hippocampal synaptic transmission and plasticity. We found that Zif268 overexpression during the establishment of memory for objects did not change the ability to form a long-term memory of objects, but enhanced the capacity to form a long-term memory of the spatial location of objects. This enhancement was paralleled by increased long-term potentiation in the dentate gyrus of the hippocampus and by increased activity-dependent expression of Zif268 and selected Zif268 target genes. These results provide novel evidence that transcriptional mechanisms engaging Zif268 contribute to determining the strength of newly encoded memories.

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Section: Discussionmentioning

confidence: 99%

Zif268 / Egr1 gain of function facilitates hippocampal synaptic plasticity and long-term spatial recognition memory

Penke

Morice

Veyrac

et al. 2014

Phil. Trans. R. Soc. B

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“…Depicted are dendritic arbors of neurons in prefrontal cortex. Early adversity in the form of disrupting infant-maternal interactions results in reduced arbors, whereas disruption later in development generates a paradoxical increase in dendritic growth (Bock et al, 2005;Xie et al, 2013). E, ELS in the first postnatal week results in an accelerated timing of a critical period for limbic circuit plasticity (Callaghan and Richardson, 2011;Bath et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Social Origins of Developmental Risk for Mental and Physical Illness

et al. 2017

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Adversity in early childhood exerts an enduring impact on mental and physical health, academic achievement, lifetime productivity, and the probability of interfacing with the criminal justice system. More science is needed to understand how the brain is affected by early life stress (ELS), which produces excessive activation of stress response systems broadly throughout the child's body (toxic stress). Our research examines the importance of sex, timing and type of stress exposure, and critical periods for intervention in various brain systems across species. Neglect (the absence of sensitive and responsive caregiving) or disrupted interaction with offspring induces robust, lasting consequences in mice, monkeys, and humans. Complementary assessment of internalizing disorders and brain imaging in children suggests that early adversity can interfere with white matter development in key brain regions, which may increase risk for emotional difficulties in the long term. Neural circuits that are most plastic during ELS exposure in monkeys sustain the greatest change in gene expression, offering a mechanism whereby stress timing might lead to markedly different long-term behaviors. Rodent models reveal that disrupted maternal-infant interactions yield metabolic and behavioral outcomes often differing by sex. Moreover, ELS may further accelerate or delay critical periods of development, which reflect GABA circuit maturation, BDNF, and circadian Clock genes. Such factors are associated with several mental disorders and may contribute to a premature closure of plastic windows for intervention following ELS. Together, complementary cross-species studies are elucidating principles of adaptation to adversity in early childhood with molecular, cellular, and whole organism resolution.

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“…It has been shown that early life stress such as maternal separation in mice can induce histone acetylation that correlates with the activation of synaptic plasticity genes Arc and Egr1 in the hippocampus of the pups [89]. The authors speculated that this adaptation of the hippocampal synaptic circuits occurs in order for the mice to cope with their stressful environment; however, direct evidence is still lacking.…”

Section: Post-natal Exposurementioning

confidence: 99%

Molecular and Epigenetic Mechanisms Underlying Cognitive and Adaptive Responses to Stress

et al. 2017

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Consolidation of contextual memories after a stressful encounter is essential for the survival of an organism and in allowing a more appropriate response to be elicited should the perceived threat reoccur. Recent evidence has explored the complex role that epigenetic mechanisms play in the formation of such memories, and the underlying signaling pathways are becoming more apparent. The glucocorticoid receptor (GR) has been shown to play a key role in these events having both genomic and non-genomic actions in the brain. GR has been shown to interact with the extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) signaling pathway which, in concert, drives epigenetic modifications and chromatin remodeling, resulting in gene induction and memory consolidation. Evidence indicates that stressful events can have an effect on the offspring in utero, and that epigenetic marks altered early in life may persist into adulthood. A new and controversial area of research, however, suggests that epigenetic modifications could be inherited through the germline, a concept known as transgenerational epigenetics. This review explores the role that epigenetic processes play in the central nervous system, specifically in the consolidation of stress-induced memories, the concept of transgenerational epigenetic inheritance, and the potential role of epigenetics in revolutionizing the treatment of stress-related disorders through the emerging field of pharmacoepigenetics and personalized medical treatment.

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Early life stress‐induced histone acetylations correlate with activation of the synaptic plasticity genes Arc and Egr1 in the mouse hippocampus

Cited by 85 publications

References 50 publications

Zif268 / Egr1 gain of function facilitates hippocampal synaptic plasticity and long-term spatial recognition memory

Zif268 / Egr1 gain of function facilitates hippocampal synaptic plasticity and long-term spatial recognition memory

Social Origins of Developmental Risk for Mental and Physical Illness

Molecular and Epigenetic Mechanisms Underlying Cognitive and Adaptive Responses to Stress

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