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Journal ArticleDOI

Stress and the brain: from adaptation to disease

TLDR
In response to stress, the brain activates several neuropeptide-secreting systems, which eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators as mentioned in this paper.
Abstract
In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.

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Early life stress, the development of aggression and neuroendocrine and neurobiological correlates: what can we learn from animal models?

TL;DR: Data suggest that social deprivation-induced inappropriate forms of aggression are associated with high or low HPA axis (re)activity and a generally lower functioning of the serotonin system in adulthood, and genetic and epigenetic modifications in HPA and serotonin systems influence the outcome of early life stress.
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Mineralocorticoid and glucocorticoid receptors at the neuronal membrane, regulators of nongenomic corticosteroid signalling.

TL;DR: Nongenomic corticosteroid actions in the brain are required for the coordination of a rapid adaptive response to stress; membrane-associated MRs and GRs play a major role herein.
Journal ArticleDOI

Cross-talk between nuclear receptors and nuclear factor |[kappa]|B

TL;DR: The molecular mechanisms of cross-talk between NRs and NF-κB and the biological relevance of thisCross-talk is described, which will lead to a new era in the field of NR research with the aim of specifically inhibiting NF-β-driven gene expression for anti-inflammatory, anti-tumor and immune-modulatory purposes.
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Gene–environment interactions: early life stress and risk for depressive and anxiety disorders

TL;DR: Overall, there is support for GxE effects of ELS on the risk for depressive and anxiety outcomes, and future studies of E LS in this context will require careful attention to methodologic considerations.
References
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Journal ArticleDOI

Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene

TL;DR: Evidence of a gene-by-environment interaction is provided, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
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How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
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Epigenetic programming by maternal behavior.

TL;DR: It is shown that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible, suggesting a causal relation among epigenomicState, GR expression and the maternal effect on stress responses in the offspring.
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Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants

TL;DR: It is shown that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants, suggesting that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neuroGenesis in the hippocampus.
Journal ArticleDOI

A Syndrome produced by Diverse Nocuous Agents

Hans Selye
- 01 Jul 1936 - 
TL;DR: If the organism is severely damaged by acute non-specific nocuous agents such as exposure to cold, surgical injury, production of spinal shock, excessive muscular exercise, or intoxications with sublethal doses of diverse drugs, a typical syndrome appears, the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed.
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