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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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Corticosteroid receptor-mediated mechanisms in the amygdala regulate anxiety and colonic sensitivity

TL;DR: The data suggest that both GR and MR play a critical role in Cort-induced anxiety and colonic hypersensitivity, and in rats with Cort implants combined with either a GR or MR antagonist, there was a significant inhibition of anxiety andColonic hypersensitivity.
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Stress and excitatory synapses: From health to disease

TL;DR: How brief and prolonged exposure to stress, in adulthood and early life, regulate the function of Excitatory synapses, and how these effects may contribute to behavioral adaptation and psychopathology is discussed.
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Animal models in translational studies of PTSD.

TL;DR: The current review covers recent translational approaches to bridge the gap between human and animal PTSD research and to create a framework for discovery of biomarkers and novel therapeutics.
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Glucocorticoid hormones decrease proliferation of embryonic neural stem cells through ubiquitin-mediated degradation of cyclin D1.

TL;DR: In embryonic brain, dexamethasone inhibited cell proliferation of NSCs, demonstrating that embryonic NSC's are critically influenced by glucocorticoids, which can have long-term effects in the brain.
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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