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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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Sericin alleviates restraint stress induced depressive- and anxiety-like behaviors via modulation of oxidative stress, neuroinflammation and apoptosis in the prefrontal cortex and hippocampus

TL;DR: Sericin treatments decreased oxygen species (ROS) and lipid peroxidation levels, restored MMP, and enhanced total antioxidant capacity (TAC) and enzyme activity of GPx and SOD in both brain regions, providing evidence for the protective effect of sericin therapy against psychopathological and behavioral changes induced by restraint stress.
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Exogenous cortisol enhances aggressive behavior in females, but not in males

TL;DR: This study provides the first evidence for a causal involvement of acute HPA axis activation in aggressive behavior in humans.
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Epigenomics of Major Depressive Disorders and Schizophrenia: Early Life Decides

TL;DR: Overall, epigenomic responses to early life adversity appear to be controlled to different degrees by genetics inMDD/SCZ, even though the potential reversibility of epigenomic processes may offer new hope for timely therapeutic interventions in MDD/ SCZ.
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Chronic exposure to stress predisposes to higher autoimmune susceptibility in C57BL/6 mice: Glucocorticoids as a double‐edged sword

TL;DR: It is demonstrated that whereas C57BL/6 female mice generally exhibit higher CORT levels and an attenuated form of EAE than males, they become less responsive to the immunosuppressive effects of CORT under chronic stress and thereby prone to a higher risk of destructive autoimmunity.
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A new model for the HPA axis explains dysregulation of stress hormones on the timescale of weeks

TL;DR: A mathematical model for the HPA axis is developed that shows the property of dynamical compensation, where gland masses adjust over weeks to buffer variation in physiological parameters, and suggests that gland‐mass dynamics may play an important role in the pathophysiology of stress‐related disorders.
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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