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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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Increased vulnerability to psychosocial stress in heterozygous serotonin transporter knockout mice

TL;DR: A mouse model of the 5-HTT-by-stress risk factor is presented and it is suggested that social avoidance represents a behavioral endophenotype of the interaction between 5- HTT and stress.
Journal ArticleDOI

Acute stress modulates genotype effects on amygdala processing in humans

TL;DR: It is shown that only carriers of a common functional deletion in ADRA2B, the gene coding for the α2b-adrenoreceptor, displayed increased phasic amygdala responses under stress, demonstrating that genetic effects on brain operations can be state dependent, such that they only become apparent under specific, often environmentally controlled conditions.
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The stressed brain of humans and rodents

TL;DR: The brain's response to stress depends on an individual's genetic background in interaction with life events, and studies in rodents point to the possibility to prevent or reverse long‐term consequences of early life adversity on cognitive processing by normalizing the balance between the two receptor types for corticosteroid hormones at a critical moment just before the onset of puberty.
Journal ArticleDOI

Chronic but not acute foot-shock stress leads to temporary suppression of cell proliferation in rat hippocampus.

TL;DR: The notion that chronic stress may lead to cumulative changes in the brain that are not seen after acute stress may indicate compromised brain plasticity and increased vulnerability to neuropathology is supported.
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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