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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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Pharmacology of glucocorticoids: beyond receptors.

TL;DR: It is concluded that the recent identification of selective glucocorticoid receptor agonists that induce distinct conformational changes to the receptors resulting in altered protein-protein interactions and consequently different regulation of gene expression will contribute to the design of safer glucocorts that retain full pharmacological properties with reduced side-effects.
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Stress and the engagement of multiple memory systems: Integration of animal and human studies

TL;DR: A model is proposed which states that the impact of stress on the relative use of multiple memory systems is due to differential effects of hormones and neurotransmitters that are released during stressful events on hippocampal and dorsal striatal memory systems, thus changing the relative strength of and the interactions between these systems.
Journal ArticleDOI

Changes in cortisol secretion during antidepressive treatment and cognitive improvement in patients with major depression: a longitudinal study.

TL;DR: Improvement of some cognitive domains during SSRI treatment was associated with decreasing cortisol secretion and was only to a lesser extent associated with improved depressive symptoms.
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Hippocampal neurogenesis and behavioural studies on adult ischemic rat response to chronic mild stress.

TL;DR: The results support a putative role for ischemia-induced neurogenesis in what may be an adaptive or compensatory process, which is influenced by post-stroke stressors and thus represents a potential target for therapy.
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Modulation of circadian glucocorticoid oscillation via adrenal opioid-CXCR7 signaling alters emotional behavior.

TL;DR: It is demonstrated that mice with adrenal subcapsular cell hyperplasia (SCH), a common histological change in the adrenals, are less anxious than mice without SCH, and recapitulating this paracrine axis by subcutaneous administration of a synthetic CXCR7 ligand is sufficient to induce anxiolytic-like behavior.
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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