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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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Pharmacological characterization of intracellular, membrane, and plasma binding sites for corticosterone in house sparrows

TL;DR: Pharmacologically characterized the three putative corticosteroid receptors in the brain, as well as a plasma corticosterone binding globulin, in the house sparrow, to extend the ability to evaluate the comparative actions of glucocorticoids, increase the understanding of mechanisms behind the tissue specificity, and offer insight into the evolution of glucOCorticoid action in vertebrates.
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Localization of mineralocorticoid receptors at mammalian synapses.

TL;DR: In this paper, the authors investigated the subcellular sites of mineralocorticoid receptors in the lateral amygdala of the Sprague-Dawley rat and found that they were expressed at both nuclear and extra nuclear sites including presynaptic terminals, neuronal dendrites, and dendritic spines.
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Effects of ghrelin on psychopathology, sleep and secretion of cortisol and growth hormone in patients with major depression

TL;DR: Ghrelin strongly affected sleep and secretion of GH and cortisol in a partly different way as previously reported in healthy subjects and may provide some initial indication that ghrelin can exert antidepressant effects in patients with major depression.
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HPA axis dysregulation associated to apolipoprotein E4 genotype in Alzheimer's disease.

TL;DR: There is a dysregulation of the hypothalamus-pituitary-adrenal axis in AD that seems to be consequence rather than cause of AD, as increases in cortisol levels were found only in AD patients.
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Corticolimbic regulation of cardiovascular responses to stress.

TL;DR: This brief review focuses on the mechanisms by which corticolimbic nuclei, critical for stress appraisal and emotional reactivity, regulate heart rate and blood pressure responses to psychological stress.
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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