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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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Citations
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Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse

TL;DR: Findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.
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The molecular neurobiology of depression

TL;DR: Recent studies combining behavioural, molecular and electrophysiological techniques reveal that certain aspects of depression result from maladaptive stress-induced neuroplastic changes in specific neural circuits and show that understanding the mechanisms of resilience to stress offers a crucial new dimension for the development of fundamentally novel antidepressant treatments.
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About sleep's role in memory

TL;DR: This review aims to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings.
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Major depressive disorder.

TL;DR: This review presents the major current approaches to understanding the biologic mechanisms of major depression and defines depression as a heterogeneous disorder with a highly variable course, an inconsistent response to treatment, and no established mechanism.
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New approaches to antidepressant drug discovery: beyond monoamines

TL;DR: A recent review summarizes the obstacles that have hindered the development of non-monoamine-based antidepressants, and provides a progress report on some of the most promising current strategies as discussed by the authors.
References
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Journal ArticleDOI

Common polymorphisms in the glucocorticoid receptor gene are associated with adrenocortical responses to psychosocial stress.

TL;DR: This is the first report documenting an impact of GR gene polymorphisms on cortisol (and perhaps ACTH) responses to psychosocial stress and these variants may contribute to the individual vulnerability for hypothalamus-pituitary-adrenal-related disorders.
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Penetration of Dexamethasone into Brain Glucocorticoid Targets Is Enhanced in mdr1A P-Glycoprotein Knockout Mice

TL;DR: It was found that brain areas expressing the glucocorticoid receptor in high abundance, such as the hippocampal cell fields and the paraventricular nucleus, showed a 10-fold increase in cell nuclear uptake of radiolabeled steroid, which supports the concept of a pituitary site of action of dexamethasone in blockade of stress-induced ACTH release.
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Chronic Treatment of Rats with the Antidepressant Amitriptyline Attenuates the Activity of the Hypothalamic-Pituitary-Adrenocortical System

TL;DR: It is hypothesized that during amitriptyline treatment a rise in limbic MR may be the initial phenomenon in a successively adjusting HPA system, as evidenced by the decreasing plasma hormone concentrations, declining adrenal size, and up-regulation of GR in particular brain regions.
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Corticotropin-releasing factor in brain: A role in activation, arousal, and affect regulation

TL;DR: It is suggested that affective regulation is exerted by CRF/urocortin systems within the brain based upon the sensitivity of local brain sites to CRf/uroCortin ligand administration and the appearance of hypothalamo-pituitary-adrenocortical activation following stressor exposure.
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Cortisol response in the combined dexamethasone/CRH test as predictor of relapse in patients with remitted depression. a prospective study.

TL;DR: An exaggerated cortisol response in the combined DEX/CRH test predicts the recurrence of depressive psychopathology and the two proposed rules for predicting relapse within the first 6 months after discharge could be optimized by including age and gender.
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