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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

Inverted-U relationship between the level of peripheral corticosterone and the magnitude of hippocampal primed burst potentiation.

TL;DR: Findings provide strong support for the hypothesis that corticosterone exerts a concentration‐dependent biphasic influence on the expression of hippocampal plasticity.
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Effects of the high-affinity corticotropin-releasing hormone receptor 1 antagonist R121919 in major depression: the first 20 patients treated.

TL;DR: The data suggested that CRH(1)-receptor blockade does not impair the corticotropin and cortisol secretory activity either at baseline or following an exogenous CRH challenge, and significant reductions in depression and anxiety scores are observed using both, patient and clinician ratings.
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Human stresscopin and stresscopin-related peptide are selective ligands for the type 2 corticotropin-releasing hormone receptor

TL;DR: Treatment with SCP or SRP suppressed food intake, delayed gastric emptying and decreased heat-induced edema, and could allow the design of drugs to ameliorate stress-related diseases.
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Repeated restraint stress suppresses neurogenesis and induces biphasic PSA-NCAM expression in the adult rat dentate gyrus.

TL;DR: Two studies subjected rats to acute or chronic restraint stress and assessed the proliferation, survival and differentiation of newly born cells in the dentate gyrus may help understand the basis for hippocampal shrinkage and raise questions about the ultimate reversibility of the effects of chronic stress.
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Repeated restraint stress facilitates fear conditioning independently of causing hippocampal CA3 dendritic atrophy.

TL;DR: Results confirmed that stress produced CA3 dendritic atrophy and tianeptine prevented it, and argued that different neural substrates underlie spatial recognition memory and fear conditioning.
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