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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

Antidepressants enhance glucocorticoid receptor function in vitro by modulating the membrane steroid transporters

TL;DR: The membrane steroid transporters that regulate access of glucocorticoids to the brain in vivo, like the multiple drug resistance p‐glycoprotein, could be a fundamental target for antidepressant action.
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Posttraumatic Stress Disorder: Acquisition, Recognition, Course, and Treatment

TL;DR: The course of PTSD, its disabling effect, its recognition and treatment, and considers possible new research directions are looked at.
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Genetic disruption of mineralocorticoid receptor leads to impaired neurogenesis and granule cell degeneration in the hippocampus of adult mice.

TL;DR: Adult MR−/− mice exhibited a significant reduction of granule cell neurogenesis to 65% of control levels, possibly mediated by GR due to elevated corticosterone plasma levels, which could attribute long‐term trophic effects of adrenal steroids on dentate granule cells to MR.
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Brain circuits involved in corticotropin-releasing factor-norepinephrine interactions during stress.

TL;DR: The results do not provide support for a feed‐forward hypothesis, and a few studies using certain tasks have indicated sensitization, and some other studies have suggested that the effect of CRF may be dose dependent.
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Corticosterone regulates expression of BDNF and trkB but not NT-3 and trkC mRNA in the rat hippocampus

TL;DR: In this article, the authors injected 30, 300, and 1,000 microg corticosterone s.c. (per kg body weight) in adrenalectomized rats and measured the mRNA levels of brain-derived neurotrophic factor (BDNF), tyrosine receptor kinase (trk)B, neurotrophin (NT)-3, and trkC in hippocampal cell fields at 6 hr after steroid administration by in situ hybridization.
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