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.read more
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Book ChapterDOI
Stress-induced changes in hippocampal function.
TL;DR: A disturbed balance between these early and late phases of the stress response as well as a shift toward the relative contribution of the dentate/amygdala pathways may explain why the normal restorative capacity fails in vulnerable people experiencing a life-threatening situation, which could contribute to the development of PTSD.
Journal ArticleDOI
Altered sirtuin deacetylase gene expression in patients with a mood disorder.
Naoko Abe,Shusaku Uchida,Koji Otsuki,Teruyuki Hobara,Hirotaka Yamagata,Fumihiro Higuchi,Tomohiko Shibata,Yoshifumi Watanabe +7 more
TL;DR: The data suggest that altered SIRT1, 2 and 6 expression is state-dependent and might be associated with the pathogenesis and/or pathophysiology of mood disorders.
Journal ArticleDOI
Psychosocial job characteristics and insomnia: a prospective cohort study using the Demand-Control-Support (DCS) and Effort-Reward Imbalance (ERI) job stress models.
Atsuhiko Ota,Takeshi Masue,Nobufumi Yasuda,Akizumi Tsutsumi,Yoshio Mino,Hiroshi Ohara,Yuichiro Ono +6 more
TL;DR: Proportionate reward for work effort and sufficient support at work assist recovery from insomnia, while overcommitment to work and high job strain cause future onset of insomnia.
Journal ArticleDOI
Glucocorticoid receptors and extinction retention deficits in the single prolonged stress model.
TL;DR: The results suggest that simple enhancements in GR expression in the hippocampus and PFC are insufficient to result in extinction retention deficits, but raise the possibility that a threshold-enhancement in hippocampal GR expression contributes to SPS-induced extinction retention deficit.
Journal ArticleDOI
Impairment of synaptic plasticity by the stress mediator CRH involves selective destruction of thin dendritic spines via RhoA signaling.
Yuncai Chen,Enikö A. Kramár,Lulu Y. Chen,Alex H. Babayan,Adrienne L. Andres,Christine M. Gall,Gary Lynch,Tallie Z. Baram +7 more
TL;DR: A novel, hippocampus-intrinsic mechanism for the selective memory defects that are provoked by stress is reported, implicate the selective loss of dendritic spine sub-populations as a novel structural and functional foundation for the clinically important effects of stress on cognitive and emotional processes.
References
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Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene
Avshalom Caspi,Karen Sugden,Terrie E. Moffitt,Alan Taylor,Ian W. Craig,Hona Lee Harrington,Joseph L. McClay,Jonathan Mill,Judy Martin,Antony W. Braithwaite,Richie Poulton +10 more
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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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Ian C. G. Weaver,Nadia Cervoni,Frances A. Champagne,Ana C. D'Alessio,Shakti Sharma,Jonathan R. Seckl,Sergiy Dymov,Moshe Szyf,Michael J. Meaney +8 more
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.
Journal ArticleDOI
Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants
Luca Santarelli,Michael Saxe,Cornelius Gross,Alexandre Surget,Fortunato Battaglia,Stephanie C. Dulawa,Noelia V. Weisstaub,James T. Lee,Ronald S. Duman,Ottavio Arancio,Catherine Belzung,René Hen +11 more
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
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.