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Journal ArticleDOI

Tianeptine attenuates stress-induced morphological changes in the hippocampus

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TLDR
Results suggest that the serotonergic system may be involved in modulating stress and corticosterone effects on dendritic morphology and that tianeptine is known to enhance neural uptake of serotonin.
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This article is published in European Journal of Pharmacology.The article was published on 1992-11-03. It has received 333 citations till now. The article focuses on the topics: Tianeptine & Corticosterone.

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Chronic Antidepressant Treatment Increases Neurogenesis in Adult Rat Hippocampus

TL;DR: Investigation of the effect of antidepressants on hippocampal neurogenesis in the adult rat using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells demonstrates that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus.
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Regulation of BDNF and trkB mRNA in Rat Brain by Chronic Electroconvulsive Seizure and Antidepressant Drug Treatments

TL;DR: The enhanced induction and prolonged expression of BDNF in response to chronic ECS and antidepressant drug treatments could promote neuronal survival, and protect neurons from the damaging effects of stress.
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A molecular and cellular theory of depression

TL;DR: These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular neurons.
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Stress and hippocampal plasticity.

TL;DR: The hippocampus is a target of stress hormones, and it is an especially plastic and vulnerable region of the brain that undergoes a selective atrophy in a number of disorders, accompanied by deficits in declarative episodic, spatial, and contextual memory performance.
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The neurobiology of stress : from serendipity to clinical relevance

TL;DR: In this article, the effects of stress on the immune system and brain are discussed and two new terms, allostasis and allostatic load, are introduced to supplement and clarify the meanings of stress and homeostasis.
References
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The Concepts of Stress and Stress System Disorders: Overview of Physical and Behavioral Homeostasis

TL;DR: The main components of the stress system are the corticotropin-releasing hormone and locus ceruleus-norepinephrine/autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system as discussed by the authors.
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Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons.

TL;DR: Repeated daily restraint stress for 21 days caused apical dendrites of CA3 pyramidal neurons to atrophy, while basal CA3 dendrite levels did not change.
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Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons

TL;DR: The changes in dendritic morphology observed may be indicative of neurons in the early stages of degeneration, as prolonged exposure to high levels of corticosterone has been shown by others to result in a loss of CA3 pyramidal cells.
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Hippocampal damage associated with prolonged and fatal stress in primates

TL;DR: This paper showed that sustained exposure to glucocorticoids (GCs), adrenal hormones secreted during stress, can cause neural degeneration in the rat hippocampus, particularly in the hippocampus, a principal neural target site for GCs.
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Calcium-binding protein (calbindin-D28k) and parvalbumin immunocytochemistry: localization in the rat hippocampus with specific reference to the selective vulnerability of hippocampal neurons to seizure activity.

TL;DR: Two neuronal calcium‐binding proteins, calbindin‐D28k (CaBP) and parvalbumin (PV), were localized in the normal rat hippocampus by using immunocytochemical methods to determine whether a correlation exists between the presence of these two calcium-binding proteins and the selective vulnerability of different hippocampal neuronal populations to experimental seizure activity.
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