Chronic psychosocial stress differentially affects apoptosis in hippocampal subregions and cortex of the adult tree shrew

Lucassen, Paul J.; Vollmann-Honsdorf, Gesa K; Gleisberg, M.; Czéh, Boldizsár; Kloet, E. Ronald de; Fuchs, Eberhard

doi:10.1046/j.0953-816x.2001.01629.x

Cited by 139 publications

(77 citation statements)

References 41 publications

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“…Thus, not only cytogenesis but also cell death, and therefore the entire process of adult dentate gyrus neuronal turnover, is affected by tianeptine treatment. In line with the antiapoptotic effect observed post-mortem by Lucassen et al, 85 tianeptine prevented the stressinduced reduction of the in vivo brain metabolite levels of N-acetylaspartate. 22 Several other studies have shown protective effects of antidepressants in different models, and mostly in the hippocampus.…”

Section: Cytoprotective Effectssupporting

confidence: 75%

“…Both stress and tianeptine had region-specific effects and tianeptine treatment reduced apoptosis in the dentate granule cell layer and subgranular zone, most likely on non-neuronal cells, but had no effect in the Ammon's Horn. These effects were not restricted to the hippocampus alone, as in the temporal cortex, chronic stress alone increased the numbers of apoptotic cells, 85 while tianeptine treatment had an antiapoptotic effect both in the stressed and unchallenged animals 84 (Figure 6). …”

Section: Cytoprotective Effectsmentioning

confidence: 96%

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Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

2005

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Recent studies have provided evidence that structural remodeling of certain brain regions is a feature of depressive illness, and the postulated underlying mechanisms contribute to the idea that there is more to antidepressant actions that can be explained exclusively by a monoaminergic hypothesis. This review summarizes recent neurobiological studies on the antidepressant, tianeptine (S-1574, [3-chloro-6-methyl-5,5-dioxo-6,11-dihydro-(c,f)-dibenzo-(1,2-thiazepine)-11-yl) amino]-7 heptanoic acid, sodium salt), a compound with structural similarities to the tricyclic antidepressant agents, the efficacy and good tolerance of which have been clearly established. These studies have revealed that the neurobiological properties of tianeptine involve the dynamic interplay between numerous neurotransmitter systems, as well as a critical role of structural and functional plasticity in the brain regions that permit the full expression of emotional learning. Although the story is far from complete, the schema underlying the effect of tianeptine on central plasticity is the most thoroughly studied of any antidepressants. Effects of tianeptine on neuronal excitability, neuroprotection, anxiety, and memory have also been found. Together with clinical data on the efficacy of tianeptine as an antidepressant, these actions offer insights into how compounds like tianeptine may be useful in the treatment of neurobiological features of depressive disorders. Molecular Psychiatry (2005) 10, 525-537.

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Section: Cytoprotective Effectssupporting

confidence: 75%

Section: Cytoprotective Effectsmentioning

confidence: 96%

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

2005

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“…Therefore, stress may perturb gene expression transiently, perhaps via epigenetic effects [97,143], but the withdrawal of the inciting stimulus leads to re-instatement of the original, fully programmed 'steady state.' In addition, whereas neuronal loss has been suspected to occur upon chronic stress in the adult [125,90], most current evidence supports the notion that the structural effects of chronic stress on hippocampal neurons involve dendritic modifications, without cell loss or profound dendritotoxicity. Thus, upon withdrawal of the molecular processes initiated by stress, recovery of both function and structure occurs in mature hippocampus [109,56,114].…”

mentioning

confidence: 52%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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“…An important feature of the present stress manipulations is their episodic nature, which differs from the life-threatening effects of continuous subordination stress (Blanchard et al, 1985;Miczek et al, 1991;Von Holst, 1998;Lucassen et al, 2001;Carr, 2002).…”

Section: Discussionmentioning

confidence: 99%

Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

Covington

Kikusui

Goodhue

et al. 2004

Neuropsychopharmacol

112

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Social stress can engender behavioral and neural sensitization and this process appears to enhance the transition to compulsive drug abuse. Exposures to brief social defeat stress in rats have significant consequences on cocaine-reinforced behavior and on the level of functional activation within regions of the mesocorticolimbic dopamine system. The objectives of the current study were to examine the enduring consequences of brief episodes of social defeat stress on cocaine bingeing (during 24 h of continuous access) and on the emergence of neural adaptations as revealed by zif268 immediate early gene expression. Adult, male Long-Evans rats were subjected to four 25 min episodes of social defeat (once every 72 h). After 2 months, cocaine binges or zif268 mRNA gene expression were studied after confirming behavioral cross-sensitization to stimulant challenge. Sensitization to social defeat increased cocaine intake during a 24 h binge, effectively abolishing the typical circadian pattern of intake. Furthermore, 60 days after exposure to the sensitizing regimen of social defeat, levels of functional activation, measured by zif268 mRNA expression, in the central and medial amygdala were increased, while levels of activation in the medial prefrontal cortex were decreased. Persistent stress-induced levels of zif268 in the central and medial amygdala were attenuated by an injection of amphetamine (1.0 mg/kg). Divergent changes in zif268 within the amygdala and cortex 2 months after social defeat stress indicate the vulnerability of distinct cellular populations in networks that modulate the behavioral actions of psychomotor stimulants.

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Chronic psychosocial stress differentially affects apoptosis in hippocampal subregions and cortex of the adult tree shrew

Cited by 139 publications

References 41 publications

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

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