Psychosocial stress, glucocorticoids, and structural alterations in the tree shrew hippocampus

Fuchs, Eberhard; Flügge, Gabriele; Ohl, Frauke; Lucassen, Paul J.; Vollmann-Honsdorf, Gesa K; Michaelis, Thomas

doi:10.1016/s0031-9384(01)00497-8

Cited by 136 publications

(82 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Psychosocial stress produces robust, measurable behavioral changes in animals analogous to behavior exhibited in depressed humans, and it closely mimics the onset of stress-related pathology in humans (Kessler, 1997;Blanchard et al, 2001). Chronic stress decreases adult neurogenesis in the hippocampus Gould et al, 1998;Czeh et al, 2001Czeh et al, , 2002Fuchs et al, 2001;Malberg and Duman, 2003;Pham et al, 2003); however, little is known about the effect of an acute episode of naturally occurring stress on neurogenesis, although it is reported to diminish neuronal proliferation in tree shrews (Gould et al, 1997). It is not known whether an acute episode of psychosocial stress could have an effect on the proliferation, differentiation, or long-term survival of newly generated neurons in hippocampal neurogenesis or whether this alteration of neurogenesis could contribute to depression.…”

Section: Introductionmentioning

confidence: 97%

Acute Psychosocial Stress Reduces Cell Survival in Adult Hippocampal Neurogenesis without Altering Proliferation

Thomas¹,

Hotsenpiller²,

Peterson³

2007

J. Neurosci.

214

143

View full text Add to dashboard Cite

Factors modulating neurogenesis may contribute to the pathophysiology of affective disorders such as major depression. Environmental stressors in animal models have been proposed to alter neurogenesis, suggesting a mechanism for this contribution. The effect of an acute psychosocial stressor on either proliferation or survival (immediate, short term, and long term) was examined along with subsequent neuronal differentiation in the hippocampus of adult male Sprague Dawley rats. Subjects were exposed to a widely used social dominance paradigm that elicits behavioral and physiological responses to an acute psychosocial stressor. This social dominance paradigm may mimic human relational stress more realistically than laboratory stressors and provides a socially relevant model. We found that exposure to an acute psychosocial stressor at the time of cell generation resulted in a decreased number of newly generated cells in the hippocampus. By using sequential thymidine analog administration to provide temporal discrimination of DNA replication, we showed that short-term survival but not initial proliferation or immediate survival was altered in response to stress. Furthermore, we determined that stress experienced subsequent to proliferation also diminished long-term survival of cells. Thus, an acute episode of a social stress produces long-lasting effects on the incorporation of new hippocampal neurons by reducing their survival.

show abstract

Section: Introductionmentioning

confidence: 97%

Acute Psychosocial Stress Reduces Cell Survival in Adult Hippocampal Neurogenesis without Altering Proliferation

Thomas¹,

Hotsenpiller²,

Peterson³

2007

J. Neurosci.

214

143

View full text Add to dashboard Cite

show abstract

“…Conditions associated with major depression in humans, such as stress (Gould et al, 1999;Fuchs et al, 2001;Coe et al, 2003;Malberg and Duman, 2003;Pham et al, 2003) and drug abuse He et al, 2005), suppress neurogenesis in the hippocampus. This may contribute to the decreased hippocampal volume (Sheline et al, 1999) and hippocampal dysfunction resulting in memory deficits (MacQueen et al, 2003) and hypothalamic-pituitary-adrenal axis hyperactivity (O'Brien et al, 1996) associated with subpopulations of patients with major depression.…”

Section: Introductionmentioning

confidence: 99%

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Perera¹,

Coplan²,

Lisanby³

et al. 2007

J. Neurosci.

406

266

View full text Add to dashboard Cite

New neurons are generated in the adult hippocampus of many species including rodents, monkeys, and humans. Conditions associated with major depression, such as social stress, suppress hippocampal neurogenesis in rodents and primates. In contrast, all classes of antidepressants stimulate neuronal generation, and the behavioral effects of these medications are abolished when neurogenesis is blocked. These findings generated the hypothesis that induction of neurogenesis is a necessary component in the mechanism of action of antidepressant treatments. To date, the effects of antidepressants on newborn neurons have been reported only in rodents and tree shrews. This study examines whether neurogenesis is increased in nonhuman primates after antidepressant treatment. Adult monkeys received repeated electroconvulsive shock (ECS), which is the animal analog of electroconvulsive therapy (ECT), the most effective short-term antidepressant. Compared with control conditions, ECS robustly increased precursor cell proliferation in the subgranular zone (SGZ) of the dentate gyrus in the monkey hippocampus. A majority of these precursors differentiated into neurons or endothelial cells, while a few matured into glial cells. The ECS-mediated induction of cell proliferation and neurogenesis was accompanied by increased immunoreactivity for the neuroprotective gene product BCL2 (B cell chronic lymphocytic lymphoma 2) in the SGZ. The ECS interventions were not accompanied by increased hippocampal cell death or injury. This study demonstrates that ECS is capable of inducing neurogenesis in the nonhuman primate hippocampus and supports the possibility that antidepressant interventions produce similar alterations in the human brain.

show abstract

“…Several components of the social landscape, such as parent-offspring interactions, social defeat, aggression, social isolation and competition are key activators of the HPA axis (47,48,(51)(52)(53)(54)(55)(56). These are considered 'social stressors'.…”

Section: Stress: What Is It and How Is It Regulated?mentioning

confidence: 99%

Developmental stress and social phenotypes: integrating neuroendocrine, behavioural and evolutionary perspectives

Spencer¹

2017

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

SummaryThe social world is filled with different types of interactions, and social experience interacts with stress on several different levels. Activation of the neuroendocrine axis that regulates the response to stress can have consequences for innumerable behavioural responses, including social decision making and aspects of sociality such as gregariousness and aggression. This is especially true for stress experienced during early life, when physiological systems are developing and highly sensitive to perturbation. Stress at this time can have persistent effects on social behaviours into adulthood. One important question remaining is to what extent these effects are adaptive. This paper initially reviews the current literature investigating the complex relationships between the hypothalamic-pituitaryadrenal (HPA) axis and other neuroendocrine systems and several aspects of social behaviour in vertebrates. In addition the review explores the evidence surrounding the potential for 'social programming' via differential development and activation of the HPA axis, providing an insight into the potential for positive effects on fitness following early life stress. Finally the paper provides a framework from which novel investigations could work to fully understand the adaptive significance of early life effects on social behaviours. BackgroundThe ability to effectively interact with conspecifics is a vital skill, which we have only just begun to explore in terms of its impact on fitness (1, 2). In humans, this ability is also highly valued and disorders known to reduce our ability *Author for correspondence (Karen.spencer@st-andrews.ac.uk). †Present address: School of Psychology & Neuroscience, University of St Andrews, South Street, St Andrews, KY16 9JP to interact or understand the emotional cues of others place sufferers at significant disadvantages, with long term impacts on health and wellbeing. Understanding the factors that give rise to individual differences in 'social competence' is therefore of fundamental importance to both our knowledge of human pathologies, but also animal welfare and population structure. Stress is a major regulator of social behaviour and in turn social influences can alter behavioural and physiological responses to stress (3-5). Activation of the vertebrate neuroendocrine axis which regulates the response to stress can cause pleiotropic effects on several aspects of social behaviour, including reduced social interaction, increased affiliative behaviours, increased aggression and altered mating behaviours (6-15). The direction and magnitude of these effects is often related to the context within which the experiment was conducted as well as the type of stressor that was experienced and the life history strategy of the species in question, however there is clear evidence to suggest that stress during all life stages can impact on sociality.One major driver of social ability in adulthood is the conditions experienced during development, when neural substrates and physiological systems...

show abstract

Psychosocial stress, glucocorticoids, and structural alterations in the tree shrew hippocampus

Cited by 136 publications

References 66 publications

Acute Psychosocial Stress Reduces Cell Survival in Adult Hippocampal Neurogenesis without Altering Proliferation

Acute Psychosocial Stress Reduces Cell Survival in Adult Hippocampal Neurogenesis without Altering Proliferation

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Developmental stress and social phenotypes: integrating neuroendocrine, behavioural and evolutionary perspectives

Contact Info

Product

Resources

About