Astrocyte plasticity induced by emotional stress: A new partner in psychiatric physiopathology?

Bender, Crhistian Luis; Calfa, Gastón; Molina, Vı́ctor A.

doi:10.1016/j.pnpbp.2015.08.005

Cited by 56 publications

(38 citation statements)

References 109 publications

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“…Mechanisms involved in the rearrangement of astrocytes possibly include astrocytic death, such as necrosis or apoptosis [29, 30]. To explore the outcome of the astroglial population, we examined a glia-specific protein called S100β, which is expressed by both protoplasmic and fibrillary astrocytes [31] The results of western blot analysis indicated that reduced expression of these proteins may be due to either: (a) reduction in cell number, or (b) decreased production of GFAP or S100βproteins without reduction in cell number in the amygdala. However, our immunohistochemistry results indicate a reduced number of GFAP + or S100 β + astrocytes.…”

Section: Discussionmentioning

confidence: 99%

RU486 Reverses Emotional Disorders by Influencing Astrocytes and Endoplasmic Reticulum Stress in Chronic Restraint Stress Challenged Rats

Dong

Wang

et al. 2017

Cell Physiol Biochem

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Aims: To investigate the effect of RU486 (mifepristone) on emotional disorders in chronic restraint stress-induced rats and to explore the mechanisms of that phenomenon. Methods: For this purpose, 80 healthy male Sprague Dawley rats were randomly divided into four groups: the normal group (Con group, The Con group members received no treatment, eating and drinking freely), the chronic restraint stress group (CRS group, normal Sprague Dawley rats treated with chronic restraint stress, 6 h/day for 21days), the propylene glycol group (CRS+propylene glycol) and the RU486 group (CRS+RU486). RU486 or propylene glycol was administered 30 mins before each CRS procedure. Twenty-four hours after CRS exposure, we investigated the effects of CRS on the anxiety-like behavior using an elevated plus-maze (EPM). To explore the mechanisms of RU486 on anxiety, we measured the expression of glial fibrillary acid protein (GFAP) and β-subunit of S100 (S100β) via immunohistochemistry and western blot analysis. Apoptosis was demonstrated by flow cytometry. In addition, endoplasmic reticulum (ER) stress markers, glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and Cysteine aspartic acid specific protease-12 (Caspase-12), were detected by western blot analysis. Results: Compared to the control group, rats in the CRS and propylene glycol group showed decreased exploratory behavior on the open arms during EPM testing, and these reductions were accompanied by significantly reduced GFAP and S100β expression, increased apoptosis and GRP78, CHOP, and caspase-12 expression in the amygdala. However, RU486 increases the exploratory behavior and reverses the changes of GFAP, S100β, GRP78, CHOP, and caspase-12 and protects cells against apoptosis. Conclusions: Taken together, these data suggest that exposure to chronic restraint stress decreases the number of astrocytes and induces apoptosis and ER stress in the amygdala, which are possible causes for psychiatric disorders. RU486 can significantly ameliorate abnormal behaviors in CRS-induced anxiety model rats. The protective effects of RU486 could be attributed to its anti-ER stress, anti-apoptosis and astrocyte increasing effects.

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Section: Discussionmentioning

confidence: 99%

RU486 Reverses Emotional Disorders by Influencing Astrocytes and Endoplasmic Reticulum Stress in Chronic Restraint Stress Challenged Rats

Dong

Wang

et al. 2017

Cell Physiol Biochem

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“…Chronic stress also leads to reduced number or weakened activity of the astrocytes [127]. This may lead to an increase in extracellular glutamate concentration in the synaptic cleft, eventually increasing the risk of excitotoxicity and cell damage.…”

Section: Neurotransmittersmentioning

confidence: 99%

Rodent models of social stress and neuronal plasticity: Relevance to depressive-like disorders

Patel

Kas

Chattarji

et al. 2019

Behavioural Brain Research

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A B S T R A C TExposure to severe or persistent social stress may lead to the development of psychiatric disorders such as anxiety and depression. These mood disorders are associated with structural alterations of neural architecture in limbic brain regions that control emotion, mood and cognition. Structural remodeling may either be a sign of successful adaptation, or of failure to do so. In neuropsychiatric disorders like depression structural remodeling involves apoptosis, reduced neurogenesis, and structural remodeling of neuronal dendrites which most likely reflects the latter. Here we review key findings from animal models of psychosocial stress that have been used to gain insights into the relation between stress-related behavioral disorders like depression and structural plasticity. Specifically, we focus on models having a high face validity like social defeat stress in the resident-intruder paradigm and chronic stress of social subordination in social housing conditions. Moderate to severe social stress appears to stimulate plasticity and neuronal growth in regions of the amygdala, whereas the effects in the hippocampus and prefrontal cortex tend to be opposite. A major focus of the current review is to characterize social stress induced structural changes in these brain regions, aiming to provide insight in pathways and factors that underlie behavioral effects of stress and depression.

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“…Chronic stress also alters astrocyte complexity and physiology in the mPFC in males . Astrocytes play a critical role in regulating synaptic stability and neurotransmission and are important in glucagon storage, glucose homeostasis, and provide metabolic support to neurones .…”

Section: Introductionmentioning

confidence: 99%

Gonadal hormones differentially regulate sex‐specific stress effects on glia in the medial prefrontal cortex

Bollinger

Salinas

Fender

et al. 2019

J Neuroendocrinology

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Women are more susceptible to various stress‐linked psychopathologies, including depression. Dysfunction of the medial prefrontal cortex (mPFC) has been implicated in depression, and studies indicate sex differences in stress effects on mPFC structure and function. For example, chronic stress induces dendritic atrophy in the mPFC in male rats, yet dendritic growth in females. Recent findings suggest glial pathways toward depression. Glia are highly responsive to neuronal activity and function as critical regulators of synaptic plasticity. Preclinical models demonstrate stress‐induced microglial activation in mPFC in males, yet deactivation in females. By contrast, stress reduces astrocyte complexity in mPFC in male rats, whereas the effects in females are unknown. Glia possess receptors for most gonadal hormones and gonadal hormones are known to modulate neuronal activity. Thus, gonadal hormones represent a potential mechanism underlying sex differences in glia, as well as divergent stress effects. Therefore, we examined the role of gonadal hormones in sex‐specific stress effects on neuronal activity (ie FosB/ ΔFosB induction) and glia in the mPFC. The findings obtained indicate greater microglial activation in mPFC in females and a greater astrocyte area in males. Basal astrocyte morphology is modulated by androgens, whereas androgens or oestrogens dampen the microglial state in males. Astrocyte morphology is associated with neuronal activity in both sexes, regardless of hormonal condition. Chronic stress induced astrocytic atrophy in males, yet hypertrophy in females, with gonadal hormones partly regulating this difference. Stress effects on microglia are oestradiol‐dependent in females. Taken together, these data suggest sex‐specific, gonadal hormone‐dependent stress effects on astrocytes and microglia in the mPFC.

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Astrocyte plasticity induced by emotional stress: A new partner in psychiatric physiopathology?

Cited by 56 publications

References 109 publications

RU486 Reverses Emotional Disorders by Influencing Astrocytes and Endoplasmic Reticulum Stress in Chronic Restraint Stress Challenged Rats

RU486 Reverses Emotional Disorders by Influencing Astrocytes and Endoplasmic Reticulum Stress in Chronic Restraint Stress Challenged Rats

Rodent models of social stress and neuronal plasticity: Relevance to depressive-like disorders

Gonadal hormones differentially regulate sex‐specific stress effects on glia in the medial prefrontal cortex

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