The postnatal origin of adult neural stem cells and the effects of glucocorticoids on their genesis

Ortega-Martínez, Sylvia; Trejo, José Luís

doi:10.1016/j.bbr.2014.11.013

Cited by 14 publications

(23 citation statements)

References 49 publications

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“…Exogenous administration of DEX during that period led to shrinkage of NSC pool in the adult hippocampus. The latter was correlated with compromised learning and memory (Ortega-Martinez, 2015; Ortega-Martinez and Trejo, 2015). This data suggests that NSCs can be harmed by pharmacological doses of glucocorticoid and exposure of neonates to this drug should be done with caution.…”

Section: Negative and Positive Effects Of Stress Hormones On Nscsmentioning

confidence: 99%

Neural stem cells respond to stress hormones: distinguishing beneficial from detrimental stress

Koutmani

Karalis

2015

Front. Physiol.

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Neural stem cells (NSCs), the progenitors of the nervous system, control distinct, position-specific functions and are critically involved in the maintenance of homeostasis in the brain. The responses of these cells to various stressful stimuli are shaped by genetic, epigenetic, and environmental factors via mechanisms that are age and developmental stage-dependent and still remain, to a great extent, elusive. Increasing evidence advocates for the beneficial impact of the stress response in various settings, complementing the extensive number of studies on the detrimental effects of stress, particularly in the developing brain. In this review, we discuss suggested mechanisms mediating both the beneficial and detrimental effects of stressors on NSC activity across the lifespan. We focus on the specific effects of secreted factors and we propose NSCs as a “sensor,” capable of distinguishing among the different stressors and adapting its functions accordingly. All the above suggest the intriguing hypothesis that NSCs are an important part of the adaptive response to stressors via direct and indirect, specific mechanisms.

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Section: Negative and Positive Effects Of Stress Hormones On Nscsmentioning

confidence: 99%

Neural stem cells respond to stress hormones: distinguishing beneficial from detrimental stress

Koutmani

Karalis

2015

Front. Physiol.

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“…Coronal sections (40 m) were cut and collected in PBS using a vibratome (Leica, VT1000S). Stereological series from the right hemisphere of the hippocampal formation were established using 96-well plates, with every sixth section for immunohistochemistry analysis, as described previously (Ortega-Martínez and Trejo, 2015;Mohammad et al, 2018).…”

Section: Perfusion and Tissue Processingmentioning

confidence: 99%

“…For Sox2/GFAP, we counted only the cells with both markers, as a colocalization analysis as previously described (Ortega-Martínez and Trejo, 2015).…”

Section: Stereological Analysismentioning

confidence: 99%

“…For each slice, cell density was calculated. We multiplied by 10 6 as previously performed (Ortega-Martínez and Trejo, 2015), for an easy interpretation.…”

Section: Neun Analysismentioning

confidence: 99%

“…Microglial depletion restores steady-state levels of AHNPCs, transit amplifying progenitors and mature neurons in mice expressing FAD-linked PS1 following EE Having demonstrated that PLX5622-mediated depletion of microglia rescues the deficits in levels of proliferation, survival, and differentiation of BrdU-labeled AHNPCs in mice expressing FAD-linked PS1 variants, we further determined the steady-state levels of AHNPCs located in the SGL of the DG by assessing the colocalization of antibodies raised against SRY (Sox2 and GFAP), as previously described (Ortega-Martínez and Trejo, 2015). The levels of Sox2/GFAP-positive neural stem cells (NSCs) in the DG of all three transgenic lines housed in SH and SC were comparable ( Fig.…”

Section: Microglial Depletion Restores Deficits In Proliferation and mentioning

confidence: 99%

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Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer's Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion

Ortega-Martínez¹,

Palla²,

Zhang³

et al. 2019

J. Neurosci.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that presently affects an estimated 5.7 million Americans. Understanding the basis for this disease is key for the development of a future successful treatment. In this effort, we previously reported that mouse prion protein-promoter-driven, ubiquitous expression of familial AD (FAD)-linked human PSEN1 variants in transgenic mice impairs environmental enrichment (EE)-induced proliferation and neurogenesis of adult hippocampal neural progenitor cells (AHN-PCs) and in a non-cell autonomous manner. These findings were confirmed in PS1 M146V/؉ mice that harbor an FAD-linked mutation in the endogenous PSEN1 gene. We now demonstrate that CSF1R antagonist-mediated microglial depletion in transgenic male mice expressing mutant presenilin 1 (PS1) or PS1 M146V/؉ "knock-in" mice leads to a complete rescue of deficits in proliferation, differentiation and survival of AHNPCs. Moreover, microglia depletion suppressed the heightened baseline anxiety behavior observed in transgenic mice expressing mutant PS1 and PS1 M146V/؉ mice to levels observed in mice expressing wild-type human PS1 or nontransgenic mice, respectively. These findings demonstrate that in mice expressing FAD-linked PS1, microglia play a critical role in the regulation of EE-dependent AHNPC proliferation and neurogenesis and the modulation of affective behaviors.

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Ablation of proliferating neural stem cells during early life is sufficient to reduce adult hippocampal neurogenesis

et al. 2018

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Environmental exposures during early life, but not during adolescence or adulthood, lead to persistent reductions in neurogenesis in the adult hippocampal dentate gyrus (DG). The mechanisms by which early life exposures lead to long-term deficits in neurogenesis remain unclear. Here, we investigated whether targeted ablation of dividing neural stem cells during early life is sufficient to produce long-term decreases in DG neurogenesis. Having previously found that the stem cell lineage is resistant to long-term effects of transient ablation of dividing stem cells during adolescence or adulthood (Kirshenbaum, Lieberman, Briner, Leonardo, & Dranovsky, ), we used a similar pharmacogenetic approach to target dividing neural stem cells for elimination during early life periods sensitive to environmental insults. We then assessed the Nestin stem cell lineage in adulthood. We found that the adult neural stem cell reservoir was depleted following ablation during the first postnatal week, when stem cells were highly proliferative, but not during the third postnatal week, when stem cells were more quiescent. Remarkably, ablating proliferating stem cells during either the first or third postnatal week led to reduced adult neurogenesis out of proportion to the changes in the stem cell pool, indicating a disruption of the stem cell function or niche following stem cell ablation in early life. These results highlight the first three postnatal weeks as a series of sensitive periods during which elimination of dividing stem cells leads to lasting alterations in adult DG neurogenesis and stem cell function. These findings contribute to our understanding of the relationship between DG development and adult neurogenesis, as well as suggest a possible mechanism by which early life experiences may lead to lasting deficits in adult hippocampal neurogenesis.

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The postnatal origin of adult neural stem cells and the effects of glucocorticoids on their genesis

Cited by 14 publications

References 49 publications

Neural stem cells respond to stress hormones: distinguishing beneficial from detrimental stress

Neural stem cells respond to stress hormones: distinguishing beneficial from detrimental stress

Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer's Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion

Ablation of proliferating neural stem cells during early life is sufficient to reduce adult hippocampal neurogenesis

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