Adverse early life environment increases hippocampal microglia abundance in conjunction with decreased neural stem cells in juvenile mice

2016 ◽  
Vol 55 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Susan Cohen ◽  
Xingrao Ke ◽  
Qiuli Liu ◽  
Qi Fu ◽  
Amber Majnik ◽  
...  
Hippocampus ◽  
2018 ◽  
Vol 28 (8) ◽  
pp. 586-601 ◽  
Author(s):  
Mary Youssef ◽  
Varsha S. Krish ◽  
Greer S. Kirshenbaum ◽  
Piray Atsak ◽  
Tamara J. Lass ◽  
...  

2019 ◽  
Vol 3 (2) ◽  
pp. 1-1
Author(s):  
Ekta Kumari ◽  
◽  
Fernando J. Velloso ◽  
Steven W. Levison ◽  
◽  
...  

2019 ◽  
Author(s):  
Pascal Bielefeld ◽  
Maralinde R. Abbink ◽  
Anna R. Davidson ◽  
Paul J. Lucassen ◽  
Aniko Korosi ◽  
...  

AbstractEarly life stress (ELS) is a potent environmental factor that can confer enduring effects on brain structure and function. Exposure to stress during early life has been linked to a wide range of physiopathological consequences later in life. In particular, ELS has been shown to have lasting effects on neurogenesis in the adult brain, suggesting that ELS is a significant regulator of adult neural stem cell function. Here, we investigated the effect of ELS on the numbers and proliferation of neural stem cells in the hypothalamus of adult mice. We show that ELS has long term negative effects on hypothalamic neural stem cell numbers and on their proliferation. Specifically, ELS reduced the total numbers of PCNA+ cells present in hypothalamic areas surrounding the 3rd ventricle; the numbers of PCNA+/Sox2+/Nestin-GFP+ cells present in the medial eminence at the base of the 3rd ventricle; and the number of β-tanycytes around the ventral 3rd ventricle, without affecting the numbers of α-tanycytes in more dorsal areas. These results suggest that a reduction of proliferation and tanycyte numbers contributes to the effects of ELS on the hypothalamus and its consequent physiological alterations.


Stress ◽  
2021 ◽  
pp. 1-7
Author(s):  
Pascal Bielefeld ◽  
Maralinde R. Abbink ◽  
Anna R. Davidson ◽  
Niels Reijner ◽  
Oihane Abiega ◽  
...  

2018 ◽  
Author(s):  
Mary Youssef ◽  
Varsha S. Krish ◽  
Greer S. Kirshenbaum ◽  
Piray Atsak ◽  
Tamara J. Lass ◽  
...  

AbstractEnvironmental 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 et al., 2014), 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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