scholarly journals Early-life stress diminishes the increase in neurogenesis after exercise in adult female mice

Hippocampus ◽  
2017 ◽  
Vol 27 (8) ◽  
pp. 839-844 ◽  
Author(s):  
M. R. Abbink ◽  
E. F. G. Naninck ◽  
P. J. Lucassen ◽  
A. Korosi
2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Yuliya A. Ryabushkina ◽  
Vasiliy V. Reshetnikov ◽  
Natalya P. Bondar

Early-life stress affects neuronal plasticity of the brain regions participating in the implementation of social behavior. Our previous studies have shown that brief and prolonged separation of pups from their mothers leads to enhanced social behavior in adult female mice. The goal of the present study was to characterize the expression of genes (which are engaged in synaptic plasticity) Egr1, Npas4, Arc, and Homer1 in the prefrontal cortex and dorsal hippocampus of adult female mice with a history of early-life stress. In addition, we evaluated the expression of stress-related genes: glucocorticoid and mineralocorticoid receptors (Nr3c1 and Nr3c2) and Nr1d1, which encodes a transcription factor (also known as REVERBα) modulating sociability and anxiety-related behavior. C57Bl/6 mice were exposed to either maternal separation (MS, 3 h once a day) or handling (HD, 15 min once a day) on postnatal days 2 through 14. In adulthood, the behavior of female mice was analyzed by some behavioral tests, and on the day after the testing of social behavior, we measured the gene expression. We found increased Npas4 expression only in the prefrontal cortex and higher Nr1d1 expression in both the prefrontal cortex and dorsal hippocampus of adult female mice with a history of MS. The expression of the studied genes did not change in HD female mice. The expression of stress-related genes Nr3c1 and Nr3c2 was unaltered in both groups. We propose that the upregulation of Npas4 and Nr1d1 in females with a history of early-life stress and the corresponding enhancement of social behavior may be regarded as an adaptation mechanism reversing possible aberrations caused by early-life stress.


Author(s):  
Ana Martín-Sánchez ◽  
Héctor González-Pardo ◽  
Laia Alegre-Zurano ◽  
Adriana Castro-Zavala ◽  
Isabel López-Taboada ◽  
...  

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Jacqueline Leachman ◽  
Sundus Ghuneim ◽  
Carolina Dalmasso ◽  
Nermin Ahmed ◽  
Mei Xu ◽  
...  

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Catherine Jensen Peña ◽  
Milo Smith ◽  
Aarthi Ramakrishnan ◽  
Hannah M. Cates ◽  
Rosemary C. Bagot ◽  
...  

Abstract Abuse, neglect, and other forms of early life stress (ELS) significantly increase risk for psychiatric disorders including depression. In this study, we show that ELS in a postnatal sensitive period increases sensitivity to adult stress in female mice, consistent with our earlier findings in male mice. We used RNA-sequencing in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of male and female mice to show that adult stress is distinctly represented in the brain’s transcriptome depending on ELS history. We identify: 1) biological pathways disrupted after ELS and associated with increased behavioral stress sensitivity, 2) putative transcriptional regulators of the effect of ELS on adult stress response, and 3) subsets of primed genes specifically associated with latent behavioral changes. We also provide transcriptomic evidence that ELS increases sensitivity to future stress through enhancement of known programs of cortical plasticity.


2020 ◽  
Vol 31 ◽  
pp. S33-S34
Author(s):  
L. Van Doeselaar ◽  
C. Engelhardt ◽  
J. Bordes ◽  
L. Brix ◽  
J. Deussing ◽  
...  

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Jaqueline R. Leachman ◽  
Eva Gatineau ◽  
Madhur Agarwal ◽  
Carolina Dalmasso ◽  
Xiu Xu ◽  
...  

2019 ◽  
Author(s):  
Catherine Jensen Peña ◽  
Milo Smith ◽  
Aarthi Ramakrishnan ◽  
Hannah M. Cates ◽  
Rosemary C. Bagot ◽  
...  

ABSTRACTAbuse, neglect, and other forms of early life stress (ELS) significantly increase risk for psychiatric disorders including depression. In this study, we show that ELS in a postnatal sensitive period increases sensitivity to adult stress in female mice, consistent with our earlier findings in male mice. We used RNA-sequencing in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of male and female mice to show that adult stress is distinctly represented in the brain’s transcriptome depending on ELS history. We identify: 1) biological pathways disrupted after ELS and associated with increased behavioral stress sensitivity, 2) putative transcriptional regulators of the effect of ELS on adult stress response, and 3) subsets of primed genes specifically associated with latent behavioral changes. We also provide transcriptomic evidence that ELS increases sensitivity to future stress through enhancement of known programs of cortical plasticity.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
María Abellán-Álvaro ◽  
Oliver Stork ◽  
Carmen Agustín-Pavón ◽  
Mónica Santos

Abstract Background Early-life stress can leave persistent epigenetic marks that may modulate vulnerability to psychiatric conditions later in life, including anxiety, depression and stress-related disorders. These are complex disorders with both environmental and genetic influences contributing to their etiology. Methyl-CpG Binding Protein 2 (MeCP2) has been attributed a key role in the control of neuronal activity-dependent gene expression and is a master regulator of experience-dependent epigenetic programming. Moreover, mutations in the MECP2 gene are the primary cause of Rett syndrome and, to a lesser extent, of a range of other major neurodevelopmental disorders. Here, we aim to study the interaction of MeCP2 with early-life stress in variables known to be affected by this environmental manipulation, namely anxiety-like behavior and activity of the underlying neural circuits. Methods Using Mecp2 heterozygous and wild-type female mice we investigated the effects of the interaction of Mecp2 haplodeficiency with maternal separation later in life, by assessing anxiety-related behaviors and measuring concomitant c-FOS expression in stress- and anxiety-related brain regions of adolescent females. Moreover, arginine vasopressin and corticotropin-releasing hormone neurons of the paraventricular hypothalamic nucleus were analyzed for neuronal activation. Results In wild-type mice, maternal separation caused a reduction in anxiety-like behavior and in the activation of the hypothalamic paraventricular nucleus, specifically in corticotropin-releasing hormone-positive cells, after the elevated plus maze. This effect of maternal separation was not observed in Mecp2 heterozygous females that per se show decreased anxiety-like behavior and concomitant decreased paraventricular nuclei activation. Conclusions Our data supports that MeCP2 is an essential component of HPA axis reprogramming and underlies the differential response to anxiogenic situations later in life.


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