scholarly journals Αlpha 2a-Adrenoceptor Gene Expression and Early Life Stress-Mediated Propensity to Alcohol Drinking in Outbred Rats

2015 ◽  
Vol 12 (7) ◽  
pp. 7154-7171 ◽  
Author(s):  
Erika Comasco ◽  
Aniruddha Todkar ◽  
Linnea Granholm ◽  
Kent Nilsson ◽  
Ingrid Nylander
2019 ◽  
Vol 25 (6) ◽  
Author(s):  
Anna K. Radke ◽  
Isabel T. Held ◽  
Elizabeth A. Sneddon ◽  
Collin A. Riddle ◽  
Jennifer J. Quinn

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mi Kyoung Seo ◽  
Jung Goo Lee ◽  
Sung Woo Park

AbstractEarly life stress (ELS) causes long-lasting changes in gene expression through epigenetic mechanisms. However, little is known about the effects of ELS in adulthood, specifically across different age groups. In this study, the epigenetic modifications of p11 expression in adult mice subjected to ELS were investigated in different stages of adulthood. Pups experienced maternal separation (MS) for 3 h daily from postnatal day 1 to 21. At young and middle adulthood, behavioral test, hippocampal p11 expression levels, and levels of histone acetylation and methylation and DNA methylation at the hippocampal p11 promoter were measured. Middle-aged, but not young adult, MS mice exhibited increased immobility time in the forced swimming test. Concurrent with reduced hippocampal p11 levels, mice in both age groups showed a decrease in histone acetylation (AcH3) and permissive histone methylation (H3K4me3) at the p11 promoter, as well as an increase in repressive histone methylation (H3K27me3). Moreover, our results showed that the expression, AcH3 and H3Kme3 levels of p11 gene in response to MS were reduced with age. DNA methylation analysis of the p11 promoter revealed increased CpG methylation in middle-aged MS mice only. The results highlight the age-dependent deleterious effects of ELS on the epigenetic modifications of p11 transcription.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Jacqueline Renee Leachman ◽  
Matthew Rea ◽  
Celia Ritter ◽  
Xiu Xu ◽  
Carolina Dalmasso ◽  
...  

2015 ◽  
Vol 22 (2) ◽  
pp. 369-380 ◽  
Author(s):  
Maria Vrettou ◽  
Linnea Granholm ◽  
Aniruddha Todkar ◽  
Kent W. Nilsson ◽  
Åsa Wallén-Mackenzie ◽  
...  

2018 ◽  
Vol 314 (3) ◽  
pp. F343-F355 ◽  
Author(s):  
Carmen De Miguel ◽  
Ijeoma E. Obi ◽  
Dao H. Ho ◽  
Analia S. Loria ◽  
Jennifer S. Pollock

Early life stress (ELS) in humans is associated with elevated proinflammatory markers. We hypothesized that ELS induces activation of the immune response in a rat model of ELS, maternal separation (MatSep), in adulthood. MatSep involves separating pups from the dam from postnatal day 2 to postnatal day 14 for 3 h/day. Control rats are nonseparated littermates. We determined circulating and renal immune cell numbers, renal immune cell activation markers, renal cytokine levels, and the renal inflammatory gene expression response to low-dose lipopolysaccharide (LPS) in male MatSep and control rats. We observed that MatSep did not change the percentage of gated events for circulating CD3+, CD4+, CD8+, and CD4+/Foxp3+ cells or absolute numbers of mononuclear and T cells in the circulation and kidneys; however, MatSep led to an increase in activation of renal neutrophils as well as CD44+ cells. Renal toll-like receptor 4 (TLR4) and interleukin 1 beta (IL-1β) was significantly increased in MatSep rats, specifically in the outer and inner medulla and distal nephron, respectively. Evaluation of renal inflammatory genes showed that in response to a low-dose LPS challenge (2 mg/kg iv) a total of 20 genes were significantly altered in kidneys from MatSep rats (17 genes were upregulated and 3 were downregulated), as opposed to no significant differences in gene expression in control vs. control + LPS groups. Taken together, these findings indicate that MatSep induces priming of the immune response in the kidney.


Stress ◽  
2016 ◽  
Vol 19 (2) ◽  
pp. 235-247 ◽  
Author(s):  
Marjorie C. Gondré-Lewis ◽  
Kaitlin T. Warnock ◽  
Hong Wang ◽  
Harry L. June ◽  
Kimberly A. Bell ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Thabisile Mpofana ◽  
Willie M. U. Daniels ◽  
Musa V. Mabandla

Early life adversity increases the risk of mental disorders later in life. Chronic early life stress may alter neurotrophic factor gene expression including those for brain derived neurotrophic factor (BDNF) and glial cell derived neurotrophic factor (GDNF) that are important in neuronal growth, survival, and maintenance. Maternal separation was used in this study to model early life stress. Following unilateral injection of a mild dose of 6-hydroxydopamine (6-OHDA), we measured corticosterone (CORT) in the blood and striatum of stressed and nonstressed rats; we also measured DNA methylation and BDNF and GDNF gene expression in the striatum using real time PCR. In the presence of stress, we found that there was increased corticosterone concentration in both blood and striatal tissue. Further to this, we found higher DNA methylation and decreased neurotrophic factor gene expression. 6-OHDA lesion increased neurotrophic factor gene expression in both stressed and nonstressed rats but this increase was higher in the nonstressed rats. Our results suggest that exposure to early postnatal stress increases corticosterone concentration which leads to increased DNA methylation. This effect results in decreased BDNF and GDNF gene expression in the striatum leading to decreased protection against subsequent insults later in life.


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