scholarly journals Social Isolation Stress in Adolescence, but not Adulthood, Produces Hypersocial Behavior in Adult Male and Female C57BL/6J Mice

2020 ◽  
Vol 14 ◽  
Author(s):  
Jean K. Rivera-Irizarry ◽  
Mary Jane Skelly ◽  
Kristen E. Pleil
2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Alessandro Ieraci ◽  
Alessandra Mallei ◽  
Maurizio Popoli

Stress is a major risk factor in the onset of several neuropsychiatric disorders including anxiety and depression. Although several studies have shown that social isolation stress during postweaning period induces behavioral and brain molecular changes, the effects of social isolation on behavior during adulthood have been less characterized. Aim of this work was to investigate the relationship between the behavioral alterations and brain molecular changes induced by chronic social isolation stress in adult male mice. Plasma corticosterone levels and adrenal glands weight were also analyzed. Socially isolated (SI) mice showed higher locomotor activity, spent less time in the open field center, and displayed higher immobility time in the tail suspension test compared to group-housed (GH) mice. SI mice exhibited reduced plasma corticosterone levels and reduced difference between right and left adrenal glands. SI showed lower mRNA levels of the BDNF-7 splice variant, c-Fos, Arc, and Egr-1 in both hippocampus and prefrontal cortex compared to GH mice. Finally, SI mice exhibited selectively reduced mGluR1 and mGluR2 levels in the prefrontal cortex. Altogether, these results suggest that anxious- and depressive-like behavior induced by social isolation stress correlates with reduction of several neuroplasticity-related genes in the hippocampus and prefrontal cortex of adult male mice.


2009 ◽  
Vol 136 (5) ◽  
pp. A-556
Author(s):  
Hiroshi Takeda ◽  
Shuichi Muto ◽  
Takehiko Katsurada ◽  
Yayoi Inagaki ◽  
Kazuaki Tsuchiya ◽  
...  

2012 ◽  
Vol 73 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Kinzo Matsumoto ◽  
Kazuya Ono ◽  
Hirofumi Ouchi ◽  
Ryohei Tsushima ◽  
Yukihisa Murakami

Author(s):  
Muhammad Imran Khan ◽  
Vahid Nikoui ◽  
Jamal Ahmad ◽  
Bashir Ahmad ◽  
Ahmad-Reza Dehpour

2021 ◽  
Vol 22 (19) ◽  
pp. 10678
Author(s):  
Francesco Matrisciano ◽  
Graziano Pinna

Social behavioral changes, including social isolation or loneliness, increase the risk for stress-related disorders, such as major depressive disorder, posttraumatic stress disorder (PTSD), and suicide, which share a strong neuroinflammatory etiopathogenetic component. The peroxisome-proliferator activated receptor (PPAR)-α, a newly discovered target involved in emotional behavior regulation, is a ligand-activated nuclear receptor and a transcription factor that, following stimulation by endogenous or synthetic ligands, may induce neuroprotective effects by modulating neuroinflammation, and improve anxiety and depression-like behaviors by enhancing neurosteroid biosynthesis. How stress affects epigenetic mechanisms with downstream effects on inflammation and emotional behavior remains poorly understood. We studied the effects of 4-week social isolation, using a mouse model of PTSD/suicide-like behavior, on hippocampal PPAR-α epigenetic modification. Decreased PPAR-α expression in the hippocampus of socially isolated mice was associated with increased levels of methylated cytosines of PPAR-α gene CpG-rich fragments and deficient neurosteroid biosynthesis. This effect was associated with increased histone deacetylases (HDAC)1, methyl-cytosine binding protein (MeCP)2 and decreased ten-eleven translocator (TET)2 expression, which favor hypermethylation. These alterations were associated with increased TLR-4 and pro-inflammatory markers (e.g., TNF-α,), mediated by NF-κB signaling in the hippocampus of aggressive mice. This study contributes the first evidence of stress-induced brain PPAR-α epigenetic regulation. Social isolation stress may constitute a risk factor for inflammatory-based psychiatric disorders associated with neurosteroid deficits, and targeting epigenetic marks linked to PPAR-α downregulation may offer a valid therapeutic approach.


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