scholarly journals Dysfunction in Ribosomal Gene Expression in the Hypothalamus and Hippocampus following Chronic Social Defeat Stress in Male Mice as Revealed by RNA-Seq

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Dmitry A. Smagin ◽  
Irina L. Kovalenko ◽  
Anna G. Galyamina ◽  
Anatoly O. Bragin ◽  
Yuriy L. Orlov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Social Stress ◽  
Ribosome Biogenesis ◽  
Social Defeat ◽  
Brain Regions ◽  
Ribosomal Gene ◽  
Rna Seq ◽  
Male Mice ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress

Chronic social defeat stress leads to the development of anxiety- and depression-like states in male mice and is accompanied by numerous molecular changes in brain. The influence of 21-day period of social stress on ribosomal gene expression in five brain regions was studied using the RNA-Seq database. MostRps, Rpl, Mprs, andMprlgenes were upregulated in the hypothalamus and downregulated in the hippocampus, which may indicate ribosomal dysfunction following chronic social defeat stress. There were no differentially expressed ribosomal genes in the ventral tegmental area, midbrain raphe nuclei, or striatum. This approach may be used to identify a pharmacological treatment of ribosome biogenesis abnormalities in the brain of patients with “ribosomopathies.”

Changes in the expression of dopaminergic genes in brain structures of male mice exposed to chronic social defeat Stress: An RNA-seq study

2016 ◽  
Vol 50 (1) ◽  
pp. 161-163 ◽  
Author(s):  
I. L. Kovalenko ◽  
D. A. Smagin ◽  
A. G. Galyamina ◽  
Yu. L. Orlov ◽  
N. N. Kudryavtseva
Keyword(s):  
Social Defeat ◽  
Brain Structures ◽  
Rna Seq ◽  
Male Mice ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress ◽  
Dopaminergic Genes

Downregulation of Serotonergic Gene Expression in the Raphe Nuclei of the Midbrain Under Chronic Social Defeat Stress in Male Mice

2013 ◽  
Vol 48 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Ul’yana A. Boyarskikh ◽  
Natalya P. Bondar ◽  
Maxim L. Filipenko ◽  
Natalia N. Kudryavtseva
Keyword(s):  
Gene Expression ◽  
Social Defeat ◽  
Raphe Nuclei ◽  
Male Mice ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress ◽  
Raphé Nuclei

scholarly journals Unique effects of social defeat stress in adolescent male mice on the Netrin-1/DCC pathway, prefrontal cortex dopamine and cognition (Social stress in adolescent vs. adult male mice)

eNeuro ◽  
2021 ◽  
pp. ENEURO.0045-21.2021
Author(s):  
Philip Vassilev ◽  
Andrea Haree Pantoja-Urban ◽  
Michel Giroux ◽  
Dominique Nouel ◽  
Giovanni Hernandez ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Adult Male ◽  
Social Stress ◽  
Social Defeat ◽  
Adolescent Male ◽  
Male Mice ◽  
Social Defeat Stress

scholarly journals Chronic stress impairs male spermatogenesis function and nectin-3 protein expression in the testis

2020 ◽  
pp. 297-306
Author(s):  
T. Li ◽  
J. Yao ◽  
Q. Zhang ◽  
Q. Li ◽  
J. Li ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Molecular Mechanisms ◽  
Social Defeat ◽  
Histological Structure ◽  
Male Mice ◽  
Corticotropin Releasing Hormone ◽  
Social Defeat Stress ◽  
Control Male ◽  
Releasing Hormone ◽  
Chronic Social Defeat Stress

Chronic stress is a crucial public issue that occurs when a person is repetitively stimulated by various stressors. Previous researches have reported that chronic stress induces spermatogenesis dysfunction in the reproductive system, but its molecular mechanisms remain unclear. The nectin protein family, including nectin-1 to nectin-4, is Ca(2+)-independent immunoglobulin-like cell adhesion molecules, that are widely expressed in the hippocampus, testicular tissue, epithelial cells and other sites. Nectin-3 contributes to the sperm development at the late stage, and the abnormal expression of nectin-3 impairs spermatogenesis. Some recent studies have demonstrated that stress induces a decrease in nectin-3 expression in the hippocampus via corticotropin-releasing hormone (CRH) to corticotropin-releasing hormone receptor 1 (CRHR1) pathway. Here, we tested whether chronic stress also caused a reduction in nectin-3 expression in the testis. We established a chronic social defeat stress paradigm, which provides naturalistic and complex chronic stress in male C57BL/6 mice. After 25 days of chronic social defeat stress, the mice showed weight loss, thymic atrophy and some other typical symptoms of chronic stress (e.g. anxiety-like behavior and social avoidance behavior). We found gonad atrophy, testicular histological structure changes and semen quality reductions in the stressed mice. The stressed male mice significantly spent more time to impregnate the female mice than the control male mice. Moreover, nectin-3 protein levels in stressed mice were significantly decreased in the testes compared with those in control mice. In addition, we found that the CRHR1 expression level was increased in the testes of stressed mice. Therefore, we demonstrated a decreased level of nectin-3 expression and an increase in CRHR1 expression in the testis after exposure to chronic stress, which may provide a potential therapeutic target for the spermatogenesis dysfunction induced by chronic stress.

scholarly journals Comparison of Gut Tight Junction Gene Expression in C57BL/6J and BALB/c Mice After Chronic Social Defeat Stress

2019 ◽  
Vol 53 (1) ◽  
pp. 41-46
Author(s):  
Naoko YAMAGISHI ◽  
Yasuhiro OMATA ◽  
Ayako AOKI-YOSHIDA ◽  
Naoko MORIYA ◽  
Tatsuhiko GOTO ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Social Defeat ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress

Blockade of D3 receptor prevents changes in DAT and D3R expression in the mesolimbic dopaminergic circuit produced by social stress- and cocaine prime-induced reinstatement of cocaine-CPP

2020 ◽  
Vol 34 (11) ◽  
pp. 1300-1315
Author(s):  
Rocío Guerrero-Bautista ◽  
Aurelio Franco-García ◽  
Juana M Hidalgo ◽  
Francisco Fernández-Gómez ◽  
M Victoria Milanés ◽  
...  
Keyword(s):  
Social Stress ◽  
Social Defeat ◽  
Behavioral Effects ◽  
The Other ◽  
D3 Receptor ◽  
Male Mice ◽  
Social Defeat Stress ◽  
Priming Dose ◽  
The Impact ◽  
The Brain

Background: Cocaine may cause persistent changes in the brain, which are more apparent in DA transporter (DAT) and DA receptor availability within the nucleus accumbens (NAc). On the other hand, the DA D3 receptor (D3R) has emerged as a promising pharmacotherapeutic target for substance use disorders. Aims: This study aims to assess the impact of selective D3R antagonism on DAT and D3R after reinstatement of cocaine preference (CPP) induced by an acute session of social defeat stress (SDS) and a cocaine prime in mice after a period of abstinence. Methods: Male mice were conditioned with 25 mg/kg of cocaine for 4 days. After 60 days of extinction training mice were pretreated with the selective D3R antagonist SB-277011A before the re-exposure to a priming dose of cocaine or to a single SDS session. CPP scores were determined and levels of DAT, D3R, phospho Akt (pAkt) and phospho mTOR (pmTOR) were assessed in the NAc shell. Results: An increase in DAT and D3R expression was seen in the NAc after both a cocaine prime- and SDS-induced reinstatement of CPP. Pretreatment with SB-277011A blocked elevated DAT and D3R expression as well as SDS-induced reinstatement. By contrast, the blockade of D3R did not modified the cocaine prime-induced CPP. Changes in DAT and D3R expression do not seem to occur via the canonic pathway involving Akt/mTOR. Conclusions: Our results suggest that the selective D3R antagonist ability to inhibit DAT and D3R up-regulation could represent a possible mechanism for its behavioral effects in cocaine-memories reinstatement induced by social stress.

scholarly journals Stress-induced sleep-like inactivity modulates stress susceptibility in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Midori Nagai ◽  
Hirotaka Nagai ◽  
Chisato Numa ◽  
Tomoyuki Furuyashiki
Keyword(s):  
Sleep Deprivation ◽  
Social Stress ◽  
Social Interest ◽  
Social Behaviors ◽  
Social Defeat ◽  
Brain Regions ◽  
Social Characteristics ◽  
Social Avoidance ◽  
Social Defeat Stress ◽  
Positive Valence

AbstractSevere environmental and social stress induces dysregulation of sleep along with mood and cognitive disturbances. However, the role and mechanism of this sleep dysregulation remain elusive. Here we evaluated sleep-like inactivity measured by voluntary movements and its relationship to social behaviors in mice without or with social defeat stress as well as the stressed mice with subsequent sleep deprivation. Social defeat stress immediately induced sleep-like inactivity with decreased body temperature. In the social interaction test, the control mice showed high social interest and its correlation with social sniffing intensity, the latter of which indicates positive valence of social sniffing. After the stress, these social characteristics were maintained in stress-resilient mice, but disrupted in stress-susceptible mice, leading to social avoidance. Sleep deprivation after the stress decreased social sniffing intensity along with reduced social interest, but enhanced the exploratory activity with the positive valence of social sniffing. We also found by c-Fos immunohistochemistry that the stress activated sleep-related brain regions, the dorsomedial hypothalamus and ventrolateral periaqueductal gray. Collectively, these findings show that stress activates sleep-related brain regions and induces sleep-like inactivity, contributing to multiple roles of stress-induced sleep for social behaviors.

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