Subchronic and mild social defeat stress downregulates peripheral expression of sweet and umami taste receptors in male mice

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.”

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

Molecular Biology ◽

10.1134/s0026893316010088 ◽

2016 ◽

Vol 50 (1) ◽

pp. 161-163 ◽

Cited By ~ 10

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

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

Physiological Research ◽

10.33549/physiolres.934287 ◽

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.

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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

Journal of Psychopharmacology ◽

10.1177/0269881120936468 ◽

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.

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Susceptibility and resilience to chronic social defeat stress in adolescent male mice: No correlation between social avoidance and sucrose preference

Neurobiology of Stress ◽

10.1016/j.ynstr.2020.100221 ◽

2020 ◽

Vol 12 ◽

pp. 100221 ◽

Cited By ~ 1

Author(s):

Leonardo Alves-dos-Santos ◽

Letícia de Souza Resende ◽

Silvana Chiavegatto

Keyword(s):

Social Defeat ◽

Sucrose Preference ◽

Adolescent Male ◽

Social Avoidance ◽

Male Mice ◽

Social Defeat Stress ◽

Chronic Social Defeat Stress

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Abnormality of social behavior and dysfunction of autism related gene expression developing under chronic social defeat stress in male mice

European Neuropsychopharmacology ◽

10.1016/s0924-977x(17)31263-4 ◽

2017 ◽

Vol 27 ◽

pp. S678-S679

Author(s):

N.N. Kudryavtseva ◽

I.L. Kovalenko ◽

D.A. Smagin ◽

A.G. Galyamina ◽

V.N. Babenko

Keyword(s):

Gene Expression ◽

Social Behavior ◽

Social Defeat ◽

Male Mice ◽

Related Gene ◽

Social Defeat Stress ◽

Chronic Social Defeat Stress

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

Molecular Neurobiology ◽

10.1007/s12035-013-8413-y ◽

2013 ◽

Vol 48 (1) ◽

pp. 13-21 ◽

Cited By ~ 45

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

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Chronic social defeat stress impairs goal-directed behavior through dysregulation of ventral hippocampal activity in male mice

Neuropsychopharmacology ◽

10.1038/s41386-021-00990-y ◽

2021 ◽

Author(s):

Keitaro Yoshida ◽

Michael R. Drew ◽

Anna Kono ◽

Masaru Mimura ◽

Norio Takata ◽

...

Keyword(s):

Social Withdrawal ◽

Social Defeat ◽

Task Completion ◽

Male Mice ◽

Social Defeat Stress ◽

Motivated Behavior ◽

Hippocampal Activity ◽

Chronic Social Defeat Stress ◽

Food Seeking ◽

Goal Directed Behavior

AbstractChronic stress is a risk factor for a variety of psychiatric disorders, including depression. Although impairments to motivated behavior are a major symptom of clinical depression, little is known about the circuit mechanisms through which stress impairs motivation. Furthermore, research in animal models for depression has focused on impairments to hedonic aspects of motivation, whereas patient studies suggest that impairments to appetitive, goal-directed motivation contribute significantly to motivational impairments in depression. Here, we characterized goal-directed motivation in repeated social defeat stress (R-SDS), a well-established mouse model for depression in male mice. R-SDS impaired the ability to sustain and complete goal-directed behavior in a food-seeking operant lever-press task. Furthermore, stress-exposed mice segregated into susceptible and resilient subpopulations. Interestingly, susceptibility to stress-induced motivational impairments was unrelated to stress-induced social withdrawal, another prominent effect of R-SDS in mouse models. Based on evidence that ventral hippocampus (vHP) modulates sustainment of goal-directed behavior, we monitored vHP activity during the task using fiber photometry. Successful task completion was associated with suppression of ventral hippocampal neural activity. This suppression was diminished after R-SDS in stress-susceptible but not stress-resilient mice. The serotonin selective reuptake inhibitor (SSRI) escitalopram and ketamine both normalized vHP activity during the task and restored motivated behavior. Furthermore, optogenetic vHP inhibition was sufficient to restore motivated behavior after stress. These results identify vHP hyperactivity as a circuit mechanism of stress-induced impairments to goal-directed behavior and a putative biomarker that is sensitive to antidepressant treatments and that differentiates susceptible and resilient individuals.

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