Effects of chronic social defeat stress on behavior and choline acetyltransferase, 78-kDa glucose-regulated protein, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice

Zhao, Tong; Huang, Guang‐Biao; Muna, Sushma Shrestha; Bagalkot, Tarique Rajasaheb; Jin, Hongmei; Chae, Han-Jung; Chung, Young‐Chul

doi:10.1007/s00213-013-3028-6

Cited by 30 publications

(24 citation statements)

References 32 publications

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“…When testing the mice on D30, no deficit in the short-term memory of CSDS-subjected animals was observed in ITI1 conditions, but the memory performances of stressed-HEC mice were significantly altered in the ITI24 ones. These data corroborated previous studies that also described impaired cognition in social-defeated mice using the NOR test1641 with mnesic alterations in that case recorded at both short and long term, but measured 5 days only after the last defeat session. Interestingly, we showed that long term memory was still affected 3 weeks after CSDS.…”

Section: Discussionsupporting

confidence: 91%

“…Following repeated exposures to aggressive resident CD-1 mice, intruder C57BL/6J mice display various behavioral deficits such as social avoidance, anxiety-like phenotype, despair-like behavior and a reduction in sweet preference111213. In addition, CSDS-exposed animals also exhibit cognitive impairments141516, related to those observed in patients subjected to social stress, that suggest a marked dysregulation of the hippocampus, a brain structure known to play a crucial role in memory processes17, and to be directly altered by social stress18.…”

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confidence: 99%

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Effect of agomelatine on memory deficits and hippocampal gene expression induced by chronic social defeat stress in mice

Martin¹,

Allaïli²,

Euvrard³

et al. 2017

Sci Rep

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Chronic stress is known to induce not only anxiety and depressive-like phenotypes in mice but also cognitive impairments, for which the action of classical antidepressant compounds remains unsatisfactory. In this context, we investigated the effects of chronic social defeat stress (CSDS) on anxiety-, social- and cognitive-related behaviors, as well as hippocampal Bdnf, synaptic plasticity markers (PSD-95, Synaptophysin, Spinophilin, Synapsin I and MAP-2), and epigenetic modifying enzymes (MYST2, HDAC2, HDAC6, MLL3, KDM5B, DNMT3B, GADD45B) gene expression in C57BL/6J mice. CSDS for 10 days provoked long-lasting anxious-like phenotype in the open field and episodic memory deficits in the novel object recognition test. While total Bdnf mRNA level was unchanged, Bdnf exon IV, MAP-2, HDAC2, HDAC6 and MLL3 gene expression was significantly decreased in the CSDS mouse hippocampus. In CSDS mice treated 3 weeks with 50 mg/kg/d agomelatine, an antidepressant with melatonergic receptor agonist and 5-HT2C receptor antagonist properties, the anxious-like phenotype was not reversed, but the treatment successfully prevented the cognitive impairments and hippocampal gene expression modifications. Altogether, these data evidenced that, in mice, agomelatine was effective in alleviating stress-induced altered cognitive functions, possibly through a mechanism involving BDNF signaling, synaptic plasticity and epigenetic remodeling.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Effect of agomelatine on memory deficits and hippocampal gene expression induced by chronic social defeat stress in mice

Martin¹,

Allaïli²,

Euvrard³

et al. 2017

Sci Rep

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“…Precedent preclinical and clinical studies revealed the involvement of ER stress in the pathophysiology of depression and stress-induced neurological complications [12,13,48,49]. Elevated ROS and cytokines can trigger the ER stress response which ultimately leads to cell damage [50,51].…”

Section: Discussionmentioning

confidence: 99%

“…However, under prolonged ER stress condition, cells may undergo apoptotic pathway through upregulation of C/EBP homologous protein (CHOP) which eventually leads to apoptosis cell death [11]. Recent studies indicated the key role of ER stress in the pathophysiology of depression and cognitive impairment [12,13]. ER stress is associated with different inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-Induced Behavioral Alterations Are Alleviated by Sodium Phenylbutyrate via Attenuation of Oxidative Stress and Neuroinflammatory Cascade

2016

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Oxido-nitrosative stress, neuroinflammation, and reduced level of neurotrophins are implicated in the pathophysiology of anxiety and depressive illness. A few recent studies have revealed the role of endoplasmic reticulum (ER) stress in the pathophysiology of stress and depression. The aim of the present study is to investigate the neuroprotective potential of sodium phenylbutyrate (SPB), an ER stress inhibitor against lipopolysaccharide (LPS)-induced anxiety and depressive-like behavior in Swiss albino mice. Anxiety and depressive-like behavior was induced by LPS (0.83 mg/kg; i.p.) administration. Various behavioral tests were conducted to evaluate the anxiety and depressive-like behavior in mice. Real-time PCR was employed for the detection and expression of ER stress markers (78-kDa glucose-regulated protein (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)). Pretreatment with SPB significantly ameliorated the LPS-induced anxiety and depressive-like behavior as revealed by behavioral paradigm results. LPS-induced oxidative stress was ameliorated by SPB pretreatment in hippocampus (HC) and prefrontal cortex (PFC) region. Neuroinflammation was significantly reduced by SPB pretreatment in LPS-treated mice as evident from reduction in proinflammatory cytokines (IL-1β and TNF-α). Importantly, LPS administration significantly up-regulated the GRP78 mRNA expression level in the HC which suggests the involvement of unfolded protein response (UPR) in LPS-evoked behavioral anomalies. These results highlight the neuroprotective potential of SPB in LPS-induced anxiety and depressive illness model which may be partially due to inhibition of oxidative stress-neuroinflammatory cascade.

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“…The procedure of social defeat stress was performed as previously reported (Golden et al, 2011; Zhao et al, 2013; Yang et al, 2015a, 2016b; Zhang et al, 2015b). Every day the C57BL/6 mice were exposed to a different CD1 aggressor mouse for 10 minutes total for 10 days.…”

Section: Methodsmentioning

confidence: 99%

Rapid and Sustained Antidepressant Action of the mGlu2/3 Receptor Antagonist MGS0039 in the Social Defeat Stress Model: Comparison with Ketamine

Dong

Zhang

Yao

et al. 2016

IJNPPY

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Background:Similar to the N-methyl-D-aspartate receptor antagonist ketamine, the metabotropic glutamate 2/3 receptor antagonist, MGS0039, shows antidepressant effects. However, there are no reports comparing these 2 compounds in the social defeat stress model of depression.Methods:We examined the effects of MGS0039 (1 mg/kg) and ketamine (10 mg/kg) on depression-like behavior in susceptible mice after repeated social defeat stress. Protein levels of brain-derived neurotrophic factor, TrkB, phospho-TrkB, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (GluA1), postsynaptic density protein 95, and dendritic spine density in selected brain regions were measured.Results:In the tail suspension and forced swimming tests, both MGS0039 and ketamine significantly attenuated the increased immobility time observed in susceptible mice, compared with vehicle-treated animals, 1 or 2 days after a single dose of drug. In the sucrose preference test, both compounds significantly improved the reduced preference typically seen in susceptible mice at 3 to 7 days after a single dose of drug. Western-blot analyses showed that similar to ketamine, MGS0039 significantly attenuated the reduced brain-derived neurotrophic factor, phospho-TrkB/TrkB ratio, GluA1 and postsynaptic density protein 95 seen in the prefrontal cortex, dentate gyrus, and CA3 of the hippocampus from susceptible mice, 8 days after a single dose. Again, in a similar manner to ketamine, MGS0039 significantly attenuated the reduction of spine density in the prelimbic regions of the medial prefrontal cortex, dentate gyrus, and CA3 of the hippocampus, but not infralimbic regions of the medial prefrontal cortex and CA1, in susceptible mice 8 days after a single dose. In contrast, neither drug elicited an effect on altered brain-derived neurotrophic factor-TrkB signaling, GluA1, and postsynaptic density protein 95 levels and did not increase spine density observed in the nucleus accumbens of susceptible mice.Conclusions:Similar to ketamine, MGS0039 shows rapid and sustained antidepressant effects in the social defeat stress model. Long-lasting synaptogenesis in the prelimbic regions of medial prefrontal cortex, dentate gyrus, and CA3 might be implicated in this sustained antidepressant effect.

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Effects of chronic social defeat stress on behavior and choline acetyltransferase, 78-kDa glucose-regulated protein, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice

Abstract: The present study demonstrated that chronic social defeat stress in mice produces stress-related behaviors. Different response patterns were noted for Grp78 and chop expression among the groups in terms of brain regions and time-course effects.

Cited by 30 publications

References 32 publications

Effect of agomelatine on memory deficits and hippocampal gene expression induced by chronic social defeat stress in mice

Effect of agomelatine on memory deficits and hippocampal gene expression induced by chronic social defeat stress in mice

Lipopolysaccharide-Induced Behavioral Alterations Are Alleviated by Sodium Phenylbutyrate via Attenuation of Oxidative Stress and Neuroinflammatory Cascade

Rapid and Sustained Antidepressant Action of the mGlu2/3 Receptor Antagonist MGS0039 in the Social Defeat Stress Model: Comparison with Ketamine

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