Effects of adolescent social stress and antidepressant treatment on cognitive inflexibility and Bdnf epigenetic modifications in the mPFC of adult mice

Xu, Hang; Wang, Jiesi; Zhang, Ke; Zhao, Mei; Ellenbroek, Bart A.; Shao, Feng; Wang, Weiwen

doi:10.1016/j.psyneuen.2017.11.013

Cited by 50 publications

(34 citation statements)

References 51 publications

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“…This activation of pERK1/2 and CREB in the DG might generate behaviors similar to depression or anxiety (Cameron & Schoenfeld, ; Gass & Riva, ). These results may throw light on the relationship of modifications of dopaminergic neurotransmission in the reward circuit (Nikulina, Lacagnina, Fanous, Wang, & Hammer, ; Xu et al., ; Yang et al., ).…”

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 96%

“…In adult mice socially defeated during adolescence, Xu et al. () observed increased levels of dimethylation of histone H3 at lysine K9 immediately downstream from the BDNF IV promoter. Equally, an upregulation of ASCT2 (D‐serine transporter) expression in chronic social defeat stress was regulated through histone hyper‐acetylation in its promoter region (Wang et al., ).…”

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

“…In one study, an increase was detected in the hippocampus 3 weeks after the last defeat experience (Montagud‐Romero, Montesinos et al., ). In another, an increment of H3K9me2/me3 in the NAc and of the promoter of the BDNF IV gene in the mPFC were produced by SD, and were associated with a repression of transcription (Pathak, Maitra, Chakravarty, & Kumar, ; Xu et al., ). Although long‐term changes in DNA methylation have not been described after SD (Wang et al., ; Xu et al., ), DNA methyltransferases 3a and 3b have been shown to undergo a significant acute decrease in their mRNA expression a few hours after SD (Jung et al., ).…”

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

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Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Montagud‐Romero

Blanco-Gandía

Reguilón

et al. 2018

Eur J of Neuroscience

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Social interaction is known to be the main source of stress in human beings, which explains the translational importance of this research in animals. Evidence reported over the last decade has revealed that, when exposed to social defeat experiences (brief episodes of social confrontations during adolescence and adulthood), the rodent brain undergoes remodeling and functional modifications, which in turn lead to an increase in the rewarding and reinstating effects of different drugs of abuse. The mechanisms by which social stress cause changes in the brain and behavior are unknown, and so the objective of this review is to contemplate how social defeat stress induces long-lasting consequences that modify the reward system. First of all, we will describe the most characteristic results of the short- and long-term consequences of social defeat stress on the rewarding effects of drugs of abuse such as psychostimulants and alcohol. Secondly, and throughout the review, we will carefully assess the neurobiological mechanisms underlying these effects, including changes in the dopaminergic system, corticotrophin releasing factor signaling, epigenetic modifications and the neuroinflammatory response. To conclude, we will consider the advantages and disadvantages and the translational value of the social defeat stress model, and will discuss challenges and future directions.

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Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 96%

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

See 1 more Smart Citation

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Montagud‐Romero

Blanco-Gandía

Reguilón

et al. 2018

Eur J of Neuroscience

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“…Many studies have shown that the expression of BDNF is involved in neuronal development and the epigenetic marker of H3K9me2/3 has a negative regulatory effect on transcription level of Bdnf gene (Walker et al, 2013;Kyzar et al, 2017). Recent studies have shown that H3K9me2 and its degree of methylation participate in regulating the occurrence of depression and anxiety symptoms in early maternally-separated separation young mice (Xu et al, 2018). More importantly, some studies suggest that stress-induced H3K9me2/3 undergoes irreversible changes, which have a regulatory effect on the expression of the Bdnf gene (Wu et al, 2019;Li et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Long-Term Effect of Post-traumatic Stress in Adolescence on Dendrite Development and H3K9me2/BDNF Expression in Male Rat Hippocampus and Prefrontal Cortex

Zhao

Wang

Jiang

et al. 2020

Front. Cell Dev. Biol.

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Exposure to a harsh environment in early life increases in the risk of post-traumatic stress disorder (PTSD) of an individual. Brain derived neurotrophic factor (BDNF) plays an important role in neurodevelopment in developmental stages. Both chronic and traumatic stresses induce a decrease in the level of BDNF and reduce neural plasticity, which is linked to the pathogenesis of PTSD. Also, studies have shown that stress alters the epigenetic marker H3K9me2, which can bind to the promoter region of the Bdnf gene and reduce BDNF protein level. However, the long-term effects of traumatic stress during adolescence on H3K9me2, BDNF expression and dendrite development are not well-known. The present study established a model of PTSD in adolescent rats using an inescapable foot shock (IFS) procedure. Anxiety-like behaviors, social interaction behavior and memory function were assessed by the open field test, elevated plus maze test, three-chamber sociability test and Morris water maze test. In addition, neuronal development and H3K9me2/BDNF expression in hippocampus (HIP) and prefrontal cortex (PFC) were evaluated by Golgi staining, western blotting, qRT-PCR analysis and CHIP-qPCR analysis. Additionally, the Unc0642, a small molecule inhibitor of histone methyltransferase (EHMT2) was used for intervention. The results showed that the IFS procedure induced the PTSD-like behaviors in rats, resulted in fewer dendrite branches and shorter dendrite length in CA1 of HIP and PFC, increased H3K9me2 level and decreased BDNF expression in HIP and PFC. Also, although all the changes can persist to adulthood, Unc0642 administration relieved most of alterations. Our study suggests that traumatic stress in adolescence leads to immediate and long-term mental disorders, neuronal morphological changes, lower BDNF level and increased H3K9me2 level in the HIP and PFC, indicating that H3K9me2/BDNF dysfunction plays a key role in pathogenesis of PTSD.

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“…SD stress induces pronounced physiological and endocrine responses, such as elevated levels of corticosterone (Lumley et al, 2000;Meerlo et al, 2002;Montagud-Romero et al, 2016b;Rodríguez-Arias et al, 2017), and alterations in the levels of BDNF (Wang et al, 2018;Xu et al, 2018). SD stress induces prolonged BDNF expression in the ventral tegmental area (VTA) (Berton et al, 2006;Fanous et al, 2010;Krishnan et al, 2007), and an enhanced expression of proBDNF in the dentate gyrus (DG) and basolateral amygdala (BLA) in adult and adolescent mice subjected to SD (Montagud-Romero et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Oxytocin prevents the increase of cocaine-related responses produced by social defeat

et al. 2019

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Effects of adolescent social stress and antidepressant treatment on cognitive inflexibility and Bdnf epigenetic modifications in the mPFC of adult mice

Cited by 50 publications

References 51 publications

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Long-Term Effect of Post-traumatic Stress in Adolescence on Dendrite Development and H3K9me2/BDNF Expression in Male Rat Hippocampus and Prefrontal Cortex

Oxytocin prevents the increase of cocaine-related responses produced by social defeat

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