Mice deficient for wild-type p53-induced phosphatase 1 display elevated anxiety- and depression-like behaviors

Ruan, Chun-Sheng; Zhou, Fiona H.; He, Zhiyong; Wang, Shufen; Yang, Chunrui; Shen, Yanjun; Guo, Yi; Zhao, Hui; Chen, L; Liu, D; Liu, J; Baune, Bernhard T.; Xiao, Zhi‐Cheng; Zhou, Xin‐Fu

doi:10.1016/j.neuroscience.2015.02.037

Cited by 20 publications

(20 citation statements)

References 72 publications

(117 reference statements)

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“…We have found that the chronic TS stress causes negative mood-related behaviours such as decreases in exploratory behaviour and increases in anxiety-like behaviour in OFT as well as increases in depression-like behaviour in FST. These results are consistent with the previous findings in mice under different chronic stress protocols such as UCMS [12], CRS [28,29] or a combined protocol of CRS and chronic TS [20]. The present study also shows that chronic TS stress causes loss of neuronal and astrocyte markers in the hippocampus, one of the most vulnerable areas in the brain in response to stress [7].…”

Section: Discussionsupporting

confidence: 93%

“…Animal models based on different chronic stress paradigms have been widely used for understanding the pathogenesis or drug development of mood disorders; and low reproducibility and complex or time-consuming producing protocol are commonly seen in the current animal models. For example, the most frequently used UCMS paradigm which has been widely applied to numerous strains of rodents have over 10 different stressors and also various stress durations including 14-day [7,8], 21-day [9,10] 28-day [11,12], 35-day [13], 42day [14,15], 49-day [16] and 56-day [17,18] protocols. The diverse of UCMS protocols suggests a fact of difficulty to reproduce the model that was confirmed by our previous study, in which we found a time-dependent recovery of behavioural and biochemical changes after 8 weeks of UCMS stress [19].…”

Section: Introductionmentioning

confidence: 99%

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A Pilot Study in Modeling Mood Disorders in Mice by Chronic Tail-Suspension Stress

Ruan¹,

Guo²,

Bobrovskaya³

et al. 2018

Neuropsychiatry

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Chronic stress has been known as a main cause for human mood disorders. The understanding of the pathogenesis of the mood disorders are primarily based on the usage of animal models. Low reproducibility and complicacy of production are commonly known shortcomings in the current models with chronic stress. Here, we tested a simple stress paradigm, daily exposure of 6-min tail-suspension (TS), in modelling chronic stress-induced mood disorders in mice. We found that after 2-3-weeks of TS stress mice displayed a significant decrease in exploratory behavior, increases in anxiety-like and depression-like behaviors as well as significant decreases of NeuN and GFAP levels in the hippocampus. We also found that longer exposure of mice to TS stress (up to 4 weeks) resulted in significant adaptation of these responses and reversal of most of the behavioural and biochemical changes. This study suggests that chronic TS stress for 2-3 weeks could be used as a model of mood disorders.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

A Pilot Study in Modeling Mood Disorders in Mice by Chronic Tail-Suspension Stress

Ruan¹,

Guo²,

Bobrovskaya³

et al. 2018

Neuropsychiatry

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“…Prior work has demonstrated the direct transcriptional repression of miR-184 by the psychiatric risk factor methyl CpG binding protein 2 (MeCP2) (Nomura et al, 2008). Additionally, the miR-34 family (including miR-34a ) has previously been linked to stress (Haramati, Navon, 2011) and is strongly induced by the TP53 gene, a key cell-cycle control gene that also regulates expression of the mood-stabilizing Wip1 gene (Rokavec et al, 2014, Ruan et al, 2015). Chronic stress is thought to act as a precipitating environmental factor for a host of mental illnesses and induces chronic elevations in circulating glucocorticoids (e.g.…”

Section: Discussionmentioning

confidence: 99%

The microRNA network is altered in anterior cingulate cortex of patients with unipolar and bipolar depression

Azevedo

Carter

Meng

et al. 2016

Journal of Psychiatric Research

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MicroRNAs (miRNAs) are small, non-coding RNAs acting as post-transcriptional regulators of gene expression. Though implicated in multiple CNS disorders, miRNAs have not been examined in any psychiatric disease state in anterior cingulate cortex (AnCg), a brain region centrally involved in regulating mood. We performed qPCR analyses of 29 miRNAs previously implicated in psychiatric illness (major depressive disorder (MDD), bipolar disorder (BP) and/or schizophrenia (SZ)) in AnCg of patients with MDD and BP versus controls. miR-132, miR-133a and miR-212 were initially identified as differentially expressed in BP, miR-184 in MDD and miR-34a in both MDD and BP (although none survived multiple correction testing and must be considered preliminary). In silico target prediction algorithms identified putative targets of differentially expressed miRNAs. Nuclear Co-Activator 1 (NCOA1), Nuclear Co-Repressor 2 (NCOR2) and Phosphodiesterase 4B (PDE4B) were selected based upon predicted targeting by miR-34a (with NCOR2 and PDE4B both targeted by miR-184) and published relevance to psychiatric illness. Luciferase assays identified PDE4B as a target of miR-34a and miR-184, while NCOA1 and NCOR2 were targeted by miR-34a and 184, respectively. qPCR analyses were performed to determine whether changes in miRNA levels correlated with mRNA levels of validated targets. NCOA1 showed an inverse correlation with miR-34a in BP, while NCOR2 demonstrated a positive correlation. In sum, this is the first study to demonstrate miRNA changes in AnCg in psychiatric illness and validate miR-34a as differentially expressed in CNS in MDD. These findings support a mechanistic role for miRNAs in the regulation of stress-responsive genes disrupted in psychiatric illness.

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“…The behavioral profiling also revealed that TA at low mobility during the night was significantly increased in zebrafish treated with ZPD and TRZ but not treated with TCS-1102 and hcrt-KO. In rodents, TA in the peripheral zone indicates non-locomotor movements of the body ( Ruan et al, 2015 ), suggesting that both ZPD and TRZ may increase non-locomotor movement of the body at low mobility during the night. It has been demonstrated that ZPD produced muscle twitching and spasticity during hypnosis in GABA-A receptor α1 –/– mice ( Kralic et al, 2002 ).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological profiling of zebrafish behavior using chemical and genetic classification of sleep-wake modifiers

et al. 2015

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Sleep-wake states are impaired in various neurological disorders. Impairment of sleep-wake states can be an early condition that exacerbates these disorders. Therefore, treating sleep-wake dysfunction may prevent or slow the development of these diseases. Although many gene products are likely to be involved in the sleep-wake disturbance, hypnotics and psychostimulants clinically used are limited in terms of their mode of action and are not without side effects. Therefore, there is a growing demand for developing new hypnotics and psychostimulants with high efficacy and few side effects. Toward this end, animal models are indispensable for use in genetic and chemical screens to identify sleep-wake modifiers. As a proof-of-concept study, we performed behavioral profiling of zebrafish treated with chemical and genetic sleep-wake modifiers. We were able to demonstrate that behavioral profiling of zebrafish treated with hypnotics or psychostimulants from 9 to 10 days post-fertilization was sufficient to identify drugs with specific modes of action. We were also able to identify behavioral endpoints distinguishing GABA-A modulators and hypocretin (hcrt) receptor antagonists and between sympathomimetic and non-sympathomimetic psychostimulants. This behavioral profiling can serve to identify genes related to sleep-wake disturbance associated with various neuropsychiatric diseases and novel therapeutic compounds for insomnia and excessive daytime sleep with fewer adverse side effects.

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Mice deficient for wild-type p53-induced phosphatase 1 display elevated anxiety- and depression-like behaviors

Cited by 20 publications

References 72 publications

A Pilot Study in Modeling Mood Disorders in Mice by Chronic Tail-Suspension Stress

A Pilot Study in Modeling Mood Disorders in Mice by Chronic Tail-Suspension Stress

The microRNA network is altered in anterior cingulate cortex of patients with unipolar and bipolar depression

Pharmacological profiling of zebrafish behavior using chemical and genetic classification of sleep-wake modifiers

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