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RNA sequencing of hippocampal sample from normal male mice, stress induced depressive male mice and male offspring born to stress-induced depressed male mice

ABSTRACT: We demonstrated that the offspring of depressed fathers display reduced resilience to stress and enhanced susceptibility to depression. To explain the observed behavioural phenotypes of depression in offspring produced by depressed fathers, molecular profiling was performed in key brain regions.We examined the hippocampal sample from normal male mice, stress induced depressive male mice and male offspring born to stress-induced depressed male mice by RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE133494 | GEO | 2020/06/28

REPOSITORIES: GEO

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RNA sequencing of hippocampal sample from normal male mice, stress induced depressive male mice and male offspring born to stress-induced depressed male mice

Project description:RNA sequencing of hippocampal sample from normal male mice, stress induced depressive male mice and male offspring born to stress-induced depressed male mice

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Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).

2014-07-01 | E-GEOD-47847 | biostudies-arrayexpress

Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected at rest

2014-07-01 | E-GEOD-47846 | biostudies-arrayexpress

Small RNA sequencing of sperm sample from normal or stress induced depressive male mice

Project description:We demonstrated that sperm sRNAs are sufficient to reproduce the effect of sperm RNAs on inducing depressive symptoms in offspring.To identify the specific subtypes of sperm sRNAs that cause abnormalities in offspring, we examined the sRNA profiles of sperm derived from normal or depressed male mice by RNA deep sequencing.

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Hypothalamic Proteomics analysis of lipopolysaccharide (LPS)-induced depressed mice

Project description:Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry were employed to detect the proteomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse. A total of 187 proteins were differentially expressed compared with the control group. The results indicated altered molecules were clustered into Ephrin receptor signalling; glutamatergic transmission, and inflammation-related signalling. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signalling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.

2020-01-09 | PXD016040 | Pride

Peripheral blood gene-expression in depressed subjects with bipolar disorder vs healthy controls.

Project description:Analysis of gene-expression changes in depressed subjects with bipolar disorder compared to healthy controls. Results provide information on pathways that may be involved in the pathogenesis of bipolar depression. Total RNA isolated from PAXgene blood RNA tubes from 20 depressed subjects with bipolar disorder and 15 healthy controls.

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The role microglia in electroconvulsive threapy (ECT) in depressed-like mice

Project description:Recent studies implicate microglia alterations in the pathogenesis and pathophysiology of depression. For example, chronic unpredictable stress (CUS) in mice can cause degeneration of microglia and depressive-like symptoms, which can be reversed by microglia stimulating drugs. To further test the causal role of microglia in CUS-induced depression and its reversal by an anti-depressive procedure, we examined the effects of microglia depletion with the CSF-1 antagonist PLX5622 or pharmacological blockade of microglial activation with minocycline on normal mood-related behavior, CUS-induced depressive-like symptoms, and the amelioration of these symptoms by electroconvulsive treatment (ECT). We report that microglia-depleted mice showed no depression, anxiety or spatial memory disturbances. Microglia depletion had no effect on the development of CUS-induced depressive-like symptoms and suppressed neurogenesis, but it completely abrogated the beneficial effects of ECT on depression and neurogenesis, as well as on the all ECT-induced transcriptomic changes. ECT induced several morphological changes in microglia, suggestive of increased activation status, and blockade of this activation by minocycline attenuated the anti-depressive and pro-neurogenesis effect of ECT and reduced the number of contacts between microglia and neurogenic cells. The immune checkpoint gene Lag3, whose expression by microglia was increased following CUS, was the only microglial transcript significantly reduced by ECT. Furthermore, treatment of depressed-like mice with a LAG3 monoclonal antibody was further tested.

2021-01-01 | GSE123027 | GEO

MicroRNA expression analysis of livers of F1 male offspring fathered from control mice or stressed mice

Project description:Psychological stress is highly prevalent in modern society. Both epidemiologic and experimental animal studies demonstrate that chronic psychological stress exerts adverse effects on the initiation and/or progression of many diseases. Here, using a mouse model of restraint stress, we report the discovery of a novel signaling pathway linking paternal stress exposure to the reprogram of hepatic gluconeogenesis in the offspring. Offspring fathered by stressed males (Stress-F1) exhibits hyperglycemia as a result of enhanced hepatic gluconeogenesis, conpared to offspring from control fathers (Control-F1). Mechanistically, protein levels of PEPCK, a key gluconeogenic enzyme, were significantly increased, while its mRNA levels were unaffected in the stress-F1 mice, pointing to a posttranscriptional regulatory mechanism. Because MicroRNAs often play an important role in regulating gene expression at the posttranscriptional level, we investigated the expression profile of MicroRNAs in livers from Control-F1 and Stress-F1 mice.

2015-09-29 | GSE73530 | GEO

Peripheral blood gene-expression in depressed subjects with bipolar disorder vs healthy controls.

2010-08-27 | GSE23848 | GEO

Sex-specific role for SLIT1 in regulating stress susceptibility

Project description:Major depressive disorder (MDD) is a pervasive and debilitating syndrome characterized by mood disturbances, anhedonia, and alterations in cognition. While the prevalence of MDD is twice as high for women compared to men, little is known about the molecular mechanisms that drive sex differences in depression susceptibility. We discovered that Slit Guidance Ligand 1 (SLIT1), a secreted protein essential for axonal navigation and molecular guidance in cellular migration, is downregulated in the ventromedial prefrontal cortex (vmPFC) of depressed women compared to healthy controls, but not depressed men. This sex-specific downregulation of Slit1 was also observed in the vmPFC of mice exposed to chronic variable stress. To identify a causal, sex-specific role for SLIT1 in depression-related behavioral abnormalities, we performed knockdown (KD) of Slit1 expression in the vmPFC of male and female mice. When combined with stress exposure, vmPFC Slit1 KD reflected the human condition by inducing a sex-specific increase in anxiety- and depression-like behavioral abnormalities in female mice with no effect seen in male mice. Further, we found that vmPFC Slit1 KD caused a pronounced reduction in dendritic arborization and concomitant alterations to electrophysiological properties of vmPFC pyramidal neurons in females. Additionally, RNA-sequencing analysis of the vmPFC following Slit1 KD in female mice revealed an augmented transcriptional stress signature. Together, our findings establish a crucial role for SLIT1 in regulating neurophysiological and transcriptional responses to stress within the vmPFC, and provide mechanistic insight into novel signaling pathways and molecular factors influencing sex differences in depression susceptibility.

2023-09-29 | GSE158993 | GEO

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