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

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

PROVIDER: PRJNA507273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8249920.fastq.gz	Fastqsanger.gz
	SRR8249930.fastq.gz	Fastqsanger.gz
	SRR8249911.fastq.gz	Fastqsanger.gz
	SRR8249921.fastq.gz	Fastqsanger.gz
	SRR8249931.fastq.gz	Fastqsanger.gz

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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

Comparison of brain and hippocampal majority proteomes from MAP6 KO mice submitted or not to electroconvulsive stimulations

Project description:For major depression, the non-drug therapy Electroconvulsive therapy (ECT) treatment is highly effective and fast-acting. Despite a large and long-standing clinical use, the neurobiological mechanisms underlining ECT curative action are still poorly understood. Thanks to a genetic animal model that constitutively exhibit behavioural and biological features relevant to some aspects of major depressive disorder, here we analyse the behavioural and biological consequences of electroconvulsive stimulations (ECS), the animal model of ECT. We found that a classical ECS treatment, with 10 stimulation over 2 weeks period, has a beneficial effect on constitutive behavioural defects. We therefore compared brain and hippocampal majority proteomes from MAP6 KO mice submitted or not to electroconvulsive stimulations.

2019-03-12 | PXD008543 | Pride

Electroconvulsive Stimulation modulates Microglia. Transcriptome analysis of Biozzi-ABH mice spinal-cord microglia following electroconvulsive-seizures.

Project description:Neurostimulation by electroconvulsive therapy is highly effective in neuropsychiatric disorders by an unknown mechanism. Microglial toxicity plays a key role in chronic neuro-inflammatory brain diseases, where there is critical shortage in therapies. To investigate the direct effect of electroconvulsive seizures (ECS) on the CNS innate immune system, we performed transcriptome analysis on spinal microglia from ECS- and sham-treated naïve mice.

2022-09-01 | GSE137184 | GEO

Electroconvulsive Stimulation modulates Microglia. Transcriptome analysis of Biozzi-ABH mice spinal-cord microglia following electroconvulsive-seizures.

Project description:Electroconvulsive Stimulation modulates Microglia. Transcriptome analysis of Biozzi-ABH mice spinal-cord microglia following electroconvulsive-seizures.

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Differential lncRNA expression in human ovarian tumors from depressed and non-depressed nude mice

Project description:Differential lncRNA expression in human ovarian tumors from depressed and non-depressed nude mice

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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: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.

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Microarray analysis to evaluate the role of USP18 in primary microglia and the microglia cell line BV-2

Project description:Microglia are tissue macrophages of the central nervous system (CNS) that control tissue homeostasis, and as such they are crucially important for organ integrity. Microglia dysregulation is thought to be causal for a group of neuropsychiatric, neurodegenerative and neuroinflammatory diseases, called ‘microgliopathies’. However, how the intracellular stimulation machinery in microglia is controlled is poorly understood. By using expression studies, we identified the ubiquitin-specific protease (Usp) 18 in white matter microglia that essentially contributes to microglial quiescence under homeostatic conditions. We further found that microglial Usp18 negatively regulated the activation of STAT1 and concomitant induction of interferon-induced genes thereby disabling the termination of IFN signalling. Unexpectedly, the Usp18-mediated feedback loop was independent from the catalytic domain of the protease but instead required the interacting region of Ifnar2. Additionally, the absence of Ifnar1 completely rescued microglial activation indicating a tonic IFN signal mediated by receptor interactions under non-diseased conditions. Finally, conditional depletion of Usp18 only in myeloid cells significantly enhanced the disease burden in a mouse model of CNS autoimmunity, increased axonal and myelin damage and determined the spatial distributions of CNS lesions that shared the same STAT1 signature as myeloid cells found in active multiple sclerosis (MS) lesions. These results identify Usp18 as novel negative regulator of microglia activation, demonstrate a protective role of the IFNAR pathway for microglia and establish Usp18 as potential therapeutic target for the treatment of MS. Primary microglia (WT, USP18ko and USP18_C61A mice) and BV-2 cells (treated with control siRNA or siRNA against USP18) were incubated with 500 U/ml IFN-b. At different timepoints (0h, 6h, and 24h) RNA samples were taken and analyzed via Microarray

2015-04-20 | E-GEOD-61500 | biostudies-arrayexpress

Sequencing of Arabidopsis ECT triple mutant

Project description:Sequencing of Arabidopsis ECT 234 triple mutant by ONT DRS

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Staphylococcus aureus subsp. aureus ECT-R 2

Project description:Staphylococcus aureus subsp. aureus ECT-R 2 genome sequencing

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Inflammatory Signatures of Microglia in the Mouse Model of Corticosterone-Induced Depression

Project description:Microglia-mediated inflammation has been recognized as a key feature of major depressive disorder. Although hypercortisolemia is commonly observed in depressed patients and can be predictive of treatment response, how such chronic exposure to this stress hormone may influence microglia is incompletely characterized. Here, we exploited a standard mouse model of depressive-like behaviors induced by repeated peripheral administration of corticosterone. Microglia in the prefrontal cortex of mice were profiled by bulk RNA sequencing, which exhibited increased expression of inflammatory markers. In addition, single-cell RNA sequencing further identified distinct molecular patterns of microglial responses. Moreover, we revealed the up-regulation of Pu.1 and Irf8, the two central transcription factors governing microglia-mediated inflammation, in the prefrontal cortex and hippocampus of corticosterone-treated mice, which similarly occurred in depressed patients' microglia. These results have established the inflammatory signatures of microglia in the mouse model recapitulating hypercortisolemia-related depression, providing new insights into developing diagnostic and therapeutic strategies.

2024-10-01 | GSE274360 | GEO

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