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Complement and microglia activation mediates stress-induced synapse loss in layer 2/3 of the medial prefrontal cortex

ABSTRACT: Complement and microglia activation mediates stress-induced synapse loss in layer 2/3 of the medial prefrontal cortex

PROVIDER: PRJNA1138783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29921873.fastq.gz	Fastqsanger.gz
	SRR29921874.fastq.gz	Fastqsanger.gz
	SRR29921875.fastq.gz	Fastqsanger.gz
	SRR29921876.fastq.gz	Fastqsanger.gz
	SRR29921877.fastq.gz	Fastqsanger.gz

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Complement and microglia activation mediates stress-induced synapse loss in layer 2/3 of the medial prefrontal cortex

Project description:Spatially heterogeneous synapse loss is a characteristic of many psychiatric and neurological disorders, but the underlying mechanisms are unclear. Here, we show that spatially-restricted complement activation mediates stress-induced heterogeneous microglia activation and synapse loss localized to the upper layers of the mouse medial prefrontal cortex (mPFC). Single cell RNA sequencing also reveals a stress-associated microglia state marked by high expression of the apolipoprotein E gene (Apoehigh) localized to the upper layers of the mPFC. Mice lacking complement component C3 are protected from stress-induced layer-specific synapse loss, and the Apoehigh microglia population is markedly reduced in the mPFC of these mice. Furthermore, C3 knockout mice are also resilient to stress-induced anhedonia and working memory behavioral deficits. Our findings suggest that region-specific complement and microglia activation can contribute to the disease-specific spatially restricted patterns of synapse loss and clinical symptoms found in many brain diseases.

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KCNH2-3.1 mediates aberrant complement activation to impair hippocampal-medial prefrontal pathway associated with schizophrenia

Project description:Although elevated KCNH2-3.1 potassium channel expression is associated with cognitive dysfunctions and with schizophrenia, little is known about the pathophysiology of synapses in patient neurons and how elevated levels of KCNH2-3.1 potassium channel could lead to synaptic deficits in humans. Here, we identified specific and delayed disruption of hippocampal-mPFC synaptic transmission and connection unexpectedly associated with age-dependent reduction of SERPING1, CFH and CD74 in the KCNH2-3.1 overexpression transgenic mice, and dysfunctional interactions between hippocampus and prefrontal cortex in the fMRI coupling signal during working memory encoding in healthy subjects carrying schizophrenia-associated risk alleles of KCNH2 potassium channel. These three genes are enriched in neurons or microglia, and reduced expression of these genes dysregulates the complement cascade activation underlying impaired synaptic connectivity of hippocampal-mPFC projections. Knockdown of these genes’ expression impairs synapse formation, and replenishing reduced CFH gene expression rescues KCNH2-3.1-induced impaired synaptogenesis. Our results uncover a previously unrecognized role of truncated KCNH2-3.1 potassium channel mediating reduced expression of three genes mentioned above, which enhances aberrant complement cascade activation during development. These results direct an important conceptual advance that truncated KCNH2-3.1 causes synapse loss mediated by abnormally activated complement system, rather than aberrant neuronal firing, may represent the therapeutic targets for a number of patients with schizophrenia.

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KCNH2-3.1 mediates aberrant complement activation to impair hippocampal-medial prefrontal pathway associated with schizophrenia

Project description:KCNH2-3.1 mediates aberrant complement activation to impair hippocampal-medial prefrontal pathway associated with schizophrenia

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Juvenile fluoxetine evoked gene expression changes in the rat medial prefrontal cortex

Project description:To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.

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Postnatal fluoxetine evoked gene expression changes in the rat medial prefrontal cortex

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Molecular mechanism for stress-induced depression assessed by sequencing miRNA and mRNA in medial prefrontal cortex (miRNA)

Project description:Major depressive disorder is a common mood disorder. Chronic stressful life is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stress to neural atrophy remain elusive. Mice were treated by chronic unpredictable mild stress (CUMS) until demonstrating depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. The sequencings of microRNA and mRNA from the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to assess the molecular profiles of major depressive disorder. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deterioration of GABAergic and dopaminergic synapses as well as axonal growth is associated to CUMS-induced depression.

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