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Impact of schizophrenia GWAS loci converge onto distinct pathways in cortical interneurons vs glutamatergic neurons during development

ABSTRACT: Genome binding/occupancy profiling was carried out by high throughput sequencing in human developmental cortical interneurons and developmental glutamatergic neurons derived from healthy control vs schizophrenia iPSCs

ORGANISM(S): Homo sapiens

PROVIDER: GSE184165 | GEO | 2022/12/21

REPOSITORIES: GEO

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Pilot transcriptome analysis of human iPSC-derived healthy control vs. schizophrenia cortical interneurons

Project description:We report specific changes in schizophrenia developmental interneurons by genome-wide transcriptome analysis.

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Genome-wide transcriptional analysis of human iPSC-derived healthy control vs. schizophrenia cortical interneurons.

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Genome-wide transcriptional analysis of human iPSC-derived healthy control vs. schizophrenia cortical interneurons

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Genome-wide transcriptome analysis of human iPSC-derived healthy control vs schizophrenia developmental glutamatergic neurons.

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Common schizophrenia risk variants are implicated in the function of glutamatergic neurons

Project description:The epigenome of human brain cells encompasses key information in understanding brain function in both healthy and diseased states. To further explore this, we used ATAC-seq to profile chromatin structure in four distinct populations of cells (glutamatergic neurons, GABAergic neurons, oligodendrocytes, and microglia/astrocytes), from three different regions of the brain. Chromatin accessibility was found to vary vastly by cell type and, more moderately, by brain region, with glutamatergic neurons showing the greatest regional variability. Transcription factor footprinting pointed to cell-specific transcriptional regulators and inferred cell-specific regulation of protein coding genes, long intergenic noncoding RNAs, and microRNAs. In vivo transgenic mouse experiments validated the cell type specificity of a number of human-derived regulatory sequences. Open chromatin regions in glutamatergic neurons were enriched for neuropsychiatric risk variants, particularly those associated with schizophrenia. Combining differential chromatin accessibility analysis using ATAC-seq data from bulk tissue increased our statistical power to confirm glutamatergic neurons as the cell type most affected in schizophrenia. Jointly, these findings illustrate the utility of studying the cell type specific epigenome in complex tissues such as the human brain and implicate an association among chromatin accessibility in glutamatergic neurons and genetic risk for schizophrenia.

2020-08-20 | GSE143666 | GEO

Genome-wide transcriptional analysis of human iPSC-derived healty control vs. schizophrenia cortical interneurons.

Project description:We report down-regulation of protocadeherins in schizophrenia interneurons by genome-wide transcriptome analysis.

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ChIP-seq profile of iPSC-derived human developmental cortical interneurons

Project description:ChIP-seq was carried out by high throughput sequencing in human developmental cortical interneurons derived from healthy control vs schizophrenia iPSCs

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Project description:Common schizophrenia risk variants are implicated in the function of glutamatergic neurons

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Genome-wide transcriptome analysis of human iPSC-derived migratory cortical interneurons.

Project description:We report changes of gene expression in migratory cortical interneurons derived from healthy control vs schizophrenia iPSCs by genome-wide transcriptome analysis.

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Project description:Unilateral Traumatic Brain Injury (TBI) causes functional disturbances of the neuronal networks spreading even to the undamaged cortical hemisphere. The phenomenon, referred to as transhemispheric diaschisis, is suggested to be mediated by an imbalance of the strength of glutamatergic, excitatory vs. GABAergic, inhibitory neurotransmission. Here we present evidence that a switch in expression of α Subunits of pore-forming L-Type voltage-gated calcium channels (VGCC), by an expression of CaV1.3 and simultaneous ablation of CaV1.2 in GABAergic interneurons could balance early cortical disturbances manifested as contralateral hyperexcitability in the early phase after TBI. The switch of the VGCC alpha Subunits in GABAergic interneurons was detected using the GAD67-GFP (Glutamate Decarboxylase 67 – Green Fluorescent Protein) Knock-in mouse line. Mice received a TBI with a Controlled Cortical Impact (CCI) to the primary motor and somatosensory cortex at postnatal day 19-21 under anesthesia in vivo. Single GFP+ interneurons located in the undamaged, contralateral cortex were isolated by Fluorescence-Activated Cell Sorting (FACS) and further analyzed by Mass Spectrometry (MS). The switch was associated with an increased excitability of Somatostatin (SST) interneurons and extracellular network activity in acute brain slices in Microelectrode Array (MEA) recordings, which could be restored in presence of isradipine (100 nM), which selectively blocks CaV1.3-containing VGCCs. These data suggest that a switch in alpha.subunits of VGCCs expressed on SST-positive interneurons stabilizes early hyperactivity of the contralateral cortical network at 72 h after TBI, thereby promoting an adaptive mechanism to counterbalance post-traumatic hyperexcitabilty that might lead to epileptogenesis.

2022-01-03 | PXD023551 | Pride

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