Levetiracetam normalized E/I imbalance in the hippocampus after cortical stroke in aged mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1008587 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25743120.fastq.gz | Fastqsanger.gz | |||
| SRR25743121.fastq.gz | Fastqsanger.gz | |||
| SRR25743122.fastq.gz | Fastqsanger.gz | |||
| SRR25743123.fastq.gz | Fastqsanger.gz | |||
| SRR25743124.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
Similar Datasets
Project description:Stroke is a prevalent disorder representing the third leading cause of death and major cause of disability. Post-stroke epilepsy (PSE) has been recognized as a common clinical issue after stroke, accounting for 30-40% of the causes of epilepsy among older adults. In this study, we determined GABAA receptor-mediated seizure susceptibility after PT cerebral stroke in aged mice. Young adult mice around 10 weeks of age are widely used in stroke experiments. However, as most strokes are diagnosed in the elderly and PSE has been recognized as a common clinical incidence after stroke, we utilized photothrombosis (PT) model of cerebral ischemia and examined seizure susceptibility. To investigate in vitro drug-induced seizure susceptibility (E/I imbalance) of GABAA receptor antagonist, gabazine (GZ), voltage-sensitive dye (VSD) imaging techniques were used in hippocampal brain slices. One month after PT stroke, in vivo aged PT stroke mice exhibited severe convulsive seizures (late-onset). in vitro GZ-induced E/I imbalance in hippocampus of aging mice increased compared to young adults. In addition, Anti-seizure medication (levetiracetam) normalized in vitro GZ-induced E/I imbalance in hippocampus of aging mice. These findings exhibited that GABAA receptor-mediated seizures susceptibility (E/I imbalance) in hippocampus after cortical PT stroke in aging mice, but not in young adults.
2023-11-27 | GSE241525 | GEO
Project description:Neurogenesis after stroke compounded with amyloid beta plaques around the cerebral vasculature has implications in delaying tissue recovery. We used single cell RNA sequencing (scRNA-seq) to understand the cellular interactions in the hippocampus during post-stroke recovery with CAA.
2024-05-26 | GSE266033 | GEO
Project description:Stroke is a prevalent disorder representing the third leading cause of death and major cause of disability. Post-stroke epilepsy (PSE) has been recognized as a common clinical issue after stroke, accounting for 30-40% of the causes of epilepsy among older adults. In this study, we determined GABAA receptor-mediated seizure susceptibility after PT cerebral stroke in aged mice. Young adult mice around 10 weeks of age are widely used in stroke experiments. However, as most strokes are diagnosed in the elderly and PSE has been recognized as a common clinical incidence after stroke, we utilized photothrombosis (PT) model of cerebral ischemia and examined seizure susceptibility and brain injury using combined behavioral (video) and EEG monitoring and histological (MRI) assessments. To investigate GABAA receptor-mediated convulsive/non-convulsive seizures, lower-doses of pentylenetetrazol (PTZ) was injected. PTZ susceptibility in aging mice increased compared to young adults. One month after PT stroke, aged PT stroke mice exhibited severe convulsive seizures (late-onset). These findings exhibited the increase of GABAA receptor-mediated seizures susceptibility in PT stroke aging mice, but not in young adults.
2023-11-27 | GSE241528 | GEO
Project description:To explore the inner mechanism of components and combination of Qingkailing inject fluid,compare the gene express and pharmacological pathway after experimental stroke mice.
2010-12-30 | E-TABM-662 | biostudies-arrayexpress
Project description:Immune imbalance in the human hippocampus in PTSD revealed by single-nucleus transcriptomics
| PRJNA1378836 | ENA
Project description:Post-traumatic stress disorder (PTSD) is increasingly recognized as a neuroimmune disorder in which disrupted neuron–glia interactions contribute to long-term cognitive and emotional dysfunction. However, the cellular and molecular basis of immune imbalance in the human hippocampus remains unclear.We performed single-nucleus RNA sequencing on postmortem hippocampal tissues from donors with PTSD and matched controls, identifying 10 major cell types, with particular emphasis on neurovascular and glial populations. Differential expression, pathway enrichment, pseudotime trajectory, and cell–cell communication analyses were applied to characterize cellular and molecular alterations.PTSD samples showed prominent activation of stress-response and inflammatory signaling across astrocytes, microglia, endothelial cells, and mural cells. Microglia and astrocytes underwent robust transcriptional reprogramming with enrichment of immune-related pathways, while endothelial and mural cells exhibited inflammation and impaired blood–brain barrier homeostasis. Trajectory analyses revealed altered state transitions in astrocytes and microglia, indicating dysregulated responses to stress. Furthermore, cell–cell communication analysis uncovered markedly reduced interactions between astrocytes or microglia with excitatory neurons and oligodendrocyte lineage cells, particularly involving stress- and inflammation-related ligand–receptor pairs.These findings demonstrate that PTSD is characterized by immune imbalance at both cellular and intercellular levels, driven by maladaptive glial activation and disrupted neuron–glia communication. Our study provides a comprehensive single-cell atlas of the hippocampal neuroimmune landscape in PTSD and highlights dysfunctional glial–neuronal interactions as a central mechanism underlying disease pathogenesis.
2025-12-17 | GSE313257 | GEO
Project description:Ischemic stroke is one of the leading causes of mortality and major healthcare and economic burden. It is a well recognized disease of aging, yet it is unclear how the age-dependent vulnerability occurs and what are the underlying mechanisms. To address these issues, we performed a comprehensive RNA-Seq analysis of aging, ischemic stroke and their interaction using a model of permanent middle cerebral artery occlusion (MCAO) in 3 and 18 month old female mice. We assessed differential gene expression across injury status and age, estimated cell type proportion changes, assayed the results against a range of transcriptional signatures from the literature and performed unsupervised co-expression analysis, identifying modules of genes with varying response to injury. We uncovered selective vulnerability of neuronal populations and increased activation of type-I interferon (IFN-I) signaling and several other inflammatory pathways in aged mice. We extended these findings via targeted expression analysis in tissue as well as acutely purified cellular populations to show differential temporal dynamics of IFN-I signaling between age groups and contribution of individual cell types. Together, these results paint a picture of ischemic stroke as a complex age related disease and provide insights into interaction of aging and stroke on cellular and molecular level.
2020-06-17 | GSE137482 | GEO
Project description:Purpose: Signaling pathways mediated by microRNAs (miRNAs) represent one of the mechanisms that regulate stroke progression and recovery. The goal of this study is to investigate miRNA expression signatures in freshly removed human stroke brain tissue. Methods: Human brain samples (5 stroke and 3 non-stroke samples) obtained at 48-72 hours after stroke onset during craniectomy and stroke-ectomy, were subjected to histopathological and immunofluorescence microscopy analyses. NGS sequencing was performed by Qiagen company and analyses were carried out using QIAseq miRNA Quantification workflow and RNA-seq Analysis tools within CLC Genomics Workbench (version 20.0.2). Reads were normalized for expression analysis using trimmed mean of M-values method (TMM). miRNA profiling was performed using the EdgeR in Bioconductor package. Whole transcriptome RNA-sequencing Analysis: The unmapped reads from the NGS miRNA analysis were extracted, deduplicated and mapped to the genome. Gene expressions were calculated by counting number of reads mapping to the annotated gene loci. Human miR-155 Targets RT2 Profiler PCR Array (Qiagen) was performed using 3 RNA samples per stroke and control groups. The PCR Array Data analysis was performed using an automated PCR Analysis Web Portal and GeneGlobe Data Analysis (Qiagen). Results: Human stroke brain tissue was characterized by classic ischemic changes, including significant neuronal and vascular damage, and prominent edema. The absence of monocytes and notable neutrophil infiltration indicated the early stage of leukocyte response to ischemia. miRNA NGS analysis detected 36 miRNAs with significantly aberrant expression in stroke tissue, as compared to non-stroke samples. Of these miRNAs, 19 were previously identified in stroke patient blood and CSF, while dysregulation of 16 miRNAs was newly detected in this study. Bioinformatics pathway enrichment analysis demonstrated a strong association of the identified miRNAs with stroke-related biological processes and signaling pathways Conclusions: Dysregulated miRNAs detected in our study could be regarded as potential candidates for biomarkers and/or targets for therapeutic intervention. The obtained data will serve for better understanding of the molecular basis of stroke and provide valuable information for the future functional studies in the experimental models of stroke.
2020-07-29 | GSE155257 | GEO
Project description:Single cell gene expression from the hippocampus of 5xFAD mice subjected to stroke
| PRJNA1105371 | ENA
Project description:The goals of this study are to compare hippocampus transcriptome profiling (RNA-seq) after cerebral ischemia for 2 h in mouse stroke model
2026-01-23 | GSE165384 | GEO