Levetiracetam normalized E/I imbalance in the hippocampus after cortical stroke in aged mice
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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 |
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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: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:It has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000
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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:Selective isolation of total RNA and then whole genome expression analysis of sprouting neurons in peri-infarct cortex of the adult rat after stroke, compared to adjacent neurons that have not sprouted a new connection, in young adult (2 months) and aged (2 years) animals. Two different fluorescent conjugates of the tracer cholera toxin B (CTb), CTb-Alexa 488 and CTb-Alexa 647 (Molecular Probes), were sequentially injected into peri-infarct cortex at the sites of post-stroke axonal sprouting using a picospritzer pressure injection system. After survival periods of 7 days and 21 days (separate cohorts of animals), CTb-647 was injected exactly within CTb-488 injection site. Seven days after the second tracer injection, laser capture microdissection (LCM) was used to capture ~300 neurons for each cell type. Total RNA was isolated from captured cells and subjected to two rounds of T7 amplification.
2010-11-15 | E-GEOD-24441 | biostudies-arrayexpress
Project description:It has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival.
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Project description:Treatments that stimulate neuronal excitability enhance motor performance after stroke.cAMP-response-element binding protein (CREB) is a transcription factor that plays a key rolein neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool ofmotor neurons enhances motor recovery after stroke, while blocking CREB signaling preventsstroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with thehM4di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue,demonstrating that it is possible to turn off and on stroke recovery by manipulating theactivity of CREB-transfected neurons. CREB transfection enhances re-mapping of injuredsomatosensory and motor circuits, and induces the formation of new connections withinthese circuits. CREB is a central molecular node in the circuit responses after stroke that leadto recovery from motor deficits.
2018-06-08 | GSE115527 | 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:Selective isolation of total RNA and then whole genome expression analysis of sprouting neurons in peri-infarct cortex of the adult rat after stroke, compared to adjacent neurons that have not sprouted a new connection, in young adult (2 months) and aged (2 years) animals.
2010-11-15 | GSE24441 | 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.
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