Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277875 | ENA |
REPOSITORIES: ENA
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Project description:Febrile seizures are the most prevalent type of seizures among children up to 5 years of age (2-4% of Western-European children). Complex febrile seizures are associated with an increased risk to develop temporal lobe epilepsy. To investigate short- and long-term effects of experimental febrile seizures (eFS), we induced eFS in highly febrile convulsion-susceptible C57BL/6J mice at post-natal day 10 by exposure to hyperthermia (HT) and compared them to normotherm-exposed (NT) mice. We detected structural re-organization in the hippocampus 14 days after eFS. To identify molecular candidates, which entrain this structural re-organization, we investigated temporal changes in mRNA expression profiles eFS 1 hour to 56 days after eFS. We identified 931 regulated genes and profiled several candidates using in situ hybridization and histology at 3 and 14 days after eFS. This is the first study to report genome-wide transcriptome analysis after eFS in mice. We identify temporal regulation of multiple processes, such as stress-, immune- and inflammatory responses, glia activation, glutamate-glutamine cycle and myelination. Identification of the short- and long-term changes after eFS is important to elucidate the mechanisms contributing to epileptogenesis. Acute, short-, and long-term effects of prolonged febrile seizures on gene expression were investigated in whole hippocampal samples. Samples were taken from C57BL/6J animals one hour (HT n = 8, NT n = 8), three days (HT n = 6, NT n = 6), fourteen days (HT n = 6, NT n = 6), and fifty-six days (HT n = 6, NT n = 6) after HT. Two-channel oligonucleotide microarray analysis was performed with an NT and HT sample on the same chip, including a dye-swap (technical replicate). 3 failed hybridizations were omitted from further analysis.
2016-01-04 | E-GEOD-66762 | biostudies-arrayexpress
Project description:Febrile seizures are the most prevalent type of seizures among children up to 5 years of age (2-4% of Western-European children). Complex febrile seizures are associated with an increased risk to develop temporal lobe epilepsy. To investigate short- and long-term effects of experimental febrile seizures (eFS), we induced eFS in highly febrile convulsion-susceptible C57BL/6J mice at post-natal day 10 by exposure to hyperthermia (HT) and compared them to normotherm-exposed (NT) mice. We detected structural re-organization in the hippocampus 14 days after eFS. To identify molecular candidates, which entrain this structural re-organization, we investigated temporal changes in mRNA expression profiles eFS 1 hour to 56 days after eFS. We identified 931 regulated genes and profiled several candidates using in situ hybridization and histology at 3 and 14 days after eFS. This is the first study to report genome-wide transcriptome analysis after eFS in mice. We identify temporal regulation of multiple processes, such as stress-, immune- and inflammatory responses, glia activation, glutamate-glutamine cycle and myelination. Identification of the short- and long-term changes after eFS is important to elucidate the mechanisms contributing to epileptogenesis.
2016-01-04 | GSE66762 | GEO
Project description:We analyzed the transcriptomic profile of CA3 explants surgically obtained from patients with refractory MTLE (mesial temporal lobe epilepsy) and HS (hippocampal sclerosis) in order to investigate if the initial precipitating injury (IPI) influences the molecular mechanisms underlying this condition. CA3 transcriptomic profile was found to be significantly different in cases with prolonged febrile seizures as the IPI (identified here as FS) when compared to correspondent data from cases without febrile seizure history (NFS). CA3 transcriptomic profiles of FS and NFS were compared in order to identify differentially expressed transcripts
2014-03-31 | E-GEOD-28674 | biostudies-arrayexpress
Project description:We analyzed the transcriptomic profile of CA3 explants surgically obtained from patients with refractory MTLE (mesial temporal lobe epilepsy) and HS (hippocampal sclerosis) in order to investigate if the initial precipitating injury (IPI) influences the molecular mechanisms underlying this condition. CA3 transcriptomic profile was found to be significantly different in cases with prolonged febrile seizures as the IPI (identified here as FS) when compared to correspondent data from cases without febrile seizure history (NFS).
2014-03-31 | GSE28674 | GEO
Project description:Prolonged febrile seizures history (FH) in early childhood is associated with refractory temporal lobe epilepsy (RTLE). FH-RTLE patients may have early (E, before 4 YOA) or late (L, mid-adolescence, early adult life) disease onset. In order to investigate molecular mechanisms underlying E and L forms we compared differentially expressed (DE) and complete (CO) transcriptional networks from hippocampal CA3 explants obtained from E and L patients.
2017-02-09 | GSE57585 | GEO
Project description:Adult neurogenesis continuously contributes new neurons to hippocampal circuits and the programmed death of a subset of immature cells provides a primary mechanism controlling this contribution. Epileptic seizures induce strong structural changes in the hippocampus, including the induction of adult neurogenesis, changes in gene expression and mitochondrial dysfunction, which may all contribute to epileptogenesis. However, a possible interplay between this factors remains largely unexplored. Here, we investigated gene expression changes in the hippocampal dentate gyrus shortly after prolonged seizures induced by kainic acid, focusing on mitochondrial functions. Using comparative proteomics, we identified networks of proteins differentially expressed shortly after seizure induction, including members of the BCL2 family and other mitochondrial proteins. Within these networks, we report for the first time that the atypical BCL2 protein BCL2L13 controls caspase-3 activity and cytochrome C release in neural stem/progenitor cells. This work has been published in Sci Rep. 2015 Jul 24;5:12448. doi: 10.1038/srep12448.
2016-03-14 | PXD003744 | Pride
Project description:This SuperSeries is composed of the following subset Series:; GSE1831: Temporal analysis of P15 hippocampus in kainate-induced seizures. Koh-2K08NS002068-04; GSE1834: Temporal analysis of hippocampus in kainate-induced seizures. Koh-7K08NS002068-05-3 Experiment Overall Design: Refer to individual Series
2007-10-10 | E-GEOD-4236 | biostudies-arrayexpress
Project description:Sudden unexplained death in childhood (SUDC) is death of a child over one year of age that is unexplained after review of clinical history, circumstances of death, and complete autopsy with ancillary testing. Multiple etiologies may cause SUDC, with parallels to sudden unexpected death in epilepsy (SUDEP) in SUDC with a history of febrile seizures, suggesting possible abnormalities in hippocampus and cortex. To identify molecular signaling pathways underlying SUDC, we performed label-free quantitative mass spectrometry on microdissected frontal cortex, hippocampal dentate gyrus (DG), and cornu ammonis (CA1-3) in SUDC (n=19) and pediatric control cases (n=19) with an explained cause of death.
2021-12-23 | MSV000088611 | MassIVE
Project description:Early childhood convulsions have been correlated with hippocampal neuron loss in patients with intractable temporal lobe epilepsy. Using a "two-hit" rat seizure model, we have shown that animals subjected to kainate (KA)- or hypoxia-induced seizures during early postnatal period showed no cell death, yet sustained more extensive neuronal death after second seizures in adulthood. An early life seizure, without causing overt cellular injury, predisposes the brain to the damaging effect of seizures in later life. Cellular and molecular changes that accompany early seizures and that lead to subsequent epileptogenesis and increased susceptibility to seizure-induced neuronal injury, however, remain poorly understood. We propose to investigate age-specific, time-dependent changes in gene expression that may underlie this priming effect of early-life seizures. We will determine the sequence of gene expression pattern in the hippocampus at various times following KA induced seizures at postnatal day (P) 15. Previous studies have shown that AMPA receptor subtype of glutamate receptors play a crucial role in the age-specific vulnerability and in the long-term epileptogenic effects of perinatal hypoxia seizures. We found that AMPA receptor antagonists block the increased susceptibility caused by early life seizures to later seizures and seizure-induced brain damage. We hypothesize that an alteration of AMPA receptor composition is one of many changes caused by early-life seizures that leads to an increase in Ca2+ permeability, which then results in cascade of downstream events and modifies array of gene expression that promote epileptogenesis and susceptibility to neuronal death in later life. We will examine three time points: 1hr, 72 hr, and 15 days following systemic KA-induced seizures at P15 as we have previously observed structural changes within the hippocampus at these time points. Within an hour of KA seizures, a marked swelling of dendrites, disassembly of dendritic microtubules and glycogen depletion are observed by electron microscopy. Within 5 days, basal dendrites of CA3 hippocampal pyramidal neurons show abnormal spine morphology and decreased branching pattern. 15 days after the seizures, aberrant growth of mossy fibers in the CA3 stratum oriens is observed in animals exposed to KA. Ten hippocampi will be pooled from five animals treated with KA (3mg/kg i.p.) and from five littermate controls injected with PBS. Animals will be decapitated and hippocampi will be rapidly dissected from the brain, flash frozen in liquid nitrogen, and stored at -80C until extraction of total RNA, which will be sent to the center. We will provide 4 tissue samples-2 controls and 2 KA, each a pool of five animals - for each time points. Mixing tissues from multiple rats will normalize single nucleotide polymorphisms and tissue heterogeneity.
2008-06-11 | E-GEOD-1831 | biostudies-arrayexpress