Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA104753 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Temporal analysis of hippocampus in kainate-induced seizures. Koh-7K08NS002068-05-3
| PRJNA104751 | ENA
Project description:Temporal analysis of P15 and P30 hippocampi in kainate-induced seizures
| PRJNA94893 | ENA
Project description:This study aims to investigate age-specific, time-dependent changes in gene expression that may underlie the priming effect of early-life seizures by looking at the sequence of gene expression patterns in the hippocampus at various times following Kainate induced seizures at postnatal day (P) 15.
2007-10-27 | E-GEOD-1156 | biostudies-arrayexpress
Project description:This study aims to investigate age-specific, time-dependent changes in gene expression that may underlie the priming effect of early-life seizures by looking at the sequence of gene expression patterns in the hippocampus at various times following Kainate induced seizures at postnatal day (P) 15. Keywords: other
2004-03-29 | GSE1156 | GEO
Project description:Mesial temporal lobe epilepsy (MTLE) is the most common medically refractory epilepsy syndrome; kainic acid (KA) induced seizures have been studied as a MTLE model as limbic seizures produced by systemic injections of KA result in a distinctive pattern of neurodegeneration in the hippocampus that resembles human hippocampal sclerosis. In our "2-hit" seizure model, animals subjected to seizures during week 2 of life become more susceptible to seizures later in life and sustain extensive hippocampal neuronal injury after second KA seizures in adulthood. Using high-density oligonucleotide gene arrays, we began to elucidate the molecular basis of this priming effect of early-life seizures and of the age-specific neuroprotection against seizure-induced neuronal injury. We seek to identify target genes for epileptogenesis and cell death by selecting transcripts that are differentially regulated at various times in the P15 and P30 hippocampus. To screen for and identify candidate genes responsible for epileptogenesis and seizure-induced cell death. We hypothesize that active process of cell death signaling and long-term synaptic changes leading to chronic epilepsy is mediated by distinct transcriptional responses in mature brain that are different from those in immature brain. We will select for transcripts that are highly regulated at 1, 6, 24, 72 and 240 hours (h) after KA-induced seizures at P30 compared to P15. These differentially regulated genes will serve as potential target genes for therapeutic intervention. Highly regulated genes identified in our array analysis will then be confirmed by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Causative roles of select genes will be directly tested by gene silencing using RNA interference technology or by gene delivery using viral vectors.
2008-06-11 | E-GEOD-1834 | biostudies-arrayexpress
Project description:It has long been established that in neurological disease models, KA is a potent excitotoxin, mediating acute limbic seizures and long-term morphologic changes in the hippocampus, which are hallmark characteristics seen in temporal lobe epilepsy (i.e. mossy-fiber sprouting, neuronal loss, and reactive gliosis; Ben-Ari and Cossart, 2000). Persuasive clinical evidence employing KA receptor agonists further substantiate the detrimental effects of kainate. For instance, domoic acid (a structural analogue of kainate) has been found to inflict detrimental damage the hippocampus through a real-life outbreak incident of toxic encephalopathy caused by ingestion of mussels contaminated with domoic acid (Pearl et al., 1990). A total of 15 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 100uM kainate over a time-course of 5h, 15h and 24h (n=3) in addition to the vehicle control (n=6).
2013-12-31 | E-GEOD-22994 | biostudies-arrayexpress
Project description:It has long been established that in neurological disease models, KA is a potent excitotoxin, mediating acute limbic seizures and long-term morphologic changes in the hippocampus, which are hallmark characteristics seen in temporal lobe epilepsy (i.e. mossy-fiber sprouting, neuronal loss, and reactive gliosis; Ben-Ari and Cossart, 2000). Persuasive clinical evidence employing KA receptor agonists further substantiate the detrimental effects of kainate. For instance, domoic acid (a structural analogue of kainate) has been found to inflict detrimental damage the hippocampus through a real-life outbreak incident of toxic encephalopathy caused by ingestion of mussels contaminated with domoic acid (Pearl et al., 1990).
2013-12-31 | GSE22994 | GEO
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