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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Kainate, NRSE ODNs vs. Kainate, scrambled ODNs]

ABSTRACT: Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were used to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and kainate injections (induced status epilepticus)

ORGANISM(S): Rattus norvegicus

SUBMITTER: Shawn McClelland

PROVIDER: E-GEOD-22897 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, NRSE ODNs]

Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and saline(controls) or kainate injections (induced status epilepticus)

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, scrambled ODNs]

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Kainate, NRSE ODNs vs. Kainate, scrambled ODNs]

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NRSF mediated epigenetic mechanisms of ion channel dysfunction in experimental temporal lobe epilepsy [Control vs. Kainate, NRSE ODNs]

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Project description:Anti-epileptogenic agents that prevent the development of epilepsy following a brain insult remain the holy grail of epilepsy therapeutics. In order to identify such drugs, it is necessary to first understand the cellular and molecular events that underlie the epileptogenic process, from initial insult to the onset of spontaneous recurrent seizures. We have employed a label-free proteomic approach that allows quantification of large numbers of brain-expressed proteins in a single analysis in the well-established kainate (KA) mouse (C57BL/6J) model of epileptogenesis. In addition, we have incorporated two putative antiepileptogenic drugs, PSD95BP and 1400W, to give an insight into how such agents might ameliorate the epileptogenesis. The test drugs were administered at appropriate time-points after induction of status epilepticus (SE) and animals were euthanized at 7 days, their hippocampi removed, and subjected to LC-MS/MS analysis. A total of 2,579 proteins were identified; their normalized abundance was compared between treatment groups using ANOVA, with correction for multiple testing by false discovery rate. Significantly altered proteins were subjected to gene ontology analysis to look for enrichment of specific biological processes. KA-induced SE was most robustly associated with an increase in proteins involved in neuroinflammation, oxidative stress, cell-cell interactions and synaptic plasticity. Treatment with PSD95BP (Tat-NR2B9c) or an iNOS inhibitor, 1400W modulated several of these proteins. Our observations require validation in a larger-scale investigation, with candidate proteins explored in more detail. Nevertheless, this study has identified several mechanisms by which epilepsy might be developed and several targets for novel drug development.

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