Document Detail


Hippocampal transcriptome after status epilepticus in mice rendered seizure damage-tolerant by epileptic preconditioning features suppressed calcium and neuronal excitability pathways.
MedLine Citation:
PMID:  18804535     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Preconditioning brain with a sub-lethal stressor can temporarily generate a damage-refractory state. Microarray analyses have defined the changes in hippocampal gene expression that follow brief preconditioning seizures, but not the transcriptome after a prolonged and otherwise injurious seizure in previously preconditioned brain. Presently, microarray analysis was performed 24 h after status epilepticus in mice that had received previously either seizure preconditioning (tolerance) or sham-preconditioning (injury). Transcriptional changes in the hippocampal CA3 subfield of >or=2 fold were detected for 1357 genes in the tolerance group compared to a non-seizure control group, with 54% up-regulated. Of these regulated genes, 792 were also regulated in the injury group. Among the remaining 565 genes regulated only in tolerance, 73% were down-regulated. Analysis of the genes differentially suppressed in tolerance identified calcium signaling, ion channels and excitatory neurotransmitter receptors, and the synapse as over-represented among pathways, functions and compartments. Finally, 12 days continuous EEG recordings determined mice with induced tolerance had fewer spontaneous electrographic seizures compared to the injury group. Our data suggest the transcriptional phenotype of neuroprotection in tolerance may be dictated by the biology of the preconditioning stressor, functions by transcriptional reduction of vulnerability to excitotoxicity, and has anti-epileptogenic effects.
Authors:
Eva M Jimenez-Mateos; Seiji Hatazaki; Martha B Johnson; Carmen Bellver-Estelles; Genshin Mouri; Caroline Bonner; Jochen H M Prehn; Robert Meller; Roger P Simon; David C Henshall
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-09-04
Journal Detail:
Title:  Neurobiology of disease     Volume:  32     ISSN:  1095-953X     ISO Abbreviation:  Neurobiol. Dis.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-11-28     Completed Date:  2009-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9500169     Medline TA:  Neurobiol Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  442-53     Citation Subset:  IM    
Affiliation:
Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin 2, Ireland.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Calcium / metabolism*
Cell Death / genetics
Cycloheximide / pharmacology
Electroencephalography
Gene Expression Profiling
Gene Expression Regulation
Hippocampus / injuries,  pathology,  physiopathology*
Ion Channels / genetics
Kainic Acid / pharmacology
Long-Term Potentiation
Mice
Microarray Analysis
Neurons / physiology*
Oligonucleotide Array Sequence Analysis
Receptors, Neurotransmitter / genetics
Status Epilepticus / genetics,  pathology,  physiopathology*
Grant Support
ID/Acronym/Agency:
NS46290/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Receptors, Neurotransmitter; 487-79-6/Kainic Acid; 66-81-9/Cycloheximide; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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