Document Detail

Role of c-Fos protein on glutamate toxicity in primary neural hippocampal cells.
MedLine Citation:
PMID:  16075465     Owner:  NLM     Status:  MEDLINE    
The hippocampus is extremely sensitive to microenvironmental signals and toxic events, including massive glutamate release. Despite the extensive literature related to the cascade of molecular events triggered in postsynaptic neurons, the distinction between proapoptotic and survival pathways is still being discussed. In this study, we have investigated the role of c-Fos in glutamate-induced toxicity in primary cultures of hippocampal neurons by using antisense oligonucleotide (ASO) technology. Exposure of cells (5 days in vitro; DIV) to glutamate 0.5 mM for 24 hr caused massive nuclear alteration. An increase in the number of caspase-3-positive cells was also observed 24 hr after glutamate treatment. The expression of c-fos and c-jun immediate-early genes was increased 30 min after glutamate exposure. The study of c-Fos and c-Jun protein expression revealed an increase in the number of cells positive for both antibodies. To investigate whether the expression of c-Fos protein after glutamate treatment was related to cell death activation or cell survival pathways, cells were exposed to 5 microM of c-fos ASO at 4 DIV, 24 hr before glutamate treatment. The presence of the ASO in the medium significantly decreased the number of altered nuclei, and this was associated with a significant reduction in the number of c-Fos-positive cells after glutamate treatment. Exposure of cells to the c-fos ASO under the conditions described above decreased caspase-3 immunostaining induced by glutamate. These results suggest that the synthesis of c-Fos protein after glutamate exposure favors cell death pathway activation in which caspase-3 is also involved.
M Fernandez; S Pirondi; T Antonelli; L Ferraro; L Giardino; L Calzà
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuroscience research     Volume:  82     ISSN:  0360-4012     ISO Abbreviation:  J. Neurosci. Res.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-10-03     Completed Date:  2006-02-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7600111     Medline TA:  J Neurosci Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  115-25     Citation Subset:  IM    
Copyright Information:
(c) 2005 Wiley-Liss, Inc.
Department of Veterinary Morphophysiology and Animal Production (DIMORFIPA), University of Bologna, Bologna, Italy.
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MeSH Terms
Analysis of Variance
Bisbenzimidazole / diagnostic use
Blotting, Northern / methods
Caspase 3
Caspases / metabolism
Cell Count / methods
Cells, Cultured
Drug Interactions
Embryo, Mammalian
Gene Expression / drug effects
Genes, jun / genetics
Glutamic Acid / toxicity*
Hippocampus / cytology*
Immunohistochemistry / methods
Neurons / drug effects*,  physiology
Oligonucleotides, Antisense / pharmacology
Proto-Oncogene Proteins c-fos / chemistry,  physiology*
RNA, Messenger / metabolism
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction / methods
Time Factors
Reg. No./Substance:
0/Oligonucleotides, Antisense; 0/Proto-Oncogene Proteins c-fos; 0/RNA, Messenger; 23491-44-3/Bisbenzimidazole; 56-86-0/Glutamic Acid; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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

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