Journal
NEUROSCIENCE LETTERS
Volume 400, Issue 1-2, Pages 177-180Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2006.02.063
Keywords
c-fos; brain-derived neurotrophic factor; kainic acid; hippocampus; immunohistochemistry; in situ hybridization
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Funding
- NIDA NIH HHS [DA13786, DA11005] Funding Source: Medline
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Excess neuronal excitation by glutamate induces neuron cell death, which may contribute to the pathogenesis of acute brain injuries and neurodegenerative diseases. Our previous Studies using a mouse with hippocampal c-fos gene deletion showed that c-fos regulates neuronal excitability and excitotoxicity. Moreover. a delayed induction of brain-derived neurotrophic factor (BDNF) protein expression in response to kainic acid (KA) treatment vas found in c-fos mutant mice compared to wildtype controls, suggesting that c-fos is important in the temporal control of BDNF induction. To further investigate mechanisms of in vivo regulation of c-fos on BDNF expression, we studied the expression of BDNF mRNA and its colocalization with c-Fos protein in the hippocampal formation in the presence and absence of KA. By in situ hybridization, we observed that the c-fos mutant and wildtype mice exhibited similar basal expression of BDNF in the absence of KA. In contrast, the KA-induced BDNF mRNA levels were significantly different in wildtype and c-fos mutant mice in CA3 and dentate gyrus regions. Our findings indicate that c-fos regulates expression of BDNF in distinct neuron populations of the hippocampal formation in vivo. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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