Nf-kappab Regulates Spatial Memory Formation and Synaptic Plasticity Through Protein Kinase A/Creb Signaling.
From: Universität Witten/Herdecke, Institut für Neurobiochemie, Stockumer Strasse 10, D-58448 Witten, Germany. c.kaltschmidt@uni-wh.de
Molecular and cellular biology
- Publish Date: Apr 2006
- ISSN: 0270-7306
- Volume: 26
- Issue: 8
- Pages: 2936-46
- Medium: Print
- Language: English
- Citation (JAMA): Kaltschmidt Barbara, Ndiaye Delphine, Korte Martin, et al. Nf-kappab Regulates Spatial Memory Formation and Synaptic Plasticity Through Protein Kinase A/Creb Signaling.. Mol. Cell. Biol. Apr 2006;26:2936-46
Abstract
Synaptic activity-dependent de novo gene transcription is crucial for long-lasting neuronal plasticity and long-term memory. In a forebrain neuronal conditional NF-kappaB-deficient mouse model, we demonstrate here that the transcription factor NF-kappaB regulates spatial memory formation, synaptic transmission, and plasticity. Gene profiling experiments and analysis of regulatory regions identified the alpha catalytic subunit of protein kinase A (PKA), an essential memory regulator, as a new NF-kappaB target gene. Consequently, NF-kappaB inhibition led to a decrease in forskolin-induced CREB phosphorylation. Collectively, these results disclose a novel hierarchical transcriptional network involving NF-kappaB, PKA, and CREB that leads to concerted nuclear transduction of synaptic signals in neurons, accounting for the critical function of NF-kappaB in learning and memory.
Mesh Headings (Keywords): Animals, Cells, Cultured, Cyclic AMP Response Element-Binding Protein, Cyclic AMP-Dependent Protein Kinases, Electrophoretic Mobility Shift Assay, Electrophysiology, Forskolin, Gene Expression Profiling, Hippocampus, Immunohistochemistry, Male, Memory, Mice, Mice, Transgenic, NF-kappa B, Phosphorylation, Synaptic Transmission
Check for Full Text / PubMed Unique Identifier (PMID): 16581769
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