Nuclear Calcium/Calmodulin Regulates Memory Consolidation

Autor: Rie Nagaoka-Yasuda, Klara Limbäck-Stokin, Edward Korzus, Mark Mayford
Rok vydání: 2004
Předmět:
Male
MAPK/ERK pathway
Calmodulin
Long-Term Potentiation
Active Transport
Cell Nucleus
Mice
Transgenic
Motor Activity
Hippocampal formation
Biology
Hippocampus
Mice
Memory
Seizures
Ca2+/calmodulin-dependent protein kinase
Avoidance Learning
Animals
Calcium Signaling
Phosphorylation
Cyclic AMP Response Element-Binding Protein
Freezing Reaction
Cataleptic
Maze Learning
Promoter Regions
Genetic
Cell Nucleus
Memory Disorders
General Neuroscience
Genes
fos
Recognition
Psychology
Long-term potentiation
Mice
Inbred C57BL
Gene Expression Regulation
Doxycycline
Calcium-Calmodulin-Dependent Protein Kinases
Exploratory Behavior
biology.protein
Conditioning
Operant
Calcium
Calmodulin-Binding Proteins
Female
Memory consolidation
Signal transduction
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Protein Processing
Post-Translational
Neuroscience
Cellular/Molecular
Zdroj: The Journal of Neuroscience. 24:10858-10867
ISSN: 1529-2401
0270-6474
DOI: 10.1523/jneurosci.1022-04.2004
Popis: The neuronal response to a Ca2+stimulus is a complex process involving direct Ca2+/calmodulin (CaM) actions as well as secondary activation of multiple signaling pathways such as cAMP and ERK (extracellular signal-regulated kinase). These signals can act in both the cytoplasm and the nucleus to control gene expression. To dissect the role of nuclear from cytoplasmic Ca2+/CaM signaling in memory formation, we generated transgenic mice that express a dominant inhibitor of Ca2+/CaM selectively in the nuclei of forebrain neurons and only after the animals reach adulthood. These mice showed diminished neuronal activity-induced phosphorylation of cAMP response element-binding protein, reduced expression of activity-induced genes, altered maximum levels of hippocampal long-term potentiation, and severely impaired formation of long-term, but not short-term, memory. Our results demonstrate that nuclear Ca2+/CaM signaling plays a critical role in memory consolidation in the mouse.
Databáze: OpenAIRE
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