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The Journal of Neuroscience, December 1, 2004, 24(48):10858-10867; doi:10.1523/JNEUROSCI.1022-04.2004

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Cellular/Molecular
Nuclear Calcium/Calmodulin Regulates Memory Consolidation

Klara Limbäck-Stokin,¹ Edward Korzus,^1,2 Rie Nagaoka-Yasuda,^1,3 and Mark Mayford^1,2,3

¹Institute for Childhood and Neglected Diseases and Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, ²Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, and ³Genomics Institute of the Novartis Research Foundation, La Jolla, California 92121

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.

Key words: calcium/calmodulin; memory; consolidation; transgenic; CREB; tetracycline

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Received March 19, 2004; revised August 2, 2004; accepted August 25, 2004.

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