| First Author | Limbäck-Stokin K | Year | 2004 |
| Journal | J Neurosci | Volume | 24 |
| Issue | 48 | Pages | 10858-67 |
| PubMed ID | 15574736 | Mgi Jnum | J:94809 |
| Mgi Id | MGI:3521549 | Doi | 10.1523/JNEUROSCI.1022-04.2004 |
| Citation | Limback-Stokin K, et al. (2004) Nuclear calcium/calmodulin regulates memory consolidation. J Neurosci 24(48):10858-67 |
| abstractText | 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. |
