© 2000 - 2011 LIN - Leibniz Institut für Neurobiologie Magdeburg

LIN: Forschungsabteilungen > Akkustik, Lernen, Sprache > Unterpunkt Ebene 3 > Unterpunkt Ebene 4

Titel: LIN Layout

Home   Print Search:
Facebook YouTube
Staff Links Sitemap

 Molecular mechanism of plasticity (AG Kreutz)

 Synapto-dendritic Ca2+

Synapto-dendritic Ca 2+ -Signaling via Caldendrin and its binding partners.

Synapto-dendritic Ca 2+ -Signaling via Caldendrin and its binding partners.

Figure: Synapto-dendritic Ca 2+ -Signaling via Caldendrin and its binding partners.

Caldendrin is a neuronal EF-hand protein that has evolved relatively late during evolution and is found only in higher vertebrates, suggesting that this might be associated with uncommon requirements for somato-dendritic Ca 2+ -signaling of mainly limbic and cortical neurons. In recent years we characterized the putative cellular function of Caldendrin. Part of this effort was the identification of Jacob. Caldendrin, but not Calmodulin, binds Jacob Ca 2+ -dependently at a central -helical region harboring an IQ-like-motif and a bipartite nuclear localization signal. Upon NMDA receptor activation Jacob is recruited to the nucleus resulting in stripping of synaptic contacts and a drastically altered morphology of the dendritic tree. We believe that this defines a novel morphogenetic pathway in limbic and cortical neurons, which links the activity of NMDA receptors to nuclear signaling events involved in modeling the synapto-dendritic input. NMDA receptor-mediated Ca 2+ signals can result in long-lasting changes of synaptic input and dendritic cytoarchitecture. At present our knowledge is sparse how these changes are accomplished at the molecular level.

last update: 2005-11-18 report a bug print this page