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Sci Rep. 2015 Jun 18;5:11135. doi: 10.1038/srep11135.

Neurogranin regulates CaM dynamics at dendritic spines.

Author information

1
Department of Cell Biology, Neurobiology and Anatomy, the Medical College of Wisconsin, Milwaukee, WI 53132.

Abstract

Calmodulin (CaM) plays a key role in synaptic function and plasticity due to its ability to mediate Ca(2+) signaling. Therefore, it is essential to understand the dynamics of CaM at dendritic spines. In this study we have explored CaM dynamics using live-cell confocal microscopy and fluorescence recovery after photobleaching (FRAP) to study CaM diffusion. We find that only a small fraction of CaM in dendritic spines is immobile. Furthermore, the diffusion rate of CaM was regulated by neurogranin (Ng), a CaM-binding protein enriched at dendritic spines. Interestingly, Ng did not influence the immobile fraction of CaM at recovery plateau. We have previously shown that Ng enhances synaptic strength in a CaM-dependent manner. Taken together, these data indicate that Ng-mediated enhancement of synaptic strength is due to its ability to target, rather than sequester, CaM within dendritic spines.

PMID:
26084473
PMCID:
PMC4471661
DOI:
10.1038/srep11135
[Indexed for MEDLINE]
Free PMC Article

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