Faculty Collaboration Database

Neurogranin regulates CaM dynamics at dendritic spines. Sci Rep 2015 Jun 18;5:11135

Date

06/19/2015

Pubmed ID

26084473

Pubmed Central ID

PMC4471661

DOI

10.1038/srep11135

Scopus ID

2-s2.0-84934900868 (requires institutional sign-in at Scopus site)   43 Citations

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.

Author List

Petersen A, Gerges NZ

Author

Nashaat Gerges PhD Chair, Professor in the School of Pharmacy Administration department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Calcium Signaling
Calmodulin
Dendritic Spines
Gene Expression
Hippocampus
Microscopy, Confocal
Neurogranin
Phosphorylation
Protein Binding
Rats
Synapses