title: Neurogranin regulates CaM dynamics at dendritic spines.
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.
authors.affiliation: Department of Cell Biology, Neurobiology and Anatomy, the Medical College of Wisconsin, Milwaukee, WI 53132.
authors.forename: Amber
authors.initials: A
authors.lastname: Petersen
authors.affiliation: Department of Cell Biology, Neurobiology and Anatomy, the Medical College of Wisconsin, Milwaukee, WI 53132.
authors.forename: Nashaat Z
authors.initials: NZ
authors.lastname: Gerges
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D002147:Calmodulin / Q000235:genetics / Q000378:metabolism*; D049229:Dendritic Spines / Q000378:metabolism*; D015870:Gene Expression; D006624:Hippocampus / Q000378:metabolism; D018613:Microscopy, Confocal; D051579:Neurogranin / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D011485:Protein Binding; D051381:Rats; D013569:Synapses / Q000378:metabolism
chemical_list: D002147:Calmodulin; D051579:Neurogranin