Abstract
Structural plasticity of excitatory synapses is a vital component of neuronal development, synaptic plasticity and behavior, and its malfunction underlies many neurodevelopmental and psychiatric disorders. However, the molecular mechanisms that control dendritic spine morphogenesis have only recently emerged. We summarize recent work that has revealed an important connection between calcium/calmodulin-dependent kinases (CaMKs) and guanine-nucleotide-exchange factors (GEFs) that activate the small GTPase Rac (RacGEFs) in controlling dendritic spine morphogenesis. These two groups of molecules function in neurons as a unique signaling cassette that transduces calcium influx into small GTPase activity and, thence, actin reorganization and spine morphogenesis. Through this pathway, CaMKs and RacGEFs amplify calcium signals and translate them into spatially and temporally regulated structural remodeling of dendritic spines.
Original language | English (US) |
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Pages (from-to) | 405-413 |
Number of pages | 9 |
Journal | Trends in Cell Biology |
Volume | 18 |
Issue number | 9 |
DOIs | |
State | Published - Sep 2008 |
Funding
We thank Kevin M. Woolfrey and Caroline Hookway (Northwestern University, http://www.northwestern.edu) for proofreading the manuscript. Research described in the text has been funded by grants from NIH MH 071316, NARSAD and NAAR (to P.P.).
ASJC Scopus subject areas
- Cell Biology