Figure 8
Model for the regulation of spine density by CaMKIIα activity. In the initial stage of spine formation, CaMKIIα has not yet been recruited to spines and Rap1 is not activated. In the subsequent step (arrow 1), glutamate receptors and CaMKIIα molecules begin to accumulate in spines, leading to the phosphorylation of synGAP, the dispersion of synGAP from postsynaptic sites, and the enhancement of local Rap1 activity. Increased Rap1 activity negatively regulates spine formation, possibly by destabilizing F-actin in spines (arrow 2). At a later stage, LTP-like spine-promoting mechanisms begin to operate (arrow 3).
