Extracellular matrix protein reelin regulate dendritic spine density through CaMKIIβ

• Reelin increased dendritic spine density by altering the puncta number of synaptophysin and PSD-95.
• Reelin increased the levels of CaMKIIβ in primary hippocampal neurons.
• CaMKIIβ shRNA transfected primary hippocampal neurons prevented the effects of Reelin on dendritic spine density.

Reelin, an extracellular matrix protein, plays an important role in brain development as well as synaptic plasticity. Interestingly, several recent studies have found that Reelin is important for dendritic spine formation in vitro and in vivo. However, the molecular mechanism by which Reelin regulates the dendritic spine density has not been studied well yet. In this study, we found that exogenous Reelin treatment was significantly increased the dendritic spine density in the primary hippocampal neurons. In addition, Reelin was increased the puncta numbers of synaptophysin and PSD-95. Moreover, we found that Reelin modulated the levels of CaMKIIβ, and CaMKIIβ siRNA prevented Reelin's effect on the dendritic spine density. Overall, our results are the first to demonstrate that CaMKIIβ might be required to enable Reelin to alter the dendritic spine density.