CaMKIIβ knockdown decreases store-operated calcium entry in hippocampal dendritic spines

Calcium/calmodulin-dependent protein kinase II (CaMKII) and neuronal store-operated calcium entry (nSOCE) have been implicated in the development of Alzheimer's disease (AD). nSOCE is involved in regulation of dendritic spine shape, particularly in stability of mushroom spines that play role in formation of strong synapses. CaMKII is involved in regulation of induction of long-term potentiation, that is needed for shaping of memory. In the present study, we demonstrated that inhibition of kinase activity of CaMKII by KN-62 decreases nSOCE amplitude in soma of primary hippocampal neurons. We have shown that knockdown of CaMKIIβ leads to the downregulation of nSOCE in dendritic spines. In agreement with previously published data, we have also observed that CaMKIIβ knockdown causes mushroom spine loss in primary hippocampal culture. The effect of CaMKIIβ knockdown on the nSOCE may be associated with a decrease of dendritic spine head size.