File:Transient vs. Sustained Dendritic Spine Growth following High-Frequency Stimulation.jpg

English: Calcium influx through NMDA receptors activates CAMKII. CAMKII then regulates several other signaling cascades that modulate the activity of the actin-binding proteins cofilin and profilin. These cascades can be divided into two primary pathways, the RhoA and Cdc42 pathways, which are mediated primarily by these members of the Rho family of GTPases. In the transient stage, the signaling cascade caused by synaptic activity results in LIMK1 phosphorylating ADF/cofilin via both the RhoA and Cdc42 pathways, which in turn inhibits the depolymerization of F-actin and increases the volume of the dendritic spine drastically while also inducing LTP. Contrastingly, the sustained stage is focused more on activating the RhoA pathway, which ultimately results in a higher concentration of profilin, which prevents additional polymerization of actin and decreases the size of the dendritic spine from the transient stage, though still allows it to remain at an elevated level compared to an unpotentiated spine.