L-type voltage-gated calcium channels (L-VGCCs) are upstream of competing pathways that promote or inhibit dendritic growth. How L-VGCCs achieve signaling specificity remains unknown. We hypothesize that modulation of ICaL determines distinct processes controlling dendritic growth. To address this issue fluorescence imaging experiments were conducted on young murine cultured hippocampal neurons. Our findings show that dihydropyridine (DHP) blockers suppress dendritic growth and overexpression of DHP-insensitive CaV1.2 mutant prevented this effect, indicating that CaV1.2 is the channel isoform underpinning dendritic development. Conversely, the channel agonist FPL 64176 enhanced the dendritic complexity whereas BayK-8644 was ineffective. Consistent with the notion that CamKII signaling restricts dendritic growth, quantitative immunofluorescence revealed that Bay-K 8644 increased phosphorylated CamKII levels (pCamKII) while FPL 64176 didn’t. We show that both BayK-8644 and FPL 64176 increase ICaL density but only FPL 64176 slows ICaL inactivation. Wider ICaL and inhibition of current inactivation were mimicked by overexpressing the channel interactor STAC2-HA. Consistently, this augmented dendritic growth and failed to recruit CamKII signaling. Furthermore, FPL 64176 reduced the surface levels of CaV1.2 in biotinylation assays, suggesting that fewer available channels may constrain pCamKII and facilitate dendritic growth. To this aim, our current results show that shRNA-induced CaV1.2 knocking down reduces pCaMKII and tends to promote dendritic growth in basal conditions. Altogether, our data suggest that CaV1.2 ICaL underlies the dendritic growth and that regulation of ICaL kinetics and amplitude may modulate CaV1.2 membrane levels restricting CaMKII signaling and facilitating dendritic growth.