The NALCN/NCA ion channel is a cation channel related to voltage-gated sodium and calcium channels. NALCN has been reported to be a sodium leak channel, but its precise cellular role and regulation are unclear. We previously found that NCA-1, one of two Caenorhabditis elegans orthologs of NALCN, is activated by a signal transduction pathway acting downstream of the heterotrimeric G protein Gq and the small GTPase Rho. Using a forward genetic screen, here we identify the GPCR kinase GRK-2 as a new player in the Gq-Rho-NCA pathway. We find that GRK-2 acts in the head acetylcholine neurons to positively regulate locomotion and Gq signaling. Using structure-function analysis, we show that the GPCR phosphorylation and membrane association domains of GRK-2 are required for its function. Our genetic epistasis data suggest that GRK-2 acts on the D2-like dopamine receptor DOP-3 to inhibit Go signaling and positively regulate NCA-1 and NCA-2 activity. We also demonstrate that dopamine, through DOP-3, negatively regulates NCA-1 and NCA-2 function. Thus, dopamine regulates activity of the NCA channels through G protein signaling pathways.