Garcia-Caballero, AgustinGandini, Maria AHuang, ShuoChen, LinaSouza, Ivana ADang, Yan LStutts, M. JZamponi, Gerald W2019-02-102019-02-102019-02-08Molecular Brain. 2019 Feb 08;12(1):12http://hdl.handle.net/1880/109896https://doi.org/10.11575/PRISM/45982Abstract This study describes the functional interaction between Cav3.2 calcium channels and the Epithelial Sodium Channel (ENaC). β-ENaC subunits showed overlapping expression with endogenous Cav3.2 calcium channels in the thalamus and hypothalamus as detected by immunostaining. Moreover, β- and γ-ENaC subunits could be co-immunoprecipitated with Cav3.2 calcium channels from brain lysates, dorsal horn and lumbar dorsal root ganglia. Mutation of a cluster of lysines present in the intracellular N-terminus region of β-ENaC (K4R/ K5R/ K9R/ K16R/ K23R) reduced interactions with Cav3.2 calcium channels. Αβγ-ENaC channels enhanced Cav3.2 calcium channel trafficking to the plasma membrane in tsA-201 cells. This effect was reciprocal such that Cav3.2 channel expression also enhanced β-ENaC trafficking to the cell surface. T-type current density was increased when fully assembled αβγ-ENaC channels were transiently expressed in CAD cells, a neuronal derived cell line. Altogether, these findings reveal ENaC as an interactor and potential regulator of Cav3.2 calcium channels expressed in neuronal tissues.Cav3.2 calcium channel interactions with the epithelial sodium channel ENaCJournal Article2019-02-10enThe Author(s).https://doi.org/10.1186/s13041-019-0433-8