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Mol Brain. 2019 Feb 8;12(1):12. doi: 10.1186/s13041-019-0433-8.

Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC.

Author information

1
Molecular Neuroscience, Department of Physiology and Pharmacology, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Dr. NW, Calgary, T2N 4N1, Canada.
2
Cystic Fibrosis Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
3
Molecular Neuroscience, Department of Physiology and Pharmacology, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Dr. NW, Calgary, T2N 4N1, Canada. zamponi@ucalgary.ca.

Abstract

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.

KEYWORDS:

Cav3.2 calcium channels; Dorsal horn; Dorsal root ganglia (DRG); Epithelial Sodium Channel (ENaC)

PMID:
30736831
PMCID:
PMC6368719
DOI:
10.1186/s13041-019-0433-8
[Indexed for MEDLINE]
Free PMC Article

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