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Individual variation and hormonal modulation of a sodium channel β subunit in the electric organ correlate with variation in a social signal
Author(s) -
Liu He,
Wu MingMing,
Zakon Harold H.
Publication year - 2007
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20404
Subject(s) - biology , alternative splicing , sodium channel , xenopus , messenger rna , rna splicing , splice , protein subunit , microbiology and biotechnology , gene expression , gene , endocrinology , medicine , sodium , genetics , rna , chemistry , organic chemistry
The sodium channel β1 subunit affects sodium channel gating and surface density, but little is known about the factors that regulate β1 expression or its participation in the fine control of cellular excitability. In this study we examined whether graded expression of the β1 subunit contributes to the gradient in sodium current inactivation, which is tightly controlled and directly related to a social behavior, the electric organ discharge (EOD), in a weakly electric fish Sternopygus macrurus . We found the mRNA and protein levels of β1 in the electric organ both correlate with EOD frequency. We identified a novel mRNA splice form of this gene and found the splicing preference for this novel splice form also correlates with EOD frequency. Androgen implants lowered EOD frequency and decreased the β1 mRNA level but did not affect splicing. Coexpression of each splice form in Xenopus oocytes with either the human muscle sodium channel gene, hNav1.4, or a Sternopygus ortholog, smNav1.4b, sped the rate of inactivation of the sodium current and shifted the steady‐state inactivation toward less negative membrane potentials. The translational product of the novel mRNA splice form lacks a previously identified important tyrosine residue but still functions normally. The properties of the fish α and coexpressed β1 subunits in the oocyte replicate those of the electric organ's endogenous sodium current. These data highlight the role of ion channel β subunits in regulating cellular excitability. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.