Expression of the sodium channel β1 subunit in rat skeletal muscle is selectively associated with the tetrodotoxin-sensitive α subunit isoform

Jane S. Yang; Paul B. Bennett; Naomasa Makita; Alfred L. George; Robert L. Barchi

doi:10.1016/0896-6273(93)90121-7

Expression of the sodium channel β₁ subunit in rat skeletal muscle is selectively associated with the tetrodotoxin-sensitive α subunit isoform

Jane S. Yang^*, Paul B. Bennett, Naomasa Makita, Alfred L. George, Robert L. Barchi

^*Corresponding author for this work

Pharmacology

Research output: Contribution to journal › Article › peer-review

63 Scopus citations

Abstract

Transcripts homologous to the rat brain sodium channel β subunit (β₁) are prominently expressed in both innervated and denervated adult skeletal muscle and in heart, but not in neonatal skeletal or cardiac muscle. Regulation of β₁ mRNA expression closely parallels that of SkM1 α during development, after denervation in adult muscle, and in primary muscle culture, but does not follow SkM2 expression under any condition examined. In oocytes, β₁ interacts functionally with SkM1 to modulate the abnormally slow inactivation kinetics observed with this α subunit expressed alone. We conclude that a common β₁, subunit is expressed in skeletal muscle, heart, and brain and that in skeletal muscle, this subunit is specifically associated with the SkM1, rather than the SkM2, sodium channel isoform.

Original language	English (US)
Pages (from-to)	915-922
Number of pages	8
Journal	Neuron
Volume	11
Issue number	5
DOIs	https://doi.org/10.1016/0896-6273(93)90121-7
State	Published - Nov 1993

Funding

This work was supported in part by NIH grants NS-08075 and NS-18013 (R. L. B.) and by a grant from the Muscular Dystrophy Association (R. L. B.). P. B. B. is an Established Investigator of the American Heart Association. A. L. C. is a Lucille P. Markey Scholar, and this work was supported in part by a grant from the Lucille P. Markey Charitable Trust. The authors thank Dr. Steven Scherer of the University of Pennsylvania for assistance with the denervation experiments reported here. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 USC Section 1734 solely to indicate this fact.

ASJC Scopus subject areas

General Neuroscience

Access to Document

10.1016/0896-6273(93)90121-7

Cite this

@article{67827c56fc784e52be1a6557bab585d8,

title = "Expression of the sodium channel β1 subunit in rat skeletal muscle is selectively associated with the tetrodotoxin-sensitive α subunit isoform",

abstract = "Transcripts homologous to the rat brain sodium channel β subunit (β1) are prominently expressed in both innervated and denervated adult skeletal muscle and in heart, but not in neonatal skeletal or cardiac muscle. Regulation of β1 mRNA expression closely parallels that of SkM1 α during development, after denervation in adult muscle, and in primary muscle culture, but does not follow SkM2 expression under any condition examined. In oocytes, β1 interacts functionally with SkM1 to modulate the abnormally slow inactivation kinetics observed with this α subunit expressed alone. We conclude that a common β1, subunit is expressed in skeletal muscle, heart, and brain and that in skeletal muscle, this subunit is specifically associated with the SkM1, rather than the SkM2, sodium channel isoform.",

author = "Yang, {Jane S.} and Bennett, {Paul B.} and Naomasa Makita and George, {Alfred L.} and Barchi, {Robert L.}",

note = "Funding Information: This work was supported in part by NIH grants NS-08075 and NS-18013 (R. L. B.) and by a grant from the Muscular Dystrophy Association (R. L. B.). P. B. B. is an Established Investigator of the American Heart Association. A. L. C. is a Lucille P. Markey Scholar, and this work was supported in part by a grant from the Lucille P. Markey Charitable Trust. The authors thank Dr. Steven Scherer of the University of Pennsylvania for assistance with the denervation experiments reported here. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 USC Section 1734 solely to indicate this fact.",

year = "1993",

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AU - Makita, Naomasa

AU - George, Alfred L.

AU - Barchi, Robert L.

N1 - Funding Information: This work was supported in part by NIH grants NS-08075 and NS-18013 (R. L. B.) and by a grant from the Muscular Dystrophy Association (R. L. B.). P. B. B. is an Established Investigator of the American Heart Association. A. L. C. is a Lucille P. Markey Scholar, and this work was supported in part by a grant from the Lucille P. Markey Charitable Trust. The authors thank Dr. Steven Scherer of the University of Pennsylvania for assistance with the denervation experiments reported here. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 USC Section 1734 solely to indicate this fact.

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N2 - Transcripts homologous to the rat brain sodium channel β subunit (β1) are prominently expressed in both innervated and denervated adult skeletal muscle and in heart, but not in neonatal skeletal or cardiac muscle. Regulation of β1 mRNA expression closely parallels that of SkM1 α during development, after denervation in adult muscle, and in primary muscle culture, but does not follow SkM2 expression under any condition examined. In oocytes, β1 interacts functionally with SkM1 to modulate the abnormally slow inactivation kinetics observed with this α subunit expressed alone. We conclude that a common β1, subunit is expressed in skeletal muscle, heart, and brain and that in skeletal muscle, this subunit is specifically associated with the SkM1, rather than the SkM2, sodium channel isoform.

AB - Transcripts homologous to the rat brain sodium channel β subunit (β1) are prominently expressed in both innervated and denervated adult skeletal muscle and in heart, but not in neonatal skeletal or cardiac muscle. Regulation of β1 mRNA expression closely parallels that of SkM1 α during development, after denervation in adult muscle, and in primary muscle culture, but does not follow SkM2 expression under any condition examined. In oocytes, β1 interacts functionally with SkM1 to modulate the abnormally slow inactivation kinetics observed with this α subunit expressed alone. We conclude that a common β1, subunit is expressed in skeletal muscle, heart, and brain and that in skeletal muscle, this subunit is specifically associated with the SkM1, rather than the SkM2, sodium channel isoform.

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