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Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman. / Chibalin, A.V.; Heiny, J.A.; Benziane, B.; Prokofiev, A.V.; Vasiliev, A.V.; Kravtsova, V.V.; Krivoi, I.I.

In: PLoS ONE, Vol. 7, No. 3, 2012, p. e33719.

Research output: Contribution to journal › Article

Harvard

Chibalin, AV, Heiny, JA, Benziane, B, Prokofiev, AV, Vasiliev, AV, Kravtsova, VV & Krivoi, II 2012, 'Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman', PLoS ONE, vol. 7, no. 3, pp. e33719. https://doi.org/doi:10.1371/journal.pone.0033719

APA

Chibalin, A. V., Heiny, J. A., Benziane, B., Prokofiev, A. V., Vasiliev, A. V., Kravtsova, V. V., & Krivoi, I. I. (2012). Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman. PLoS ONE, 7(3), e33719. https://doi.org/doi:10.1371/journal.pone.0033719

Vancouver

Chibalin AV, Heiny JA, Benziane B, Prokofiev AV, Vasiliev AV, Kravtsova VV et al. Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman. PLoS ONE. 2012;7(3):e33719. https://doi.org/doi:10.1371/journal.pone.0033719

Author

Chibalin, A.V. ; Heiny, J.A. ; Benziane, B. ; Prokofiev, A.V. ; Vasiliev, A.V. ; Kravtsova, V.V. ; Krivoi, I.I. / Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman. In: PLoS ONE. 2012 ; Vol. 7, No. 3. pp. e33719.

BibTeX

@article{0e26d5265d8b4dd8a01d41d40edb54a8,
title = "Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman",
abstract = "Our previous finding that the muscle nicotinic acetylcholine receptor (nAChR) and the Na,K-ATPase interact as a regulatory complex to modulate Na,K-ATPase activity suggested that chronic, circulating nicotine may alter this interaction, with long-term changes in the membrane potential. To test this hypothesis, we chronically exposed rats to nicotine delivered orally for 21–31 days. Chronic nicotine produced a steady membrane depolarization of ~3 mV in the diaphragm muscle, which resulted from a net change in electrogenic transport by the Na,K-ATPase α2 and α1 isoforms. Electrogenic transport by the α2 isoform increased (+1.8 mV) while the activity of the α1 isoform decreased (−4.4 mV). Protein expression of Na,K-ATPase α1 or α2 isoforms and the nAChR did not change; however, the content of α2 subunit in the plasma membrane decreased by 25%, indicating that its stimulated electrogenic transport is due to an increase in specific activity. The physical association between the nAChR, the Na,K-ATPase α1 or α2 subu",
author = "A.V. Chibalin and J.A. Heiny and B. Benziane and A.V. Prokofiev and A.V. Vasiliev and V.V. Kravtsova and I.I. Krivoi",
year = "2012",
doi = "doi:10.1371/journal.pone.0033719",
language = "English",
volume = "7",
pages = "e33719",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "3",

}

RIS

TY - JOUR

T1 - Chronic nicotine exposure modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman

AU - Chibalin, A.V.

AU - Heiny, J.A.

AU - Benziane, B.

AU - Prokofiev, A.V.

AU - Vasiliev, A.V.

AU - Kravtsova, V.V.

AU - Krivoi, I.I.

PY - 2012

Y1 - 2012

N2 - Our previous finding that the muscle nicotinic acetylcholine receptor (nAChR) and the Na,K-ATPase interact as a regulatory complex to modulate Na,K-ATPase activity suggested that chronic, circulating nicotine may alter this interaction, with long-term changes in the membrane potential. To test this hypothesis, we chronically exposed rats to nicotine delivered orally for 21–31 days. Chronic nicotine produced a steady membrane depolarization of ~3 mV in the diaphragm muscle, which resulted from a net change in electrogenic transport by the Na,K-ATPase α2 and α1 isoforms. Electrogenic transport by the α2 isoform increased (+1.8 mV) while the activity of the α1 isoform decreased (−4.4 mV). Protein expression of Na,K-ATPase α1 or α2 isoforms and the nAChR did not change; however, the content of α2 subunit in the plasma membrane decreased by 25%, indicating that its stimulated electrogenic transport is due to an increase in specific activity. The physical association between the nAChR, the Na,K-ATPase α1 or α2 subu

AB - Our previous finding that the muscle nicotinic acetylcholine receptor (nAChR) and the Na,K-ATPase interact as a regulatory complex to modulate Na,K-ATPase activity suggested that chronic, circulating nicotine may alter this interaction, with long-term changes in the membrane potential. To test this hypothesis, we chronically exposed rats to nicotine delivered orally for 21–31 days. Chronic nicotine produced a steady membrane depolarization of ~3 mV in the diaphragm muscle, which resulted from a net change in electrogenic transport by the Na,K-ATPase α2 and α1 isoforms. Electrogenic transport by the α2 isoform increased (+1.8 mV) while the activity of the α1 isoform decreased (−4.4 mV). Protein expression of Na,K-ATPase α1 or α2 isoforms and the nAChR did not change; however, the content of α2 subunit in the plasma membrane decreased by 25%, indicating that its stimulated electrogenic transport is due to an increase in specific activity. The physical association between the nAChR, the Na,K-ATPase α1 or α2 subu

U2 - doi:10.1371/journal.pone.0033719

DO - doi:10.1371/journal.pone.0033719

M3 - Article

VL - 7

SP - e33719

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 3

ER -

ID: 5352489