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Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.

Berthier C, Kutchukian C, Bouvard C, Okamura Y, Jacquemond V - J. Gen. Physiol. (2015)

Bottom Line: However, in Ci-VSP-expressing fibers challenged by 5-s-long depolarizing pulses, the Ca(2+) level late in the pulse (3 s after initiation) was significantly lower at 120 mV than at 20 mV.Our results indicate that the PtdIns(4,5)P2 level is tightly maintained in the transverse tubule membrane of the muscle fibers, and that VSP-induced depletion of PtdIns(4,5)P2 impairs voltage-activated Ca(2+) release from the SR.Because Ca(2+) release is thought to be independent from InsP3 signaling, the effect likely results from an interaction between PtdIns(4,5)P2 and a protein partner of the E-C coupling machinery.

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Affiliation: Centre National de la Recherche Scientifique UMR 5534, Université Lyon 1, Centre de Génétique et de Physiologie Moléculaire et Cellulaire, 69100 Villeurbanne, France.

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Membrane current during trains of depolarizing steps in VSP-negative fibers and Ci-VSP–expressing fibers. Mean value for the membrane current measured at the end of each depolarizing pulse during the control and test protocols shown in Fig. 4. The horizontal axis is positioned at the zero-current level. Error bars represent ± SEM.
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fig5: Membrane current during trains of depolarizing steps in VSP-negative fibers and Ci-VSP–expressing fibers. Mean value for the membrane current measured at the end of each depolarizing pulse during the control and test protocols shown in Fig. 4. The horizontal axis is positioned at the zero-current level. Error bars represent ± SEM.

Mentions: We asked whether the presence and/or activation of VSP had consequences on the membrane current flowing during the pulses. We measured membrane current near the end of each depolarizing pulse applied during the control and test protocol, and values were normalized to fiber capacitance. Corresponding mean values are presented in Fig. 5. There was no indication that either the presence of Ci-VSP in the membrane or its activation by the pulses to 100 mV produced any modification of the membrane current.


Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.

Berthier C, Kutchukian C, Bouvard C, Okamura Y, Jacquemond V - J. Gen. Physiol. (2015)

Membrane current during trains of depolarizing steps in VSP-negative fibers and Ci-VSP–expressing fibers. Mean value for the membrane current measured at the end of each depolarizing pulse during the control and test protocols shown in Fig. 4. The horizontal axis is positioned at the zero-current level. Error bars represent ± SEM.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4380211&req=5

fig5: Membrane current during trains of depolarizing steps in VSP-negative fibers and Ci-VSP–expressing fibers. Mean value for the membrane current measured at the end of each depolarizing pulse during the control and test protocols shown in Fig. 4. The horizontal axis is positioned at the zero-current level. Error bars represent ± SEM.
Mentions: We asked whether the presence and/or activation of VSP had consequences on the membrane current flowing during the pulses. We measured membrane current near the end of each depolarizing pulse applied during the control and test protocol, and values were normalized to fiber capacitance. Corresponding mean values are presented in Fig. 5. There was no indication that either the presence of Ci-VSP in the membrane or its activation by the pulses to 100 mV produced any modification of the membrane current.

Bottom Line: However, in Ci-VSP-expressing fibers challenged by 5-s-long depolarizing pulses, the Ca(2+) level late in the pulse (3 s after initiation) was significantly lower at 120 mV than at 20 mV.Our results indicate that the PtdIns(4,5)P2 level is tightly maintained in the transverse tubule membrane of the muscle fibers, and that VSP-induced depletion of PtdIns(4,5)P2 impairs voltage-activated Ca(2+) release from the SR.Because Ca(2+) release is thought to be independent from InsP3 signaling, the effect likely results from an interaction between PtdIns(4,5)P2 and a protein partner of the E-C coupling machinery.

View Article: PubMed Central - HTML - PubMed

Affiliation: Centre National de la Recherche Scientifique UMR 5534, Université Lyon 1, Centre de Génétique et de Physiologie Moléculaire et Cellulaire, 69100 Villeurbanne, France.

Show MeSH
Related in: MedlinePlus