التفاصيل البيبلوغرافية
| العنوان: |
Pharmacological Dissection of the Crosstalk between Na V and Ca V Channels in GH3b6 Cells. |
| المؤلفون: |
Réthoré, Léa1 (AUTHOR) lea.rethore@univ-angers.fr, Park, Joohee1 (AUTHOR) pakjoohee25@gmail.com, Montnach, Jérôme2 (AUTHOR) jerome.montnach@univ-nantes.fr, Nicolas, Sébastien2 (AUTHOR) sebastien.nicolas@univ-nantes.fr, Khoury, Joseph1,3 (AUTHOR) joseph-0-khoury@hotmail.com, Le Seac'h, Elodie1 (AUTHOR) elodieleseach@gmail.com, Mabrouk, Kamel4 (AUTHOR) kamel.mabrouk@univ-amu.fr, De Pomyers, Harold5 (AUTHOR) harold.pomyers@latoxan.com, Tricoire-Leignel, Hélène1 (AUTHOR) helene.tricoire-leignel@univ-angers.fr, Mattei, César1 (AUTHOR) cesar.mattei@univ-angers.fr, Henrion, Daniel1 (AUTHOR) daniel.henrion@univ-angers.fr, Fajloun, Ziad3,6 (AUTHOR), De Waard, Michel2,7 (AUTHOR) michel.dewaard@univ-nantes.fr, Legendre, Claire1 (AUTHOR) claire.legendre@univ-angers.fr, Legros, Christian1 (AUTHOR) claire.legendre@univ-angers.fr |
| المصدر: |
International Journal of Molecular Sciences. Jan2022, Vol. 23 Issue 2, p827-N.PAG. 1p. |
| مصطلحات موضوعية: |
*CALCIUM channels, *SODIUM channels, *ELECTRIC stimulation, *NEUROTOXIC agents, *TETRODOTOXIN, *DISSECTION, *IMMUNOBLOTTING |
| مستخلص: |
Thanks to the crosstalk between Na+ and Ca2+ channels, Na+ and Ca2+ homeostasis interplay in so-called excitable cells enables the generation of action potential in response to electrical stimulation. Here, we investigated the impact of persistent activation of voltage-gated Na+ (NaV) channels by neurotoxins, such as veratridine (VTD), on intracellular Ca2+ concentration ([Ca2+]i) in a model of excitable cells, the rat pituitary GH3b6 cells, in order to identify the molecular actors involved in Na+-Ca2+ homeostasis crosstalk. By combining RT-qPCR, immunoblotting, immunocytochemistry, and patch-clamp techniques, we showed that GH3b6 cells predominantly express the NaV1.3 channel subtype, which likely endorses their voltage-activated Na+ currents. Notably, these Na+ currents were blocked by ICA-121431 and activated by the β-scorpion toxin Tf2, two selective NaV1.3 channel ligands. Using Fura-2, we showed that VTD induced a [Ca2+]i increase. This effect was suppressed by the selective NaV channel blocker tetrodotoxin, as well by the selective L-type CaV channel (LTCC) blocker nifedipine. We also evidenced that crobenetine, a NaV channel blocker, abolished VTD-induced [Ca2+]i elevation, while it had no effects on LTCC. Altogether, our findings highlight a crosstalk between NaV and LTCC in GH3b6 cells, providing a new insight into the mode of action of neurotoxins. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
Full Text Finder