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Sodium-calcium exchanger and R-type Ca(2+) channels mediate spontaneous [Ca(2+)]i oscillations in magnocellular neurones of the rat supraoptic nucleus

S. Kortus, C. Srinivasan, O. Forostyak, M. Zapotocky, Y. Ueta, E. Sykova, A. Chvatal, A. Verkhratsky, G. Dayanithi,

. 2016 ; 59 (6) : 289-98. [pub] 20160331

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17031804

Isolated supraoptic neurones generate spontaneous [Ca(2+)]i oscillations in isolated conditions. Here we report in depth analysis of the contribution of plasmalemmal ion channels (Ca(2+), Na(+)), Na(+)/Ca(2+) exchanger (NCX), intracellular Ca(2+) release channels (InsP3Rs and RyRs), Ca(2+) storage organelles, plasma membrane Ca(2+) pump and intracellular signal transduction cascades into spontaneous Ca(2+) activity. While removal of extracellular Ca(2+) or incubation with non-specific voltage-gated Ca(2+) channel (VGCC) blocker Cd(2+) suppressed the oscillations, neither Ni(2+) nor TTA-P2, the T-type VGCC blockers, had an effect. Inhibitors of VGCC nicardipine, ω-conotoxin GVIA, ω-conotoxin MVIIC, ω-agatoxin IVA (for L-, N-, P and P/Q-type channels, respectively) did not affect [Ca(2+)]i oscillations. In contrast, a specific R-type VGCC blocker SNX-482 attenuated [Ca(2+)]i oscillations. Incubation with TTX had no effect, whereas removal of the extracellular Na(+) or application of an inhibitor of the reverse operation mode of Na(+)/Ca(2+) exchanger KB-R7943 blocked the oscillations. The mitochondrial uncoupler CCCP irreversibly blocked spontaneous [Ca(2+)]i activity. Exposure of neurones to Ca(2+) mobilisers (thapsigargin, cyclopiazonic acid, caffeine and ryanodine); 4-aminopyridine (A-type K(+) current blocker); phospholipase C and adenylyl cyclase pathways blockers U-73122, Rp-cAMP, SQ-22536 and H-89 had no effect. Oscillations were blocked by GABA, but not by glutamate, apamin or dynorphin. In conclusion, spontaneous oscillations in magnocellular neurones are mediated by a concerted action of R-type Ca(2+) channels and the NCX fluctuating between forward and reverse modes.

Citace poskytuje Crossref.org

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$a Srinivasan, Chinnapaiyan $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Forostyak, Oksana $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic.
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$a Zapotocky, Martin $u Institute of Physiology, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Institute of Biophysics and Informatics, First Medical Faculty, Charles University in Prague, Salmovska 1, 12000 Prague, Czech Republic.
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$a Ueta, Yoichi $u Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
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$a Sykova, Eva $u Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic; Department of Neuroscience, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Chvatal, Alexandr $u Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic; Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Dayanithi, Govindan $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Institut National de la Santé et de la Recherche Médicale, Unité de recherche U1198, Université Montpellier, 34095 Montpellier, France; Ecole Practique des Hautes Etudes, Sorbonne, 75014 Paris, France. Electronic address: gdaya@univ-montp2.fr.
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