Sodium-calcium exchanger and R-type Ca(2+) channels mediate spontaneous [Ca(2+)]i oscillations in magnocellular neurones of the rat supraoptic nucleus
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
27052156
DOI
10.1016/j.ceca.2016.03.010
PII: S0143-4160(16)30036-7
Knihovny.cz E-zdroje
- Klíčová slova
- 1,4,5-Trisphosphate, Ca(2+) channel toxins, Ca(2+) clearance, Ca(2+) homeostasis, Ca(2+) imaging, Ca(2+) oscillations, Ca(2+) signalling, GABA, Glutamate, Hypothalamus, Mitochondria, Na(+)/Ca(2+) exchanger, Oxytocin, Plasma membrane calcium pump, Sarcoendoplasmic reticulum Ca(2+)-ATPase, Supraoptic nucleus, Tetrodotoxin, Transgenic rats, Vasopressin, Voltage-gated Ca(2+) channels,
- MeSH
- adenylátcyklasy metabolismus MeSH
- biologický transport MeSH
- draslíkové kanály metabolismus MeSH
- fosfolipasy typu C metabolismus MeSH
- gating iontového kanálu MeSH
- intracelulární prostor metabolismus MeSH
- neurony metabolismus MeSH
- neurotransmiterové látky metabolismus MeSH
- nucleus supraopticus metabolismus MeSH
- potkani Wistar MeSH
- pumpa pro výměnu sodíku a vápníku metabolismus MeSH
- sodík metabolismus MeSH
- sodíkové kanály metabolismus MeSH
- systémy druhého messengeru MeSH
- vápník metabolismus MeSH
- vápníková signalizace * MeSH
- vápníkové kanály - typ R metabolismus MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adenylátcyklasy MeSH
- draslíkové kanály MeSH
- fosfolipasy typu C MeSH
- neurotransmiterové látky MeSH
- pumpa pro výměnu sodíku a vápníku MeSH
- sodík MeSH
- sodíkové kanály MeSH
- vápník MeSH
- vápníkové kanály - typ R MeSH
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.
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