Sodium-calcium exchanger and R-type Ca(2+) channels mediate spontaneous [Ca(2+)]i oscillations in magnocellular neurones of the rat supraoptic nucleus
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
27052156
DOI
10.1016/j.ceca.2016.03.010
PII: S0143-4160(16)30036-7
Knihovny.cz E-resources
- Keywords
- 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
- Adenylyl Cyclases metabolism MeSH
- Biological Transport MeSH
- Potassium Channels metabolism MeSH
- Type C Phospholipases metabolism MeSH
- Ion Channel Gating MeSH
- Intracellular Space metabolism MeSH
- Neurons metabolism MeSH
- Neurotransmitter Agents metabolism MeSH
- Supraoptic Nucleus metabolism MeSH
- Rats, Wistar MeSH
- Sodium-Calcium Exchanger metabolism MeSH
- Sodium metabolism MeSH
- Sodium Channels metabolism MeSH
- Second Messenger Systems MeSH
- Calcium metabolism MeSH
- Calcium Signaling * MeSH
- Calcium Channels, R-Type metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adenylyl Cyclases MeSH
- Potassium Channels MeSH
- Type C Phospholipases MeSH
- Neurotransmitter Agents MeSH
- Sodium-Calcium Exchanger MeSH
- Sodium MeSH
- Sodium Channels MeSH
- Calcium MeSH
- Calcium Channels, R-Type 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.
References provided by Crossref.org
