Abstract
Bovine chromaffin cells can be stimulated by acetylcholine to allow Na(superscript +) influx and the opening of voltage-gated Ca(superscript 2+) channels (VGCC). Ca2+ entry via VGCC dramatically increases [Ca(superscript 2+)]c by the process of Ca(superscript 2+)-induced Ca(superscript 2+) release (CICR) and the increase in [Ca(superscript 2+)]c promotes exocytosis. At the same time, Na(superscript +) influx through acetylcholine receptor temporarily induces the reverse mode activity of Na(superscript +)/Ca(superscript 2+) exchanger (NCX), which also contributes to part of Ca(superscript 2+) influx. It is controversial whether the reverse mode of NCX also can promote CICR. Here our results show that the elevation of [Ca(superscript 2+)]c by the reverse mode of NCX was inhibited by emptying ER with Thapsigargin. Besides, [Ca(superscript 2+)]c rising could be inhibited by the treatment of either Ryanodine (Ry), a Ryanodine receptor (RyR) inhibitor or 2-APB, an IP3 receptor (IP3R) inhibitor. The effect of treating 2-APB and Ry simultaneously had no significant difference from that of treating 2-APB alone. We concluded that the reverse mode of NCX can promote the release of Ca(superscript 2+) from ER through RyR and IP3 receptor (IP3R). Furthermore, IP3R may function as a modulator of the opening of RyR. The crosstalk of NCX, RyR, and IP3R has important effects on intracellular calcium homeostasis.
Published Version
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