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  • Title: Inositol 1,4,5-trisphosphate but not ryanodine-receptor agonists induces calcium release from rat liver Golgi apparatus membrane vesicles.
    Author: Surroca A, Wolff D.
    Journal: J Membr Biol; 2000 Oct 01; 177(3):243-9. PubMed ID: 11014862.
    Abstract:
    We investigated the direct effect of inositol 1,4,5-trisphosphate (IP(3)) and ryanodine receptor agonists on Ca(2+) release from vesicles of a rat liver Golgi apparatus (GA) enriched fraction, which were actively loaded with (45)Ca(2+). Results in GA were compared with those obtained in a rat liver endoplasmic reticulum (ER) enriched fraction. The addition of IP(3) at concentrations ranging from 100 nm to 100 microm, in the presence of thapsigargin, a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPases, promoted a rapid decrease in the Ca(2+) content of GA vesicles. The amount of Ca(2+) released from the vesicles was a function of IP(3) concentration, reaching about 60% in both GA and ER fractions at 100 microm IP(3). Calcium release was inhibited by heparin, an antagonist of IP(3) receptors. Calcium exhibited a bell-shaped effect on IP(3)-dependent Ca(2+) released from GA vesicles: it activated Ca(2+) release at concentrations up to 1 microm, and inhibited it at higher concentrations. In contrast to that found in the endoplasmic reticulum fraction, none of the ryanodine receptor agonists tested (cyclic ADP-ribose, caffeine and ryanodine) significantly induced Ca(2+) release from GA fraction vesicles in the presence of thapsigargin. Our results indicate the presence of an IP(3)-sensitive Ca(2+) release mechanism in the Golgi apparatus membrane analogous to that of the ER. However, a Ca(2+) release mechanism sensitive to ryanodine receptor agonists like that of ER is not evident in the GA membrane.
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