Ca2+ release from inositol trisphosphate-sensitive stores is not modulated by intraluminal [Ca2+].
In a recent model developed to explain the apparent "quantal" nature of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-induced Ca2+ release from specific intracellular stores, it was proposed that Ca2+ release from the stores may itself be modulated by intraluminal levels of Ca2+, possibly via an action at a binding site on the Ins(1,4,5)P3 receptor/Ca2+ channel complex. Essential predictions of this model include a specific effect of intraluminal Ca2+ levels on the sensitivity of Ins(1,4,5)P3-induced Ca2+ release and a non-exponential decay of passive Ca2+ loss from the store following inhibition of the Ca2+ pump on the store. However, in measurements of Ins(1,4,5)P3-induced Ca2+ release and passive Ca2+ loss in permeabilized preparations of a model exocrine cell under conditions of thapsigargin-induced store depletion, we found that neither of these predicted behaviors could be demonstrated.
Shuttleworth
T J
TJ
Department of Physiology, University of Rochester School of Medicine and Dentistry, New York 14642.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000187:drug effects; D002273:Carcinogens / Q000494:pharmacology; D002478:Cells, Cultured; D004372:Ducks; D005456:Fluorescent Dyes; D015544:Inositol 1,4,5-Trisphosphate / Q000502:physiology*; D013729:Terpenes / Q000494:pharmacology; D019284:Thapsigargin
D002273:Carcinogens; D005456:Fluorescent Dyes; D013729:Terpenes; D019284:Thapsigargin; D015544:Inositol 1,4,5-Trisphosphate; D000252:Calcium-Transporting ATPases; D002118:Calcium