Abstract
A model is proposed for the mechanism by which activation of surface membrane receptors causes sustained Ca 2+ entry into cells from the extracellular space. Reassessment of previously published findings on the behavior of receptor-regulated intracellular Ca 2+ pools leads to the conclusion that when such pools are empty, a pathway from the extracellular space to the pool is opened; conversely when the pool is filled, the pathway is closed and it becomes relatively stable to depletion by low Ca 2+ media or chelating agents. The biphasic nature of agonist-activated Ca 2+-mobilization is thus seen as an initial emptying of the intracellular Ca 2+ pool by inositol (1,4,5) trisphosphate, followed by rapid entry of Ca 2+ into the pool and, in the continued presence of inositol (1,4,5) trisphosphate, into the cytosol. On withdrawal of agonist, inositol (1,4,5) trisphosphate is then rapidly degraded, the pathway from the pool to the cytosol is closed, and rapid entry from the outside continues until the Ca 2+ content of the pool reaches a level that inactivates Ca 2+ entry. This capacitative model allows for Ca 2+ release and Ca 2+ entry to be controlled by a single messenger, inositol (1,4,5) trisphosphate.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call