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Ca 2+ influx drives agonist‐activated [Ca 2+ ] i oscillations in an exocrine cell
Author(s) -
Martin Shaun C.,
Shuttleworth Trevor J.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00913-9
Subject(s) - agonist , intracellular , biophysics , depolarization , chemistry , quenching (fluorescence) , receptor , physics , biochemistry , biology , fluorescence , quantum mechanics
In current models describing agonist‐induced oscillations in [Ca 2+ ] i , Ca 2+ entry is generally assumed to have a simple sustaining role, replenishing Ca 2+ lost from the cell and recharging intracellular Ca 2+ stores. In cells from the avian nasal gland, a model exocrine cell, we show that inhibition of Ca 2+ entry by La 3+ , SK&F 96365, or by membrane depolarization, rapidly blocks [Ca 2+ ] i oscillations but does so without detectible depletion of agonist‐sensitive Ca 2+ stores. As the rate of Mn 2+ quenching during [Ca 2+ ] i oscillations is constant, Ca 2+ entry is not directly contributing to the [Ca 2+ ] i changes and, instead, appears to be involved in inducing the repetitive release of Ca 2+ from internal stores. Together, these data contradict current models in that (i) at the low agonist concentrations where [Ca 2+ ] i oscillations are seen, generated levels of Ins(1,4,5)P 3 are themselves inadequate to result in a regenerative [Ca 2+ ] i signal, and (ii) Ca 2+ entry is necessary to actually drive the intrinsic oscillatory mechanism.