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Inhibition of trichocyst exocytosis and calcium influx in Paramecium by amiloride and divalent cations
Author(s) -
Kerbœuf Daniel,
Cohen Jean
Publication year - 1996
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/j.1768-322x.1996.tb00953.x
Subject(s) - exocytosis , secretagogue , divalent , veratridine , amiloride , paramecium , biology , biophysics , ionomycin , microbiology and biotechnology , calcium , chromaffin cell , biochemistry , aequorin , secretion , chemistry , sodium , intracellular , endocrinology , adrenal medulla , sodium channel , catecholamine , organic chemistry
Summary— Regulated exocytosis of defensive secretory organelles, the trichocysts, as well as a transient Ca 2+ ‐influx can be induced in Paramecium by aminoethyldextran (Kerbœuf and Cohen, J Cell Biol (1990) 111, 2527). Knoll et al (Febs Lett (1992) 304, 265) reported that veratridine was also a secretagogue for Paramecium . Here we show that, like aminoethyldextran, veratridine induces a transient Ca 2+ ‐influx. Both aminoethyldextran‐and veratridine‐induced exocytosis and associated Ca 2+ ‐influx were: i) blocked in the nd12 thermosensitive mutant at the non‐permissive temperature; and ii) inhibited by amiloride and four divalent cations, Ba 2+ , Mg 2+ , Sr 2+ and Co 2+ . This suggests that, although of different chemical nature, aminoethyldextran and veratridine act through the same physiological pathway. In addition, the inhibitory doses are comparable to the ones found to inhibit a hyperpolarization‐sensitive Ca 2+ ‐current described in Paramecium (Preston et al (1992) J Gen Physiol 100, 233). The possibility that the activation of this Ca 2+ ‐current by the secretagogue represents an early step in the regulation of trichocyst exocytosis is discussed.