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Differential effects of maitotoxin on calcium entry and ciliary beating in the rabbit ciliated tracheal epithelium
Author(s) -
Venant Annick,
Dazy AnneCatherine,
Diogène Georges,
Marano Francelyne
Publication year - 1995
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 - 10.1016/0248-4900(96)85281-6
Subject(s) - biology , verapamil , calcium , arachidonic acid , calmodulin , stimulation , okadaic acid , trifluoperazine , tetrodotoxin , endocrinology , bapta , fura 2 , medicine , pharmacology , biochemistry , intracellular , enzyme , phosphatase , cytosol
Summary— The marine toxin maitotoxin (MTX) induces stimulation of ciliary beating in primary cultures of rabbit tracheal epithelial cells. The response is time‐ and concentration‐dependent. External calcium is an absolute requirement, although at a very low concentration (50 μM for maximal effect). Pretreatment of the cells with MTX induces an early (5 min) and sustained (≥ 24 h) homologous desensitization. The response to MTX is strongly inhibited by trifluoperazin (an inhibitor of Ca‐calmodulin‐dependent enzymes) and by chelation of [Ca] i with BAPTA. However, the magnitude and kinetics of [Ca] i rise elicited by MTX do not correlate with those of the ciliary beat frequency (CBF) increase: the CBF increase is transient (with a peak at 5–10 min) while the [Ca] i rise is sustained; the CBF increase occurs at concentrations of MTX which are without an effect on [Ca] i ; the CBF increase is not inhibited by 200 μM verapamil, genistein or okadaic acid, which inhibit the MTX‐induced [Ca] i rise. The CBF increase is strongly inhibited by antagonists of arachidonic acid metabolism, mepacrine and nordiguaiaretic acid. However, MTX does not stimulate cAMP synthesis. These results suggest that calcium is not the only factor involved in the biological effects of MTX and even suggest that MTX may primarily stimulate phospholipid breakdown in the cell membrane.