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Journal of Experimental Biology, Vol 202, Issue 11 1535-1544, Copyright © 1999 by Company of Biologists
JOURNAL ARTICLES |
WS Marshall, TR Emberley, TD Singer, SE Bryson and SD Mccormick
Department of Biology, St Francis Xavier University, Antigonish, Nova Scotia, Canada B2G 2W5, Vanderbilt University, Department of Anaesthesiology, Laboratory of Cellular and Molecular Physiology, 1313 21st Avenue South, Nashville, TN 37232-21.
Freshwater-adapted killifish (Fundulus heteroclitus) were transferred directly from soft fresh water to full-strength sea water for periods of 1 h, 3 h, 8 h and 1, 2, 7, 14 and 30 days. Controls were transferred to fresh water for 24 h. Measured variables included: blood [Na+], osmolality, glucose and cortisol levels, basal and stimulated rates of ion transport and permeability of in vitro opercular epithelium, gill Na+/K+-ATPase and citrate synthase activity and chloride cell ultrastructure. These data were compared with previously published killifish cystic fibrosis transmembrane conductance regulator (kfCFTR) expression in the gills measured over a similar time course. Plasma cortisol levels peaked at 1 h, coincident with a rise in plasma [Na+]. At 8 h after transfer to sea water, a time at which previous work has shown kfCFTR expression to be elevated, blood osmolality and [Na+] were high, and cortisol levels and opercular membrane short-circuit current (Isc; a measure of Cl- secretion rate) were low. The 24 h group, which showed the highest level of kfCFTR expression, had the highest plasma [Na+] and osmolality, elevated plasma cortisol levels, significantly lower opercular membrane resistance, an increased opercular membrane ion secretion rate and collapsed tubule inclusions in mitochondria-rich cells, but no change in gill Na+/K+-ATPase and citrate synthase activity or plasma glucose levels. Apparently, killifish have a rapid (<1 h) cortisol response to salinity coupled to subsequent (8-48 h) expression of kfCFTR anion channel proteins in existing mitochondria-rich cells that convert transport from ion uptake to ion secretion.
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