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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 285 (1996), S. 75-82 
    ISSN: 1432-0878
    Keywords: Key words: Gill ; Chloride cell ; Gas transfer ; Diffusing capacity ; Oncorhynchus mykiss (Teleostei)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Rainbow trout (Oncorhynchus mykiss) were exposed to ion-poor (soft) water to test the hypothesis that naturally induced proliferation of branchial chloride cells causes a thickening of the blood-to-water diffusion barrier. This was achieved by using a combination of scanning and transmission electron-microscopic techniques. Fish were exposed to soft-water conditions ([Na+]= 0.055 mmol l-1, [Cl–]≈0.029 mmol 1–1, [Ca2+]≈ 0.059 mmol 1–1, and [K+]≈0.007 mmol 1–1) for 1, 2, and 4 weeks. Marked chloride cell proliferation was evident at all sampling times with an approximate doubling of the gill epithelial surface area covered by chloride cells exposed to the water (”chloride cell fractional area”). The increases in chloride cell fractional area resulted from both increased numbers of cells and expanded apical surfaces of exposed individual cells. As a result of chloride cell proliferation, soft-water exposure was associated with a doubling of the lamellar blood-to-water diffusion distance from 3.26±0.08 μm to 6.58±0.43 μm as determined from transmission electron micrographs. These data demonstrated a positive correlation between chloride cell fractional area and blood-to-water diffusion distance. We conclude that, in trout, chloride cell proliferation during soft-water exposure, while presumably benefiting ionic regulation, may impair gas transfer owing to the associated thickening of the blood-to-water diffusion barrier.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-5168
    Keywords: fish gills ; calcium transport ; Ca-pump ; Ca-ATPase ; stanniectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Description / Table of Contents: Abstract The branchial Ca2+ uptake by teleost fish is under inhibitory control by the hormone stanniocalcin (STC) which is generated by the corpuscles of Stannius (CS). Removal of the CS in North American eel, Anguilla rostrata LeSueur, induced a rapid rise in blood calcium levels. Branchial Ca2+ influx following the extirpation of the CS (stanniectomy, STX) increased during the first four days and stayed elevated thereafter (in agreement with previous studies). The transepithelial potential (TEP) across the gills did not change after STX and this means that the electrochemical gradient for Ca2+ is less favourable for passive influx of Ca2+ in STX eel. Therefore, the Ca2+ influx in STX eels is a transcellular flux, with Ca2+ crossing the apical and basolateral membrane barrier. The kinetics of ATP-driven Ca2+-transport across basolateral plasma membranes from eel gills did not change after STX. Thus, the increased Ca2+-influx after STX is not correlated with changes in ATP-dependent Ca2+-extrusion across the basolateral membrane, suggesting a regulation at the apical membrane. Moreover, STC did not affect ATP-driven Ca2+-transport in isolated basolateral membranes (in vitro). STC (0.1 nM) reduced cAMP levels in dispersed eel gill cells. It had no significant effect on the IP3 levels in these cells. We postulate that STC controls the permeability to Ca2+ of the apical membranes of the Ca2+ transporting cells of fish gills by controlling second messenger operated Ca2+ channels in the apical membrane.
    Notes: Résumé L'entrée de calcium au niveau des branchies est sous le controle inhibiteur de la stanniocalcine (STC) qui est synthétisée au niveau des corpuscules de Stannius (CS). L'ablation des CS chez l'anguille d'Amérique du Nord, Anguilla rostrata LeSueur, induit une augmentation rapide des niveaux de calcium dans le sang. Le flux entrant branchial de calcium consécutif à l'ablation des CS (stanniectomie, STX) augmente pendant les 4 premiers jours et reste élevé au-delà (en accord avec des études antérieures). Le potentiel transépithélial (TEP) à travers les branchies ne change pas après STX, ceci indiquant que le gradient électrochimique du Ca2+ est moins favorable pour le flux entrant passif du Ca2+ chez l'anguille STX. En conséquence, le flux entrant de Ca2+ chez l'anguille STX est un flux transcellulaire, avec le Ca2+ traversant la barrière membranaire apicale et basolatérale. La cinétique du transport de Ca2+ conduit par l'ATP à travers les membranes plasmatiques basolatérales de branches d'anguille n'est pas modifiée après STX. Ainsi, l'augmentation du flux entrant de Ca2+ après STX n'est pas corrlée avec des modifications de l'excrétion de Ca2+ conduit par l'ATP à travers la membrane basolatérale, suggérant donc une régulation au niveau de la membrane apicale. De plus, la STC ne modifie pas le transport de Ca2+ conduit par l'ATP dans des membranes basolatérales isolées (in vitro). La STC (0.1 nM) réduit les niveaux d'AMPc dans des cellules dispersées de branchies d'anguille. Cette hormone n'a pas d'effet significatif sur les niveaux d'IP3 dans ces cellules. Nous suggérons que la STC régule la perméabilité au Ca2+ des membranes apicales des cellules branchiales transporteuses de Ca2+ en controlant un second messager agissant sur les canaux calciques de la membrane apicale.
    Type of Medium: Electronic Resource
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