Control of ion transport by mitochondrion-rich chloride cells of eurythermic teleost fish: Cold shock vs. cold acclimation

Seawater-acclimated eurythermic mummichogs (Fundulus heteroclitus L) were acclimated to cold and warm conditions (5 and 20 degrees C, 4 weeks). Opercular epithelia (OE) from 20 degrees C-acclimated animals, containing numerous mitochondrion-rich chloride cells were mounted in Ussing-style membrane chambers, cooled to 16, 13, 10,5 and 2.5 degrees C, then subjected to hypotonic shock that normally inhibits Cl- secretion (as short-circuit current, I-sc). Cold exposure to 10 degrees C slowed Cl- secretion (Q(10) = 1.62 +/- 0.204 95% CI) and OEs responded rapidly and reversibly to hypotonic shock, but below 8.0 degrees C a sharp decrease (Q(10) = 5.63 +/- 0.736) occurred and the tissue was unresponsive to hypotonicity. By immunocytochemistry, Focal Adhesion Kinase (FAK) phosphorylated at tyrosine-407 (pY(407)) colocalized with CFTR in apical membrane and dephosphorylated with hypotonic shock at 20 degrees C but failed to dephosphorylate at 5 degrees C, while opercular epithelia from cold-acclimated fish at 5 and 20 degrees C responded normally to hypotonic shock. Cold-shock of warm-acclimated OEs also stimulated covering over of mitochondrion- rich cell apical crypts, detected by SEM. Cold-acclimation increased C18:1 and decreased C18:0 fatty acids in liver, indicating homeoviscous adaptation. Eurythermic fish acclimate osmoregulatory systems to cold by maintaining membrane fluidity and preserving complex transport regulation pathways. (C) 2012 Elsevier Inc. All rights reserved.