We acclimated the estuarine mussel Geukensia demissa to a regime of sinusoidal salinity cycling (12 h cycle between 100 % and 60 % seawater) and correlated changes in the volume of gill cells with changes in several indicators of the functional status of gill cells (rate of O2 consumption, ATP content and amino acid transport). There was no indication of short-term volume regulation in the gill cells of mussels acclimated to salinity cycling. When exposed to cycling salinity, cell water space consistently increased to approximately 3 ml g-1 dry mass during the cycle troughs (60 % seawater) and returned to approximately 2 ml g-1 dry mass at the cycle peaks (100 % seawater). In mussels acclimated for 2 weeks to cycling salinity, the gill contents of betaine, taurine and K+ were unchanged (approximately 240, 230 and 160 micromol g-1 dry mass, respectively) between the 60 % and 100 % seawater portions of the salinity cycle. The changes in cell volume did not appear to be associated with large perturbations in the functional status of cells. The rate of O2 consumption was approximately 100 microl O2 g-1 dry mass min-1, and ATP content was approximately 30 micromol g-1 protein, in all salinities to which mussels were exposed. Rates of uptake of taurine, leucine and phenylalanine decreased by approximately 50 % during the first sinusoidal decrease to 60 % seawater, but recovered following re-exposure to 100 % seawater. Uptake rates of all three amino acids were unaffected by any subsequent salinity cycles. These results suggest (1) that the regulation of gill cell volume is normally absent from mussels exposed to repeated, gradual salinity changes, and (2) that any effects of changes in cell volume are not severe enough to justify the energetic expenditure that would be associated with repeated regulation of cell volume. Unlike the response of gill cells to cycling salinity, there was a decrease in the solute contents of ventricles during the salinity troughs compared with the salinity peaks, suggesting that the presence of short-term volume regulation may be more critical in the ventricle.

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