P3.158 Friday, Jan. 6 Na,K-ATPase Isoform Switching is Critical for the Development of Salinity Tolerance in Juvenile Atlantic Salmon. MCCORMICK, S.D.*; REGISH, A.M.; CHRISTENSEN, A.K.; BJORNSSON, B.T.; USGS, Conte Anadromous Fish Res Ctr, Turners Falls, MA; USGS; USGS; University of Goteborg, Sweden email@example.com
The sodium pump, Na+,K+-ATPase (NKA), in the gills of teleost fish is involved in ion regulation in both freshwater and seawater. Freshwater and seawater isoforms of the alpha subunit of Na+/K+-ATPase have previously been identified in gill ionocytes of Atlantic salmon. We examined the abundance and cellular localization of these isoforms during the parr-smolt transformation, a developmental process which is preparatory for seawater entry. NKA activity increased 2.5-fold during smolt development, and salinity tolerance was higher in smolt than in parr. The abundance of NKAa1a was lower in smolts than in parr, but remained relatively constant during spring and decreased in summer. NKAa1b increased ten-fold in smolts during spring, peaking in early May at the time of downstream migration and salinity tolerance, then decreased in summer. NKAa1b increased a further two-fold after seawater exposure of smolts, whereas NKAa1a decreased by 98%. The abundance of NKAa1b-positive and NKAa1b and NKAa1a colabeled ionocytes increase during smolt development, whereas NKAa1a cells decrease. After seawater exposure of smolts, NKAa1b-positive ionocytes increase, whereas colabeled cells disappear and NKA&alpha1a-positive cells decrease. Plasma growth hormone and cortisol increased during spring in smolts, but not in parr, peaking just prior to the highest levels of NKAa1b. The results indicate that the increase in the abundance of NKAa1b during smolt development is directly linked to the increase in salinity tolerance that occurs at this stage, and that significant changes also occur after seawater exposure. Spring increases in circulating levels of growth hormone, IGF-I and cortisol indicate these hormones are involved in upregulation of NKAa1b during smolt development.