Abstract

We previously reported that the marine, longhorn sculpin, Myoxocephalus octodecemspinosus, can acclimate to 20% SW for days with no change in plasma osmolality, ion concentrations, or hematocrit level. Sculpin, however, lose ions during acclimation to 10% SW for 24 and 72 h and this reaches a lethal level after 6 days. During these acclimations, the sculpin is incapable of down‐regulating gill NKCC or CFTR, suggesting that they cannot turn off their gill ion secreting mechanisms. The counterpart to this is whether they can upregulate the transporters necessary for ion uptake during acclimation to low salinity water, such as the Na+/H+ exchangers (NHE), anion exchanger 1 (AE1) or H+‐ATPase (HAT), and thus maintain proper ion and water balance. We determined that sculpin upregulate gill NHE3 mRNA and NHE2c, while significantly down regulating AE1 during acclimation to 20% SW, and have undetectable levels of NHE2b during acclimation to 10% SW. There were no significant changes in HAT or NHE8. These transporters were immunolocalized in the sculpin gill, and we determined that during acclimation to 10 or 20% SW they are distributed in different aspects of the ion transporting cells of the gill. We conclude that longhorn sculpin are incapable of properly regulating gill ion transporters; thus, this is a physiological barrier from living in low‐salinity (below 10% SW) or fresh water.

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