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Temperature fluctuations and climate change impacts may substantially affect spawning success of fish, especially migratory species with a limited spawning window. Factors affecting American shad (Alosa sapidissima) spawning success and survival were investigated at different temperatures and periods (peak- and late-spawning periods) during the Connecticut River, USA, spawning migration in 2017. Wild caught American shad were exposed to constant temperatures regimes of 15, 18, 21, 24 and 27 °C for 2 weeks. During the peak-spawning period, an increase in temperature (15–24 °C) was shown to increase spawning success factors, including spawning probability, number of eggs, and fertilization success, but decreased egg size. Temperatures between 18 and 27 °C did not affect these factors during the late-spawning period. Glochidia infection by the alewife floater (Anodonta implicata) was much higher in the late-spawning period and significantly decreased the survival of American shad. Further research should investigate the parasite-host relationship between the alewife floater and American shad to determine annual variability of glochidia infections and how they affect American shad from physiological and passage perspectives. Higher temperatures were shown to increase spawning success of American shad during the peak-spawning period, but temperature had no effect during the late-spawning period. However, any effect during the late-spawning period may have been masked by a high level of glochidia infection.

Hatchery salmonid smolts are often reared using groundwater with elevated temperatures to maximize growth. Previous work has shown that rearing hatchery smolts in surface water with a more natural thermal regime resulted in increased return rates of adult landlocked Atlantic salmon (Salmo salar). We evaluated whether landlocked Atlantic salmon reared in surface water with a natural temperature regime have altered physiological smolt characteristics compared with fish reared in groundwater with elevated winter temperatures. Hatchery fish were sampled three consecutive years from January to May. Additional fish were released as smolts, recaptured, and compared with fry-stocked smolts. Surface water smolts had earlier peaks of plasma T4, lower T3 levels, later peak cortisol, and lower gill Na+/K+-ATPase activity as compared with groundwater smolts. After release and recapture, surface water fish had elevated plasma T4 and gill Na+/K+-ATPase activity compared with groundwater fish, but less than stream-reared fish. Elevated plasma T4 in surface water fish in the hatchery and after release may have promoted imprinting and other aspects of smolt development, contributing to the higher adult return rates of a cohort reared in surface water.

Migrating adult Pacific salmon (Oncorhynchus spp.) are sensitive to warm water (>18 °C), with a range of consequences from decreased spawning success to early mortality. We examined the proportion of Yukon River Chinook salmon (O. tshawytscha) exhibiting evidence of heat stress to assess the potential that high temperatures contribute to freshwater adult mortality in a northern Pacific salmon population. Water temperatures greater than 18 °C have occurred almost annually in the Yukon River and correspond with low population abundance since the 1990s. Using gene transcription products and heat shock protein 70 biomarkers validated by field experiment, we identified heat stress in half of Chinook salmon examined (54%, n = 477) across three mainstem locations and three tributaries in 2016–2017. Biomarkers tracked wide variation in water temperature (14–23 °C) within a tributary. The proportion of salmon with heat stress differed between years at four of the six locations, with more prevalent heat stress in the warmer year. This work demonstrates that warming water temperatures are currently affecting northern populations of Pacific salmon.

Juvenile American shad (Alosa sapidissima) experience a wide range of temperatures in rivers before migrating to the ocean. Temperatures in these freshwater environments can vary greatly spatially, seasonally, year-to-year, and can be impacted by anthropogenic factors such as power plant discharge or climate change. Currently, there is uncertainty concerning juvenile American shad thermal tolerance due to a lack of a well-controlled study. Here, we report results of laboratory experiments to establish the upper thermal tolerance and heat shock protein response of juvenile American shad exposed to gradually increasing temperatures. Upper thermal tolerance was determined to be 35 °C (median; range = 34–36 °C) when fish were acclimated to 25 °C and temperatures were raised 1 °C day−1. Heat shock protein response was indicated by changes in branchial mRNA abundance of the inducible heat shock protein 90 alpha (hsp90α), which was significantly elevated (more than 5-fold increase) at 30 °C, and highest in fish that had reached their upper thermal maximum between 34 and 36 °C. Our findings indicate a higher upper thermal tolerance than previously reported for juvenile American shad, and an onset temperature of hsp90α induction at 30 °C, a temperature juvenile American shad commonly experience during summer months.

The gill is one of the most important organs for growth and survival of fishes. Early life stages in coral reef fishes often exhibit extreme physiological and demographic characteristics that are linked to well-established respiratory and ionoregulatory processes. However, gill development and function in coral reef fishes is not well understood. Therefore, we investigated gill morphology, oxygen uptake and ionoregulatory systems throughout embryogenesis in two coral reef damselfishes, Acanthochromis polyacanthus and Amphiprion melanopus (Pomacentridae). In both species, we found key gill structures to develop rapidly early in the embryonic phase. Ionoregulatory cells appear on gill filaments 3–4 days post-fertilization and increase in density, whilst disappearing or shrinking in cutaneous locations. Primary respiratory tissue (lamellae) appears 5–7 days post-fertilization, coinciding with a peak in oxygen uptake rates of the developing embryos. Oxygen uptake was unaffected by phenylhydrazine across all ages (pre-hatching), indicating that haemoglobin is not yet required for oxygen uptake. This suggests that gills have limited contribution to respiratory functions during embryonic development, at least until hatching. Rapid gill development in damselfishes, when compared with that in most previously investigated fishes, may reflect preparations for a high-performance, challenging lifestyle on tropical reefs, but may also make reef fishes more vulnerable to anthropogenic stressors.

Our current understanding of the hormonal control of ion regulation in aquatic vertebrates comes primarily from studies on teleost fishes, with relatively little information on more basal fishes. We investigated the role of cortisol in regulating seawater tolerance and its underlying mechanisms in an anadromous chondrostean, the Atlantic sturgeon (Acipenser oxyrinchus). Exposure of freshwater-reared Atlantic sturgeon to seawater (25 ppt) resulted in transient (1–3 day) increases in plasma chloride, cortisol and glucose levels and long-term (6–14 day) increases in the abundance of gill Na+/K+/2Cl− cotransporter (NKCC), which plays a critical role in salt secretion in teleosts. The abundance of gill V-type H+-ATPase, which is thought to play a role in ion uptake in fishes, decreased after exposure to seawater. Gill Na+/K+-ATPase activity did not increase in 25 ppt seawater, but did increase in fish gradually acclimated to 30 ppt. Treatment of Atlantic sturgeon in freshwater with exogenous cortisol resulted in dose-dependent increases in cortisol, glucose and gill NKCC and H+-ATPase abundance. Our results indicate that cortisol has an important role in regulating mechanisms for ion secretion and uptake in sturgeon and provide support for the hypothesis that control of osmoregulation and glucose by corticosteroids is a basal trait of jawed vertebrates.

The growth hormone (Gh)/insulin-like growth-factor (Igf)/Igf binding protein (Igfbp) system regulates growth and osmoregulation in salmonid fishes, but how this system interacts with other endocrine systems is largely unknown. Given the well-documented consequences of mounting a glucocorticoid stress response on growth, we hypothesized that cortisol inhibits anabolic processes by modulating the expression of hepatic igfbp mRNAs. Atlantic salmon (Salmo salar) parr were implanted intraperitoneally with cortisol implants (0, 10, and 40 μg g−1 body weight) and sampled after 3 or 14 days. Cortisol elicited a dose-dependent reduction in specific growth rate (SGR) after 14 days. While plasma Gh and Igf1 levels were unchanged, hepatic igf1 mRNA was diminished and hepatic igfbp1b1 and -1b2 were stimulated by the high cortisol dose. Plasma Igf1 was positively correlated with SGR at 14 days. Hepatic gh receptor (ghr), igfbp1a, -2a, -2b1, and -2b2 levels were not impacted by cortisol. Muscle igf2, but not igf1 or ghr, levels were stimulated at 3 days by the high cortisol dose. As both cortisol and the Gh/Igf axis promote seawater (SW) tolerance, and particular igfbps respond to SW exposure, we also assessed whether cortisol coordinates the expression of branchial igfbps and genes associated with ion transport. Cortisol stimulated branchial igfbp5b2 levels in parallel with Na+/K+-ATPase (NKA) activity and nka-α1b, Na+/K+/2Cl--cotransporter 1 (nkcc1), and cystic fibrosis transmembrane regulator 1 (cftr1) mRNA levels. The collective results indicate that cortisol modulates the growth of juvenile salmon via the regulation of hepatic igfbp1s whereas no clear links between cortisol and branchial igfbps previously shown to be salinity-responsive could be established.

Chinook salmon (Oncorhynchus tshawytscha) declines are widespread and may be attributed, at least in part, to warming river temperatures. Water temperatures in the Yukon River and tributaries often exceed 18°C, a threshold commonly associated with heat stress and elevated mortality in Pacific salmon. Untangling the complex web of direct and indirect physiological effects of heat stress on salmon is difficult in a natural setting with innumerable system challenges but is necessary to increase our understanding of both lethal and sublethal impacts of heat stress on populations. The goal of this study was to characterize the cellular stress response in multiple Chinook salmon tissues after acute elevated temperature challenges. We conducted a controlled 4-hour temperature exposure (control, 18°C and 21°C) experiment on the bank of the Yukon River followed by gene expression (GE) profiling using a 3′-Tag-RNA-Seq protocol. The full transcriptome was analysed for 22 Chinook salmon in muscle, gill and liver tissue. Both the 21°C and 18°C treatments induced greater activity in genes associated with protein folding (e.g. HSP70, HSP90 mRNA) processes in all tissues. Global GE patterns indicate that transcriptomic responses to heat stress were highly tissue-specific, underscoring the importance of analyzing multiple tissues for determination of physiological effect. Primary superclusters (i.e. groupings of loosely related terms) of altered biological processes were identified in each tissue type, including regulation of DNA damage response (gill), regulation by host of viral transcription (liver) and regulation of the force of heart contraction (muscle) in the 21°C treatment. This study provides insight into mechanisms potentially affecting adult Chinook salmon as they encounter warm water during their spawning migration in the Yukon River and suggests that both basic and more specialized cellular functions may be disrupted.

Chinook salmon (Oncorhynchus tshawytscha) declines are widespread and may be attributed, at least in part, to warming river temperatures. Water temperatures in the Yukon River and tributaries often exceed 18°C, a threshold commonly associated with heat stress and elevated mortality in Pacific salmon. Untangling the complex web of direct and indirect physiological effects of heat stress on salmon is difficult in a natural setting with innumerable system challenges but is necessary to increase our understanding of both lethal and sublethal impacts of heat stress on populations. The goal of this study was to characterize the cellular stress response in multiple Chinook salmon tissues after acute elevated temperature challenges. We conducted a controlled 4-hour temperature exposure (control, 18°C and 21°C) experiment on the bank of the Yukon River followed by gene expression (GE) profiling using a 3′-Tag-RNA-Seq protocol. The full transcriptome was analysed for 22 Chinook salmon in muscle, gill and liver tissue. Both the 21°C and 18°C treatments induced greater activity in genes associated with protein folding (e.g. HSP70, HSP90 mRNA) processes in all tissues. Global GE patterns indicate that transcriptomic responses to heat stress were highly tissue-specific, underscoring the importance of analyzing multiple tissues for determination of physiological effect. Primary superclusters (i.e. groupings of loosely related terms) of altered biological processes were identified in each tissue type, including regulation of DNA damage response (gill), regulation by host of viral transcription (liver) and regulation of the force of heart contraction (muscle) in the 21°C treatment. This study provides insight into mechanisms potentially affecting adult Chinook salmon as they encounter warm water during their spawning migration in the Yukon River and suggests that both basic and more specialized cellular functions may be disrupted.

Human activity has resulted in increasing atmospheric carbon dioxide (CO2 ), which will result in reduced pH and higher levels of CO2 in the ocean, a process known as ocean acidification. Understanding the effects of ocean acidification (OA) on fishes will be important to predicting and mitigating its consequences. Anadromous species such as salmonids may be especially at risk because of their rapid movements between fresh water and seawater, which could minimize their ability to acclimate. In the present study, we examine the effect of future OA on the salinity tolerance and early seawater growth of Atlantic salmon Salmo salar smolts. Exposure to 610 and 1010 μatm CO2 did not alter salinity tolerance but did result in slightly lower plasma chloride levels in smolts exposed to seawater compared with controls (390 μatm). Gill Na+ -K+ -ATPase activity, plasma cortisol, glucose and haematocrit after seawater exposure were not altered by elevated CO2 . Growth rate in the first 2 weeks of seawater exposure was greater at 1010 μatm CO2 than under control conditions. This study of the effects of OA on S. salar during the transition from fresh water to seawater indicates that elevated CO2 is not likely to affect osmoregulation negatively and may improve early growth in seawater.

Atlantic salmon (Salmo salar) smolts are sensitive to acid rain and associated increases in dissolved inorganic aluminum (Al) resulting in decreased seawater tolerance at this critical life stage. Salmon have two major isoforms of the catalytic alpha subunit of Na+/K+-ATPase (NKA), with NKAα1a being the major freshwater (FW) isoform and NKAα1b the major seawater (SW) isoform. Here we evaluate physiological markers of SW preparedness and NKAα1a and NKAα1b isoforms after short-term exposure to acidified water and acidified water with added Al (acid–Al). Atlantic salmon smolts were exposed to low ion FW (Control), low ion acidic water (pH 5.2; acid), and low ion acidic water (pH 5.2) with moderate levels of added inorganic Al (35 μg·L−1; acid–Al) for 4 days. Acid exposure resulted in loss of salinity tolerance (higher plasma chloride (Cl) after SW exposure) and significantly decreased the levels of gill NKAα1b but not NKAα1a protein abundance. Acid–Al exposure resulted in loss of plasma Cl in FW and higher plasma Cl in SW and decreased NKAα1a and NKAα1b abundance. The loss of salinity tolerance in smolts can be explained by the differential sensitivity of NKA isoforms to acid.

Lipid content forms the most important energy reserve in anadromous fish and can limit survival, migration and reproductive success. A fat meter was evaluated and compared with a traditional extractive method of measuring available lipid for migrating American shad Alosa sapidissima in the Connecticut River, U.S.A. The fat meter gives rapid (

Cortisol is the final product of the hypothalamic-pituitary-interrenal (HPI) axis and acts as a gluco- and mineralo-corticoid in fish. Long-term elevations of cortisol have been linked to reduced growth in fishes, but the mechanism(s) and relative sensitivities of species are still unclear. We carried out experiments to examine the relative effects of cortisol on growth and gill NKA activity in two salmonids: Atlantic salmon (Salmo salar) and brook trout (Salvelinus fontinalis). Treatment with intraperitoneal cortisol implants for 30 days resulted in reduced growth in both species, but with greater sensitivity to cortisol in brook trout. Gill NKA activity was strongly upregulated by cortisol in Atlantic salmon, and weakly upregulated in brook trout but with no statistically significant effect. Cortisol treatment resulted in reduced plasma levels of insulin-like growth factor I and increased plasma growth hormone levels in Atlantic salmon. Our results demonstrate that there are species differences in the sensitivity of growth and osmoregulation to cortisol, even among species in the same family (Salmonidae).

Thermal acclimation is known to elicit metabolic adjustments in ectotherms, but the cellular mechanisms and endocrine control of these shifts have not been fully elucidated. Here we examined the relationship between thermal acclimation, thyroid hormones and oxidative metabolism in juvenile lake whitefish. Impacts of thermal acclimation above (19°C) or below (8°C) the thermal optimum (13°C) and exposure to exogenous thyroid hormone (60µg T4/g body weight) were assessed by quantifying citrate synthase and cytochrome c oxidase activities in liver, red muscle, white muscle and heart. Warm acclimation decreased citrate synthase activity in liver and elevated both citrate synthase and cytochrome c oxidase activities in red muscle. In contrast, induction of hyperthyroidism in warm-acclimated fish stimulated a significant increase in liver citrate synthase and heart cytochrome c oxidase activities, and a decrease in the activity of both enzymes in red muscle. No change in citrate synthase or cytochrome c oxidase activities was observed following cold acclimation in either the presence or absence of exogenous thyroid hormones. Collectively, our results indicate that thyroid hormones influence the activity of oxidative enzymes more strongly in warm-acclimated than in cold-acclimated lake whitefish, and they may play a role in mediating metabolic adjustments observed during thermal acclimation.

Populations of anadromous fish have become landlocked in relatively recent geological history (+/K+-ATPase increased in spring in both strains but was greater in anadromous salmon. Hormones associated with seawater acclimation (adrenocorticotropic hormone, cortisol and growth hormone) increased in spring in both strains but were higher in anadromous salmon, whereas plasma thyroid hormones did not differ. Hypothalamic urotensin I mRNA levels also increased in spring and were higher in the anadromous strain. The results provide evidence that salinity tolerance and associated physiological traits are regulated by seasonal stimulation of the hypothalamic-pituitary-interrenal axis, and that relaxed selection on seawater entry traits has decreased this stimulation in landlocked salmon.

As stream temperatures increase due to factors such as heated runoff from impervious surfaces, deforestation, and climate change, fish species adapted to cold water streams are forced to move to more suitable habitat, acclimate or adapt to increased thermal regimes, or die. To estimate the potential for adaptation, a (within individual) repeatable metric of thermal tolerance is imperative. Critical thermal maximum (CTmax) is a dynamic test that is widely used to measure thermal tolerance across many taxa and has been used in fishes for decades, but its repeatability in most species is unknown. CTmax tests increase water temperature steadily over time until loss of equilibrium (LOE) is achieved. To determine if CTmax is a consistent metric within individual fish, we measured CTmax on the same lab-held individually-marked adult brook trout Salvelinus fontinalis at three different times (August & September 2016, September 2017). We found that CTmax is a repeatable trait (Repeatability ± S.E.: 0.48 ± 0.14). CTmax of individuals males was consistent over time, but the CTmax of females increased slightly over time. This result indicates that CTmax is a robust, repeatable estimate of thermal tolerance in a cold-water adapted fish.

Smolting Atlantic salmon exhibit a seasonal increase in seawater tolerance that is associated with changes in the abundance of major gill ion-transporter transcripts and proteins. In the present study, we investigate how the transcript and protein abundance of specific ion-transporter isoforms relate to each other during smolt development and seawater acclimation, and how each correlates to seawater tolerance. We show that during smolt development both mRNA and protein abundance of gill Na+/K+-ATPase α1a subunit (NKAα1a) decreased but the decrease in the mRNA was five-times greater than that of the protein. Gill NKAα1b mRNA levels increased only slightly (1.5-fold) throughout development whereas protein abundance increased 30-fold at its peak. Gill Na+/K+/2Cl− co-transporter 1 (NKCC1) increased at the mRNA and protein level (5- and 12-fold) in smolts. The abundance of a gill ion-transporter's mRNA and protein changed in the same direction through development and after seawater transfer, but the changes were not always strongly correlated: NKAα1a (r = 0.768), NKAα1b (r = 0.40), and NKCC1 (r = 0.898). The maintenance of plasma chloride concentration correlated most strongly with the abundance of NKAα1a mRNA, and the ratio of NKAα1b to NKAα1a mRNA and protein. Growth performance after seawater transfer correlated most strongly with the abundance of NKAα1b protein and the ratio of NKAα1b to NKAα1a protein. Our results indicate that the abundance of ion-transporter mRNA and protein do not always correlate well and a decrease in the abundance of gill NKAα1a mRNA and increase in NKAα1b protein are strong predictors of seawater tolerance and growth performance after seawater transfer.

Smolting in Atlantic salmon Salmo salar is a critical life-history stage that is preparatory for downstream migration and entry to seawater that is regulated by abiotic variables including photoperiod and temperature. The present study was undertaken to determine the interaction of temperature and salinity on salinity tolerance, gill osmoregulatory proteins and cellular and endocrine stress in S. salar smolts. Fish were exposed to rapid changes in temperature (from 14 to 17, 20 and 24°C) in fresh water (FW) and seawater (SW), with and without prior acclimation and sampled after 2 and 8 days. Fish exposed simultaneously to SW and 24°C experienced 100% mortality, whereas no mortality occurred in any of the other groups. The highest temperature also resulted in poor ion regulation in SW with or without prior SW acclimation, whereas no substantial effect was observed in FW. Gill Na+ -K+ -ATPase (NKA) activity increased in SW fish compared to FW fish and decreased with high temperature in both FW and SW. Gill Nkaα1a abundance was high in FW and Nkaα1b and Na+ -K+ -2Cl- cotransporter high in SW, but all three were lower at the highest temperature. Gill Hsp70 levels were elevated in FW and SW at the highest temperature and increased with increasing temperature 2 days following direct transfer to SW. Plasma cortisol levels were elevated in SW at the highest temperature. Our results indicate that there is an important interaction of salinity and elevated temperature on osmoregulatory performance and the cellular stress response in S. salar, with an apparent threshold for osmoregulatory failure in SW above 20°C.

Field studies were conducted to determine levels of gill aluminium as an index of acidification effects on migrating Atlantic salmon Salmo salar smolts in the north-eastern U.S.A. along mainstem river migration corridors in several major river basins. Smolts emigrating from the Connecticut River, where most (but not all) tributaries were well buffered, had low or undetectable levels of gill aluminium and high gill Na(+) /K(+) -ATPase (NKA) activity. In contrast, smolts emigrating from the upper Merrimack River basin where most tributaries are characterized by low pH and high inorganic aluminium had consistently elevated gill aluminium and lower gill NKA activity, which may explain the low adult return rates of S. salar stocked into the upper Merrimack catchment. In the Sheepscot, Narraguagus and Penobscot Rivers in Maine, river and year-specific effects on gill aluminium were detected that appeared to be driven by underlying geology and high spring discharge. The results indicate that episodic acidification is affecting S. salar smolts in poorly buffered streams in New England and may help explain variation in S. salar survival and abundance among rivers and among years, with implications for the conservation and recovery of S. salar in the north-eastern U.S.A. These results suggest that the physiological condition of outmigrating smolts may serve as a large-scale sentinel of landscape-level recovery of atmospheric pollution in this and other parts of the North Atlantic region.

The timing of downstream migration and detection rates of hatchery-reared Atlantic salmon Salmo salar smolts and stream-reared smolts (stocked 2 years earlier as fry) were examined in the Connecticut River (U.S.A.) using passive integrated transponder (PIT) tags implanted into fish and then detected at a downstream fish bypass collection facility at Turners Falls, MA (river length 192 km). In two successive years, hatchery-reared smolts were released in mid-April and early May at two sites: the West River (river length 241 km) or the Passumpsic (river length 450 km). Hatchery-reared smolts released higher in the catchment arrived 7 to 14 days later and had significantly lower detection rates than smolts stocked lower in the catchment. Hatchery-reared smolts released 3 weeks apart at the same location were detected downstream at similar times, indicating that early-release smolts had a lower average speed after release and longer residence time. The size and gill Na(+) /K(+) -ATPase (NKA) activity of smolts at the time of release were significantly greater for detected fish (those that survived and migrated) than for those that were not detected. Stream-reared pre-smolts (>11·5 cm) from four tributaries (length 261-551 km) were tagged in autumn and detected during smolt migration the following spring. Stream-reared smolts higher in the catchment arrived later and had significantly lower detection rates. The results indicate that both hatchery and stream-reared smolts from the upper catchment will arrive at the mouth of the river later and experience higher overall mortality than fish from lower reaches, and that both size and gill NKA activity are related to survival during downstream migration.

Freshwater and seawater isoforms of the alpha subunit of Na+/K+-ATPase (NKA) have previously been identified in gill ionocytes of Atlantic salmon ( Salmo salar ). In the present study we examine the abundance and cellular localization of these isoforms during the parr–smolt transformation, a developmental process that is preparatory for seawater entry. The abundance of NKAα1a was lower in smolts than in parr, remained relatively constant during spring and decreased in summer. NKAα1b increased tenfold in smolts during spring, peaking in late April, coincident with downstream migration and increased salinity tolerance. NKAα1b increased a further twofold after seawater exposure of smolts, whereas NKAα1a decreased by 98%. The abundance of NKAα1b-positive, and NKAα1b and NKAα1a co-labeled ionocytes increased during smolt development, whereas the number of NKAα1a cells decreased. After seawater exposure of smolts, NKAα1b-positive ionocytes increased, NKAα1a-positive cells decreased, and co-labeled cells disappeared. Plasma growth hormone and cortisol increased during spring in smolts, but not in parr, peaking just prior to the highest levels of NKAα1b. The results indicate that the increase in the abundance of NKAα1b during smolt development is directly linked to the increase in salinity tolerance that occurs at this stage, but that significant changes also occur after seawater exposure. Spring increases in circulating levels of growth hormone and cortisol indicate that these hormones may be instrumental in upregulating NKAα1b during smolt development. * CFTR : cystic fibrosis transmembrane regulator GH : growth hormone NKA : Na+/K+-ATPase NKCC : Na+/K+/Cl− co-transporter

Billions of hatchery salmon smolts are released annually in an attempt to mitigate anthropogenic impacts on freshwater habitats, often with limited success. Mortality of wild and hatchery fish is high during downstream and early ocean migration. To understand changes that occur during migration, we examined physiological and endocrine changes in Atlantic salmon (Salmo salar) smolts during hatchery rearing, downstream migration, and early ocean entry in two successive years. Gill Na+/K+-ATPase activity increased in the hatchery during spring, increased further after river release, and was slightly lower after recapture in the ocean. Plasma growth hormone levels increased in the hatchery, were higher in the river, and increased further in the ocean. Plasma IGF-I remained relatively constant in the hatchery, increased in the river, then decreased in the ocean. Plasma thyroid hormones were variable in the hatchery, but increased in both river- and ocean-captured smolts. Naturally reared fish had lower condition factor, gill NKA activity, and plasma thyroxine than hatchery fish in the river but were similar in the ocean. This novel data set provides a vital first step in understanding the role and norms of endocrine function in smolts and the metrics of successful marine entry.

The growth hormone (Gh)/insulin-like growth-factor (Igf) system plays a central role in the regulation of growth in fishes. However, the roles of Igf binding proteins (Igfbps) in coordinating responses to food availability are unresolved, especially in anadromous fishes preparing for seaward migration. We assayed plasma Gh, Igf1, thyroid hormones and cortisol along with igfbp mRNA levels in fasted and fed Atlantic salmon (Salmo salar). Fish were fasted for 3 or 10days near the peak of smoltification (late April to early May). Fasting reduced plasma glucose by 3days and condition factor by 10days. Plasma Gh, cortisol, and thyroxine (T4) were not altered in response to fasting, whereas Igf1 and 3,5,3'-triiodo-l-thyronine (T3) were slightly higher and lower than controls, respectively. Hepatic igfbp1b1, -1b2, -2a, -2b1 and -2b2 mRNA levels were not responsive to fasting, but there were marked increases in igfbp1a1 following 3 and 10days of fasting. Fasting did not alter hepatic igf1 or igf2; however, muscle igf1 was diminished by 10days of fasting. There were no signs that fasting compromised branchial ionoregulatory functions, as indicated by unchanged Na(+)/K(+)-ATPase activity and ion pump/transporter mRNA levels. We conclude that dynamic hepatic igfbp1a1 and muscle igf1 expression participate in the modulation of Gh/Igf signaling in smolts undergoing catabolism.

Although the negative effects of acid and aluminum (Al) on smolt development have been known for some time, the thresholds for impact of short-term exposure of several days that may occur during episodic acidification have not been systematically examined. In order to determine the levels of acid and Al that impact juvenile Atlantic salmon, smolts and yolk-sac larvae were exposed to three pH levels (6.0, 5.7, and 5.3) and four added Al levels (0, 40, 80 and 175 μg/L total Al) for 48 h. Following this treatment, 10 smolts were sampled in freshwater and another 10 were subjected to a 24 h seawater challenge (35 ppt). Survival of yolk-sac larvae was > 96% in all acid and Al treatments. All smolts died within 48 h at pH 5.3, 175 μg L − 1 Al. There were some mortalities in freshwater at pH 5.3, 80 μg L − 1 Al and pH 5.7, 175 μg L − 1 Al, and further mortalities when these fish were transferred to seawater. Mortalities in these groups were associated with decreased plasma chloride in freshwater and higher plasma chloride in seawater, indicating that these smolts had lost seawater tolerance. Gill Na + /K + -ATPase (NKA) activity decreased at pH 5.7, 175 μg L − 1 Al in freshwater, and further decreases were observed at more moderate pH and Al exposures after transfer to seawater. Hematocrit and plasma glucose were the most sensitive physiological responses, increasing at all Al treatments at pH 5.7 and 5.3 in freshwater. There was no detectable increase in gill Al levels at pH 6.0 with added Al, whereas substantial increases in gill Al were observed in all added Al groups at pH 5.7 and 5.3. Our results demonstrate a critical interaction between acid and Al in their effects on smolts, and that episodic acidification events will negatively impact smolt survival in freshwater and after seawater entry.

It has long been held that cortisol, acting through a single receptor, carries out both glucocorticoid and mineralocorticoid actions in teleost fish. The recent finding that fish express a gene with high sequence similarity to the mammalian mineralocorticoid receptor (MR) suggests the possibility that a hormone other than cortisol carries out some mineralocorticoid functions in fish. To test for this possibility, we examined the effect of in vivo cortisol, 11-deoxycorticosterone (DOC) and aldosterone on salinity tolerance, gill Na(+),K(+)-ATPase (NKA) activity and mRNA levels of NKA alpha 1a and alpha 1b in Atlantic salmon. Cortisol treatment for 6-14 days resulted in increased, physiological levels of cortisol, increased gill NKA activity and improved salinity tolerance (lower plasma chloride after a 24h seawater challenge), whereas DOC and aldosterone had no effect on either NKA activity or salinity tolerance. NKA alpha 1a and alpha 1b mRNA levels, which increase in response to fresh water and seawater acclimation, respectively, were both upregulated by cortisol, whereas DOC and aldosterone were without effect. Cortisol, DOC and aldosterone had no effect on gill glucocorticoid receptor GR1, GR2 and MR mRNA levels, although there was some indication of possible upregulation of GR1 by cortisol (p=0.07). The putative GR blocker RU486 inhibited cortisol-induced increases in salinity tolerance, NKA activity and NKA alpha 1a and alpha 1b transcription, whereas the putative MR blocker spironolactone had no effect. The results provide support that cortisol, and not DOC or aldosterone, is involved in regulating the mineralocorticoid functions of ion uptake and salt secretion in teleost fish.