RESULTS Mass and length There was no significant difference in mass Acid

Results mass and length there was no significant

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RESULTS Mass and length There was no significant difference in mass (Acid-Al=29.6±4.3g, control=29.0±3.5g; t -test: t 1,18 =0.36, P =0.72) or fork length (Acid- Al=14.4±0.8cm, control=14.2±0.6cm; t -test: t 1,18 =0.88, P =0.39) of fish after 2weeks of treatment. Physiology Gill aluminum Gill Al levels were higher in the Acid-Al exposed fish compared with the control fish ( t -test: t 1,17 =23.04, P <0.01; Table3). Plasma glucose Fish from the Acid-Al treatment were hyperglycemic, whereas those from the control treatment were not ( t -test: t 1,18 =3.83, P =0.01; Table3). Plasma cortisol Fish from the Acid-Al treatment had higher plasma cortisol levels than control fish (Mann–Whitney: U =11.0, P <0.01; Table3). NKA activity Fish from the Acid-Al treatment had significantly lower NKA activity than control fish ( t -test: t 1,18 =5.82, P <0.01; Table3). NeuroD1 mRNA Fish from the Acid-Al treatment had significantly lower neuroD1 mRNA levels (relative to RPL 23) than control fish (Acid- Al=4.6±1.4, control=6.9±2.3; t -test: t 1,18 =2.67, P =0.02; Fig.2). Behavior For both the control and Acid-Al fish, the average number of arms visited decreased across trials, suggesting that performance improved as the fish became more experienced with the maze (ANOVA: F 5,407 =3.57, P <0.01). Examining the behavior of the fish across the two blocks (block 1: trials 1–3 and block 2: trials 4–6) revealed a significant effect of treatment across block 2 trials, with Acid-Al fish making more mistakes on average than control fish (Acid- Al=3.6±0.3, control=2.9±0.2, ANOVA: F 1,67 =4.23, P =0.04; Fig.3). There was no effect of treatment across block 1 trials (ANOVA: F 1,68 =0.03, P =0.86). DISCUSSION Two weeks of exposure to Al in acidified water caused Al accumulation on the gills and impaired the spatial learning ability of smolting Atlantic salmon. The Acid-Al-exposed fish made more mistakes, indicating that acquisition of the task was inhibited, and had reduced neural plasticity indicators in their forebrain. Exposure to Al imposed a physiological stress, as levels of plasma glucose Table3. Summary of physiological parameters in control and Acid-Al fish Physiological parameter Control Acid-Al P Gill Al (μmolg –1 dry mass) 0.11±0.01 2.00±0.15 <0.01 Gill NKA activity ( m molADPh –1 mg –1 protein) 14.6±1.6 9.3±2.4 <0.01 Plasma glucose (mmoll –1 ) 5.3±0.5 7.7±2.8 0.01 Plasma cortisol (ngml –1 ) 14.5 43.0 <0.01 All values are reported as means ± s.d. excluding the plasma cortisol levels, which are median values. Control Acid-Al Treatment * 10 9 8 7 6 5 4 3 2 1 0 NeuroD mRNA (23RPL) Fig.2. Relative NeuroD1 mRNA expression in the telencephalon for control and Acid-Al fish (mean ± s.d.). *Significant difference between treatments ( P <0.05). THE JOURNAL OF EXPERIMENTAL BIOLOGY
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3153 Al exposure and Atlantic salmon and cortisol increased. Together, these data suggest that exposure to Al toxicity in acidified water has a negative impact on both the brain and learning behavior in salmon. Such an effect is likely to have a negative influence on the ability of the fish to cope with the transition from freshwater to the marine environment, a time when the fish need to perform critical behaviors such as predator avoidance, social interactions and navigation (McCormick et al., 1998; Ebbesson and Braithwaite, 2012). Furthermore, it is possible
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  • Winter '20
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