As atmospheric CO2 levels rise, the CO2 concentration in ocean surface waters increases through a process commonly referred to as ocean acidification. Recently, surprising behavioural modifications has been detected in the early life stages of tropical coral reef fish exposed to ocean acidification-relevant CO2 concentrations, but it has been unclear if this effect could occur in temperate waters. Here we show several severe behavioural disturbances, including effects on boldness, exploratory behaviour, lateralisation, and learning in a temperate fish, the three-spined stickleback (Gasterosteus aculeatus). The behavioural effects were consistent throughout the exposure period and increased in effect size with exposure time. We observed the effects on adult sticklebacks, a species known to be tolerant to other environmental stressors. Our findings suggest that behavioural abnormalities that stem from CO2 exposure are not restricted to sensitive tropical species or early life stages and may therefore affect fish on a global scale. The severity of disturbances and the possibility of a serious behavioural problem for fish across the globe is cause for concern.

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Ocean acidification and warming are both primarily caused by increased levels of atmospheric CO2, and marine organisms are exposed to these two stressors simultaneously. Although the effects of temperature on fish have been investigated over the last century, the long-term effects of moderate CO2 exposure and the combination of both stressors are almost entirely unknown. A proteomics approach was used to assess the adverse physiological and biochemical changes that may occur from the exposure to these two environmental stressors. We analysed gills and blood plasma of Atlantic halibut (Hippoglossus hippoglossus) exposed to temperatures of 12°C (control) and 18°C (impaired growth) in combination with control (400 µatm) or high-CO2 water (1000 µatm) for 14 weeks. The proteomic analysis was performed using two-dimensional gel electrophoresis (2DE) followed by Nanoflow LC-MS/MS using a LTQ-Orbitrap. The high-CO2 treatment induced the up-regulation of immune system-related proteins, as indicated by the up-regulation of the plasma proteins complement component C3 and fibrinogen β chain precursor in both temperature treatments. Changes in gill proteome in the high-CO2 (18°C) group were mostly related to increased energy metabolism proteins (ATP synthase, malate dehydrogenase, malate dehydrogenase thermostable, and fructose-1,6-bisphosphate aldolase), possibly coupled to a higher energy demand. Gills from fish exposed to high-CO2 at both temperature treatments showed changes in proteins associated with increased cellular turnover and apoptosis signalling (annexin 5, eukaryotic translation elongation factor 1γ, receptor for protein kinase C, and putative ribosomal protein S27). This study indicates that moderate CO2-driven acidification, alone and combined with high temperature, can elicit biochemical changes that may affect fish health.

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Oceans are warming and pH levels are decreasing as a consequence of increasing levels of dissolved CO2 concentrations. The CO2 emissions are predicted to be produce in greater and faster changes in the ocean than any other event in geological and historical records over the past 300 million years. Marine organisms will need to respond to multiple stressors but the potential consequences of global change-related effects in fish are not fully understood. Since fish are affected by many biotic and abiotic environmental variables, including temperature and CO2 fluctuations, it is critical to investigate how these variables may affect physiological and biochemical processes. We investigated the effects of elevated CO2 levels (pH of 8.0, which served as a control, or 7.6, which is predicted for the year 2100) combined with exposure to different temperatures (5, 10, 12, 14, 16, and 18 °C ) in the Atlantic halibut (Hippoglossus hippoglossus) during a three month experiment. We assessed effects on antioxidant and cholinesterase enzymes (AChE and BChE), and CYP1A enzyme activities (EROD). The treatments resulted in oxidative stress, and damage was evident in the form of protein carbonyls which were consistently higher in the elevated CO2-treated fish at all temperatures. Analyses of antioxidant enzymes did not show the same results, suggesting that the exposure to elevated CO2 increased ROS formation but not defences. The antioxidant defence system was insufficient, and the resulting oxidative damage could impact physiological function of the halibut on a cellular level.

Early restriction of nutrients during the perinatal period has marked repercussions on CNS ontogeny, leading to impaired functions. This study investigated the effects of pre- and postnatal (up to 75 days) undernutrition (diet: 8% protein; normonourished group: 25% protein) on some glutamatergic and behavioral parameters of rats. Undernutrition reduced: (i) seizures caused by ICV quinolinic acid (QA) administration; (ii) Na-independent [3H]glutamate binding in cell plasma membranes of cerebral cortex, and (ii) basal [3H]glutamate release from synaptosomal preparation. Behavioral parameters related to locomotion, anxiety, or memory were not affected. These results indicate that our model of undernutrition decreased the sensitivity to QA as convulsing agent and point to some putative glutamatergic parameters involved in this effect.

We have investigated the glycine, serine and leucine metabolism in slices of various rat brain regions of 14-day-old or adult rats, using [1-14C]glycine, [2-14C]glycine, L-[3-14C]serine and L-[U-14C]leucine. We showed that the [1-14C]glycine oxidation to CO2 in all regions studied occurs almost exclusively through its cleavage system (GCS) in brains of both 14-day-old and adults rats. In 14-day-old rats, the highest oxidation of [1-14C]glycine was in cerebellum and the lowest in medulla oblongata. In these animals, the L-[U-14C]leucine oxidation was lower than the [1-14C]glycine oxidation, except in medulla oblongata where both oxidations were the same. Serine was the amino acid that showed lowest oxidation to CO2 in all structure studied. In adult rats brains, the highest oxidation of [1-14C]glycine was in cerebral cortex and the lowest in medulla oblongata. We have not seen difference in the lipid synthesis from both glycine labeled, neither in 14-day-old rats nor in adult ones, indicating that the lipids formed from glycine were not neutral. Lipid synthesis from serine was significantly high than lipid synthesis and from all other amino acids studied in all studied structures. Protein synthesis from L-[U-14C]leucine was significantly higher than that from glycine in all regions and ages studied.