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The hypoxia-inducible factor (HIF) is considered key in the transcriptional response to low oxygen. Yet, the role of HIF in the absence of oxygen (anoxia) and in preparation for reoxygenation remains unclear. Recent studies suggest that mounting a HIF response may be counterproductive for anoxia survival. We here studied one of the champions of anoxia survival, the crucian carp (Carassius carassius), and hypothesized that expression of prolyl hydroxylase domains (PHDs; the upstream regulators of HIF) are upregulated to circumvent an energy-costly activation of HIF in anoxia and to prepare for reoxygenation. We measured whole brain mRNA and protein levels of the three isoforms PHD1, PHD2, and PHD3, coded for by multiple paralogs of the genes egln2, egln1, and egln3, using quantitative PCR and Western blotting in the brain of crucian carps exposed to 5 days normoxia or anoxia, and 5 days anoxia followed by 3 or 24 h of reoxygenation. The mRNA levels of most egln paralogs were increased in anoxia and upon reoxygenation, with egln3 showing the largest increase in mRNA level (up to 17-fold) and highest relative mRNA abundance (up to 75% of expressed egln). The protein level of all PHDs was maintained in anoxia and increased upon reoxygenation. We then explored PHD distribution in different brain regions and found PHD immunoreactivity to be associated with axonal branches and showing region-specific changes during anoxia-reoxygenation. Our results support an overall upregulation of egln under prolonged anoxia and PHDs upon reoxygenation in crucian carp, likely aimed at suppressing HIF responses, although regional differences are apparent in such a complex organ as the brain. [ABSTRACT FROM AUTHOR]

Recent studies suggest that projected rises of aquatic CO2 levels cause acid-base regulatory responses in fishes that lead to altered GABAergic neurotransmission and disrupted behaviour, threatening fitness and population survival. It is thought that changes in Cl- and HCO3- gradients across neural membranes interfere with the function of GABA-gated anion channels (GABAA receptors). So far, such alterations have been revealed experimentally by exposing species living in low-CO2 environments, like many oceanic habitats, to high levels of CO2 (hypercapnia). To examine the generality of this phenomenon, we set out to study the opposite situation, hypothesizing that fishes living in typically hypercapnic environments also display behavioural alterations if exposed to low CO2 levels. This would indicate that ion regulation in the fish brain is fine-tuned to the prevailing CO2 conditions.We quantified pH regulatory variables and behavioural responses of Pangasianodon hypophthalmus, a fish native to the hypercapnic Mekong River, acclimated to high-CO2 (3.1 kPa) or low-CO2 (0.04 kPa) water. We found that brain and blood pH was actively regulated and that the low-CO2 fish displayed significantly higher activity levels, which were reduced after treatment with gabazine, a GABAA receptor blocker. This indicates an involvement of the GABAA receptor and altered Cl- and HCO3- ion gradients. Indeed, Goldman calculations suggest that low levels of environmental CO2 may cause significant changes in neural ion gradients in P. hypophthalmus. Taken together, the results suggest that brain ion regulation in fishes is fine-tuned to the prevailing ambient CO2 conditions and is prone to disruption if these conditions change. [ABSTRACT FROM AUTHOR]

Tropical coral reef organisms are predicted to be especially sensitive to ocean warming because many already live close to their upper thermal limit, and the expected rise in ocean CO2 is proposed to further reduce thermal tolerance. Little, however, is known about the thermal sensitivity of a diverse and abundant group of reef animals, the gastropods. The humpbacked conch (Gibberulus gibberulus gibbosus), inhabiting subtidal zones of the Great Barrier Reef, was chosen as a model because vigorous jumping, causing increased oxygen uptake (ṀO2), can be induced by exposure to odour from a predatory cone snail (Conus marmoreus). We investigated the effect of present-day ambient (417–454 µatm) and projected-future (955–987 µatm) PCO2 on resting (ṀO2,rest) and maximum (ṀO2,max) ṀO2, as well as ṀO2 during hypoxia and critical oxygen tension (PO2,crit), in snails kept at present-day ambient (28°C) or projectedfuture temperature (33°C). ṀO2,rest and ṀO2,max were measured both at the acclimation temperature and during an acute 5°C increase. Jumping caused a 4- to 6-fold increase in ṀO2, and ṀO2,max increased with temperature so that absolute aerobic scope was maintained even at 38°C, although factorial scope was reduced. The humpbacked conch has a high hypoxia tolerance with a PO2,crit of 2.5 kPa at 28°C and 3.5 kPa at 33°C. There was no effect of elevated CO2 on respiratory performance at any temperature. Long-term temperature records and our field measurements suggest that habitat temperature rarely exceeds 32.6°C during the summer, indicating that these snails have aerobic capacity in excess of current and future needs. [ABSTRACT FROM AUTHOR]

The Alaska blackfish (Dallia pectoralis) is an air-breathing fish native to Alaska and the Bering Sea islands, where it inhabits lakes that are ice-covered in the winter, but enters warm and hypoxic waters in the summer to forage and reproduce. To understand the respiratory physiology of this species under these conditions and the selective pressures that maintain the ability to breathe air, we acclimated fish to 5°C and 15°C and used respirometry to measure: standard oxygen uptake (ṀO2) in normoxia (19.8 kPa Po2) and hypoxia (2.5 kPa), with and without access to air; partitioning of standard Mo2 in normoxia and hypoxia; maximum Ṁo2 and partitioning after exercise; and critical oxygen tension (Pcrit). Additionally, the effects of temperature acclimation on haematocrit, haemoglobin oxygen affinity and gill morphology were assessed. Standard Ṁo2 was higher, but air breathing was not increased, at 15°C or after exercise at both temperatures. Fish acclimated to 5°C or 15°C increased air breathing to compensate and fully maintain standard Ṁo2 in hypoxia. Fish were able to maintain ṀO2 through aquatic respiration when air was denied in normoxia, but when air was denied in hypoxia, standard Ṁo2 was reduced by ~30-50%. Pcrit was relatively high (5 kPa) and there were no differences in Pcrit, gill morphology, haematocrit or haemoglobin oxygen affinity at the two temperatures. Therefore, Alaska blackfish depends on air breathing in hypoxia and additional mechanisms must thus be utilised to survive hypoxic submergence during the winter, such as hypoxia-induced enhancement in the capacities for carrying and binding blood oxygen, behavioural avoidance of hypoxia and suppression of metabolic rate. [ABSTRACT FROM AUTHOR]

Lactate ions are involved in several physiological processes, including a direct stimulation of the carotid body, causing increased ventilation in mammals. A similar mechanism eliciting ventilatory stimulation in other vertebrate classes has been demonstrated, but it remains to be thoroughly investigated. Here, we investigated the effects of lactate ions on the cardiorespiratory system in swimming rainbow trout by manipulating the blood lactate concentration. Lactate elicited a vigorous, dose-dependent elevation of ventilation and bradycardia at physiologically relevant concentrations at constant pH. After this initial confirmation, we examined the chiral specificity of the response and found that only l-lactate induced these effects. By removal of the afferent inputs from the first gill arch, the response was greatly attenuated, and a comparison of the responses to injections up- and downstream of the gills collectively demonstrated that the lactate response was initiated by branchial cells. Injection of specific receptor antagonists revealed that a blockade of serotonergic receptors, which are involved in the hypoxic ventilatory response, significantly reduced the lactate response. Finally, we identified two putative lactate receptors based on sequence homology and found that both were expressed at substantially higher levels in the gills. We propose that lactate ions modulate ventilation by stimulating branchial oxygen-sensing cells, thus eliciting a cardiorespiratory response through receptors likely to have originated early in vertebrate evolution.

With the occurrence of global change, research aimed at estimating the performance of marine ectotherms in a warmer and acidified future has intensified. The concept of oxygen- and capacity-limited thermal tolerance, which is inspired by the Fry paradigm of a bell-shaped increase-optimum-decrease-type response of aerobic scope to increasing temperature, but also includes proposed negative and synergistic effects of elevated CO2 levels, has been suggested as a unifying framework. The objectives of this meta-analysis were to assess the following: (i) the generality of a bell-shaped relationship between absolute aerobic scope (AAS) and temperature; (ii) to what extent elevated CO2 affects resting oxygen uptake MO2rest and AAS; and (iii) whether there is an interaction between elevated temperature and CO2. The behavioural effects of CO2 are also briefly discussed. In 31 out of 73 data sets (both acutely exposed and acclimated), AAS increased and remained above 90% of the maximum, whereas a clear thermal optimum was observed in the remaining 42 data sets. Carbon dioxide caused a significant rise in MO2rest in only 18 out of 125 data sets, and a decrease in 25, whereas it caused a decrease in AAS in four out of 18 data sets and an increase in two. The analysis did not reveal clear evidence for an overall correlation with temperature, CO2 regime or duration of CO2 treatment. When CO2 had an effect, additive rather than synergistic interactions with temperature were most common and, interestingly, they even interacted antagonistically on MO2rest and AAS. The behavioural effects of CO2 could complicate experimental determination of respiratory performance. Overall, this meta-analysis reveals heterogeneity in the responses to elevated temperature and CO2 that is not in accordance with the idea of a single unifying principle and which cannot be ignored in attempts to model and predict the impacts of global warming and ocean acidification on marine ectotherms.

Ocean acidification poses a range of threats to marine invertebrates; however, the potential effects of rising carbon dioxide (CO2) on marine invertebrate behaviour are largely unknown. Marine gastropod conch snails have a modified foot and operculum allowing them to leap backwards rapidly when faced with a predator, such as a venomous cone shell. Here, we show that projected near-future seawater CO2 levels (961 µatm) impair this escape behaviour during a predator-prey interaction. Elevated-CO2 halved the number of snails that jumped from the predator, increased their latency to jump and altered their escape trajectory. Physical ability to jump was not affected by elevated-CO2 indicating instead that decision-making was impaired. Antipredator behaviour was fully restored by treatment with gabazine, a GABA antagonist of some invertebrate nervous systems, indicating potential interference of neurotransmitter receptor function by elevated-CO2, as previously observed in marine fishes. Altered behaviour of marine invertebrates at projected future CO2 levels could have potentially far-reaching implications for marine ecosystems.