Resilience to an acid-base disturbance and the development and plasticity of acid-base regulatory pathways in estuarine teleosts

Since the industrial revolution marine environments have displayed marked increases in CO₂ levels. Changes in ocean chemistry – collectively termed ocean acidification (OA) – are predicted to have numerous effects on marine fish, including critical behavioral endpoints and survival, with the most severe impacts hypothesized to occur in the vulnerable early life stages. However, many regions around the globe routinely have CO₂ levels in excess of those predicted by climate change, including the estuaries in the Gulf of Mexico, which are essential habitat for many ecologically and commercially important fish species. We hypothesize that the species that inhabit these environments contain physiological traits that confer resilience to OA. Thus, it is imperative that we understand the resilience of these species as well as the underlying mechanisms that may inform on the adaptive capacity of fish in general. The underlying physiological cause for many of the outcomes of OA is a systemic acid-base disturbance, which causes an elevated arterial pCO₂ and plasma [HCO₃⁻]. Because embryos and early life stage fish lack gills and practice cutaneous gas exchange, acid-base disturbances could be exacerbated in these life stages. Furthermore, little is known about the ontogeny, development, plasticity of acid-base regulatory mechanisms in early life stage marine fish, raising many questions about their ability to compensate for disturbance. Here we present work that shows tolerance of early life stage estuarine species to elevated CO₂ levels, including survival, standard length, and yolk size. However, we did observe significant heart rates in both studied estuarine species, and although we saw no immediate impacts, the long-term impacts of elevated heart rate are of keen interest. We also observed that alterations in acid-base regulatory machinery were the largely the result of development, rather than in response to exposure to an acid-base disturbance, including an acidosis and alkalosis. Although we did observe significant increases in NHE2 and VHA as the result of exposure to elevated CO₂ levels. Of interest is that H⁺ excretion was significant elevated in response to exposure to hypercapnia, and we hypothesize that this H⁺ excretion is the result of both the NHE and VHA pathway, from data obtained via the scanning ion-selective electrode technique (SIET) and pharmacological inhibition, but this must be further investigatedMarine Scienc

The early life stages of an estuarine fish, the red drum (Sciaenops ocellatus), are tolerant to high pCO2

Ocean acidification (OA) and other climate change induced environmental alterations are resulting in unprecedented rates of environmental deterioration. This environmental change is generally thought to be too fast for adaptation using typical evolutionary processes, and thus sensitivity may be dependent on the presence of existing tolerant genotypes and species. Estuaries undergo natural pCO2 fluctuations over a variety of time scales, and levels regularly exceed the predicted end of the century values. Interestingly, estuarine fish species have been overlooked in reference to the impacts of OA. Here, we use the estuarine red drum (Sciaenops ocellatus) as a model to explore the hypothesis that early life stages of estuarine species have intrinsic tolerance to elevated pCO2. Our sensitivity endpoints included: survival, growth, yolk consumption, heart rate, and scototaxis. Survival was significantly decreased when exposed to 1300 μatm and 3000 μatm, and coincided with a significant increase in heart rate at the 3000 μatm exposure. However, these effects were less pronounced than the findings of previous studies on other marine fish species. Yolk depletion rate and standard length were not significantly affected by pCO2. Scototaxis behaviour was also not significantly affected by exposure to elevated levels of pCO2 under both acute and acclimated exposure scenarios. Overall, these results support the hypothesis that estuarine life history and habitat usage may play a critical role in determining sensitivity of fish species to OA. Furthermore, estuarine species may provide present-day insight into the physiological and ecological foundation of OA tolerance.</jats:p

The early life stages of the orange-spotted grouper,<i>Epinephelus coioides</i>, exhibit robustness to hypercapnia

AbstractOcean acidification (OA) and other climate change-induced environmental alterations are resulting in unprecedented rates of environmental degradation. This environmental change is generally thought to be too fast for adaptation using evolutionary process dependent on natural selection, and thus, resilience may be related to the presence of existing tolerant genotypes and species. Estuaries undergo natural partial pressure carbon dioxide (pCO2) fluctuations, with levels regularly exceeding predicted end of the century values. In this study, we use the estuarine orange-spotted grouper (Epinephelus coioides) to explore the intrinsic resilience to elevated pCO2. Our sensitivity endpoints included: survival, heart rate, growth, and yolk consumption. Furthermore, we attempted to determine whether their acid–base regulatory machinery was plastic in response to elevated pCO2 by analysing the gene expression of key transporters and ionocyte density. Survival was not significantly altered by exposure to elevated pCO2. Interestingly, the heart rate was significantly elevated at both 1500 and 3100 μatm exposure. However, other metrics of energetic consumption, such as yolk consumption and growth, were not significantly altered. Furthermore, we found no changes in gene expression in vha, nhe3, and nbc, as well as ionocyte density at elevated pCO2. Overall, these results support the hypothesis that estuarine species are resilient to the impacts of OA.</jats:p

Pulsatile urea excretion in Gulf toadfish: the role of circulating serotonin and additional 5-HT receptor subtypes

The neurochemical serotonin (5-HT) is involved in stimulating pulsatile urea excretion in Gulf toadfish (Opsanus beta) through the 5-HT2A receptor; however, it is not known if (1) the 5-HT signal originates from circulation or if (2) additional 5-HT receptor subtypes are involved. The first objective was to test whether 5-HT may be acting as a hormone in the control of pulsatile urea excretion by measuring potential fluctuations in circulating 5-HT corresponding with a urea pulse, which would suggest circulating 5-HT may be involved with urea pulse activation. We found that plasma 5-HT significantly decreased by 38% 1 h after pulse detection when branchial urea excretion was significantly elevated and then returned to baseline. This suggests that 5-HT is removed from the circulation, possibly through clearance or excretion, and may be involved in the termination of pulsatile urea excretion. There appeared to be no pulsatile release of 5-HT from peripheral tissues to trigger a urea pulse. The second objective was to determine if additional 5-HT receptor subtypes, such as an additional 5-HT2 receptor (5-HT2C receptor) or the 5-HT receptors that are linked to cAMP (5-HT4/6/7 receptors), played a role in the stimulation of urea excretion. Intravenous injection of 5-HT2C, 5-HT4, 5-HT6, and 5-HT7 receptor agonists did not result in a urea pulse, suggesting that these receptors, and thus cAMP, are not involved in stimulating urea excretion. The involvement of circulating 5-HT and the 5-HT2A receptor in the regulation of pulsatile urea excretion may provide insight into its adaptive significance