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Heart rate of the freshwater turtle (Trachemys scripta) is markedly depressed with anoxia exposure and arises in part from a resetting of intrinsic heart rate. Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels ("pacemaker" channels) constitute an important component in the control of cardiac rhythmicity. HCN channels are tetramers, and four HCN channel subunit isoforms exist, which are encoded for by four genes (HCN1-4). The four isoforms can form homotetramers and heterotetramers, resulting in a number of HCN channels with distinct biophysical properties. Using real-time RT-PCR, we examined the effects of anoxia and subsequent reoxygenation on the expression of HCN1-4 mRNA in the cardiac chambers (sinus venosus, right atrium, left atrium and ventricle) of 21°C- and 5°C-acclimated turtles. With 24 h of anoxia at 21°C, the relative abundance of HCN2 increased in all cardiac chambers, and following 24 h reoxygenation, HCN2 expression returned to control levels. In contrast, at 5°C, few and only minor changes in HCN channel sub-unit expression occurred with anoxia (14 d) and reoxygenation (13 d). However, compared to 21°C normoxic turtles, cardiac chambers of 5°C normoxic turtles exhibited a pronounced increase in the relative abundance of HCN2. Combined, the findings suggest that modified HCN expression with cold acclimation may prime the turtle cardiac muscle for the approaching anoxic winter, and that cardiac anoxia survival at 21°C may be aided by the circumvention of this priming and through rapid induction of similar changes in HCN expression. The altered HCN expression may serve to facilitate a slowed heart rate during anoxia by fine-tuning the sensitivity of HCN channels to the changing levels of intracellular and extracellular modulators of HCN activity that occurs with anoxia exposure. Indeed, the turtle HCN isoforms show high sequence similarity to their mammalian counterparts, notably at the location of key regulatory motifs. [ABSTRACT FROM AUTHOR]

Average sea-surface temperature and the amount of CO2 dissolved in the ocean are rising due to increasing concentrations of atmospheric CO2. Many coral reef fishes appear to be living close to their thermal optimum, and for some of them, even relatively moderate increases in temperature (2-4°C) lead to significant reductions in aerobic scope (i.e. the difference between resting and maximum rates of oxygen uptake). Reduced aerobic capacity could affect population sustainability since less energy can be devoted to feeding and reproduction. Coral reef fish seem to have limited capacity to acclimate to elevated temperature as adults, but recent research shows that developmental and transgenerational plasticity occur, which might enable some species to adjust to rising ocean temperatures. A mayde even greater worry is that, even at maintained water temperatures, predicted future rises in ocean CO2 levels have been found to alter sensory responses and behaviour of marine fishes. Changes include increased boldness and activity, loss of behavioural lateralization, altered auditory preferences and impaired olfactory function. It has been found that impaired olfactory function makes larval coral reef fish attracted to odours they normally avoid, including ones from predators and unfavourable habitats. These behavioural alterations have significant effects on mortality that may have far-reaching implications for populations. However, the underlying mechanism linking high CO2 to these diverse responses has been unknown until recently. I will present results showing that abnormal olfactory preferences and loss of behavioural lateralization exhibited by two species of larval coral reef fish exposed to high CO2 can be rapidly and effectively reversed by treatment with an antagonist of the GABA-A receptor. GABA-A is a Cl-/bicarbonate channel and a major neurotransmitter receptor in the vertebrate brain. These results indicate that high CO2 interferes with brain ion-balance and thereby neurotransmitter function, a hitherto unrecognized threat to marine populations and ecosystems. Given the ubiquity and conserved function of GABA-A receptors, this predicts that rising CO2 levels could cause sensory and behavioural impairment in a wide range of marine animals. [ABSTRACT FROM AUTHOR]