UC San Diego

Experimental exposure to ocean and freshwater acidification affects the behaviour of multiple aquatic organisms in laboratory tests. One proposed cause involves an imbalance in plasma chloride and bicarbonate ion concentrations as a result of acid-base regulation, causing the reversal of ionic fluxes through GABA_A receptors, which leads to altered neuronal function. This model is exclusively based on differential effects of the GABA_A receptor antagonist gabazine on control animals and those exposed to elevated CO₂ However, direct measurements of actual chloride and bicarbonate concentrations in neurons and their extracellular fluids and of GABA_A receptor properties in aquatic organisms are largely lacking. Similarly, very little is known about potential compensatory mechanisms, and about alternative mechanisms that might lead to ocean acidification-induced behavioural changes. This article reviews the current knowledge on acid-base physiology, neurobiology, pharmacology and behaviour in relation to marine CO₂-induced acidification, and identifies important topics for future research that will help us to understand the potential effects of predicted levels of aquatic acidification on organisms.