Altered brain ion gradients following compensation for elevated CO(2) are linked to behavioural alterations in a coral reef fish

Neurosensory and behavioural disruptions are some of the most consistently reported responses upon exposure to ocean acidification-relevant CO(2) levels, especially in coral reef fishes. The underlying cause of these disruptions is thought to be altered current across the GABA(A) receptor in neuronal cells due to changes in ion gradients (HCO(3)(−) and/or Cl(−)) that occur in the body following compensation for elevated ambient CO(2). Despite these widely-documented behavioural disruptions, the present study is the first to pair a behavioural assay with measurements of relevant intracellular and extracellular acid-base parameters in a coral reef fish exposed to elevated CO(2). Spiny damselfish (Acanthochromis polyacanthus) exposed to 1900 μatm CO(2) for 4 days exhibited significantly increased intracellular and extracellular HCO(3)(−) concentrations and elevated brain pH(i) compared to control fish, providing evidence of CO(2) compensation. As expected, high CO(2) exposed damselfish spent significantly more time in a chemical alarm cue (CAC) than control fish, supporting a potential link between behavioural disruption and CO(2) compensation. Using HCO(3)(−) measurements from the damselfish, the reversal potential for GABA(A) (E(GABA)) was calculated, illustrating that biophysical properties of the brain during CO(2) compensation could change GABA(A) receptor function and account for the behavioural disturbances noted during exposure to elevated CO(2).