Altered brain ion gradients following compensation for elevated CO₂ are linked to behavioural alterations in a coral reef fish

Abstract

AbstractNeurosensory and behavioural disruptions are some of the most consistently reported responses upon exposure to ocean acidification-relevant CO₂ levels, especially in coral reef fishes. The underlying cause of these disruptions is thought to be altered current across the GABAA receptor in neuronal cells due to changes in ion gradients (HCO3− and/or Cl−) that occur in the body following compensation for elevated ambient CO₂. 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 CO₂. Spiny damselfish (Acanthochromis polyacanthus) exposed to 1900 μatm CO₂ for 4 days exhibited significantly increased intracellular and extracellular HCO3− concentrations and elevated brain pHi compared to control fish, providing evidence of CO₂ compensation. As expected, high CO₂ exposed damselfish spent significantly more time in a chemical alarm cue (CAC) than control fish, supporting a potential link between behavioural disruption and CO₂ compensation. Using HCO3− measurements from the damselfish, the reversal potential for GABAA (EGABA) was calculated, illustrating that biophysical properties of the brain during CO₂ compensation could change GABAA receptor function and account for the behavioural disturbances noted during exposure to elevated CO₂.