Downstream impacts of elevated CO2 on neurosensory and behavioural endpoints in marine fish

Chair: Ivan Nagelkerken

Rachael M. Heuer (1)*, Jodie L. Rummer (2), Megan J. Welch (2), Philip L. Munday (2), Martin Grosell (3)

1 Department of Biological Sciences, University of North Texas, Denton, Texas 76203, USA
2 ARC Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland, 4811, Australia
3 RSMAS, University of Miami, Miami, FL, 33149, USA

Neurosensory and behavioural disruptions have been some of the most well-documented and consistent responses to elevated ambient CO2, especially in coral reef species. The underlying physiological mechanism for these behavioural abnormalities is thought to result from a reversal of HCO3 and/or Cl ion movement through the GABAA receptor in neurons following compensation for a CO2-induced acidosis. This current reversal is thought to mediate a depolarizing, excitatory response that is linked to behavioural abnormalities in marine fish.

Brain HCO3 (mM), brain pHi, and plasma HCO3 representing both intracellular and extracellular ion conditions in the Spiny damselfish (Acanthochromis polyacanthus) were measured following exposure to control or 1900 atm CO2 for 4 days. Concurrently, damselfish were assessed with a behavioural assay to test their avoidance response to a chemical alarm cue (CAC). Measurements from this study were also used to calculate the reversal potential for GABAA (EGABA) under control and high CO2 conditions.

Spiny damselfish exhibited significantly increased intracellular and extracellular HCO3 concentrations, providing evidence of CO2 compensation. Damselfish exposed at this CO2 level also spent significantly more time in a chemical alarm cue compared to control fish. Calculations of EGABA using values from the present study demonstrated that altered ion gradients during compensation for CO2 could reverse ion movement through the GABAA receptor and account for behavioural disturbances noted during low-level CO2 exposure.

The present study is the first to report intracellular and extracellular HCO3 levels in a coral reef species exposed to an ocean acidification-relevant CO2 exposure that also exhibits behavioural alterations. Furthermore, this study demonstrates the utility of estimating EGABA using measured values under physiologically relevant scenarios to support existing studies implicating GABAA receptor involvement in CO2-induced behavioural alternations.