Abstract
Neurosensory 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.
Highlights
Neurosensory and behavioural disruptions are some of the most consistently reported responses upon exposure to ocean acidification-relevant CO2 levels, especially in coral reef fishes
In the model proposed by Nilsson and colleagues, following stimulation by GABAA receptor and its associated neurotransmitter (GABA), HCO3− and/or Cl− ions enter the cell through the GABAA receptor under control conditions, leading to cellular hyperpolarization, and a concomitant inhibitory response that is associated with a normal behavioural phenotype in fish
Our results show that spiny damselfish, compensate for a CO2 induced acidosis by elevating plasma and brain HCO3− following exposure to 1900 μatm CO2 for 4 days (Fig. 1)
Summary
Neurosensory 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. Expected changes in extracellular and/or intracellular HCO3− and Cl− that occur during CO2 compensation are thought to reverse ion movement through the GABAA receptor, leading to a depolarizing excitatory response and a disrupted behavioural phenotype[34]. Even an attenuation of the normal inhibitory response of the GABAA receptor due to changes in ion gradients could alter the function of neurons and account for noted behavioural disruptions
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