Neurosensory Impacts of Ocean Acidification on Fish

Many recent studies have linked CO₂ exposure to broad neurological disruptions in fish, across multiple sensory systems and behavioral endpoints. The underlying physiological mechanism for this disruption is suspected to be related to acid-base compensation following a CO₂ induced acidosis, where fish effectively defend pH but retain sustained elevated levels of HCO₃^- and PCO₂ in both extracellular and intracellular fluids. A growing number of studies have hypothesized this compensatory response may alter ion gradients and affect the direction of ion movement (HCO₃^- and/or Cl^-) through the ubiquitously distributed GABA_A receptor, possibly causing a reversal from inhibitory to excitatory response during GABA (γ-Aminobutyric acid) binding. These hypotheses have largely been tested by the administration of GABA_A receptor pharmaceutical agonists and/or antagonists paired with an assay designed to demonstrate the alleviation or enhancement of a particular behavior. Interestingly, theoretical treatment of the reversal potential for the GABA_A receptor using measured and calculated values for extracellular and intracellular HCO₃^-, Cl^-, and pH during low-level CO₂ exposure supports the idea that inhibitory responses could potentially become excitatory, aligning with results from previous behavioral studies. In addition to ion gradient alterations, other potential causes for noted behavioral disturbances will also be discussed.