Physiological Downstream Consequences and Tradeoffs Associated with CO2 Compensation in Marine Fish

• Main Author: Heuer, Rachael M
• Other Authors: Martin Grosell, M. Danielle McDonald, Lynne A. Fieber, Colin J. Brauner, Diego Lirman
• Format: Other/Unknown Material
• Language: unknown
• Published: Scholarly Repository 2016
• Subjects: CO2; carbon dioxide; ocean acidification; fish; GABA; osmoregulation; Ocean acidification
• Online Access: https://scholarlyrepository.miami.edu/oa_dissertations/1566; https://scholarlyrepository.miami.edu/cgi/viewcontent.cgi?article=2584&context=oa_dissertations

Fish are renowned for their ability to defend blood pH following exposure to elevated ambient CO2, a trait that has undoubtedly led to their ability to thrive successfully in a wide variety of habitats. While the defense of internal pH is critical for survival, the sustained elevation of HCO3- and PCO2 that occurs as a part of this compensatory response could potentially lead to sub-lethal impacts. This point is underscored by a growing number of studies demonstrating negative effects of CO2, even at relatively low CO2 tensions. The goal of this dissertation was to assess potential downstream consequences and/or tradeoffs associated with compensation for CO2 exposure in marine fish. This was achieved by examining the intestinal response of the Gulf toadfish (Opsanus beta) and the neurological response of the Spiny damselfish (Acanthochromis polyacanthus). Results from this dissertation indicate that ocean acidification relevant CO2 exposure levels predicted for year 2300 stimulates HCO3- loss through the intestine that is seemingly counterproductive to whole-animal acid-base balance. This base loss incurred an increased energetic demand on isolated intestinal tissue, providing evidence that low level CO2 exposure could lead to increases in baseline metabolism. Increasing the range of tested CO2 levels in the toadfish (up to 20,000 microatm CO2; ~2 kPa) led to the first broad characterization of intestinal transport physiology during elevated CO2. Despite a consistent increase in intestinal HCO3- secretion with CO2 exposure, the quantity and composition of intestinally produced carbonates did not change. Finally, the last portion of this dissertation involved a shift in focus to downstream impacts of CO2 compensation in the brain. To my knowledge, this dissertation provides the first direct measurements of extracellular and intracellular HCO3- in a coral reef species exposed to an ocean acidification relevant CO2 level (1900 microatm CO2; 0.19 kPa) that also induces a behavioral disturbance. These measurements support the hypothesis that CO2 compensation leads to changes in gradients across neuronal membranes that alter behavior. Overall, results from this dissertation indicate that CO2 compensation may lead to an unexpected sensitivity for certain tested endpoints. The potential for sub-lethal impacts on fish is particularly topical, since it is unclear how fast fish will adapt in response to oceans that are currently undergoing acidification at a rapid rate.