| Summary: | Fish and some invertebrates have demonstrated to be strong acid‐base regulators following exposure to ocean acidification‐relevant carbon dioxide (CO 2 ) levels through the accumulation of bicarbonate (HCO 3 − ) in extracellular and intracellular fluids. This allows for pH compensation, however, internal p CO 2 and HCO 3 − remain elevated. This compensation has been hypothesized to cause negative behavioral impairments, by altering ion gradients (HCO 3 − /Cl − ) along neuronal cell membranes that affect the function of the GABA A receptor, an important inhibitory receptor in the central nervous system of vertebrates and invertebrates. Aplysia californica , known for their simple and well‐mapped nervous system, have the potential to be strong model organisms to examine the relationship between CO 2 compensation and impaired behavior in invertebrates. We hypothesized that CO 2 ‐exposed animals would compensate for an acidosis by accumulating HCO 3 − . In the second portion of the study, we hypothesized that two important behaviors, the righting reflex and tail‐withdrawal reflex, would be impaired following CO 2 exposure, since this has been noted in many other species. Aplysia were exposed for 4–11 days to either control (400 μatm), 1,200 μatm (close to end of century predictions), or 3,000 μatm CO 2 . Hemolymph pH was measured using a custom gas‐tight chamber with a fiber‐optic pH microsensor, and HCO 3 − and p CO 2 were calculated using pH and measurements of total CO 2 using the Henderson‐Hasselbach equation. The amount of time it took the animal to right following release from the water column (righting reflex), and the amount of time it took the animal to relax its tail to 50% of the original length (tail‐withdrawal reflex) following a mild tail depression were recorded. We observed that animals were able to fully compensate pH at 1,200 μatm CO 2 , but experienced a significant but mild acidosis at the 3,000 μatm level. Hemolymph HCO 3 − and p CO 2 increased at both CO 2 levels, and were statistically ...
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