Independent effects of seawater pH and high PCO2on olfactory sensitivity in fish: possible role of carbonic anhydrase

Abstract

Ocean acidification may alter olfactory-driven behaviour in fish by direct effects on the peripheral olfactory system; olfactory sensitivity is reduced in CO2-acidified seawater. The current study tested whether this is due to elevated PCO2or the consequent reduction in seawater pH and, if the former, the possible involvement of carbonic anhydrase, the enzyme responsible for the hydration of CO2and production of carbonic acid. Olfactory sensitivity to amino acids was assessed by extracellular multi-unit recording from the olfactory nerve of the gilthead seabream (Sparus aurata L.) in normal seawater (pH ∼8.2), and after acute exposure to acidified seawater (pH ∼7.7) but normal PCO2(∼340 μatm) or to high PCO2seawater (∼1400 μatm) at normal pH (∼8.2). Reduced pH in the absence of elevated PCO2caused a reduction in olfactory sensitivity to L-serine, L-leucine, L-arginine and L-glutamine, but not L-glutamic acid. Increased PCO2in the absence of changes in pH caused reduced olfactory sensitivity to L-serine, L-leucine and L-arginine, including increases in their threshold of detection, but had no effect on sensitivity to L-glutamine and L-glutamic acid. Inclusion of 1 mmol l-1 acetazolamide (a membrane-permeant inhibitor of carbonic anhydrase) in the seawater reversed the inhibition of olfactory sensitivity to L-serine caused by high PCO2. Ocean acidification may reduce olfactory sensitivity by reductions in seawater pH and intracellular pH (of olfactory receptor neurones); the former by reducing odorant-receptor affinity, and the latter by reducing the efficiency of olfactory transduction. The physiological role of carbonic anhydrase in the olfactory receptor neurones remains to be explored.