CO2-Induced Ocean Acidification Alters the Burrowing Behavior of Manila Clam Ruditapes philippinarum by Reversing GABAA Receptor Function

Biological burrowing behavior is an important drivershaping ecosystemsthat is being threatened by CO2-induced ocean acidification;however, the effects of ocean acidification on burrowing behaviorand its neurological mechanism remain unclear. This study showed thatelevated pCO(2) significantly affected theburrowing behaviors of the Manila clam Ruditapes philippinarum, such as increased foot contraction, burrowing time, and intrabottommovement and decreased burrowing depth. Delving deeper into the mechanism,exposure to elevated pCO(2) significantlydecreased extracellular pH and increased [HCO3 (-)]. Moreover, an indicator GABA(A) receptor, a neuroinhibitorfor movement, was found to be closely associated with behavioral changes. In situ hybridization confirmed that the GABA(A) receptor was widely distributed in ganglia and foot muscles, andelevated pCO(2) significantly increasedthe mRNA level and GABA concentration. However, the increase in GABA(A) receptor and its ligand did not suppress the foot movement,but rather sent "excitatory" signals for foot contraction.The destabilization of acid-base homeostasis was demonstratedto induce an increase in the reversal potential for GABA(A) receptor and an alteration in GABA(A) receptor functionunder elevated pCO(2). This study revealedthat elevated pCO(2) affects the burrowingbehavior of Manila clams by altering GABA(A) receptor functionfrom inhibitory to excitatory. Little is knownabout the behavioral manifestations of infaunaunder ocean acidification and its mechanisms. This study reports elevated pCO(2) alters the burrowing behavior of Manilaclams by reversing GABA(A) receptor function induced by theinstability of acid-base homeostasis.