Ocean Acidification Impairs Olfaction in the Large Yellow Croaker, Larimichthys crocea , by Disrupting Sensory Integrity and Neural Processing

Abstract Ocean acidification (OA) poses a significant threat to marine organisms, yet its effects on fish sensory systems remain poorly understood. This study investigated the effects of elevated pCO2 on olfactory function in the large yellow croaker, Larimichthys crocea. Elevated pCO2 reduced peripheral olfactory sensitivity, as evidenced by suppressed electro-olfactogram responses. This impairment was accompanied by epithelial disorganization, cellular damage, increased apoptosis in the olfactory epithelium, and reduced expression of olfactory neuron markers. In vitro analyses using a selected recombinant L. crocea odorant receptor LORA1–1 showed that acidified pH altered its physicochemical properties and odorant-specific receptor–ligand interaction dynamics. OA also downregulated genes associated with odorant receptor expression, G protein-mediated signaling, calcium-related transduction, and neuronal maturation. Telencephalic responses included altered ion-transport ATPase activities, histopathological abnormalities, oxidative stress, enhanced apoptotic activity, and reduced neuropeptide Y expression. Transcriptomic and proteomic analyses further identified telencephalic molecular changes associated with altered neuroactive ligand–receptor interaction, calcium signaling, glutathione metabolism, apoptosis, mitophagy, MAPK signaling, and olfactory transduction. Our findings suggest that epithelial injury, altered odorant recognition, and disrupted peripheral signaling contribute to OA-induced olfactory impairment in L. crocea, with potential consequences for migration and reproduction that depend on olfactory cues.