RESUMEN
Ocean acidification is progressing rapidly in the California Current System (CCS), a region already susceptible to reduced aragonite saturation state due to seasonal coastal upwelling. Results from a high-resolution (~ 3 km), coupled physical-biogeochemical model highlight that the intensity, duration, and severity of undersaturation events exhibit high interannual variability along the central CCS shelfbreak. Variability in dissolved inorganic carbon (DIC) along the bottom of the 100-m isobath explains 70-90% of event severity variance over the range of latitudes where most severe conditions occur. An empirical orthogonal function (EOF) analysis further reveals that interannual event variability is explained by a combination coastal upwelling intensity and DIC content in upwelled source waters. Simulated regional DIC exhibits low frequency temporal variability resembling that of the Pacific Decadal Oscillation, and is explained by changes to water mass composition in the CCS. While regional DIC concentrations and upwelling intensity individually explain 9 and 43% of year-to-year variability in undersaturation event severity, their combined influence accounts for 66% of the variance. The mechanistic description of exposure to undersaturated conditions presented here provides important context for monitoring the progression of ocean acidification in the CCS and identifies conditions leading to increased vulnerability for ecologically and commercially important species.
RESUMEN
Fish rely heavily on their sense of smell to maintain behaviors essential for survival, such as predator detection and avoidance, prey selection, social behavior, imprinting, and homing to natal streams and spawning sites. Due to its direct contact with the outside environment, the peripheral olfactory system of fish is particularly susceptible to dissolved contaminants. In particular, environmental exposures to copper (Cu) can cause a rapid loss of olfactory function. In this study, confocal imaging of double-transgenic zebrafish larvae with differentially labeled ciliated and microvillous olfactory sensory neurons (OSNs) were used to examine cell death and regeneration following Cu exposure. Changes in cell morphologies were observed at varying degrees within both ciliated and microvillous OSNs, including the presence of round dense cell bodies, cell loss and fragmentation, retraction or loss of axons, disorganized cell arrangements, and loss of cells and fluorescence signal intensity, which are all indicators of cell death after Cu exposure. A marked loss of ciliated OSNs relative to microvillous OSNs occurred after exposure to low Cu concentrations for 3 h, with some regeneration observed after 72 h. At higher Cu concentrations and 24-h exposures, ciliated and microvillous OSNs were damaged with increased severity of injury with longer Cu exposures. Interestingly, microvillous, but not ciliated OSNs, regenerated rapidly within the 72-h time period of recovery after death from Cu exposure, suggesting that microvillous OSNs may be replaced in lieu of ciliated OSNs. An increase in bromodeoxyuridine labeling was observed 24 h after Cu-induced OSN death, suggesting that increased proliferation of the olfactory stem cells replaced the damaged OSNs. Olfactory behavioral analyses supported our imaging studies and revealed both initial loss and restoration of olfactory function after Cu exposures. In summary, our studies indicate that following zebrafish OSN damage by Cu, regeneration of microvillous OSNs may occur exceeding ciliated OSNs, likely via increased proliferation of the cellular reservoir of neuronal OSC precursors. Transgenic zebrafish are a valuable tool to study metal olfactory injury and recovery and to characterize sensitive olfactory neuron populations in fish exposed to environmental pollutants.