Fragile X syndrome (FXS) is a genetic disorder caused by loss-of-function mutations of the FMR1 gene and is the most common genetic cause of autism spectrum disorder. Prenatal maternal stress, resulting in increased embryonic cortisol exposure, may also be related to the development of intellectual disability, however, the impact of cortisol on the neurodevelopment of individuals with FXS is not well characterized. To investigate the interaction of cortisol and FXS genotype, wildtype zebrafish embryos and FMR1 knockout zebrafish embryos were treated with cortisol concentrations of 5 µM, 0.5 µM, 0.05 µM, or a vehicle solution between 6 hours post-fertilization (hpf) and 5 days post-fertilization (dpf). At 5dpf, zebrafish were placed in a 96-well plate and evoked swimming velocities were captured across alternating light-dark cycles using a commercial motor tracking system. While zebrafish larvae showed significant difference in light vs dark swimming behaviors, there was no difference in velocity at any cortisol concentration for both AB and fmr1 strains. These results indicate cortisol exposure does not impact swimming behavior development in wildtype or FMR1 knockout zebrafish strains, suggesting no interaction of cortisol and FXS genotype for this phenotype.
