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Eutrophication and climate change are increasing the incidence of severe hypoxia in fish nursery habitats, yet the programming effects of hypoxia on stress responsiveness in later life are poorly understood. In this study, to investigate whether early hypoxia alters the developmental trajectory of the stress response, zebrafish embryos were exposed to 4 h of anoxia at 36 h post-fertilization and reared to adults when the responses to secondary stressors were assessed. While embryonic anoxia did not affect basal cortisol levels or the cortisol response to hypoxia in later life, it had a marked effect on the responses to a social stressor. In dyadic social interactions, adults derived from embryonic anoxia initiated more chases, bit more often, entered fewer freezes and had lower cortisol levels. Adults derived from embryonic anoxia also performed more bites towards their mirror image, had lower gonadal aromatase gene expression and had higher testosterone levels. We conclude that acute embryonic anoxia has long-lasting consequences for the hormonal and behavioural responses to social interactions in zebrafish. Specifically, we demonstrate that acute embryonic anoxia favours the development of a dominant and aggressive phenotype, and that a disruption in sex steroid production may contribute to the programming effects of environmental hypoxia.

Acute embryonic anoxia exposure favours the development of a dominant and aggressive phenotype in adult zebrafish