Abstract

To further our understanding of the development of the stress axis and the responsiveness of embryonic and larval fish to environmental stressors, this study examined the ontogeny of whole-body cortisol levels and of the corticotropin-releasing factor (CRF) system in rainbow trout, as well as the endocrine and cellular stress responses to hypoxia. After depletion of a maternal deposit, de novo synthesis of cortisol increased exponentially between the ‘eyed’ stage and first feeding. Whole body CRF mRNA levels dominated over those of the related peptide urotensin I (UI) from hatch through complete yolk sac absorption. The mRNA levels of CRF-binding protein (CRF-BP) closely paralleled those of CRF and UI throughout ontogeny except at first feeding when an increase in CRF gene expression was not matched by change in CRF-BP transcript abundance. In the hypoxia challenge, fish were exposed to 15% O2 saturation for either 90min or 24h at three key developmental stages: hatch, swim up and first feeding. While the embryos were unaffected, chronic hypoxia elicited a transient 2-fold increase in whole-body cortisol levels in the larval stages. The hypoxia challenge also generally suppressed the mRNA levels of CRF and CRF-BP, had no effect on the expression of UI, but had a marked stimulatory effect on heat shock protein 70 (Hsp70) gene expression. Taken together, these results suggest a role for the CRF system in the ontogenic regulation of corticosteroidogenesis and show that hypoxia has developmental stage-specific effects on the endocrine and cellular stress responses in rainbow trout.

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