Corticotropin-releasing factor and neuropeptide Y mRNA levels are modified by glucocorticoids in rainbow trout, Oncorhynchus mykiss

The primary stress response involves neuronal activation that ultimately leads to the release of glucocorticoids. Circulating glucocorticoids are thought to influence their own synthesis and release through a negative feedback mechanism that inhibits the activity of the hypothalamic and pituitary components of the stress axis. This study was designed to address the hypothesis that glucocorticoids modify corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) mRNA levels in the rainbow trout (Oncorhynchus mykiss) brain. Cortisol implantation significantly reduced CRF1 and NPY mRNA levels in fish exposed to an isolation stress. In contrast, cortisol implantation did not prevent the stress-induced elevation of CRF1 and NPY mRNA levels during confinement. Treatment with the glucocorticoid receptor antagonist RU-486 reduced CRF1 mRNA levels in both isolated and confined fish, but had no effect on NPY mRNA. Although the cytochrome P450 inhibitor metyrapone reduced ACTH-induced cortisol secretion in vitro, plasma cortisol levels were elevated in isolated trout treated with metyrapone. Nevertheless, metyrapone implantation increased CRF1 and NPY mRNA levels in confined fish. Together, these results implicate cortisol as a modulator of CRF and NPY mRNA levels in the preoptic area of the trout brain, but that cortisol is only one such regulating mechanism.