9810326 Borski The investigator addresses novel mechanisms by which a steroid, cortisol, rapidly inhibits prolactin secretion in fish. Steroid hormones typically act on target tissues by altering DNA, a genomic process requiring hours or days to occur. Dr. Borski shows cortisol acts within minutes to inhibit prolactin release. He postulates that cortisol may also act through nongenomic, membrane receptor-associated pathways typically described for rapidly acting neurotransmitter and peptide hormones. Dr. Borski will test this hypothesis and define biochemical pathways by which cortisol and other steroids rapidly alter cell function. In many fish, prolactin is critical to survival in fresh water, while cortisol is central to seawater osmoregulation. Rapid attenuation of a freshwater hormone, prolactin, and stimulation of seawater adaptation by cortisol is likely essential for allowing fish to survive rapid increases in salinity. Conversely, stress-induced elevations in cortisol could prove maladaptive for animals living in fresh water conditions which cause high mortality of commercially valuable finfish due to handling and live transport. Completion of this work will advance understanding of the detailed workings underlying osmoregulation, an ancient and universal process critical to physiological adaptation as well as provide an integrative model for "stress hormone" effects that impair physiological processes including reproduction, behavior, and immune function.
