Meeting Abstract

132.3  Monday, Jan. 7  Direct Effects of Cortisol on Appetite Regulation in the Brain of Tilapia, Oreochromis mossambicus DUNCAN , C.A.**; RILEY, L.G.; Fresno State Univ.; Fresno State Univ. cduncan@csufresno.edu

Food intake in vertebrates is under the regulation of appetite stimulating (e.g. neuropeptide Y, ghrelin) and appetite inhibiting (e.g. corticotropin-releasing hormone) signals in the brain. The efficacy of these brain signals are influenced by environmental and social factors as well as the hormonal milieu within the animal. Previous work has established that stress and cortisol consistently decrease food intake in fish. However, the link between cortisol and appetite is not well understood in any species of fish. The response to acute stressors is likely adaptive, but when exposed to chronic stress, the adaptive value might be lost. A recent report from our laboratory has shown that a single injection of cortisol decreased food intake in tilapia, which appears to be mediated by a reduction in the ghrelin signaling pathway via NPY in the telencephalon region of the brain. The present study was designed to test the direct effects of cortisol on regions of the brain known to regulate appetite. The telencephalon and hypothalamus were individually dissected from tilapia and cultured separately in cortisol-containing media for 24 h. Following treatment, mRNA levels of genes involved in appetite regulation were quantified from each brain region. In the telencephalon, cortisol decreased NPY mRNA levels while increasing the ghrelin signaling pathway. In the hypothalamus, cortisol decreased CRH and NPY mRNA levels. This study is novel because it is the first to report the direct effects of cortisol in fish. Furthermore, these data suggest that the direct actions of cortisol on appetite might be mediated by a decrease in NPY and hypothalamic CRH as well as an increase in the ghrelin signaling pathway in the telencephalon. Supported by USDA to LGR.