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We examined the effects of environmental salinity on circulating levels of the two prolactins (tPRL177 and tPRL188) and levels of pituitary tPRL177 and tPRL188 mRNA in the euryhaline tilapia, Oreochromis mossambicus. Fish were sham-operated or hypophysectomized and the rostral pars distalis (RPD) autotransplanted onto the optic nerve. Following post-operative recovery in (1/4) seawater, tilapia were transferred to fresh water (FW), (1/4) seawater (SW) or SW. Serum tPRL177 and tPRL188 levels in sham-operated and RPD-autotransplanted fish were highest in FW and decreased as salinity was increased. tPRL177 and tPRL188 mRNA levels in RPD implants as well as in pituitaries from the sham-operated fish were also highest in FW and decreased with increasing salinity. Serum osmolality increased with salinity, with the highest levels occurring in the seawater groups. We conclude that some plasma factor (probably plasma osmolality), in the absence of hypothalamic innervation, exerts a direct regulatory action on prolactin release and gene expression in the pituitary of O. mossambicus. This regulation is in accord with the actions of the two prolactins in the freshwater osmoregulation of the tilapia.
Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Ocean Research Institute, University of Tokyo, Nakano, Tokyo 164-8639, Japan
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To clarify the role of ghrelin in the fish immune system, the in vitro effect of ghrelin was examined in phagocytic leukocytes of rainbow trout (Oncorhynchus mykiss). Administration of trout ghrelin and des-VRQ-trout ghrelin, in which three amino acids are deleted from trout ghrelin, increased superoxide production in zymosan-stimulated phagocytic leukocytes from the head kidney. Gene expression of growth hormone (GH) secretagogue-receptor (GHS-R) was detected by RT–PCR in leukocytes. Pretreatment of phagocytic leukocytes with a GHS-R antagonist, [D-Lys3]-GHRP-6, abolished the stimulatory effects of trout ghrelin and des-VRQ-trout ghrelin on superoxide production. Ghrelin increased mRNA levels of superoxide dismutase and GH expressed in trout phagocytic leukocytes. Immunoneutralization of GH by addition of anti-salmon GH serum to the medium blocked the stimulatory effect of ghrelin on superoxide production. These results suggest that ghrelin stimulates phagocytosis in fish leukocytes through a GHS-R-dependent pathway, and also that the effect of ghrelin is mediated, at least in part, by GH secreted by leukocytes.
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