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Levels of two types of gonadotropin-releasing hormone (salmon GnRH and chicken GnRH-II) in the brain and pituitary, and content of gonadotropin (GTHIβ and IIβ) in the pituitary were measured in male masu salmon from hatching to gonadal maturation for three years in order to clarify the involvement of GnRHs in precocious maturation. Underyearling precocious males were distinguishable in summer of year 1 and were marked by an increased GSI. Spermiation was observed among these individuals thereafter every autumn. Pituitary GTHIβ content in both precocious and immature males, and GTHIIβ content in precocious males showed seasonal fluctuations — high in autumn and low in winter. Pituitary GTHIIβ content was low in immature males. Pituitary sGnRH content in precocious males increased from spring to autumn during the three-year period. sGnRH concentrations in discrete brain areas showed seasonal changes — high during autumn to winter and low in summer. Concentrations in the olfactory bulbs and hypothalamus increased significantly in association with testicular maturation during year 3. sGnRH concentrations in the hypothalamus were significantly higher in precocious males than in immature males; this was possibly due to positive feedback of steroid hormones. cGnRH-II was undetectable in the pituitary and no distinct changes were observed in its concentration in the brain in relation to maturation. The phenomenon of underyearling precocious maturation is considered to be triggered before the onset of early summer. It is suggested that males which mature precociously are larger in size and contain much sGnRH in the pituitary before the outward signs of precocity appear; sGnRH may stimulate GTH II synthesis and induce precocious maturation.  相似文献   
2.
This study describes the development and validation of competitive antigen capture enzyme-linked immunosorbent assay (ELISA) for growth hormone (GH) of the catfish, Clarias batrachus. Isolated GH was characterized first through bioassay, amino acid sequencing, immunoblotting and immunocytochemistry, and then used to raise antibody to develop ELISA. The lowest detection limit of the assay system was 0.17 ng ml−1, and the standard curve had an ED50 value of 0.35 ng ml−1. Repeated determination of GH in a plasma pool exhibited intra- and interassay co-efficient of variation of 8.1% and 7.09% (n=5), respectively. Dose–response inhibition curves resulting from dilutions of plasma and pituitary homogenate of C. batrachus were parallel to the standard curve, while such parallelism in the case of Cyprinus carpio and H. fossilis was absent revealing no cross reaction of them in the present ELISA. In vivo effects of sGnRH, testosterone, 5-HT and morphine on plasma GH were also examined to validate the ELISA physiologically. sGnRH, testosterone and morphine increased, while 5-HT decreased GH level in a dose-dependent manner.  相似文献   
3.
The objective of the present study was to confirm previous results on the mediation of GnRH signal in tilapia by providing evidence from experiments in cultured pituitary cells and from perifusion experiments using a GnRH-antagonist. After 4 days in culture under identical conditions, cells taken from pituitaries of fish maintained at 26°C were more sensitive to GnRHa ([D-Ala6, Pro9-NEt]-LHRH) than those taken from fish maintained at 19°C. Cells from female pituitaries were more responsive than those from males. taGTH release in culture was augmented by Ca2+ ionophore (A23187; 1–100 μM) or ionomycin (0.02–10 μM). The response of perifused pituitary to GnRH was reduced by nimodipine (1–10 μM) indicating that Ca2+ influx via voltage-sensitive Ca2+ channels is involved in the stimulation of GTH release. Activation of protein kinase C by OAG (1-oleyl-2-acetyl glycerol; 0.16–160 μM) or TPA (1-O-tetra-decanoyl phorbol-13-acetate; 1.25–125 nM) resulted in a dose-dependent stimulation of taGTH release from cultured cells. Arachidonic acid (0.33–330 μM) also augmented the release of taGTH from the culture. Four sequential pulses of sGnRH (100 nM) at 2h intervals resulted in surges of taGTH release from perifused pituitary fragments; the surges were similar in magnitude with no signs of desensitization. Sequential stimulation with graded doses of sGnRH (0.1 nM to 1 μM) in the presence of GnRH-antagonist ([Pro2,6, Trp3]-GnRH) resulted in an attenuation of taGTH release. However, the GnRH-antagonist did not alter the pattern of forskolin-stimulated GTH release, indicating that forskolin stimulation is exerted at the level of the adenohypophyseal cells. It is concluded that, as in other vertebrates, the transduction of GnRH stimulation of GTH release involves Ca2+ influx through voltage-sensitive Ca2+ channels, mobilization of the ion from intracellular sources, arachidonic acid and activation of PKC. Adenylate cyclase-cAMP system us also involved in the mediation but its relationship with other transduction cascades requires further investigations.  相似文献   
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