The feeding response of obese mice (genotype, ob ob) and their wild-type littermates to cholecystokinin (pancreozymin).
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Biomedical subjects
Publications and source records attributed to R F Parrott.
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A method is described for the intracerebroventricular infusion of labelled testosterone in conscious sheep. Our objective was to establish whether the infused testosterone entered the nuclei of cells in the hypothalamic region. Since the results from castrated males showed testosterone to be taken up by cell nuclei, in the hypothalamic region, the method promises to be useful for the study of the hypothalamic metabolism of androgens in relation to the sexual behaviour and neuroendocrine function in large animals.
At different times of the year, groups of wethers were treated with 20 mg testosterone, dihydrotestosterone or 19-hydroxytestosterone propionates/day or 2 mg oestradiol dipropionate/day, or the oil vehicle, for 6 weeks after a 2-week control period. LH and FSH values were determined by radioimmunoassay of serum samples collected at regular intervals. Oestradiol and dihydrotestosterone reduced LH and FSH concentrations whereas 19-hydroxytestosterone and testosterone had no effect.
Prolactin concentrations were measured in serum from wethers at various times of the year before and during treatment with testosterone proprionate, dihydrotestosterone propionate, 19-hydroxytestosterone dipropionate and oestradiol dipropionate. Levels of prolactin in serum were lower in untreated wethers during short (October) than during long (April-August) days. Seasonal differences persisted throughout the experiment but became less obvious during tretment with oestradiol dipropionate and 19-hydroxytestosterone dipropionate, both of which raised prolactin concentrations. Neither testosterone propionate nor dihydrotestosterone propionate altered the levels of prolactin.
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Five groups of rats were observed for sexual behavior as intact subjects and in the 3 weeks following castration. Particular emphasis was placed upon ultrasonic vocalization recorded during the refractory period (RP) following ejaculation. All rats received daily injections (100 mug test steroid + 100 mug dihydrotestosterone propionate, DHTP) from the day of castration. Treatment groups were: Testosterone propionate (TP) + DHTP, N = 5; 19-hydroxytestosterone propionate (19HTP) + DHTP, N = 6; Oestradiol dipropionate (OP) + DHTP, N = 5; DHTP (200 mug/day), N = 6; Vehicle only, N = 7. Ejaculation and normal RPs were maintained with TP, 19HTP and OP treatments. In rats treated with DHTP alone or vehicle only ejaculatory ability declined and RPs increased in length. Ultrasonic vocalization was normal in all rats except those treated with OP, where it was either reduced or absent. In Week 4 treatments in TP + DHTP and OP + DHTP groups were reversed. During Weeks 5-7 vocalization was gradually restored in rats that previously received OP and partially inhibited in animals previously treated with TP. These results indicate that; (1) vocalization may not be dependent on the presence of testicular androgens and, (2) OP has a gradual inhibitory effect on vocalization when given at high doses and this effect is reversible.
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Groups of neonatal female rats were treated for the first 5 days of life with oestradiol-17beta, oestradiol benzoate or a synthetic oestrogen, 11beta-methoxy-17-ethynyl-1,3,5(10)-oestratriene-3,17beta-diol (RU 2858), in daily doses ranging from 0-5 to 1000 ng. Oestradiol-17beta had no effect on adult ovarian cyclicity or sexual receptivity after ovariectomy and oestrogen+ progesterone treatment. Ovarian cyclicity was prevented by 100 ng or more oestradiol benzoate/day, and by all doses of RU 2858. Only rats receiving 50 ng oestradiol benzoate/day or 0-5 ng RU 2858/day showed normal receptivity. The defeminizing action of RU 2858 was at least 100 times greater than that of oestradiol benzoate; it is suggested that this greater potency is due to the low affinity of RU 2858 for the oestradiol-binding protein in the plasma of neonatal rats. These results indicate that defeminization of the neonatal rat brain can be induced by physiological amounts of oestrogen, and are discussed with reference to the action of testosterone.
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