REGULATION OF PROLACTIN BINDING SITES IN THE SEMINAL VESICLE, PROSTATE GLAND, TESTIS AND LIVER OF INTACT AND CASTRATED ADULT RATS: EFFECT OF ADMINISTRATION OF TESTOSTERONE, 2-BROMO-α-ERGOCRYPTINE AND FLUPHENAZINE

1979 ◽  
Vol 81 (1) ◽  
pp. 11-18 ◽  
Author(s):  
R. J. BARKEY ◽  
J. SHANI ◽  
D. BARZILAI

The effect of hormonal manipulations on prolactin binding to its specific binding sites in the seminal vesicle, prostate gland, testis and liver of adult male rats was studied. Castration significantly reduced prolactin binding to the seminal vesicle and prostate, whereas it greatly increased its binding to the liver. Testosterone replacement therapy restored the reduced level of binding to that found in the liver of intact rats, whereas binding to the seminal vesicle and the prostate was raised to the high levels found in the testosterone-treated intact rats. In contrast, testosterone administration to intact rats significantly reduced the binding of prolactin to the testicular homogenate. The administration of 2-bromo-α-ergocryptine (CB 154) to either intact or testosterone-treated castrated rats caused no significant change in binding of prolactin to any of the organs tested. Fluphenazine enanthate or CB 154 +ovine prolactin increased the binding of prolactin to the liver, when compared with untreated rats, whereas in the testis these treatments resulted in a minor decrease as compared with untreated rats. In the testosterone-treated castrated rats, fluphenazine caused no apparent effect on the binding of prolactin to any of the organs tested. In conclusion, testosterone is essential for the maintenance of prolactin binding sites in the seminal vesicle and prostate of the adult rat. Prolactin, however, does not appear to regulate its own receptor in the accessory sex glands, neither alone nor in synergism with testosterone. In the testis, exogenous testosterone exerted a negative effect on prolactin binding, as did raised serum prolactin levels. In the liver of the male rat, testosterone seemed to be the major cause of the low level of prolactin binding sites, while prolactin was capable of inducing its own sites in that organ.

1980 ◽  
Vol 239 (4) ◽  
pp. E237-E237

Male rat adipose tissues contain cytoplasmic estrogen binding sites comparable to those found in females. This bindng is of high affinity (Kd = 1.7 x 10(-10) M) and is estrogen specific. Binding of 17 beta-estradiol was inhibited by radioinert estrogens (17 beta-estradiol and R 2858) but not by other steroids (progesterone, 5 alpha-dihydrotestosterone, and corticosterone). Estrogen binding sites were found in all fat pads studied, but levels were highest in the epididymal pads. Treatment of female rats with 17 beta-estradiol benzoate (E2B) induced cytoplasmic progestin receptors in adipose tissues, but in three separate experiments, E2B treatment (20 microgram/day for 3 days) failed to induce measurable progestin ([3H]R 5020) binding sites in males. E2B treatment reduced lipoprotein lipase (LPL) activity by approximately 75% in epididymal (male) and parametrial (female) fat pads. Concurrent progesterone treatment increased parametrial LPL activity in E2B-treated females, but progesterone had no effect on epididymal fat pad LPL activity in males. These findings are consistent with the hypothesis that in male rats aromatized (estrogenic) metabolites of testosterone may reduce body fat content and alter lipid metabolism by direct actions on adipose tissues.


Author(s):  
O. Tkachenko ◽  
V. Kovalenko

Comparative study of embryo-fetal death in females fertilized by males with metabolic syndrome, induced in adult or juvenile age has shown that the offspring of adult rats did not have significant abnormalities in embrio- and fetogenesis. At the same time it has been revealed 4% postimplantation death of offspring in male rats with metabolic syndrome induced in the juvenile age. The pre-implantation loss in this group was 6 folds higher than in control. Accordingly, the total mortality of the offspring rose 2.4 times in comparison with control.


1966 ◽  
Vol 35 (3) ◽  
pp. 217-222 ◽  
Author(s):  
U. ZOR ◽  
H. AILABOUNI ◽  
F. G. SULMAN

SUMMARY The mechanism by which combined treatment with monoamine oxidase inhibitors and a corticosteroid reduces the weight of the accessory sex glands in intact rats by about one half has been studied. Phenelzine sulphate in combination with hydrocortisone acetate given for 30 days to ovariectomized rats reduced the pituitary stores of luteinizing hormone (LH) by 33%. Similar reductions in somatotrophic hormone, corticotrophin and thyroid-stimulating hormone content were found after comparable treatment, whereas luteotrophic hormone increased. The increase of weight of the seminal vesicles and prostate gland produced by human chorionic gonadotrophin could be partly antagonized by the simultaneous administration of mebanazine and dexamethasone, but the action of testosterone on these glands in castrated animals was not inhibited. Interference with the production and effectiveness of LH is therefore the most likely mode of action by which these drugs effect the reduction of the weight of the accessory sex glands.


1981 ◽  
Vol 98 (3) ◽  
pp. 441-445 ◽  
Author(s):  
Ulrich Müller ◽  
Th. Bauknecht ◽  
Jan Willem Siebers

Abstract. Ovaries of adult rats specifically bind PGF2α while those of immature animals do not. Induction of luteinization by hCG in juvenile animals, however, results in specific binding of PGF2α It is suggested that luteal cells are the only cell type of the ovary, which is endowed with specific receptors for PGF2α The number of PGF2α binding sites varies during the ovarian cycle. Most free receptors are detectable in early pro-oestrus, least in the oestrus stage. The oscillation of receptors disappears after inhibition of prostaglandin synthesis by indomethacin. Therefore the apparent cyclic variation of prostaglandin receptors must be ascribed to occupancy of the receptors by varying amounts of endogenous prostaglandin F2α.


1976 ◽  
Vol 156 (2) ◽  
pp. 375-380 ◽  
Author(s):  
L M Lewin ◽  
Y Yannai ◽  
S Sulimovici ◽  
P F Kraicer

Radioactive myo-inositol was injected intraperitoneally into nephrectomized rats. The radioactive material present in liver, spleen, brain, heart, diaphragm, seminal vesicle, coagulating gland, prostate, epididymis, vas deferens and testis was shown to consist exclusively of myo-inositol and its derivatives, as shown by paper chromatography of hydrolysates and trichloroacetic acid extracts of these tissues. Radioactive myo-inositol was accumulated rapidly within 1 h by the thyroid, coagulating gland and seminal vesicle. Other tissues, such as the pituitary, prostate gland, liver and spleen, concentrated myo-inositol less actively. The muscle tissues studied (diaphragm and heart) concentrated little inositol, whereas brain, testis, and epididymal fat-pad did not concentrate it at all. The lipid fraction of liver contained most of the radio-labelled myo-inositol. In the other organs most of the radioactivity was found in the aqueous trichloroacetic acid extract, largely as free myo-inositol.


1973 ◽  
Vol 58 (2) ◽  
pp. 227-231 ◽  
Author(s):  
H. M. LLOYD ◽  
J. D. MEARES ◽  
JOAN JACOBI

SUMMARY The effects of a single injection of 1 mg diethylstilboestrol dipropionate on pituitary mitotic activity and on secretion of growth hormone and prolactin were investigated in male rats on each of the first 15 days following the single dose and then at intervals for a total period of 63 days. Mitotic activity increased to a maximum on day 4 and then gradually diminished. Serum growth hormone was moderately increased during the 2nd week and serum prolactin showed a gradual rise with a return to normal on day 63. In the pituitary gland, growth hormone concentration diminished until day 28, whereas prolactin rose quickly at first, maintained a raised level and increased further on day 43. During the first 12 days, pituitary weight was significantly correlated with serum growth hormone and prolactin concentration. During days 13–28, serum prolactin, but not growth hormone, was significantly correlated with the pituitary mitotic index.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2014 ◽  
Author(s):  
Stefano Sartini ◽  
Davide Lattanzi ◽  
Michael Di Palma ◽  
David Savelli ◽  
Silvia Eusebi ◽  
...  

Creatine plays a crucial role in developing the brain, so much that its genetic deficiency results in mental dysfunction and cognitive impairments. Moreover, creatine supplementation is currently under investigation as a preventive measure to protect the fetus against oxidative stress during difficult pregnancies. Although creatine use is considered safe, posing minimal risk to clinical health, we found an alteration in morpho-functional maturation of neurons when male rats were exposed to creatine loads during brain development. In particular, increased excitability and enhanced long-term potentiation (LTP) were observed in the hippocampal pyramidal neurons of weaning pups. Since these effects were observed a long time after creatine treatment had been terminated, long-lasting modifications persisting into adulthood were hypothesized. Such modifications were investigated in the present study using morphological, electrophysiological, and calcium imaging techniques applied to hippocampal Cornu Ammonis 1 (CA1) neurons of adult rats born from dams supplemented with creatine. When compared to age-matched controls, the treated adult offspring were found to retain enhanced neuron excitability and an improved LTP, the best-documented neuronal substrate for memory formation. While translating data from rats to humans does have limitations, our findings suggest that prenatal creatine supplementation could have positive effects on adult cognitive abilities.


1970 ◽  
Vol 63 (2) ◽  
pp. 207-215 ◽  
Author(s):  
Kjell J. Tveter

ABSTRACT The distribution of radioactive material in the prostate gland and the seminal vesicles has been studied by autoradiography after intramuscular administration of [1,2-3H] testosterone in vivo to adult castrated male rats. Positive autoradiographs were obtained from 7½ min to 8 h after the administration. As early as after 15 min, there appeared to be a selective localization of radioactivity in the epithelial cells, with much of the labelling associated with the nuclei; the stromal labelling was markedly less. This picture was even more significant ½, 1 and 2 h after the injection, when the autoradiographs demonstrated a preferential labelling of the nuclei of the epithelial cells. A distinct labelling of the epithelial cells was also found 8 h after the injection. The same qualitative pattern of distribution of radioactivity was seen in the four prostatic lobes and the seminal vesicles. No significant labelling of the secretions in the glandular lumina was observed.


1982 ◽  
Vol 95 (2) ◽  
pp. 267-274 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey

Measurement of pituitary gonadotrophin releasing hormone (Gn-RH) receptor content provides a qualitative index of prior exposure of the pituitary gland to endogenous Gn-RH. The effect of moderate hyperprolactinaemia (serum prolactin = 95–250 μg/l), achieved with three pituitary grafts beneath the renal capsule, on the pituitary Gn-RH receptor content and serum LH responses to gonadectomy of adult rats has been studied. In males the presence of hyperprolactinaemia for 7 days completely prevented the increase in Gn-RH receptor content 3 days after castration and inhibited the serum LH rise by 45%. By 6 days after castration, Gn-RH receptors had increased in the hyperprolactinaemic castrated animals but values were 33% lower than in sham-grafted controls, while the serum LH increase was attenuated by 30%. Pituitary LH content was also lower in grafted castrated animals 6 days after castration. Hyperprolactinaemia for 3 weeks had no effect on Gn-RH receptors or pituitary LH content of intact male rats, although basal serum LH was decreased by 50%. Hyperprolactinaemia also attenuated the increases in Gn-RH receptors, serum LH and pituitary LH which occurred 6 days after ovariectomy in female rats. In all experiments the pituitary content of prolactin was reduced by 80–90% in animals bearing pituitary grafts. These results suggest that hyperprolactinaemia restricts the Gn-RH receptor response to gonadectomy by decreasing endogenous hypothalamic Gn-RH secretion.


1979 ◽  
Vol 81 (1) ◽  
pp. 75-81 ◽  
Author(s):  
B. D. GREENSTEIN

Available high-affinity binding sites for 5α-dihydrotestosterone (DHT) were measured in cytosols obtained from the amygdala, hypothalamus, anterior pituitary gland and ventral prostate gland of 12-week-old rats at various times after orchidectomy, and in the corresponding tissues of 18-month-old male rats. It is suggested that the lower affinity of the DHT binding reaction in brain and ventral prostatic cytosols after orchidectomy or ageing respectively, may explain, at least in part, the changes in the responsiveness of the tissues to androgens.


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