Effect of corticosterone on the hypothalamic-pituitary-gonadal system of male Japanese quail exposed to either short or long photoperiods

1982 ◽  
Vol 95 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Pierre Deviche ◽  
Renato Massa ◽  
Luciana Bottoni ◽  
Jean-Claude Hendrick

Male quail were bred under short photoperiods of 8 h light: 16 h darkness (8L : 16D; SD) for the first 4 weeks of life and were then transferred to either long photoperiods of 16L : 8D (LD) or maintained under the SD regime. Both groups of birds were treated for 2 weeks with a daily dose of either 0·25 or 1·0 mg corticosterone. The conversion of [14C]testosterone in vitro into 5α- and 5β-dihydrotestosterone (5α- and 5β-DHT), 5α- and 5β-androstane-3α,17β-diol, and androstenedione was then measured in the pituitary and cloacal glands of all birds. In the hyperstriatum and posterior hypothalamus only 5β-reduced metabolites and androstenedione were detected. Transfer to LD and injection of corticosterone affected the metabolism of testosterone only in the pituitary and cloacal glands. In the pituitary gland, exposure to LD increased the production of 5α-reduced metabolites but not of either 5β-reduced metabolites or androstenedione. In both SD and LD birds, injections of corticosterone enhanced the production of 5β-reduced steroids and decreased the production of androstenedione. In LD birds corticosterone also decreased the production of 5α-androstane-3α,17β-diol. Plasma levels of LH and FSH were higher in the LD than in the SD birds. In the SD birds treatment with corticosterone increased the level of LH after 14 days of treatment. Exposure to LD decreased the production of 5β-androstane-3α,17β-diol and androstenedione in the cloacal gland and increased the conversion of testosterone into 5α-DHT Treatment with corticosterone increased the production of androstenedione in the cloacal gland of LD birds but decreased it in that of SD birds. Corticosterone also partially blocked the photoinduced growth of the cloacal gland, but it slightly stimulated the growth of the gland in the SD birds. After 2 weeks of treatment SD (but not LD) corticosterone-treated birds had higher testicular weights than the corresponding controls. It is suggested that treatment with corticosterone might affect the hypothalamic-pituitary-gonadal axis partly through changes in the metabolism of testosterone.

1990 ◽  
Vol 127 (3) ◽  
pp. 487-496 ◽  
Author(s):  
S. C. Wilson ◽  
R. A. Chairil ◽  
F. J. Cunningham ◽  
R. T. Gladwell

ABSTRACT The contents of LHRH-I and -II in the anterior hypothalamus and posterior hypothalamus (including the mediobasal hypothalamus and median eminence) were measured at 90, 180 and 360 min after the i.m. injection of laying hens with progesterone. Whilst no changes were observed in the content of LHRH-I in the anterior hypothalamus, LHRH-I in the posterior hypothalamus tended to fall at 90 and 180 min after injection of progesterone in hens maintained on 16 h light:8 h darkness (16L:8D) and 8L:16D respectively. Pretreatment of laying hens with tamoxifen significantly increased the hypothalamic contents of LHRH-I and -II, raised the basal plasma concentration of LH and modified the LH response to progesterone injection. In hens in which tamoxifen prevented an increase in the plasma concentration of LH after progesterone injection, the content of LHRH-I in the posterior hypothalamus remained unchanged. In contrast, in hens in which progesterone stimulated a steep increase in LH within 90 min, there was a pronounced and significant fall in LHRH-I content of the posterior hypothalamus. No change in the hypothalamic content of LHRH-II was observed during the progesterone-induced surge of LH until plasma concentrations had attained maximal values or started to decline. Then, in hens maintained on 16L:8D, a significant fall in the content of LHRH-II in the anterior hypothalamus was found at both 180 and 360 min after injection with progesterone. Tests in vitro and in vivo of the responsiveness of the pituitary gland to synthetic LHRH-I and -II revealed no change at 90 min after injection of laying hens with progesterone, when plasma concentrations of LH were increasing, but a pronounced reduction when plasma LH concentrations were maximal or falling. These results suggest that LHRH-I mediates in the progesterone-induced increase in the plasma concentration of LH. Although the subsequent decline in plasma LH was associated with a reduced responsiveness of the pituitary gland to LHRH, a significant correlation between the contents of LHRH-I and -II in the anterior hypothalamus and a fall in the hypothalamic content of LHRH-II when plasma LH was maximal or declining allows the possibility of an involvement of this peptide in the neuroendocrine events preceding ovulation. Journal of Endocrinology (1990) 127, 487–496


1980 ◽  
Vol 84 (2) ◽  
pp. 223-230 ◽  
Author(s):  
R. MASSA ◽  
D. T. DAVIES ◽  
L. BOTTONI

A cloacal gland complex whose growth and development is androgen-dependent exists in the Japanese quail. In-vitro incubation studies of the cloacal gland using 4-14C-labelled testosterone as substrate allowed the positive identification of five metabolites: androstenedione, 5β-dihydrotestosterone (5β-DHT), 5β-androstane-3α,17β-diol, 5α-DHT and 5α-androstane-3α,17β-diol. More polar metabolites, not yet chemically identified, were detected in trace amounts. Androstenedione appeared to be the main testosterone metabolite in immature birds while in mature birds on long daylengths testosterone was preferentially metabolized to 5α-DHT. This change may have been in response to the higher levels of plasma steroids found in mature birds. When various testosterone metabolites, contained in silicone elastomer capsules, were implanted s.c. into castrated birds maintained on a photostimulatory light régime, 5α-DHT, 5α-androstane-3,17-dione, androstenedione and 5α-androstan-3α-ol-17-one were shown to be equipotent with testosterone in stimulating the development of the cloacal gland. 5α-Androstane-3α,17β-diol and 5α-androstan-3β-ol-17-one stimulated some growth while 5β-DHT, 5α-androstane-3β,17β-diol, 5α-androstane-3α,17β-diol, 5β-androstane-3,17-dione, androst-5-en-3β-ol-17-one and androst-5-ene-3β,17β-diol were completely ineffective.


1984 ◽  
Vol 100 (1) ◽  
pp. 13-18 ◽  
Author(s):  
J. Balthazart ◽  
M. Schumacher

ABSTRACT Testosterone metabolism in the brain and pituitary and cloacal glands of male and female Japanese quail was studied in vitro during sexual maturation (from 1 day to 5 weeks after hatching). The production of 5α-dihydrotestosterone in the hyperstriatum and cloacal gland and that of androstenedione in the cloacal gland of males was highest at 1 day after hatching, which could be related to the peak of plasma androgens previously demonstrated in neonatal quail. 5β-Reductase activity was very high in the brain, but not the pituitary or cloacal glands of young chicks and decreased markedly, especially in the hypothalamus, during sexual maturation. As 5β-reduced metabolites of testosterone are inactive androgens, it is suggested that the decrease of 5β-reductase activity with age corresponds to a potentiation of the effects of testosterone at the level of the brain. J. Endocr. (1984) 100, 13–18


2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Avishek Biswas ◽  
O. S. Ranganatha ◽  
Jag Mohan

A study was conducted to determine the effect of foam extract on sperm motility in the male Japanese quail (Coturnix coturnix japonica). Adult male quails (12 weeks) of heavy body weight strain were housed in individual cages and divided into 5 groups according to the size of their cloacal glands. The data indicated that the size of the cloacal gland was positively correlated with the frequency of foam secretion and total foam production. One gram of freshly collected clean foam was mixed with 1.0 mL of normal saline and homogenized for 10 minutes. After centrifugation at 35 000 rpm, the supernatant was used as 100% foam extract. The extract was diluted to 1:40, 1:20, 1:10, and 1:4 with normal saline to produce 2.5, 5.0, 10, and 25% foam extracts, respectively. 5% foam extract enhanced sperm survival at room temperature (30°–35°C) for 2 to 3 hrs, whereas higher concentrations (10% and above) suppressed sperm motility. From this study, it may be concluded that foam secretion and quantity of foam are directly proportional to the size of the cloacal gland and that the foam enhances and prolongs sperm motility, in vitro at an optimum concentration of 5%.


1975 ◽  
Vol 64 (1) ◽  
pp. 87-101 ◽  
Author(s):  
W. R. GIBSON ◽  
B. K. FOLLETT ◽  
BARBARA GLEDHILL

SUMMARY Plasma levels of luteinizing hormone (LH) were measured by radioimmunoassay in gonadectomized male and female Japanese quail, exposed either to 8 h light: 16 h darkness per day (8L:16D; short days) or to 20L:4D (long days). In both sexes, exposure to long days increased LH levels and in the gonadectomized quail LH continued to rise over several weeks. Eventually the castrated quail had levels about five times higher than the control birds and the ovariectomized quail had levels about 14 times higher than their controls. Quail kept on short days had low LH levels while birds kept on long days and returned to short days resumed low levels after a delay of some days. Since very high levels of LH occurred in gonadectomized quail only when they were on long days, we conclude that the photoperiodic regulation of LH secretion does not operate solely by adjusting sensitivity to gonadal feedback, but works in a more direct manner. Ovariectomized females whether on long days (high LH) or short days (low LH) grew masculine plumage and castrated males retained male plumage. This confirms that the ovary is responsible for sexual dimorphism of plumage and shows that the action of the ovary is not mediated by LH (through feedback). The remaining rudimentary (right) gonad in ovariectomized females did not undergo visible hypertrophy and did not secrete enough hormone to stimulate the cloacal gland or oviduct.


1992 ◽  
Vol 67 (02) ◽  
pp. 258-263 ◽  
Author(s):  
Raffaele De Caterina ◽  
Rosa Sicari ◽  
An Yan ◽  
Walter Bernini ◽  
Daniela Giannessi ◽  
...  

SummaryIndobufen is an antiplatelet drug able to inhibit thromboxane production and cyclooxygenase-dependent platelet aggregation by a reversible inhibition of cyclooxygenase. Indobufen exists in two enantiomeric forms, of which only d-indobufen is active in vitro in inhibiting cyclooxygenase. In order to verify that also inhibition of platelet function is totally accounted for by d-indobufen, ten patients with proven coronary artery disease (8 male, 2 female, age, mean ± S.D., 58.7 ± 7.5 years) were given, in random sequence, both 100 mg d-indobufen and 200 mg dl-indobufen as single administrations in a double-blind crossover design study with a washout period between treatments of 72 h. In all patients thromboxane (TX) B2 generation after spontaneous clotting (at 0, 1, 2, 4, 6, 8, 12, 24 h), drug plasma levels (at the same times), platelet aggregation in response to ADP, adrenaline, arachidonic acid, collagen, PAF, and bleeding time (at 0, 2, 12 h) were evaluated after each treatment. Both treatments determined peak inhibition of TXB2 production at 2 h from administration, with no statistical difference between the two treatments (97 ±3% for both treatments). At 12 h inhibition was 87 ± 6% for d-indobufen and 88 ± 6% for dl-indobufen (p = NS). Inhibition of TXB2 production correlated significantly with plasma levels of the drugs. Maximum inhibitory effect on aggregation was seen in response to collagen 1.5 pg/ml (63 ± 44% for d-indobufen and 81 ± 22% for dl-indobufen) and arachidonic acid 0.5-2 mM (78 ± 34% for d-indobufen and 88 ± 24% for dl-indobufen) at 2 h after each administration. An effect of both treatments on platelet aggregation after 12 h was present only for adrenaline 2 μM (55 ± 41% for d-indobufen and 37 ± 54% for dl-indobufen), collagen 1.5 pg/ml (69 ± 30% for d-indobufen and 51 ± 61% for dl-indobufen), arachidonic acid 0.5-2 mM (56 ± 48% for d-indobufen and 35 ± 49% for dl-indobufen). The extent of inhibition of TX production and the extent of residual platelet aggregation were never significantly different between treatments. Bleeding time prolongation was similar in the two treatment groups without showing a pronounced and long lasting effect (from 7.0 ± 2.0 min to 10.0 ± 3.0 min at 2 h and 8.0 ± 2.0 min at 12 h for d-indobufen; from 6.0 ±1.0 min to 8.5 ± 2.0 min at 2 h and 8.0 ± 1.0 min at 12 h for dl-indobufen). These results demonstrate that the biological activity of dl-indobufen as an antiplatelet agent in vivo is totally accounted for by d-indobufen.


1985 ◽  
Vol 54 (04) ◽  
pp. 808-812 ◽  
Author(s):  
Ulf Berglund ◽  
Henning von Schenck ◽  
Lars Wallentin

SummaryThe effects of ticlopidine (T) (500 mg daily) on platelet function were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. The in vitro platelet reactivity to aggregating agents, the platelet sensitivity to prostacyclin and the plasma levels of platelet specific proteins and fibrinogen were determined before and after 4 and 8 weeks of treatment. T exerted a potent inhibitory effect on ADP- and collagen-induced platelet aggregation. The effect of T was proportional to the pretreatment reactivity to ADP and collagen. The inhibitory effect of T on the epinephrine response was less pronounced. The plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen were not influenced by T. The platelet inhibition of prostacyclin was potentiated by T, and it was demonstrated that T and prostacyclin had synergistic inhibitory effects on platelet aggregation.


1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.


1970 ◽  
Vol 64 (4) ◽  
pp. 687-695 ◽  
Author(s):  
Junzo Kato

ABSTRACT The anterior, middle, and posterior hypothalamus, the cortex cerebri, the anterior hypophysis as well as the diaphragm of adult ovariectomized rats were incubated in vitro with tritiated 17β-oestradiol. The uptake of tritiated oestradiol was differentially distributed intracerebrally with higher accumulation in the anterior hypothalamus and the hypophysis. Lowering the temperature of the incubation medium caused a reduction in the uptake of radioactivity by the anterior hypothalamus as compared to that found in other brain tissues. Tritiated oestradiol taken up in vitro by the anterior hypothalamus and the hypophysis tended to be retained after further incubation in a steroid-free medium. The addition of non-radioactive 17β-oestradiol to the medium inhibited the uptake of tritiated oestradiol by these tissues. Moreover, pretreatment with non-radioactive 17β-oestradiol in vivo prevented the preferential accumulation of tritiated oestradiol in vitro in the anterior hypothalamus and the hypophysis. These results indicate that oestradiol is preferentially taken up in vitro by the anterior hypothalamus and the hypophysis of the rat.


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