scholarly journals Modulation of K+ conductances by Ca2+ and human chorionic gonadotrophin in Leydig cells from mature rat testis.

1996 ◽  
Vol 495 (1) ◽  
pp. 23-35 ◽  
Author(s):  
J F Desaphy ◽  
C Rogier ◽  
M Joffre
Keyword(s):  
Leydig Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Rat Testis

BINDING OF HUMAN CHORIONIC GONADOTROPHIN BY RAT TESTIS: EFFECT OF SEXUAL MATURATION, CRYPTORCHIDISM AND HYPOPHYSECTOMY

1975 ◽  
Vol 64 (1) ◽  
pp. 59-66 ◽  
Author(s):  
JOACHIM FROWEIN ◽  
WOLFGANG ENGEL
Keyword(s):  
Dissociation Constant ◽  
Sexual Maturation ◽  
Leydig Cells ◽  
Binding Capacity ◽  
Specific Binding ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Scatchard Analysis ◽  
Rat Testis ◽  
Relative Binding

SUMMARY The specific binding of 125I-labelled human chorionic gonadotrophin (HCG) by rat testicular homogenate as compared with isolated Leydig cells differs with respect to total binding capacity but not to the dissociation constant (KD) as revealed by Scatchard analysis. The maximal binding capacity for [125I]HCG of crude testicular homogenate was 95 ng/g rat testis. Hypophysectomy causes a decline in binding capacity within the first three days but on the 20th and 30th day after hypophysectomy the relative binding capacity no longer differs from that of controls. Binding capacity is enhanced in cryptorchid testes relative to normal, and increases during sexual maturation to a peak shortly before puberty.

Regulation of testicular human chorionic gonadotrophin binding in prolactin-deficient Snell dwarf mice

1982 ◽  
Vol 95 (3) ◽  
pp. 301-309 ◽  
Author(s):  
A. G. Amador ◽  
A. Bartke
Keyword(s):  
Leydig Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Direct Effects ◽  
Down Regulation ◽  
Drug Induced ◽  
Congenital Deficiency ◽  
Similar Dose ◽  
Snell Dwarf ◽  
Dwarf Mice

The regulation of binding of 125I-labelled human chorionic gonadotrophin (hCG) to testis was studied in mutant mice with congenital deficiency of prolactin (dw/dw), in mice with prolactin deficiency induced by treatment with bromocriptine and in normal untreated mice. After injection of hCG, normal mice showed a dose-related decrease in testicular hCG binding and subsequent recovery from down-regulation, similar to previous findings in the rat. Mice with congenital prolactin deficiency had a similar dose–response curve of receptor loss after hCG administration, but recovered from down-regulation faster than the normal mice. Induction of prolactin deficiency with bromocriptine prevented down-regulation of hCG binding. The differential effects of congenital and drug-induced prolactin deficiency could be related to a difference in the duration of the deficiency or to its severity. However, this difference could also suggest direct effects of the dw mutation and/or bromocriptine on the Leydig cells.

ISOLATION OF RAT LEYDIG CELLS BY DENSITY GRADIENT CENTRIFUGATION

1982 ◽  
Vol 92 (2) ◽  
pp. 293-NP ◽  
Author(s):  
J. S. GALE ◽  
J. ST J. WAKEFIELD ◽  
H. C. FORD
Keyword(s):  
Density Gradient ◽  
Binding Sites ◽  
Leydig Cells ◽  
Interstitial Cell ◽  
Density Gradient Centrifugation ◽  
Gradient Centrifugation ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Collagenase Treatment

A rapid method for preparing Leydig cells from rat testes is described. An interstitial cell suspension, prepared by collagenase treatment of decapsulated testes, was centrifuged for 10 min over a cushion of 60% (v/v) Percoll to remove red blood cells, and then centrifuged for 20 min in a 0–60% linear density gradient of Percoll. Seventy-four per cent of the cells present in that fraction of the gradient comprising 35–50% Percoll were Leydig cells; the yield from each testis was about 1·5 × 106 cells. The Leydig cells appeared viable, excluded Trypan blue, possessed high-affinity binding sites for human chorionic gonadotrophin (hCG) and synthesized increased quantities of testosterone in response to hCG. The cells could be stored overnight in 20% (v/v) glycerol at −20 °C, with only minimal effect on the specific activities of a number of enzymes used as markers of subcellular components. Testosterone production in vitro by the cells after storage for 20 h was greater than that of hCG-stimulated fresh cells and was not further increased by hCG.

Studies on the testicular source of inhibin and its route of secretion in rams: failure of the Leydig cell to secrete inhibin in response to a human chorionic gonadotrophin/LH stimulus

1991 ◽  
Vol 130 (1) ◽  
pp. 107-114 ◽  
Author(s):  
A. J. Tilbrook ◽  
D. M. de Kretser ◽  
I. J. Clarke
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Jugular Vein ◽  
Plasma Concentrations ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Spermatic Vein ◽  
Jugular Veins ◽  
Testicular Vein ◽  
Peripheral Plasma

ABSTRACT To determine whether Leydig cells produce inhibin in the ram, Leydig cells were stimulated by administering human chorionic gonadotrophin (hCG) or raising the levels of endogenous LH by an injection of gonadotrophin releasing hormone (GnRH). Plasma concentrations of testosterone increased in the 72 h after either a single injection (P < 0·05) or two injections (P < 0·01) of hCG. Plasma concentrations of inhibin were not significantly influenced by either one or two injections of hCG. Administration of GnRH (1 μg) caused an 11-fold increase in plasma concentrations of LH but did not influence concentrations of inhibin in either the jugular or testicular veins (pampiniform plexus). In contrast, concentrations of testosterone were increased by about fourfold in both jugular (P < 0·01) and testicular (P < 0·05) veins. The concentrations of inhibin in the testicular vein were 1·3-fold higher than in the peripheral plasma (P < 0·05) both before and following treatment with GnRH whereas the concentrations of testosterone were 18- to 21-fold greater than in peripheral concentrations. In view of the difference in concentrations of inhibin between testicular and jugular veins, in a further experiment a sample was taken from the jugular vein, a vein located in the tunica vasculosa of the testis (testicular vein) and from a vein (spermatic vein) and lymph vessels located in the spermatic cord. The mean (± s.e.m.) concentrations of inhibin were highest in the testicular lymph (45·93±4·21 μg/l; P < 0·001) compared with the peripheral (4·14±0·31 μg/l), spermatic (8·0±1·17 μg/l) or testicular (6·4±0·82 μg/l) plasma. Plasma concentrations of inhibin were significantly higher in the spermatic vein than in the testicular vein (P < 0·05) and jugular vein (P < 0·01), and concentrations of inhibin in the testicular vein were significantly (P < 0·05) higher than in the jugular vein. There were no significant differences in the concentrations of testosterone in the spermatic vein, testicular vein or testicular lymph but the concentrations of testosterone in the peripheral plasma were significantly (P < 0·05) less than in the testicular plasma or lymph. These results suggest that, in the ram, the Leydig cell does not respond to hCG or endogenous LH by secreting inhibin or by influencing other cells within the testis to secrete inhibin within the time-frame of these experiments. The low testicular to jugular differences in the concentration of inhibin and the high concentrations of inhibin in the testicular lymph suggest that the lymph may be an important route of secretion of inhibin from the testis in the ram. Journal of Endocrinology (1991) 130, 107–114

Regulation of testosterone production in Leydig cells from fetal mice under dynamic conditions: effect of human chorionic gonadotrophin and 8-bromo-cyclic AMP

1985 ◽  
Vol 107 (3) ◽  
pp. 409-414 ◽  
Author(s):  
G. Pointis ◽  
M. T. Latreille
Keyword(s):  
Cyclic Amp ◽  
Leydig Cells ◽  
Time Lag ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Continuous Exposure ◽  
Testosterone Secretion ◽  
Testosterone Production ◽  
Peak Value ◽  
Fetal Leydig Cells

ABSTRACT The temporal release of testosterone by Leydig cells from 18-day-old mouse fetuses in response to human chorionic gonadotrophin (hCG) and to 8-bromo-cyclic AMP (8-bromo-cAMP) was investigated under short-term incubation (180 min) conditions. A rapid and large increase in testosterone release was induced by a 5-min exposure to hCG (20 i.u./l) or 8-bromo-cAMP (10 mmol/l). The testosterone response of fetal Leydig cells to the two gonadotrophic stimuli was Gaussian in distribution with a peak value of testosterone by 15–20 min. Repeated exposure to hCG resulted in a reduced testosterone response but an increased accumulation of cAMP. The apparent resistance of fetal Leydig cells to hCG could not be overcome either by increasing the hCG concentration (to 2000 i.u./l) or by exposing the cells to 8-bromo-cAMP (10 mmol/l). Continuous exposure to hCG (200 i.u./l) divided into multiple small doses (each 8 i.u./l) induced testosterone secretion with different kinetic characteristics: a three-fold longer time-lag between hormone exposure and the peak value; a twofold greater testosterone response (P<0·001) and a gradual decrease of testosterone secretion. Oestradiol significantly reduced basal and hCG-stimulated testosterone production only at a high concentration (10 μmol/l). These results indicate that continuous or pulsatile exposure to hCG can induce refractoriness of fetal Leydig cells. The similarity between the actions of hCG and 8-bromo-cAMP on fetal steroidogenesis suggests that this rapid defect is not primarily due to a depletion of gonadotrophin receptors but results from disruption of regulatory mechanisms at the post-receptor level. J. Endocr. (1985) 107, 409–414

scholarly journals DIRECT BINDING OF RADIOIODINATED HUMAN CHORIONIC GONADOTROPHIN TO FROZEN SECTIONS OF RAT TESTIS

Reproduction ◽  
1975 ◽  
Vol 43 (1) ◽  
pp. 123-126 ◽  
Author(s):  
A. D. LAGO ◽  
M. T. ROLANDI ◽  
M. BORTOLUSSI ◽  
S. GALLI
Keyword(s):  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Frozen Sections ◽  
Rat Testis ◽  
Direct Binding

Phospholipid methylation decreases in human chorionic gonadotrophin-induced desensitized rat Leydig cells

1993 ◽  
Vol 138 (1) ◽  
pp. 65-71 ◽  
Author(s):  
A. M. Ronco ◽  
L. E. Valladares
Keyword(s):  
Enzymatic Activity ◽  
Leydig Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
High Dose ◽  
Minimal Amount ◽  
Methyltransferase Activity ◽  
Single High Dose ◽  
Surface Receptors ◽  
Cellular Changes

ABSTRACT Phospholipid methylation in Leydig cells from desensitized rats was studied. The incorporation of l-[methyl-3H] methionine into phospholipids in intact Leydig cells decreased when animals were injected with a single high dose of human chorionic gonadotrophin (hCG). This effect was detected on the first day after hCG injection and remained up to 12 days after treatment. The inhibition was not due to a reduced uptake of l-[methyl-3H]methionine. A decreased phospholipid methylation with unaltered phospholipid methyltransferase activity was observed on days 1, 6 and 12 after the hCG. On day 3 after hCG injection, phospholipid methyltransferase activity and phospholipid methylation in intact Leydig cells were both inhibited by 40%. Also, a minimal amount of LH free receptors and the lowest number of total receptors was observed at this time. Thus, a relationship between the reduced enzymatic activity and the maximal decrease in LH surface receptors is suggested. In addition, the decreased incorporation of l-[methyl-3H]methionine into phospholipids on days 1, 6 and 12 after hCG injection, could be associated with other cellular changes related to the desensitization process. Journal of Endocrinology (1993) 138, 65–71

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