Acute and short-term actions of serotonin administration on the pituitary-testicular axis in the adult rat

1995 ◽  
Vol 7 (5) ◽  
pp. 1101 ◽  
Author(s):  
MP Hedger ◽  
S Khatab ◽  
G Gonzales ◽  
Kretser DM de
Keyword(s):  
Serum Testosterone ◽  
Fold Increase ◽  
Significant Inhibition ◽  
Male Rats ◽  
Minor Role ◽  
Testis Weight ◽  
Serum Concentrations ◽  
Adult Rat ◽  
Serum Lh ◽  
A Minor

In this study, adult male rats were injected intraperitoneally with a single dose of serotonin (5-hydroxytryptamine, 5HT; 10 mg kg-1 bodyweight) for 2 h or 18 h, or daily with graded doses of 5HT (0.1-10 mg kg-1) for four days before being killed. Serum and testicular interstitial fluid (IF) concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone and immunoreactive-inhibin were measured by radioimmunoassay, and one testis was removed for histological examination. At 2 h after a single injection, 5HT caused a significant inhibition of serum concentrations of LH and inhibin, recovered IF volume and intratesticular testosterone concentrations; testis weight and serum concentrations of testosterone and FSH were unaffected. At 18 h after injection, all parameters had returned to normal, with the exception of intratesticular testosterone concentration which remained lower than normal. The lowest 5HT dose (0.1 mg kg-1) had no effect on any parameter following four daily injections. At a dose of 1.0 mg kg-1 5HT, there was a four-fold increase in the concentration of serum LH, but testis weight, recovered IF volume, testosterone and inhibin concentrations and serum concentrations of FSH were not significantly affected. At the highest dose of 5HT (10 mg kg-1) after four daily injections, testis weight decreased, and IF volume increased nearly three-fold. Testis concentrations of inhibin and serum testosterone were reduced, whereas serum concentrations of both LH and FSH were elevated; intratesticular testosterone concentrations did not differ from controls. Only at the highest dose of 5HT was disruption to the seminiferous epithelium observed, with focal damage ranging in severity from increased degeneration of spermatogenic cell profiles, to complete loss of the germinal epithelium; however, many tubule profiles displayed completely normal spermatogenesis. The acute IF volume reduction and spermatogenic disruption in 5HT-treated rats were consistent with localized ischaemia due to constriction of the testicular arterial supply. The eventual increase in IF volume observed after 5HT treatment appeared to be secondary to the loss of germ cells. Although 5HT also inhibited pituitary LH release and Leydig cell steroidogenesis, these effects appeared to play only a minor role in the induction of spermatogenic damage.

HYPOTHALAMIC-PITUITARY-TESTICULAR SYSTEM FOLLOWING TESTICULAR X-IRRADIATION

1976 ◽  
Vol 83 (1) ◽  
pp. 190-200 ◽  
Author(s):  
H. L. Verjans ◽  
K. B. Eik-Nes
Keyword(s):  
Interstitial Cell ◽  
Serum Testosterone ◽  
Male Rats ◽  
Ventral Prostate ◽  
Testis Weight ◽  
X Ray ◽  
Serum Lh ◽  
Testicular Weight ◽  
Unknown Factor ◽  
X Irradiation

ABSTRACT Testes of adult, male rats were exposed to a total dose of 1500 R of X-irradiation. Testicular weight decreased from day 8 after X-ray treatment. This decrease was, however, preceded by an increment of the testis weight on day 4 following treatment. X-ray treatment of testes was associated with significant increases in serum FSH. Testicular irradiation had, however, no effect on ventral prostate and seminal vesicles weights. Serum testosterone increased only on day 1, 2 and 4 after irradiation, while serum LH levels tended to increase from day 8 post-irradiation. These changes were not significant, however, when compared with non-irradiated controls. At 7, 13 and 20 days following 1500 R of bilateral, testicular X-irradiation, the hypothalamic-pituitary unit was still capable of responding to exogenous gonadotrophin releasing factor. Serum FSH may in male rats be regulated at least partly by circulating steroids of testicular origin and partly by an unknown factor of non-interstitial cell nature.

The contribution of corticosterone and testosterone to the suppression of serum LH in hyperprolactinaemic adult male rats with pituitary transplants

1987 ◽  
Vol 113 (1) ◽  
pp. 111-116 ◽  
Author(s):  
R. F. A. Weber ◽  
M. P. Ooms ◽  
J. T. M. Vreeburg
Keyword(s):  
Adult Male ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Male Rats ◽  
Male Rat ◽  
Serum Concentrations ◽  
Testosterone Secretion ◽  
Accessory Sex Glands ◽  
Serum Lh ◽  
Stimulation Of

ABSTRACT The effects of hyperprolactinaemia on serum levels of LH were investigated in adult male rats of the R × U strain. Hyperprolactinaemia was induced by three pituitary grafts under the kidney capsule, transplanted on day 0 of each experiment. Special attention was paid to the contribution of prolactin-stimulated testes, adrenals and corticosterone. In experiment 1, hyperprolactinaemia significantly reduced the serum concentrations of LH in intact rats. In spite of a significant increase in the serum levels of corticosterone, serum testosterone was not significantly affected by hyperprolactinaemia. The weights of both the adrenals and accessory sex glands were significantly increased at autopsy. In experiment 2, treatment with 10 mg corticosterone s.c. daily from day 14 to day 28 after pituitary grafting significantly reduced serum levels of both LH and testosterone. The suppression of testosterone in the hyperprolactinaemic corticosterone-treated animals was significantly less than in the corticosterone-treated control animals. The weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 3, rats were adrenalectomized and half of them were substituted with corticosterone. Serum testosterone levels significantly increased in both hyperprolactinaemic adrenalectomized rats and in adrenalectomized corticosterone-treated animals without any significant effect on serum LH. Again the weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 4, rats were adrenalectomized, gonadectomized and corticosterone treated on day 0 and then implanted with a 2, 1·5 or 1 cm silicone elastomer capsule containing testosterone. On day 28 after pituitary grafting, LH levels were significantly suppressed in animals with a 2 or 1·5 cm testosterone implant. The weights of the accessory sex glands were not increased in the hyperprolactinaemic animals. These results show that in the male rat the inhibitory effects of hyperprolactinaemia on serum LH levels may be due to (1) increased sensitivity of the hypothalamic-pituitary axis to the negative feedback action of testosterone by prolactin and by the prolactin-stimulated corticosterone secretion and (2) stimulation of testicular testosterone secretion by prolactin, which can also explain the increased weights of the accessory sex glands. Even in the presence of high serum concentrations of corticosterone, stimulation of testicular testosterone secretion by prolactin was observed. J. Endocr. (1987) 113,111–116

Leydig cell resistance to the cytotoxic effect of ethylene dimethanesulphonate in the adult rat testis

1985 ◽  
Vol 105 (3) ◽  
pp. 311-NP ◽  
Author(s):  
I. D. Morris
Keyword(s):  
Seminal Vesicle ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Serum Testosterone ◽  
Male Rats ◽  
Cell Physiology ◽  
Testis Weight ◽  
Endocrine Activity ◽  
Adult Rat ◽  
Seminal Vesicle Weight

ABSTRACT Weekly doses of the Leydig cell cytotoxic ethylene dimethanesulphonate (EDS) were administered to adult male rats in an attempt to study the endocrine activity of the testis in the absence of Leydig cells. One week after the first dose serum testosterone and LH concentrations and seminal vesicle weights were close to levels in castrated rats and testicular human chorionic gonadotrophin (hCG) binding was severely depressed. These changes were maintained for a further week but subsequently began to return to, but did not achieve, control levels. After six weekly doses seminal vesicle weight and serum testosterone concentrations were significantly higher than in the castrated rats. Serum LH concentrations were declining towards control values at 4 weeks but had risen again at 6 weeks. Serum FSH concentrations were raised to about 50% of the value in castrated rats throughout the period studied. Testis weight and hCG binding, which initially fell, were partially restored at 6 weeks and spermatogenesis was recovering. The data show that responses of the testis to multiple doses of EDS are similar to those after a single dose. This apparent resistance indicates that the regenerating Leydig cells are functionally different from the mature Leydig cell. The similarities between the maturing Leydig cell seen after EDS destruction and those in the immature rat suggest that EDS will provide a valuable model for the investigation of Leydig cell physiology. J. Endocr. (1985) 105, 311–316

Testosterone maintains pituitary and serum FSH and spermatogenesis in gonadotrophin-releasing hormone antagonist-suppressed rats

1986 ◽  
Vol 108 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. A. Rea ◽  
G. R. Marshall ◽  
G. F. Weinbauer ◽  
E. Nieschlag
Keyword(s):  
Serum Testosterone ◽  
Treated Group ◽  
Male Rats ◽  
Testis Weight ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Hypophysectomized Rats ◽  
Gonadotrophin Releasing Hormone ◽  
Vehicle Treated Control

ABSTRACT Groups of adult male rats were treated continuously for 30 days with either vehicle or the potent gonadotrophin-releasing hormone (GnRH) antagonist, (N-Ac-d-Nal(2)1,d-pCl-Phe2,d-Trp3,d-hArg (Et2)6,d-Ala10)-GnRH (RS 68439; 35 μg/day). In addition, groups of vehicle- and antagonist-treated rats received s.c. testosterone implants sufficient to maintain serum testosterone concentrations 3·5- to 5-fold higher than those of vehicle-treated control rats. After 30 days of antagonist treatment serum LH, FSH and testosterone concentrations were at or below the detection limits of their respective assays and pituitary FSH content and GnRH receptor binding were reduced, relative to control animals, by 77 and 98% respectively. Testis weight in antagonist-treated rats was reduced by 75% and spermatogenesis was suppressed to an extent comparable to that observed in hypophysectomized rats. Testosterone, which caused a 40% reduction in serum FSH relative to control animals, prevented the antagonist-induced fall in both serum and pituitary FSH, but not GnRH receptors, below that observed in the vehicle plus testosterone-treated group. Furthermore, spermatogenesis in the antagonist plus testosterone-treated group was indistinguishable from that observed in control animals. It is concluded that testosterone is capable of maintaining serum and pituitary FSH levels in vivo, under conditions which presumably render the pituitary insensitive to hypothalamic GnRH. J. Endocr. (1986) 108, 101–107

Cimetidine-induced prolactin release in rats The effect of sex and gonadal steroids

1987 ◽  
Vol 114 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Hajime Watanobe ◽  
Kazuo Takebe
Keyword(s):  
Anterior Pituitary ◽  
Male Rats ◽  
Minor Role ◽  
Adult Males ◽  
Adult Age ◽  
Significant Difference ◽  
Males And Females ◽  
Plasma Prl ◽  
A Minor

Abstract. The cimetidine-induced plasma Prl response was examined in rats of both sexes. First, 10 week old intact adult males and females (dioestrous) were compared. There was no significant difference in the Prl response to cimetidine between the two groups, despite the fact that in adult females the anterior pituitary Prl content was 4 times greater than in males. Second, the effect of gonadal state in adult age on the Prl response to cimetidine was examined in both sexes. In male rats, gonadectomy at the age of 6 weeks significantly reduced the plasma Prl response as well as the pituitary Prl content, both of which were sufficiently restored by testosterone replacement. However, in females, neither gonadectomy at the age of 6 weeks nor subsequent oestradiol replacement affected the Prl response to cimetidine, despite the fact that gonadectomy significantly reduced and oestradiol treatment significantly enhanced the pituitary Prl content. Third, possible permanent effects of the postnatal gonadal milieu on the cimetidine-induced Prl response and the pituitary Prl content were examined in both sexes by castration at varying postnatal ages. The ratio of plasma Prl response to pituitary Prl content was similar in all castrated males. In females, however, the ratio decreased with increasing castration age. In conclusion, the mechanism of cimetidine-induced Prl release is less sex-dependent than are the mechanisms of Prl release by other Prl secretagogues. First, this may be due to a minor role of oestrogen in females in determining the Prl response to cimetidine. Second, the postnatal ovarian secretions may exert a permanent inhibition of the development of the cimetidine-mobilized anterior pituitary Prl pool.

Effects and Mechanisms of Acupuncture and Moxibustion on Reproductive Endocrine Function in Male Rats with Partial Androgen Deficiency

2016 ◽  
Vol 34 (2) ◽  
pp. 136-143 ◽  
Author(s):  
Yi Ren ◽  
Xiaoguang Yang ◽  
Yu Zhang ◽  
Ying Wang ◽  
Xuezhi Li
Keyword(s):  
Protein Expression ◽  
Mrna Expression ◽  
Serum Testosterone ◽  
Hydroxysteroid Dehydrogenase ◽  
Endocrine Function ◽  
Male Rats ◽  
Acupuncture Points ◽  
Total Testosterone ◽  
Androgen Deficiency ◽  
Serum Lh

Objectives Partial androgen deficiency of the aging male (PADAM) is characterised by a deficiency in serum androgen levels. Both electroacupuncture (EA) and mild moxibustion (MM) can raise serum testosterone levels in PADAM. We investigated the mechanisms underlying the use of EA and MM in a rodent model of PADAM. Methods Fifty rats received cyclophosphamide injection over 5 consecutive days to induce PADAM, which was verified by comparing total testosterone (TT) and free testosterone (FT) levels with 10 non-PADAM healthy control rats (CON). Successful modelling was confirmed in 43 of 50 rats, 40 of which were randomly divided into untreated (PADAM), EA-treated (PADAM+EA), MM-treated (PADAM+MM), and androlin (AD)-treated (PADAM+AD) groups (n=10 each). EA and MM were administered at BL23 and CV4 acupuncture points for 8 weeks, and no treatment was given to rats in the PADAM and CON groups. Serum levels of luteinising hormone (LH) and follicle-stimulating hormone (FSH), mRNA expression of cytochrome P450c17 (P450c17) and 3β-hydroxysteroid dehydrogenase 1 (3β-HSD1), and protein levels of cytochrome P450 side chain cleavage (P450scc), 17β-hydroxysteroid dehydrogenase 3 (17β-HSD3) and steroidogenic factor 1 (SF-1) were evaluated after 8 weeks. Results Both EA and mild MM significantly increased serum TT and FT levels with MM displaying superiority. P450scc, 17β-HSD3 and SF-1 protein expression, and P450c17 and 3β-HSD1 mRNA expression, were significantly increased and serum LH and FSH levels were significantly decreased in PADAM+EA and PADAM+MM relative to PADAM rats. Moreover, serum LH and FSH levels were significantly lower and 17β-HSD3 protein expression significantly higher in PADAM+MM relative to PADAM+EA rats. Conclusions EA and MM at the BL23 and CV4 acupuncture points appear to be effective treatments for PADAM, and MM displays superior efficacy to EA.

scholarly journals Betamethasone modulation of sphingomyelin hydrolysis up-regulates CTP:cholinephosphate cytidylyltransferase activity in adult rat lung

1996 ◽  
Vol 318 (1) ◽  
pp. 333-341 ◽  
Author(s):  
Rama K MALLAMPALLI ◽  
Satya N MATHUR ◽  
Lorna J WARNOCK ◽  
Ronald G SALOME ◽  
Gary W HUNNINGHAKE ◽  
...  
Keyword(s):  
Hydrolysis Product ◽  
Fold Increase ◽  
Acid Sphingomyelinase ◽  
Male Rats ◽  
Reversible Inhibitor ◽  
Serine Palmitoyltransferase ◽  
Adult Rat ◽  
Surfactant Synthesis

Glucocorticoids appear to play an integral role in stimulating surfactant synthesis by activating the rate-regulatory enzyme for phosphatidylcholine synthesis, CTP:cholinephosphate cytidylyltransferase (CT). The activity of liver CT, in vitro, has been shown to be inhibited by the sphingomyelin hydrolysis product, sphingosine. In order to investigate the mechanisms by which glucocorticoids alter CT activity, in vivo, we administered betamethasone (1 mg/kg intraperitoneally) sequentially to adult male rats for 5 days. Betamethasone increased CT activity 2-fold relative to control in whole lung. The hormone also increased membrane-bound activity, but did not affect cytosolic enzyme activity. Betamethasone modestly increased CT mRNA as determined by the reverse-transcription PCR and Southern analysis of PCR products, but did not alter the levels of immunoreactive enzyme in lung membranes as demonstrated by Western blotting. The hormone did, however, produce a nearly 3-fold increase in membrane-associated sphingomyelin, and co-ordinately a substantial decrease in the levels of sphingosine in lung membranes. Sphingosine, but not sphinganine, was a competitive, reversible inhibitor of lung CT with respect to the enzyme activator, phosphatidylglycerol. Betamethasone decreased the activities of the sphingomyelin hydrolases: acid sphingomyelinase by 33% and of alkaline ceramidase by 21%. The hormone also inhibited the generation of sphingosine from lysosphingomyelin in lung membranes. There was no significant effect of the hormone on serine palmitoyltransferase activity, the first committed enzyme for sphingolipid biosynthesis. Further, administration of l-cycloserine, an inhibitor of sphingosine formation, was shown to stimulate CT activity by 74% and increase disaturated phosphatidylcholine in alveolar lavage by 52% relative to control. These observations suggest that glucocorticoids up-regulate surfactant synthesis at the level of a key regulatory enzyme by significantly altering the availability of inhibitory metabolites resulting from sphingomyelin hydrolysis.

Reproductive toxicity and tissue concentrations of 3,3',4,4'-tetrachlorobiphenyl (PCB 77) in male adult rats

1998 ◽  
Vol 17 (3) ◽  
pp. 151-156 ◽  
Author(s):  
A S Faqi ◽  
P R Dalsenter ◽  
W Mathar ◽  
B Heinrich-Hirsch ◽  
I Chahoud
Keyword(s):  
Adult Male ◽  
Weight Control ◽  
Reproductive Toxicity ◽  
Serum Testosterone ◽  
Male Rats ◽  
Testis Weight ◽  
Adult Rats ◽  
Male Adult ◽  
Reproductive Effects ◽  
Investigation Period

1 The aim of this study was to ascertain the reproductive effects of PCB 77 on adult male rats and to determine its concentration in the liver and testis. Adult male rats (n=15/group) were treated subcutaneously with a singledoseof18 mg/kgbw(PC18)orwith60 mg/kg bw (PC60). The substance was dissolved in a 10 ml volume of peanut oil/kg. Control rats received the same volume of the vehicle. The reproductive effects as well as the concentration of PCB 77 in the liver and testis were investigated 1, 4 and 8 weeks after treatment. 2 In both groups, the daily sperm production (DSP; 6106) remained permanently reduced in the PC18 as well as in the PC60 groups throughout the entire investigation period (DSP week 8: control: 31+7; PC18: 22+5; PC60: 20+7). The sperm number (6106) per cauda epididymis was affected only at the 1st and 4th week after treatment (control week 1: 211+67; PC18 week 1: 135+62; PC60 week 1: 142+49). Moreover, a significant increase in the percentage of abnormal sperm was observed 4 weeks following treatment in the PC18 and PC60 groups and 8 weeks after treatment in the PC60 group. Abnormal tails were the most frequent changes observed. 3 The relative testicular and prostata weights (g) were slightly increased in the PC60 group at the 1st and 4th week following treatment (testis weight: control/I: 0.46+0.02; PC60/I: 0.51+0.03). 4 The serum testosterone concentrations and effects on testis morphology were not reported. 5 The maximum concentration of PCB 77 was detected in the liver and testis 1 week after treatment. The concentration declined 4 weeks after treatment in both organs, but still a significant amount of PCB 77 was detectable in the liver as well as in the testis 8 weeks after treatment. 6 The results demonstrate that PCB 77 affects sperm variables when applied to adult rats and that the elimination of PCB 77 in the testis parallels that of the liver.

Metabolic and haemodynamic effects of α2-adrenoceptor stimulation and antagonism in man

1985 ◽  
Vol 68 (s10) ◽  
pp. 137s-139s ◽  
Author(s):  
M. J. Brown ◽  
A. D. Struthers ◽  
L. Di Silvio ◽  
T. Yeo ◽  
M. Ghatei ◽  
...  
Keyword(s):  
Physiological Role ◽  
Fold Increase ◽  
Plasma Noradrenaline ◽  
Minor Role ◽  
Hormone Release ◽  
Plasma Growth Hormone ◽  
Similar Reduction ◽  
Α2 Adrenoceptor ◽  
Baseline Values ◽  
A Minor

1. Six healthy volunteers received a 60 min infusion of guanfacine (α2-agonist) on two occasions, preceded by either idazoxan (α2-antagonist) or vehicle. 2. Idazoxan elevated blood pressure by 8/7 mmHg, but there was no change on either day during guanfacine infusion. 3. Guanfacine reduced plasma noradrenaline by approximately 30%, and this was not antagonized by idazoxan. By contrast, the 30-fold increase in plasma growth hormone caused by guanfacine was almost completely blocked by idazoxan. 4. Guanfacine caused a two- to three-fold increase in plasma glucagon and a similar reduction in plasma insulin. Only the latter was antagonized by idazoxan. No consistent changes in plasma ACTH were observed after either idazoxan or guanfacine. 5. Idazoxan itself elevated plasma noradrenaline up to twice baseline values, but did not affect the other metabolic measurements. 6. α2-Adrenoceptor stimulation plays a minor role in control of hormone release but has a greater physiological role in regulating release of the neurotransmitter, noradrenaline.

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