Naloxone-induced secretion of LH in the male Syrian hamster: modulation by photoperiod and gonadal steroids

1985 ◽  
Vol 106 (2) ◽  
pp. 243-248 ◽  
Author(s):  
A. C. Roberts ◽  
M. H. Hastings ◽  
N. D. Martensz ◽  
J. Herbert
Keyword(s):  
Syrian Hamster ◽  
Serum Testosterone ◽  
Opiate Receptor ◽  
Gonadal Steroids ◽  
Endogenous Opiates ◽  
Serum Lh ◽  
Testicular Regression ◽  
Lh Release ◽  
Long Photoperiod

ABSTRACT The role of endogenous opiates in the regulation of photoperiodically induced testicular regression was studied in the male Syrian hamster. In reproductively active hamsters exposed to a long photoperiod (LD; 16 h light: 8 h darkness) or to short days (SD; 8 h light: 16 h darkness) for 20 weeks or to SD after pinealectomy, administration of naloxone, a competitive opiate receptor antagonist, at doses of 2·5–20 mg/kg, significantly increased serum LH concentrations. In marked contrast, these doses of naloxone did not produce any change in LH levels in reproductively quiescent hamsters exposed to SD for 8 weeks. The influence of gonadal steroids on the LH response to naloxone was studied in hamsters castrated or castrated and implanted s.c with a capsule containing testosterone. Naloxone did not induce LH release in castrated hamsters maintained in LD or in SD, but this response was restored in LD but not SD when serum testosterone concentrations were maintained at levels similar to those observed in intact reproductively active hamsters. These results show that inhibition of reproduction by the photoperiod prevents naloxone-induced LH release in the male hamster. This lack of response to naloxone is not due, however, to the lower testosterone titres present in these animals compared with reproductively active animals. Responsiveness to naloxone can be restored when the animal is rendered insensitive to the inhibitory photoperiod either by removal of the pineal gland or by induction of photorefractoriness by extended exposure to SD. J. Endocr. (1985) 106, 243–248

ABSENCE OF POSITIVE FEEDBACK EFFECT OF OESTROGEN ON LH RELEASE IN PATIENTS WITH TESTICULAR FEMINIZATION SYNDROME

1978 ◽  
Vol 87 (2) ◽  
pp. 259-267 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takayuki Kinugasa ◽  
Keiichi Kurachi ◽  
Keishi Matsumoto
Keyword(s):  
Sex Differentiation ◽  
Serum Testosterone ◽  
Normal Male ◽  
Testicular Feminization ◽  
Serum Lh ◽  
Exogenous Oestrogen ◽  
Lh Release ◽  
Normal Males ◽  
Lh Rh

ABSTRACT The response of serum LH to exogenous oestrogen administration was studied in 5 patients with testicular feminization syndrome (TFS). The serum LH levels were elevated in all the patients, while serum testosterone levels were within the normal male range. Serum FSH levels were elevated in 4 patients and normal in one patient. Intravenous administration of 100 μg of LH-RH provoked a further increase in both LH and FSH. Following intravenous injection of 20 mg of conjugated oestrogen (Premarin®), the LH levels were serially determined until 120 h in TFS patients, 5 normal males, and 10 normal females during the mid-follocular phase (D7-9). Both TFS patients and normal males showed no LH release following oestrogen injection in contrast to normal females who displayed a significant increase in LH with a peak at 48 to 56 h after the injection. These results seem to suggest that the insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. The possible role of oestradiol conversion from testosterone in the hypothalamus is discussed.

Effect of testosterone on gonadotropin response to DBcAMP, cAMP binding, and cAMP production in pituitary cultures

1984 ◽  
Vol 247 (3) ◽  
pp. E312-E317 ◽  
Author(s):  
L. K. Tang ◽  
A. C. Martellock ◽  
F. Y. Tang
Keyword(s):  
Young Female ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Intracellular Camp ◽  
Camp Production ◽  
Monolayer Cultures ◽  
Minimal Dose ◽  
Lh Release ◽  
Release Data

The role of testosterone (T) in the modulation of pituitary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) sensitivity to DBcAMP was examined in the pituitary monolayer cultures prepared from intact young female rats. Hormone contents in media and cell homogenates were determined by radioimmunoassays. Incubation with 8 and 4 mM DBcAMP for 4 h consistently induced a significant (P less than 0.05) increase in FSH and LH release, respectively. Pretreatment with 10 nM T for 4 days reduced the minimal dose of DBcAMP required to stimulate FSH release (2 vs. 8 mM) but had no effect on the DBcAMP-induced LH release. Data indicate that T treatment for 4 or 7 days stimulated total FSH contents (sum of hormone contents in medium and cells). Similarly, incubation with 10 mM DBcAMP for 4 h significantly increased total FSH content per dish in both the T-treated and non-T-treated cultures. Neither T nor DBcAMP had any effect on LH production under these conditions. Intracellular cAMP was significantly increased to three- to eightfold of control after T treatment for 3 or 6 h, respectively. Furthermore, cAMP-binding activities were significantly increased after T treatment for 1 or 4 days (174 or 422% of control). Our previous data indicate that estrogen increases LH production, cAMP binding, cAMP production, and LH sensitivity to DBcAMP, and these data indicate that T exerts stimulatory effects on FSH in a similar fashion. These results support the concept that the two gonadotropins are regulated independently via different gonadal steroids.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

A possible role of clomiphene citrate in the control of pre-ovulatory LH surge during induction of ovulation

1985 ◽  
Vol 109 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Naoki Terakawa ◽  
Ikuya Shimizu ◽  
Hirohisa Tsutsumi ◽  
Toshihiro Aono ◽  
Keishi Matsumoto
Keyword(s):  
Nuclear Receptor ◽  
Clomiphene Citrate ◽  
Ovariectomized Rats ◽  
Receptor Complex ◽  
Oestrogen Receptors ◽  
Lh Surge ◽  
Serum Lh ◽  
Lh Release

Abstract. A possible role of clomiphene citrate (clomiphene) in the control of ovulation in anovulatory women was investigated. Since a single ip administration of 5 μg oestradiol-17β (E2) to long-term ovariectomized rats did not induce LH surge, the following studies were designed to determine whether pretreatment with clomiphene followed by administration of E2 could induce LH surge in the ovariectomized rats. Changes in cytoplasmic and nuclear oestrogen receptors (ER) were also examined in the pituitaries of these animals. An ip injection of 200 μg clomiphene suppressed serum LH levels significantly for 72 h. The clomiphene injection rapidly caused an elevation of nuclear ER with a concomitant depletion of cytoplasmic ER level in the pituitary and the ER levels remained almost unchaged for 72 h. An administration of E2 12 or 24 h after the clomiphene injection had no significant effects on either the serum LH levels or the cytoplasmic and nuclear ER levels, compared with those induced by clomiphene alone. However, LH surge and the depletion of nuclear ER in the pituitary occurred 24 h later when E2 was injected 48 h after the clomiphene administration. The E2-induced LH release seems to be induced by a replacement of clomiphene by E2 on the nuclear receptor complex. These results suggest that clomiphene may exert actions directly on the pituitary gland to augment oestrogeninduced LH release.

Effect of pinealectomy on photoperiodic gonadal response of Indian palm squirrel, Funambulus pennanti

1987 ◽  
Vol 65 (4) ◽  
pp. 833-836 ◽  
Author(s):  
C. Haldar-Misra ◽  
M. Srivastava
Keyword(s):  
Pineal Gland ◽  
Experimental Period ◽  
Short Photoperiod ◽  
Gonadal Activity ◽  
Reproductive Axis ◽  
Testicular Regression ◽  
Long Photoperiod

The role of the pineal gland in mediating the effects of photoperiod on the reproductive axis is not well established in tropical mammals. Indian palm squirrels (Funambulus pennanti) were exposed to experimental long (16L:8D) and short (6L:18D) photoperiods. It was observed that the testes regressed in response to short photoperiod, while during the long photoperiod the gonads were active. When squirrels were maintained for a long experimental period (130 days) under the short photoperiodic schedule (6L:18D), gonadal regrowth eventually occurred even though the photoperiod was the same one that initially induced testicular regression. Pinealectomized animals maintained the gonadal activity even in short photoperiod, suggesting that the effect of photoperiod is mediated through the pineal gland.

Neuroendocrinological effects of ketoconazole in rats

1990 ◽  
Vol 122 (3) ◽  
pp. 409-413 ◽  
Author(s):  
Gabor Irsy ◽  
Lajos Koranyi
Keyword(s):  
Female Rats ◽  
Ovariectomized Rats ◽  
Male Rat ◽  
Hormone Release ◽  
Steroid Biosynthesis ◽  
Steroid Synthesis ◽  
Serum Lh ◽  
Dopamine Content ◽  
Lh Release

Abstract The effect of ketoconazole on steroid synthesis was studied in intact (sham-operated) and castrated male and ovariectomized female rats. Rats were given 25 mg/kg ketoconazole twice a day im for 5 days. The influence of ketoconazole was also investigated on hormone release altered by GnRH, estradiol and haloperidol. The following hormones were measured: serum LH, PRL, testosterone, corticosterone, 17-OH-progesterone, estradiol, and dopamine content of the tubero-infundibular area. Ketoconazole treatment resulted in a significant decrease of testerone level (from 7.93 ± 1.99 to 3.83 ± 0.94 nmol/l), whereas LH, PRL, corticosterone and 17-OH-progesterone remained unchanged in the male rat. The effect of castration on LH level was reduced by ketoconazole in male (from 590 ± 35 to 390 ± 25 μg/l) and female rats (from 468 ± 22 to 346 ± 39 μg/l), but the GnRH-stimulated LH release in castrated and ovariectomized animals was unchanged. The suppressive action of estradiol on LH in ovariectomized rats was enhanced (from 160 ± 41 to 64.6 ± 12.9 μg/l), and its priming effect on PRL release was diminished by ketoconazole (from 598 ± 81 to 281 ± 66 μg/l). Ketoconazole failed to modify the tubero-infundibular dopamine content and haloperidol-induced PRL release. It can be assumed that in addition to its inhibitory role of steroid biosynthesis ketoconazole has an influence on central mechanisms underlying LH and PRL release.

The role of sex hormones in the mechanism of inhibited LH release in female patients with anorexia nervosa

1982 ◽  
Vol 99 (3) ◽  
pp. 334-338 ◽  
Author(s):  
B. Baranowska ◽  
S. Zgliczyński
Keyword(s):  
Anorexia Nervosa ◽  
Serum Testosterone ◽  
Sex Hormone Binding Globulin ◽  
Control Group ◽  
Hormonal Changes ◽  
Female Patients ◽  
Serum Lh ◽  
Before And After ◽  
Lh Release ◽  
Lh Secretion

Abstract. In order to elucidate the mechanism of impaired LH secretion, 60 female patients with anorexia nervosa were investigated. A control group consisted of 14 women of the same age, examined in the follicular phase of the menstrual cycle. The serum LH, FSH, prolactin, TSH, testosterone, dihydrotestosterone, dehydroepiandrosterone, Δ 4-androstenedione, oestrone, oestradiol, oestriol, progesterone, thyroxine, triiodothyronine, reverse T3 and serum sex hormone binding globulin (SHBG) concentrations were measured. The results showed a significant increase in serum dehydroepiandrosterone, testosterone, oestriol and reverse T3 concentrations. However, oestrone, oestradiol, progesterone, SHBG and triiodothyronine levels were significantly lower than those of the control group. The mean serum LH concentration in patients with anorexia nervosa before and after LRH stimulation was significantly lower than that in the control group, but FSH secretion in response to LRH was normal. All hormonal changes in anorexia nervosa disappeared after weight gain during cyproheptadine treatment. Dramatically increased dehydroepiandrosterone levels suggest that the high testosterone in women with anorexia nervosa is derived from adrenal rather than from gonadal steroids. There was no correlation between serum testosterone, dehydroepiandrosterone, oestriol and LH concentrations indicating that steroid hormone disturbances do not cause impaired LH release in anorexia nervosa.

Proliferation, apoptosis, and number of Sertoli cells in the Syrian hamster during recrudescence after exposure to short photoperiod†‡

2019 ◽  
Vol 102 (3) ◽  
pp. 588-597 ◽  
Author(s):  
Jesús Martínez-Hernández ◽  
Vicente Seco-Rovira ◽  
Ester Beltrán-Frutos ◽  
Concepción Ferrer ◽  
María Isabel Serrano-Sánchez ◽  
...  
Keyword(s):  
Syrian Hamster ◽  
Normal Population ◽  
Similar Rate ◽  
The Other ◽  
Short Photoperiod ◽  
Control Group ◽  
Bright Field ◽  
Testicular Regression ◽  
Testicular Recrudescence ◽  
Long Photoperiod

Abstract The Sertoli cell (Sc) has been described as a quiescent cell once the animal has reached sexual maturity. Syrian hamster is an animal that displays testicular regression due to short photoperiod, during which process germ cells and Sc are removed through apoptosis. The aim of this work was to investigate histochemically whether the spontaneous testicular recrudescence processes after exposure to a short photoperiod lead to an increase in Sc proliferative activity in order to restore the normal population. Three spontaneous recrudescence groups were established: initial (IR), advanced (AR), and total (TR) recrudescence, which were compared with animal undergoing the regression process (mild: MRg, strong: SRg, and total: TRg) and animals in long photoperiod (Controls). Histological sections were submitted to histochemical techniques for detecting apoptotic and proliferative Sc with bright-field and fluorescence microscopy. For each group, the proliferative Sc index (PScI) and apoptotic Sc index (AScI), and the total number of Sc were obtained. The results revealed the existence of Vimentin+/TUNEL+ as well as Vimentin+/PCNA+ cells. The PScI was significantly higher in TRg and IR than in the other groups. The AScI was only significantly higher in MRg and SRg with respect to the other groups. The total number of Sc increased among TRg, IR, and AR, reaching values similar to those of the Controls. In conclusion, the increase in Sc proliferation from final regression and recrudescence, accompanied by a similar rate of apoptosis to the Control group, is the cause of the restoration of the Sc population during spontaneous recrudescence.

Effects of catecholamine synthesis inhibitors and adrenergic receptor antagonists on restraint-induced LH release

1995 ◽  
Vol 144 (3) ◽  
pp. 511-515 ◽  
Author(s):  
A I Martín ◽  
J Fernández-Ruiz ◽  
A López-Calderón
Keyword(s):  
Adrenergic Receptor ◽  
Acute Stress ◽  
Male Rats ◽  
Receptor Antagonists ◽  
Catecholamine Synthesis ◽  
Serum Lh ◽  
Propranolol Treatment ◽  
Lh Release ◽  
Lh Secretion

Abstract Acute stress is known to increase LH secretion and the release of central norepinephrine (NE) in intact rats. Studies were performed to analyse the role of catecholamines in acute stress-induced LH release in male rats. Injection of α-methyl-p-tyrosine (αMPT) and diethyldithiocarbamate (DDC), catecholamine synthesis inhibitors, significantly decreased both hypothalamic concentration of NE and serum LH. Restraint for 30 min evoked an increase in serum LH in saline-treated rats, whereas αMPT and DDC administration blocked the stress-induced LH release. The effects of α1-, α2- and β-adrenoreceptor antagonists on the LH response to restraint stress were also studied. Propranolol treatment did not modify serum LH in either unstressed or stressed rats. The two α-adrenergic receptor antagonists prazosin and yohimbine prevented the restraint-induced LH release; however, prazosin but not yohimbine significantly decreased the serum concentration of LH in unstressed rats. These data suggest that the acute stress-induced increase in LH secretion is mediated through the activation of α2-adrenergic receptors. Journal of Endocrinology (1995) 144, 511–515

Function of pituitary-gonadal axis in zinc-deficient rats

1976 ◽  
Vol 230 (6) ◽  
pp. 1730-1732 ◽  
Author(s):  
KY Lei ◽  
A Abbasi ◽  
AS Prasad
Keyword(s):  
Luteinizing Hormone ◽  
Body Weight Gain ◽  
Specific Effect ◽  
Zinc Content ◽  
Serum Testosterone ◽  
Gonadal Function ◽  
Luteinizing Hormone Releasing Hormone ◽  
Serum Lh ◽  
Testicular Steroidogenesis

The role of zinc in gonadal function was investigated in rats. The increases in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone were assayed after intravenous administration of synthetic luteinizing-hormone-releasing hormone (LHRH) to zinc-deficient and restricted-fed control rats. Body weight gain, zinc content of testes, and weight of testes were significantly lower in the zinc-deficient rats compared with the controls. The serum LH and FSH response to LHRH administration were higher in the zinc-deficient rats but serum testosterone response was lower in comparison with the restricted-fed controls. These studies indicate a specific effect of zinc on testes and suggest that gonadal function in zinc-deficient state is affected through some alteration of testicular steroidogenesis.

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