Role of the organum vasculosum laminae terminalis in the control of gonadotrophin secretion in rats

1982 ◽  
Vol 93 (3) ◽  
pp. 355-NP ◽  
Author(s):  
F. Piva ◽  
P. Limonta ◽  
L. Martini
Keyword(s):  
Ovariectomized Rats ◽  
Adult Rats ◽  
Organum Vasculosum Laminae Terminalis ◽  
Serum Lh ◽  
Parallel Increase ◽  
Gonadotrophin Secretion ◽  
Radiofrequency Lesions ◽  
Organum Vasculosum

The organum vasculosum laminae terminalis (OVLT) was destroyed by radiofrequency lesions in regularly cycling and in long-term ovariectomized adult rats. After OVLT lesion practically all cyclic females (16 out of 22) became dioestrous, as indicated by vaginal smears. At the time of killing these animals (8 days after the lesion) serum LH levels were undetectable, while serum FSH was as low as in cyclic animals in dioestrus. In the few OVLT-lesioned animals which exhibited some sort of oestrous cyclicity, serum LH showed a small subphysiological increase at pro-oestrus: this was not accompanied by a parallel increase in serum FSH and in these animals a delayed peak of FSH occurred on the day of oestrus. Ovariectomized rats bearing OVLT lesions had serum titres of LH and FSH as high as those of ovariectomized control rats. It is suggested that the OVLT may play a role in the control of the cyclic release of gonadotrophins but is not involved in the tonic regulation of gonadotrophin secretion.

Role of the subcommissural organ in the control of gonadotrophin secretion in the female rat

1982 ◽  
Vol 95 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Patrizia Limonta ◽  
Roberto Maggi ◽  
Luciano Martini ◽  
Flavio Piva
Keyword(s):  
Subcommissural Organ ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Female Rat ◽  
Thermal Lesions ◽  
Gonadotrophin Secretion

Thermal lesions were placed in the subcommissural organ (SCO) of female rats with normal cycles and long-term ovariectomized rats. In normal female rats SCO lesions disrupted the oestrous cycle in more than half of the animals, the majority of which entered a state of prolonged dioestrus. In these animals, serum gonadotrophin levels were similar to those of rats with regular cycles on day 2 of dioestrus. In animals in which the oestrous cycle was maintained, a delayed LH surge occurred on the day of pro-oestrus and the pro-oestrous FSH surge was absent. The usual increase in FSH on the day of oestrus was present. Lesions in the SCO did not change the high gonadotrophin levels typical of ovariectomized animals. These results suggested that the SCO may play a role in the control of the cyclic but not the tonic release of the gonadotrophins. In particular, it appears that the SCO might be involved in the regulation of the hypersecretion of FSH during the day of pro-oestrus.

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 opioid peptides on gonadotrophin secretion

1982 ◽  
Vol 99 (3) ◽  
pp. 321-325 ◽  
Author(s):  
M. Motta ◽  
L. Martini
Keyword(s):  
Opioid Peptides ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Intraventricular Injection ◽  
Experimental Conditions ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Intraventricular Injections ◽  
Lh Release

Abstract. The intraventricular injection of 25 μg of Methionine-Enkephalin (Met-Enk) induces a significant increase of serum LH levels in long-term ovariectomized rats 15, 30 and 60 min following administration. The synthetic Met-Enk agonistic analogue [D-Ala2]Methionine-Enkephalinamide ([D-Ala2]Met-Enk) also enhances significantly serum LH levels at 30 and 60 min; under the same experimental conditions neither Met-Enk nor [D-Ala2]Met-Enk modifies serum levels of FSH following intraventricular injections into ovariectomized animals. It is concluded that, under particular circumstances, opioid peptides of the Met-Enk family may stimulate LH release.

Suppression of pituitary-testis function in rats treated neonatally with a gonadotrophin-releasing hormone agonist and antagonist: acute and long-term effects

1989 ◽  
Vol 123 (1) ◽  
pp. 83-91 ◽  
Author(s):  
K.-L. Kolho ◽  
I. Huhtaniemi
Keyword(s):  
Body Weight ◽  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Long Term Effects ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Accessory Sex Organs ◽  
Gonadotrophin Releasing Hormone

ABSTRACT The acute and long-term effects of pituitary-testis suppression with a gonadotrophin-releasing hormone (GnRH) agonist, d-Ser(But)6des-Gly10-GnRH N-ethylamide (buserelin; 0·02, 0·1, 1·0 or 10 mg/kg body weight per day s.c.) or antagonist, N-Ac-d-Nal(2)1,d-p-Cl-Phe2,d-Trp3,d-hArg(Et2)6,d-Ala10-GnRH (RS 68439; 2 mg/kg body weight per day s.c.) were studied in male rats treated on days 1–15 of life. The animals were killed on day 16 (acute effects) or as adults (130–160 days; long-term effects). Acutely, the lowest dose of the agonist decreased pituitary FSH content and testicular LH receptors, but with increasing doses pituitary and serum LH concentrations, intratesticular testosterone content and weights of testes were also suppressed (P< 0·05–0·01). No decrease was found in serum FSH or in weights of accessory sex organs even with the highest dose of the agonist, the latter finding indicating continuing secretion of androgens. The GnRH antagonist treatment suppressed pituitary LH and FSH contents and serum LH (P< 0·05–0·01) but, as with the agonist, serum FSH remained unaltered. Testicular testosterone and testis weights were decreased (P <0·01) but testicular LH receptors remained unchanged. Moreover, the seminal vesicle and ventral prostate weights were reduced, in contrast to the effects of the agonists. Pituitary LH and FSH contents had recovered in all adult rats treated neonatally with agonist and there was no effect on serum LH and testosterone concentrations or on fertility. In contrast, in adult rats treated neonatally with antagonist, weights of testis and accessory sex organs remained decreased (P <0·01–0·05) but hormone secretion from the pituitary and testis had returned to normal except that serum FSH was increased by 80% (P <0·01). Interestingly, 90% of the antagonist-treated animals were infertile. It is concluded that treatment with a GnRH agonist during the neonatal period does not have a chronic effect on pituitary-gonadal function. In contrast, GnRH antagonist treatment neonatally permanently inhibits the development of the testis and accessory sex organs and results in infertility. Interestingly, despite the decline of pituitary FSH neonatally, neither of the GnRH analogues was able to suppress serum FSH values and this differs from the concomitant changes in LH and from the effects of similar treatments in adult rats. Journal of Endocrinology (1989) 123, 83–91

The role of oestrogens on gonadotrophin secretion in the testicular feminization syndrome1

1980 ◽  
Vol 95 (3) ◽  
pp. 314-318 ◽  
Author(s):  
Martha Medina ◽  
Alfredo Ulloa-Aguirre ◽  
Maria A. Fernández ◽  
Gregorio Pérez-palacios
Keyword(s):  
Clomiphene Citrate ◽  
Poor Response ◽  
Testicular Feminization ◽  
Normal Response ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Before And After ◽  
Complete Form ◽  
Lh Secretion

Abstract. The role of oestrogens on gonadotrophin secretion was assessed in three related patients with the complete form of testicular feminization syndrome. Serum LH and FSH levels were measured before and after I.RH stimulation as well as before, during and after chronic clomiphene citrate administration. Moderately elevated LH basal levels with a significant LH rise following I.RH were observed. Normal or even low FSH level with poor response to LRH were found in all subjects. Administration of clomiphene citrate resulted in a significant serum LH increase without any change of FSH. Following castration both LH and FSH rose and a normal response to LRH was observed. These results were interpreted as demonstrating that, while endogenous oestrogens modulate LH secretion in patients with androgen unresponsiveness, it plays no role in regulating FSH secretion and suggested that a factor of testicular origin without androgenic or oestrogenic activity is responsible for FSH regulation.

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

Effects of oestradiol benzoate and progesterone on luteinizing hormone release and catecholamine turnover in the preoptic-hypothalamic brain area of ovariectomized rats

1983 ◽  
Vol 97 (3) ◽  
pp. 437-445 ◽  
Author(s):  
C. Hiemke ◽  
D. Frohne ◽  
D. Bruder ◽  
R. Ghraf
Keyword(s):  
Brain Area ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Time Interval ◽  
Dopamine Turnover ◽  
Noradrenaline Turnover ◽  
Serum Lh ◽  
Short Term Exposure ◽  
Oestradiol Benzoate

At noon, long-term (4–6 weeks) ovariectomized rats were exposed for 6–78 h to a single subcutaneous injection of oestradiol benzoate (20 μg) which significantly reduced the serum levels of LH over the whole time-interval investigated. The negative feedback action of oestradiol was accompanied by reduced turnover of both noradrenaline and dopamine in the preoptic-anterior hypothalamic brain area (POAH), but not in the mediobasal hypothalamus, 6, 68 and 72 h after administration of the hormone. Between 72 and 78 h after oestradiol-priming an afternoon increase of noradrenaline turnover was observed in the POAH. In rats primed with oestradiol benzoate for 72 h, short-term exposure (6 h) to progesterone (2·5 mg) induced a marked surge of serum LH and FSH in the late afternoon. In the POAH of these rats progesterone did not interfere with the afternoon increase of noradrenaline turnover induced by oestradiol-priming. However, it markedly increased the dopamine turnover rate of primed rats, thus reversing the inhibitory action of oestradiol benzoate on the dopaminergic system of the POAH. It is concluded that both the noradrenergic and the dopaminergic neurones of the POAH are involved in the negative and positive feedback actions of oestradiol and progesterone on LH and FSH release. The paper discusses whether the oestradiol-induced afternoon increase in noradrenaline turnover represents a prerequisite for the induction of LH surges by progesterone.

Influence of pinealectomy on the suppression of gonadotrophin secretion induced by hyperprolactinaemia in the adult male rat

1983 ◽  
Vol 97 (3) ◽  
pp. 401-407 ◽  
Author(s):  
A. S. McNeilly ◽  
D. W. Lincoln
Keyword(s):  
Pineal Gland ◽  
Adult Male ◽  
Male Rats ◽  
Male Rat ◽  
Gonadotrophin Secretion ◽  
Adult Male Rat ◽  
Pituitary Glands ◽  
Hypothalamic Pituitary Axis

To investigate the role of the pineal gland in the long-term suppression of gonadotrophin secretion induced by prolactin, the effects of pinealectomy were studied in adult male rats with hyperprolactinaemia produced by the transplantation of two pituitary glands under the kidney capsule. Pinealectomy had no effect on basal levels of LH, FSH or prolactin. The presence of pituitary transplants induced a significant twofold increase in prolactin levels and a prolonged suppression in both LH and FSH. These changes were not affected by pinealectomy. Castration resulted in a similar rise in plasma levels of LH and FSH in rats with and without pituitary transplants. In control rats this rise in LH and FSH was reduced by testosterone-containing silicone elastomer implants (s.c) of 10 mm in length and delayed by implants of 30 mm. These rises in LH and FSH were significantly delayed (10-mm implant) or abolished (30-mm implant) in rats with pituitary transplants indicating an increase in sensitivity of the hypothalamic-pituitary axis to the negative feedback effects of testosterone in these animals compared to controls. These responses were not affected by pinealectomy. These results suggest that the pineal gland is not involved in the mechanism whereby pituitary grafts, possibly through their secretion of prolactin, cause long-term suppression of gonadotrophin secretion.

ROLE OF OESTROGENS AND GONADOTROPHINS IN PERPHENAZINE-INDUCED MAMMOGENESIS

1970 ◽  
Vol 48 (3) ◽  
pp. 365-371 ◽  
Author(s):  
A. DANON ◽  
C. P. WELLER ◽  
F. G. SULMAN
Keyword(s):  
Median Eminence ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Gonadotrophin Secretion

SUMMARY Treatment of intact or recently (1 day) ovariectomized female rats with 5 mg perphenazine (Trilafon)/kg/day for 5 days resulted in marked lobulo—alveolar differentiation of the mammary glands. Perphenazine failed to stimulate mammogenesis in chronically (12 days) ovariectomized rats, unless they had been primed with oestradiol. However, mammogenic effects in chronically ovariectomized rats were obtained after implantation of minute amounts (2 μg) of oestradiol into the median eminence, or after treatment for 16 days with the non-steroid pituitary gonadotrophin-inhibitor methallibure (ICI 33828; 20 mg/kg/day). Since these latter procedures counteract the gonadotrophin surge after ovariectomy, it would appear that inhibition of gonadotrophin secretion is necessary before prolactin secretion can be stimulated by perphenazine. Castrated male rats responded to perphenazine with lobulo—alveolar differentiation similar to that in intact males. The implications of this difference with regard to the mechanism of pituitary response to gonadectomy are discussed.

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