Repeated convulsions induce pseudopregnancy in the intact rat and inhibit steroid-mediated gonadotrophin secretion in the ovariectomized rat

1982 ◽  
Vol 95 (1) ◽  
pp. 43-48 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson
Keyword(s):  
Reproductive Function ◽  
Shock Therapy ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Basal Serum ◽  
Gonadotrophin Secretion ◽  
Acute Seizure ◽  
Gonadotrophin Releasing Hormone ◽  
Positive Feedback Effect

We have investigated the effects of repeated flurothyl-induced seizures on reproductive function in the female rat. This treatment rapidly induced a state of pseudopregnancy in intact cyclic rats. Prolactin is clearly implicated in this response since treatment with bromocriptine readily counteracted the influence of the convulsions. The mechanism of action of repeated seizures was further characterized in experiments on ovariectomized rats. Thus, 11 daily convulsions, but not a single acute seizure, were able to inhibit the positive feedback effect of progesterone on LH and FSH release in oestrogen-primed animals. In this model also the pituitary gland response to gonadotrophin releasing hormone in vitro was significantly reduced. However, the convulsions had no effect on basal serum or basal in-vitro secretion of LH and FSH in ovariectomized or oestrogen-treated ovariectomized rats. Thus, repeated seizures modified the hypothalamo-pituitary axis in such a way as to prevent it from responding to stimulation. Our results indicate that normal reproductive function in the female rat is very sensitive to repeated seizures and suggest that similar effects may be evident in women subjected to electroconvulsive shock therapy. The successful use of bromocriptine in reversing the influence of seizures in the rat suggests its use in man also.

Flurothyl-induced convulsions delay the onset of sexual maturation in the female rat

1982 ◽  
Vol 95 (1) ◽  
pp. 37-41 ◽  
Author(s):  
M. Wilkinson ◽  
R. Bhanot ◽  
J. A. Pincock ◽  
L. Donald
Keyword(s):  
Sexual Maturation ◽  
Serum Levels ◽  
Female Rats ◽  
Female Rat ◽  
Basal Serum ◽  
Age Related ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Related Increase

We have investigated whether sexual maturation in female rats is affected by repeated flurothyl-induced convulsions. This treatment had no effect on the normal age-related increase in body weight though puberty (vaginal opening) was significantly delayed when compared with non-convulsed control rats. In an attempt to probe the mechanism of this delaying effect we observed that (1) anterior pituitary response to gonadotrophin releasing hormone in vitro was normal in terms of LH release but FSH secretion was impaired and (2) progesterone injection in oestrogen-primed convulsed rats failed to generate an ovulatory-type surge of LH or FSH. Basal serum levels and basal in-vitro secretion of LH and FSH were normal. We conclude that repeated convulsions adversely affect the hypothalamo-pituitary-gonadotrophin system of immature female rats.

IN-VITRO STUDIES OF THE EFFECTS OF OESTROGEN PRETREATMENT ON THE SENSITIVITY OF THE IMMATURE FEMALE RAT PITUITARY GLAND TO STIMULATION WITH GONADOTROPHIN RELEASING HORMONE

1977 ◽  
Vol 74 (1) ◽  
pp. 11-21 ◽  
Author(s):  
M. WILKINSON ◽  
D. DE ZIEGLER ◽  
DANIELLE CASSARD ◽  
K. B. RUF
Keyword(s):  
Pituitary Gland ◽  
Brain Lesion ◽  
Culture Technique ◽  
Female Rats ◽  
Female Rat ◽  
Immature Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Unilateral Brain Lesion

The effects of oestrogen priming on the sensitivity of the anterior pituitary gland to stimulation with gonadotrophin releasing hormone (GnRH) was investigated in immature female rats using a new organ culture technique. Hemipituitary glands obtained from animals primed with a single dose of oestradiol benzoate (OB; 20 μg/100 g body weight) released significantly more LH when pulsed with GnRH (4 nmol/l) than did control hemipituitary glands. This potentiating effect was detectable as early as 5 days after birth. After a second stimulation, LH secretion remained high. These results were compared with those obtained from animals treated to induce increased levels of endogenous oestrogen on day 26 of life. Thus, hemipituitary glands were obtained from animals given two injections of OB, an injection of pregnant mare serum gonadotrophin (PMSG) or a unilateral brain lesion placed in the basal hypothalamus. Pituitary tissue was stimulated as before with a pulse of GnRH. Two injections of OB enhanced the sensitivity to stimulation. Conversely, both PMSG and lesion treatment severely reduced the sensitivity to GnRH, although PMSG-treated and lesioned animals have been used as models for the study of ovulation.

scholarly journals Regulation of gonadotrophin secretion by inhibin, testosterone and gonadotrophin-releasing hormone in pituitary cell cultures of male monkeys

1998 ◽  
Vol 159 (1) ◽  
pp. 103-110 ◽  
Author(s):  
U Fingscheidt ◽  
GF Weinbauer ◽  
HL Fehm ◽  
E Nieschlag
Keyword(s):  
Dose Response ◽  
Pituitary Cells ◽  
Basal Secretion ◽  
Response Curves ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Dose Response Curves ◽  
Male Rhesus

The effects of bovine inhibin, testosterone and GnRH on gonadotrophin secretion by primate pituitary cells were characterized in vitro using pituitaries from six male rhesus monkeys and one male cynomolgus monkey. The effect of inhibin on basal secretion of FSH and LH was investigated. Dose-response curves in monkeys and rats were compared. GnRH dose-response curves in the presence and absence of testosterone were also examined in monkeys. In monkey pituitary cells, testosterone at a concentration of 10(-7) M had no effect on LH or FSH secretion. Inhibin suppressed FSH secretion to 50.8% of that of controls with no effect on LH. In rats, FSH secretion was suppressed to 45.0% of that of controls with a median effective dose (ED50, 95% range) of 1.298 (1.064-1.584) U/ml, compared with 1.024 (0.7204-1.455) U/ml in monkeys. In monkey pituitary cells, LH release was stimulated 9.9-fold and FSH 3.3-fold by GnRH. Testosterone had no effect on basal or GnRH-stimulated gonadotrophin release. These results support the view that the pituitary is not the target organ for the negative feedback action of testosterone in the male. In vitro, inhibin is the major regulator of FSH secretion at the pituitary level.

Long-term effects of a gonadotrophin-releasing hormone agonist ([d-Ser(But)6]GnRH(1–9)nonapeptide-ethylamide) on gonadotrophin secretion from human pituitary gonadotroph cell adenomas in vitro

1988 ◽  
Vol 118 (3) ◽  
pp. 491-496 ◽  
Author(s):  
M. Daniels ◽  
P. Newland ◽  
J. Dunn ◽  
P. Kendall-Taylor ◽  
M. C. White
Keyword(s):  
Gnrh Agonist ◽  
In Vitro Release ◽  
Long Term Effects ◽  
Human Pituitary ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Gonadotrophin Releasing Hormone

ABSTRACT We have studied the effects of TRH and native gonadotrophin-releasing hormone (GnRH), and of a GnRH agonist (Buserelin; [d-Ser(But)6]GnRH(1–9) nonapeptide-ethylamide), on LH, FSH, α subunit and LH-β subunit secretion from three human gonadotrophin-secreting pituitary adenomas in dispersed cell culture. During a 24 h study, treatment with 276 nmol TRH/1 resulted in a significant (P < 0·05) stimulated release of FSH and α subunit from all three adenomas, and LH from the two adenomas secreting detectable concentrations of this glycoprotein; treatment with 85 nmol GnRH/l significantly (P < 0·05) stimulated the release of α subunit from all three, but FSH from only two and LH from only one adenoma. During a long-term 28-day study, basal FSH and α subunit concentrations were maintained, but secretion of LH, and LH-β (detectable from one tumour only), declined with time from two of the three adenomas. Addition of Buserelin to the cultures resulted in the continuous (P < 0·05) stimulation of α subunit secretion from all three adenomas, and of LH and FSH from two, whilst a transient stimulatory effect on LH and FSH secretion was seen from a third adenoma, with subsequent secretion rates declining towards control values. These data show that human gonadotrophin-secreting adenomas demonstrate variable stimulatory responses to hypothalamic TRH and GnRH, and that during chronic treatment with a GnRH agonist the anticipated desensitizing effect of the drug was not observed in two out of three adenomas studied. The mechanism for this is not clear, but such drugs are unlikely to be of therapeutic value in the management of gonadotrophin-secreting tumours. The data also suggest that GnRH and GnRH agonists have a differential effect on the in-vitro release of intact gonadotrophins and the common α subunit. J. Endocr. (1988) 118, 491–496

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.

PROGESTERONE TREATMENT INCREASES PITUITARY OESTRADIOL RETENTION IN THE OVARIECTOMIZED NORMAL FEMALE RAT BUT NOT IN THE MALE NOR IN THE ANDROGEN- OR OESTROGEN-STERILIZED FEMALE RAT

1977 ◽  
Vol 84 (2) ◽  
pp. 268-280 ◽  
Author(s):  
Robert D. Lisk ◽  
Lawrence A. Reuter
Keyword(s):  
Testosterone Propionate ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Nuclear Fraction ◽  
Female Rat ◽  
Treatment Conditions ◽  
Oestradiol Benzoate ◽  
Pre Treatment

ABSTRACT Pituitary retention of [3H]oestradiol in ovariectomized rats was measured following in vivo progesterone pre-treatment and found to be significantly increased after 48, 72, 96 and 120 h of pre-treatment. Increased [3H]oestradiol retention was also observed for at least up to 72 h after removal of the progesterone pre-treatment source. This retention was measured as dpm per mg dry tissue weight. [3H]Oestradiol retention was also measured in the nuclear fraction of tissues incubated with [3H]oestradiol in vitro. Following 72 h of in vivo progesterone pre-treatment, the nuclear fraction from the pituitary was found to retain significantly more [3H]oestradiol than corresponding fractions from non-treated animals. In contrast to ovariectomized females, no increase in [3H]oestradiol retention was found in the pituitary of orchidectomized males pre-treated with progesterone for 72 h. [3H]Oestradiol retention by pituitaries of ovariectomized rats injected on the day of birth with 200 μg oestradiol benzoate (OeB) or 500 μg testosterone propionate (TP) was significantly decreased in comparison to control animals. When the rats were pre-treated in vivo with oestradiol for 6 or 72 h and [3H]oestradiol retention was measured 6 or 24 h after this pre-treatment, the OeB and TP treated animals retained significantly less [3H]oestradiol under most treatment conditions. Progesterone pretreatment for 24 or 72 h in vivo followed by measurement of [3H]oestradiol retention immediately or 6 or 24 h later resulted in a significant increase in [3H]oestradiol retention for the control animals. In contrast, the neonatally OeB or TP treated animals differed significantly by not showing increased retention. When [3H]oestradiol retention of the pituitary was measured in vitro following homogenization at 0°C and incubation at 37°C for 1 h, the nuclear fraction from both OeB and TP treated animals was found to retain less hormone per unit DNA; however, this decrease was significant only for the TP animals. Thus, males and androgen- or oestrogensterilized females have an altered and reduced augmentation of pituitary oestradiol retention in response to both oestrogen and progesterone pretreatments.

Effects of melatonin in the mediobasal hypothalamus on the secretion of gonadotrophins in sheep: role of dopaminergic pathways

1995 ◽  
Vol 146 (3) ◽  
pp. 543-552 ◽  
Author(s):  
D J Tortonese ◽  
G A Lincoln
Keyword(s):  
Reproductive Function ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Mediobasal Hypothalamus ◽  
Time Treatment ◽  
Gonadotrophin Secretion ◽  
Treatment Interaction ◽  
Micro Implants

Abstract Previous studies have shown that treatment with microimplants of melatonin in the mediobasal hypothalamus (MBH) of sexually inactive Soay rams exposed to long days induces an increase in the secretion of FSH and reactivation of the testicular axis, as normally occurs in response to short days. The current study was conducted to investigate the possible involvement of hypothalamic dopaminergic (DA) systems in this melatonin-induced effect. At 10 weeks under long days, sexually inactive Soay rams were treated in the MBH with micro-implants containing bromocriptine (DA agonist) or sulpiride (DA antagonist), given alone or in combination with melatonin, to establish whether the DA drugs would mimic or negate the effects of melatonin. All micro-implants were inserted bilaterally and left in place for 14 weeks; the study lasted a total of 28 weeks (14 weeks implant period and 14 weeks post-implant period) while the animals remained under long days. The ability of the micro-implants to release bromocriptine and sulpiride for 14 weeks was confirmed by incubating implants in vitro and testing for the presence of the compounds in the incubate using a pituitary cell bioassay. Profiles of FSH, determined in blood samples collected three times weekly, were significantly different among treatments (time × treatment interaction, P<0·001, ANOVA). Melatonin in the MBH induced a marked increase in the concentrations of FSH during the implant period, and a decrease during the post-implant period (P<0·001). Bromocriptine given alone in the MBH induced a decrease in the concentrations of FSH which became statistically different from the control during the post-implant period (P<0·05). Treatment with sulpiride alone also resulted in a suppressive effect during the post-implant period (P<0·01). When given in combination with melatonin, bromocriptine or sulpiride significantly reduced the melatonin-induced increase in the concentrations of FSH observed during the implant period (P<0·001). The results support the view that DA pathways in the MBH play an important role in the inhibitory regulation of gonadotrophin secretion in the ram. The inhibitory effect of bromocriptine is likely to result from the direct activation of the hypothalamic DA receptors linked to GnRH neurones regulating the secretion of FSH. The apparent paradoxical inhibitory effect of sulpiride is thought to be due to enhanced gonadal steroid negative feedback resulting from blockade of the inhibitory DA pathways, as evidenced by significantly increased secretion of testosterone (P<0·05) in the animals receiving sulpiride in combination with melatonin. The observation that DA drugs modified the effects of melatonin in the MBH provides evidence that hypothalamic DA pathways may participate in the mechanism by which melatonin mediates the effects of photoperiod on reproductive function in the ram. Journal of Endocrinology (1995) 146, 543–552

Gonadotrophin-releasing activity of neurohypophysial hormones: II. The pituitary oxytocin receptor mediating gonadotrophin release differs from that of corticotrophs

1989 ◽  
Vol 122 (1) ◽  
pp. 107-116 ◽  
Author(s):  
J. J. Evans ◽  
K. J. Catt
Keyword(s):  
Calcium Concentration ◽  
Phosphodiesterase Inhibitor ◽  
Pituitary Cells ◽  
Neurohypophysial Hormones ◽  
Gonadotrophin Secretion ◽  
Agonist And Antagonist ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Type Receptor

ABSTRACT Neurohypophysial hormones stimulate gonadotrophin release from dispersed rat anterior pituitary cells in vitro, acting through receptors distinct from those which mediate the secretory response to gonadotrophin-releasing hormone (GnRH). The LH response to oxytocin was not affected by the presence of the phosphodiesterase inhibitor, methyl isobutylxanthine, but was diminished in the absence of extracellular calcium and was progressively increased as the calcium concentration in the medium was raised to normal. In addition, the calcium channel antagonist, nifedipine, suppressed oxytocin-stimulated secretion of LH. It is likely that the mechanisms of LH release induced by GnRH and neurohypophysial hormones are similar, although stimulation of gonadotrophin secretion is mediated by separate receptor systems. Oxytocin was more active than vasopressin in releasing LH, but less active in releasing ACTH. The highly selective oxytocin agonist, [Thr4,Gly7]oxytocin, elicited concentration-dependent secretion of LH but had little effect on corticotrophin secretion. The neurohypophysial hormone antagonist analogues, [d(CH2)5Tyr(Me)2]-vasopressin, [d(CH2)5Tyr(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2Val4,Cit8]vasopressin, inhibited the LH response to both oxytocin and vasopressin. However, [d(CH2)5Tyr(Me)2]vasopressin was much less effective in inhibiting the ACTH response to the neurohypophysial hormones, and [d(CH2)5Tyr-(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2,Val4, Cit8]vasopressin exhibited no inhibitory activity against ACTH release. Thus, agonist and antagonist analogues of neurophypophysial hormones display divergent activities with regard to LH and ACTH responses, and the neuropeptide receptor mediating gonadotroph activation is clearly different from that on the corticotroph. Whereas the corticotroph receptor is a vasopressin-type receptor an oxytocin-type receptor is responsible for gonadotrophin release by neurohypophysial hormones. Journal of Endocrinology (1989) 122, 107–116

Effects of the synthetic glucocorticoid dexamethasone on reproductive function in the ewe

1990 ◽  
Vol 126 (2) ◽  
pp. 289-295 ◽  
Author(s):  
D. J. Phillips ◽  
I. J. Clarke
Keyword(s):  
Reproductive Function ◽  
Ovulation Rate ◽  
Dexamethasone Treatment ◽  
Domestic Species ◽  
Gonadotrophin Secretion ◽  
Gonadotrophin Releasing Hormone ◽  
Breeding Seasons ◽  
Lh Secretion ◽  
Pregnant Mare Serum Gonadotrophin ◽  
Synthetic Glucocorticoid

ABSTRACT Glucocorticoids have been found to inhibit reproductive function in most domestic species studied but, in the ewe, preliminary reports suggest that glucocorticoids may have little or no effect. This study investigated the effects of the synthetic glucocorticoid dexamethasone on oestrus and ovulation rate in ewes during the breeding season and gonadotrophin secretion in the breeding and non-breeding seasons. In cyclic ewes, dexamethasone treatment at rates of up to 2 mg/day did not affect the natural or pregnant mare serum gonadotrophin-stimulated ovulation rate, or the timing and incidence of behavioural oestrus (P>0·05). Dexamethasone administration (2 mg/day) had no effect on LH secretion or the plasma LH response to a 1 μg injection of gonadotrophin-releasing hormone (GnRH) in ovariectomized ewes in the breeding and non-breeding seasons, and did not compromise the inhibition of plasma LH levels during chronic treatment with oestrogen. Similarly, dexamethasone had no effect on plasma FSH concentrations, but significantly (P<0·05) reduced the plasma FSH response to a 1 μg GnRH injection during chronic negative treatment with oestrogen in ovariectomized ewes. Collectively, these data show that in these experiments dexamethasone did not significantly modify reproductive function in the ewe, a finding that is in contrast to that found in other domestic species. Journal of Endocrinology (1990) 126, 289–295

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