THE EFFECT OF OVARIAN STEROIDS ON HYPOTHALAMIC THRESHOLDS FOR OVULATION IN THE FEMALE RAT

1971 ◽  
Vol 49 (3) ◽  
pp. 421-429 ◽  
Author(s):  
P. G. McDONALD ◽  
D. P. GILMORE

SUMMARY Electrochemical stimulation of the basal and preoptic hypothalamus, under sodium pentobarbitone anaesthesia, was carried out on the day of pro-oestrus in normal cycling and in ovarian hormone-treated female rats. Control rats ovulated in response to 25, 50 and 100 μA for 60 s in the median eminence and to 10 μA for 60 s in the preoptic area. Oestradiol (1 μg) given 24 h before median eminence stimulation significantly increased the number of rats ovulating. An injection of progesterone (1 mg) 24 h before median eminence stimulation did not affect the number of animals ovulating or the number of ova shed. In contrast, there was a significant reduction in the number of animals ovulating after preoptic stimulation. Stimulation of the median eminence 2–4 h after progesterone administration increased the number of animals ovulating. The results suggest that both oestradiol and progesterone exert a positive feedback effect at or below the level of the median eminence and that the negative feedback effect of progesterone is exerted on the preoptic area.

1976 ◽  
Vol 70 (3) ◽  
pp. 501-511 ◽  
Author(s):  
NANCY M. SHERWOOD ◽  
SHARON A. CHIAPPA ◽  
G. FINK

SUMMARY The effects of sex steroid hormones on the responsiveness of the neural mechanism responsible for the secretion of LH-RF have been examined in the female rat. Responsiveness was determined at pro-oestrus by measuring the increments in immunoreactive LH-RF of pituitary stalk blood produced by electrical stimulation of the medial preoptic area or median eminence. Ovariectomy on the morning of dioestrus reduced the LH-RF response to preoptic stimulation while oestradiol benzoate (OB) or testosterone propionate (TP) administered immediately after ovariectomy significantly augmented the response. The facilitatory effect of TP was possibly due to its conversion to an aromatized derivative since 5α-dihydrotestosterone monobenzoate was ineffective. Progesterone did not facilitate preoptic responsiveness, and, when administered to animals ovariectomized at 12.00 h of pro-oestrus, reduced the LH-RF response at 18.00 h the same day. Stimulation of the median eminence produced a significantly greater increment in LH-RF than stimulation of the preoptic area. The facilitatory action of OB on the LH-RF response was less marked for median eminence compared with preoptic stimulation. The administration of ICI 46474 at 17.00 h of dioestrus did not reduce preoptic responsiveness on the morning of the next day, suggesting that this compound does not act as an 'antioestrogen' at the level of the preoptic area.


1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.


1992 ◽  
Vol 263 (3) ◽  
pp. E507-E511 ◽  
Author(s):  
D. Dondi ◽  
P. Limonta ◽  
R. Maggi ◽  
F. Piva

These experiments were performed to analyze whether treatments of ovariectomized female rats with ovarian steroid regimens able to induce either an increase (positive feedback effect) or a decrease (negative feedback effect) of serum levels of luteinizing hormone (LH) have some impact on the characteristics of mu-opioid binding sites in circumscribed areas of the brain. The increase of serum levels of LH elicited by a treatment with estradiol benzoate (EB) plus progesterone (P; positive feedback effect) was accompanied by a significant decrease in the number of mu-binding sites in the hypothalamus and in the corpus striatum. The decrease in serum levels of LH induced by a treatment with EB alone (negative feedback effect) brought about a significant increase of the number of mu-binding sites in the thalamus and in the hippocampus. These results seem to suggest that the release of LH induced by EB plus P may involve a decrease of hypothalamic mu-binding sites. Apparently, the inhibitory effect on LH release exerted by EB alone does not involve any change of the density of these binding sites in the hypothalamus.


1983 ◽  
Vol 97 (3) ◽  
pp. 319-325 ◽  
Author(s):  
E. Aguilar ◽  
C. Fernández Galaz ◽  
M. D. Vaticón ◽  
A. Tejero ◽  
A. Oriol

Neonatally oestrogenized female rats showed hyperprolactinaemia (prolactin, 230 μg/l), normal LH levels and absence of a positive feedback effect of oestrogen on secretion of LH at 5 months of age. Bromocriptine treatment for 13 days (1 mg/kg per day) caused no changes in LH levels and prolactin levels decreased to normal values (33 μg/l). This decrease in prolactin concentration was not followed by the recovery of phasic LH response to oestrogens. The effectiveness of oestrogens to induce prolactin secretion was greater in the neonatally oestrogenized rats than in the control group. In both cases the effect diminished after bromocriptine treatment. These results indicate that hyperprolactinaemia is not the cause of the anovulatory state in oestrogenized rats and that neonatal treatment with oestrogens alters oestrogen–prolactin relations, probably involving dopamine.


1962 ◽  
Vol 39 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roger A. Gorski ◽  
Charles A. Barraclough

ABSTRACT We have previously suggested that the failure of the androgen-sterilized, persistent-oestrous rat to ovulate, following electrical stimulation of the median eminence structures of the hypothalamus, is due to an insufficiency in adenohypophyseal LH concentration. Using the ovarian ascorbic acid technique for quantitative determination of pituitary LH content, the present studies have demonstrated that the sterile rat pituitary gland contains one-third the LH content of the normal prooestrous gland. Furthermore, not only does progesterone priming of this persistent-oestrous rat result in a 75 % increase in LH concentration, but on hypothalamic stimulation sufficient LH is released to induce ovulation. The decrease in LH concentration which accompanies ovulation in the progesterone-primed, sterile rat is approximately 45 % of the total gland content as compared with a 51 % decrease in pituitary content in the normal cyclic rat.


Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 323-335 ◽  
Author(s):  
Bruna Kalil ◽  
Aline B. Ribeiro ◽  
Cristiane M. Leite ◽  
Ernane T. Uchôa ◽  
Ruither O. Carolino ◽  
...  

Abstract In rodents, kisspeptin neurons in the rostral periventricular area of the third ventricle (RP3V) of the preoptic area are considered to provide a major stimulatory input to the GnRH neuronal network that is responsible for triggering the preovulatory LH surge. Noradrenaline (NA) is one of the main modulators of GnRH release, and NA fibers are found in close apposition to kisspeptin neurons in the RP3V. Our objective was to interrogate the role of NA signaling in the kisspeptin control of GnRH secretion during the estradiol induced LH surge in ovariectomized rats, using prazosin, an α1-adrenergic receptor antagonist. In control rats, the estradiol-induced LH surge at 17 hours was associated with a significant increase in GnRH and kisspeptin content in the median eminence with the increase in kisspeptin preceding that of GnRH and LH. Prazosin, administered 5 and 3 hours prior to the predicted time of the LH surge truncated the LH surge and abolished the rise in GnRH and kisspeptin in the median eminence. In the preoptic area, prazosin blocked the increases in Kiss1 gene expression and kisspeptin content in association with a disruption in the expression of the clock genes, Per1 and Bmal1. Together these findings demonstrate for the first time that NA modulates kisspeptin synthesis in the RP3V through the activation of α1-adrenergic receptors prior to the initiation of the LH surge and indicate a potential role of α1-adrenergic signaling in the circadian-controlled pathway timing of the preovulatory LH surge.


2015 ◽  
Vol 42 (12) ◽  
pp. 3138-3148 ◽  
Author(s):  
M. Dean Graham ◽  
James Gardner Gregory ◽  
Dema Hussain ◽  
Wayne G. Brake ◽  
James G. Pfaus

1971 ◽  
Vol 51 (1) ◽  
pp. 31-39 ◽  
Author(s):  
R. E. PETER

SUMMARY The effect on thyroid activity of a systemically ineffective dose of thyroxine (T4) implanted in the hypothalamus or pituitary of goldfish was tested. Thyroid activity was decreased by T4 implantation in either location, indicating that T4 has a negative feedback effect on the pituitary causing a decrease in thyrotrophin secretion, and a positive feedback effect on the hypothalamus stimulating the secretion of thyrotrophin inhibitory factor (TIF). Fish with a T4 or blank-control implant in the pituitary that had a damaged pituitary stalk, as a result of the operative procedures, were hyperthyroid, suggesting either that TIF is more effective in suppressing thyrotroph activity than T4 and that the effect of T4 was masked by the absence of TIF, or, less likely, that T4 negative feedback in the pituitary is not effective independent of TIF. The results were compared with the information about T4 feedback in mammals.


Sign in / Sign up

Export Citation Format

Share Document