SHORT-LOOP FEEDBACK MECHANISM OF LUTEINIZING HORMONE: LH STIMULATES HYPOTHALAMIC L-CYSTINE ARYLAMIDASE TO INACTIVATE LH-RH IN THE RAT HYPOTHALAMUS

1975 ◽  
Vol 78 (4) ◽  
pp. 649-663 ◽  
Author(s):  
Herbert Kuhl ◽  
Hans-Dieter Taubert
Keyword(s):  
Enzyme Activity ◽  
Feedback Mechanism ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Maximal Increase ◽  
Short Loop ◽  
Male And Female Rats ◽  
Loop Feedback ◽  
Lh Rh ◽  
Cystine Arylamidase

ABSTRACT The effect of the intravenous administration of several hormones on L-cystine arylamidase in the hypothalamus of the rat was examined. The injection of 10 μg LH into adult male and female rats was followed within 90 min by an increase of the enzyme activity by 50 %, while infantile animals were not affected. When prepuberal rats were pre-treated sc with testosterone and oestrogen respectively, the iv injection of LH brought about a rise in hypothalamic arylamidase activity. When ovariectomized rats were tested, no response was seen after LH injection unless the animals had been pre-treated with oestrogen and progesterone. The iv injection of 0.1 μg oestradiol-17β into female, and of 0.5 μg testosterone into male intact mature rats also resulted in an increase of hypothalamic enzyme activity. The maximal increase in enzyme activity was seen 16 h after steroid treatment. As it had previously been shown that L-cystine arylamidase inactivates LH-RH, it may be assumed that this enzyme is involved in the short-loop feedback of LH. This assumption is based on the observation that an elevation of plasma LH brings about an activation of the enzyme system, which subsequently leads to increased inactivation of LH-RH in the hypothalamus. This mechanism seems to depend on the presence of certain plasma levels of oestrogen in female, and of testosterone in male animals.

Failure of Prolactin Short Loop Feedback Mechanism to Operate in Old as Compared to Young Female Rats*

Endocrinology ◽  
1983 ◽  
Vol 113 (4) ◽  
pp. 1452-1458 ◽  
Author(s):  
DIPAK K. SARKAR ◽  
NOBUHIRO MIKI ◽  
JOSEPH MEITES
Keyword(s):  
Young Female ◽  
Feedback Mechanism ◽  
Female Rats ◽  
Short Loop ◽  
Loop Feedback

THE REGULATORY FUNCTION OF A PITUITARY LH-RH-DEGRADING ENZYME SYSTEM IN THE FEEDBACK CONTROL OF GONADOTROPHINS

1977 ◽  
Vol 86 (1) ◽  
pp. 60-70 ◽  
Author(s):  
Herbert Kuhl ◽  
Christian Rosniatowski ◽  
Hans-Dieter Taubert
Keyword(s):  
Enzyme Activity ◽  
Enzyme System ◽  
Significant Rise ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Regulatory Function ◽  
Specific Response ◽  
Degrading Enzyme ◽  
Lh Rh ◽  
Cystine Arylamidase

ABSTRACT It had previously been shown that a luteinizing hormone-releasing hormone (LH-RH)-inactivating enzyme in the rat hypothalamus, L-cystine arylamidase, is in all probability involved in the short-loop feedback mechanism of LH. Since this enzyme system was also shown to be present in the pituitary, the effect of the iv injection of several sex hormones upon its activity was investigated. The basal arylamidase activity was found to be considerably higher in the neurohypophysis as compared to the adenohypophysis. The injection of 10 μg LH brought about a significant rise in arylamidase activity (+60 %) only in the latter. There was a dose-dependent increase in the pituitary enzyme activity 2 h after the iv administration of LH, and 16 h after the injection of oestradiol and progesterone into dioestrous rats. Contrary to previous findings obtained with hypothalamic homogenates, the effect of LH upon the enzyme in the pituitary proved to be not dependent on the presence of sex steroids, as the iv application of 10 μg LH into ovariectomized rats resulted in an increase of pituitary L-cystine arylamidase by about 30 %. The injection of testosterone, oestradiol and - to a lesser degree - progesterone into adult male rats caused a significant increase of enzyme activity in the hypophysis. Progesterone proved to be ineffective in the hypothalamus. This indicates that in contrast to the hypothalamus there is no sex-specific response of the LH-RH-degrading enzyme in the pituitary. It is concluded that this enzyme system seems to play an important part in the mechanisms regulating gonadotrophin release in the pituitary.

scholarly journals Influence of sex, estrous cycle, and estrogen on intracranial dural mast cells

Cephalalgia ◽  
2012 ◽  
Vol 32 (12) ◽  
pp. 924-931 ◽  
Author(s):  
Tanner Boes ◽  
Dan Levy
Keyword(s):  
Mast Cells ◽  
Estrous Cycle ◽  
Potential Role ◽  
Ovarian Hormones ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Migraine Headaches ◽  
Male And Female Rats ◽  
Quantitative Analyses

Background: The frequency of migraine headaches is higher in women than in men and in susceptible women attacks are related to changes in ovarian hormone levels. Intracranial mast cells (MCs) are likely to have a role in migraine headache genesis, and changes in the dural MC population might influence headache susceptibility. The present study thus tested the hypothesis that sex and ovarian hormones influence the density and phenotypic makeup of dural MCs. Methods: Histochemistry combined with quantitative analyses was used to investigate sex differences, estrous cycle and ovarian hormones on dural MC density, phenotype and degranulation level in male and female rats. Results: Our data show that in female rats, dural MC density fluctuates during the estrous cycle and is overall higher than in males. In ovariectomized rats, estradiol, but not progesterone, promoted an increase in dural MC density. This effect was abolished by a splenectomy, suggesting estrogen-related recruitment of MCs from the spleen. Finally, our data suggest that the phenotypic make up of dural MCs, which represents the level of cellular maturity, is also governed by changes in estrogen levels. Conclusions: Given the potential role of dural MCs in triggering headache, our data suggest that estrogen-related modulation of dural MC density and phenotypic makeup could have a role in mediating the higher frequency and severity of headaches such as migraine, in women.

DISSOCIATION IN THE REGULATION OF LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE IN A HYPERPROLACTINAEMIC RAT MODEL: INTERRELATIONSHIPS BETWEEN GONADOTROPHIN AND PROLACTIN CONTROL

1981 ◽  
Vol 90 (1) ◽  
pp. 41-51 ◽  
Author(s):  
J. A. F. TRESGUERRES ◽  
A. I. ESQUIFINO
Keyword(s):  
Positive Feedback ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Female Wistar Rats ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

Male and female Wistar rats were made hyperprolactinaemic by grafting two pituitary glands of litter-mate donors under the kidney capsule at 30 days of age. Other animals were sham-operated at the same age to serve as controls. Plasma levels of prolactin, LH and FSH were measured by double-antibody radioimmunoassay. Basal preoperative prolactin levels of ∼ 10 ng/ml increased after the transplantation in both male and female rats, reaching values of ∼ 180 ng/ml. Levels of LH were significantly reduced in these hyperprolactinaemic rats, whereas an increase in FSH values was seen. After administration of LH releasing hormone (LH-RH) a reduced LH response was seen but there was no response of FSH to LH-RH or even a decrease in FSH values. Prolactin levels were also reduced by LH-RH injection. Although an increase in prolactin levels was observed in control animals after a challenge with oestradiol benzoate, reduced increments were seen in experimental animals. The positive feedback effect of oestradiol benzoate on LH in females was reduced in pituitary-grafted rats but a potentiation of the FSH positive feedback could be clearly detected. This study suggests a dissociation of LH and FSH regulation in hyperprolactinaemia.

scholarly journals Neuroendocrine control of the pituitary gonadotropic function in experimental diabetes

2019 ◽  
Vol 43 (3) ◽  
pp. 43-47
Author(s):  
V. N. Babichev ◽  
E. I. Adamskaya ◽  
T. A. Kuznetsova ◽  
I. V. Shishkina
Keyword(s):  
Nuclear Receptors ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Female Rats ◽  
Maximal Response ◽  
Basal Secretion ◽  
Male And Female Rats ◽  
Lh Rh ◽  
Lh Secretion

The hypothalamo-pituitary-gonadal system was examined in male and female rats with experimental diabetes in­duced by streptozotocin (STZ). Injection of STZ caused a decrease of testosterone (T) concentration and of T nuclear receptors in the pituitary. The levels of luteinizing and follicle stimulating hor­mones (LH and FSH) in the blood of diabetic rats did not differ from those in intact animals. In vitro experiments showed that the development of diabetes did not change the basal secretion of LH by the pituitary in males. Maximal response to LH-RH was record­ed in control males after 3-hour incubation, whereas the rate of LH secretion in experimental rats did not differ from basal values. In­jection of STZ to cycling females disordered the estrous cycle and involved decreases of the basal and cyclic secretion of LH, FSH, and sex hormones. The concentrations of estradiol nuclear receptors in the preoptic anterohypothalamic region and pituitary decreased, whereas the number of T-binding sites decreased only in the pitui­tary. Sex hormone-stimulated gonadotropin wave in oophorect- omized females was decreased in diabetes, which was due to changed activity of the LH-RH producing system. The authors hy­pothesize that changes in the mechanism of regulation of the hy­pothalamo-pituitary-gonadal system in experimental diabetes are re­lated to pituitary disorders in males, whereas changed basal and cy­clic secretion of LH and FSH in females is caused by disordered activity of the LH-RH production and receptor binding at the level of the hypothalamo-pituitary complex.

The Effect of Estradiol Benzoate on the Pituitary Responsiveness to LH-RH in Male and Female Rats

1974 ◽  
Vol 15 (3-4) ◽  
pp. 182-188 ◽  
Author(s):  
J.A.M.J. van Dieten ◽  
J. Steijsiger ◽  
J. Dullaart ◽  
G.P. van Rees
Keyword(s):  
Estradiol Benzoate ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Lh Rh

HORMONAL MODULATION OF HYPOTHALAMIC UNIT ACTIVITY AND EEG RESPONSE TO VAGINAL STIMULATION IN THE DEERMOUSE

1971 ◽  
Vol 49 (1) ◽  
pp. 59-69 ◽  
Author(s):  
A. J. ZOLOVICK ◽  
B. E. ELEFTHERIOU
Keyword(s):  
Luteinizing Hormone ◽  
Unit Activity ◽  
Discharge Rate ◽  
Inhibitory Response ◽  
Feedback Mechanism ◽  
Short Loop ◽  
Hormonal Modulation ◽  
Loop Feedback ◽  
Vaginal Stimulation

SUMMARY The EEG after-reaction to vaginal stimulation occurred during oestrus and was inhibited during dioestrus or abolished by pregnancy or ovariectomy. Hypothalami of oestrous animals were more responsive to vaginal stimulation than the hypothalami of dioestrous or pregnant animals. The increase in the number of responsive neurones in oestrous animals was attributed to an increase in the number of neurones that exhibited a delayed decline in their discharge rate in response to vaginal probing. These neurones were located along the midline in the anterior and basal hypothalamus. Administration of oestrogen to ovariectomized animals was moderately successful in reinstating the delayed inhibitory response of the hypothalamic neurones to vaginal stimulation while the EEG response was almost completely restored. The importance of this hypothalamic activity is discussed in relation to the luteinizing hormone short loop feedback mechanism and the EEG after-reaction.

Effects of vasopressin on arterial blood pressure and cardiac output in male and female rats

1991 ◽  
Vol 261 (5) ◽  
pp. R1118-R1125 ◽  
Author(s):  
K. Toba ◽  
J. T. Crofton ◽  
M. Inoue ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Arterial Blood ◽  
Male And Female Rats ◽  
Cycle Dependent

This study was performed to investigate further the mechanisms underlying the sexual dimorphism of the pressor responses to vasopressin. We have confirmed our earlier findings that the pressor response to graded infusions of vasopressin in conscious unrestrained male rats is similar to that in estrous females and greater than in diestrus, proestrus, and metestrus. This difference was due primarily to greater increases in total peripheral resistance (TPR) in males and estrous females, since there were no sex- or cycle-related differences in the vasopressin-induced reductions in cardiac output. Gonadectomy was without effect in males but, in females, increased blood pressure responses to vasopressin to levels found in males. Chronic treatment of ovariectomized rats with estradiol reduced pressor responsiveness to vasopressin; treatment with progesterone was without effect. These differences were also due to differences in TPR. It is concluded that the sex- and cycle-dependent differences in vasopressin-induced increases in blood pressure are due largely to attenuation of increases in TPR by estrogen.

Identification of target cells for growth hormone's action in the arcuate nucleus

1995 ◽  
Vol 269 (4) ◽  
pp. E716-E722
Author(s):  
K. A. Burton ◽  
E. B. Kabigting ◽  
R. A. Steiner ◽  
D. K. Clifton
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Arcuate Nucleus ◽  
Feedback Mechanism ◽  
Target Cells ◽  
Growth Hormone Releasing Hormone ◽  
Short Loop ◽  
Loop Feedback ◽  
The Brain

Growth hormone (GH) participates in the regulation of its own secretion by acting through a short-loop feedback mechanism to regulate the synthesis and secretion of somatostatin (SS) and growth hormone-releasing hormone (GHRH). The mechanism of GH's action in certain peripheral targets involves the induction of c-fos. Similarly, we hypothesized that GH induces the expression of c-fos mRNA in SS and GHRH neurons in the hypothalamus. Using in situ hybridization, we observed a significant induction of c-fos mRNA in the arcuate nucleus of human GH-treated compared with control animals. Contrary to our hypothesis, only 11% of GHRH mRNA-containing and 5% of SS mRNA-containing neurons colabeled for c-fos mRNA. These findings indicate that GH feedback on the hypothalamus includes the induction of c-fos mRNA primarily in neurons other than GHRH and SS in the arcuate nucleus and suggest that these unidentified neurons located in the arcuate nucleus are directly involved in transducing the effects of GH in the brain.

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