THE EFFECT OF NEONATAL ANDROGEN ON THE ACTIVITY OF CERTAIN ENZYMES IN THE RAT HYPOTHALAMUS

1972 ◽  
Vol 70 (4) ◽  
pp. 767-774 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper
Keyword(s):  
Enzyme Activity ◽  
Luteinizing Hormone ◽  
Particulate Fraction ◽  
Female Rats ◽  
Testosterone Treatment ◽  
Rat Hypothalamus ◽  
Hypothalamic Control ◽  
Activity Of Enzymes ◽  
Lh Secretion

ABSTRACT The activity of enzymes inactivating oxytocin in the hypothalamus changes with stimuli known to release gonadotrophins and may be related to luteinizing hormone-releasing factor (LH-RF) release (Frith & Hooper 1971a,b; Griffiths & Hooper 1972). In the work presented here, enzyme activity was determined following neonatal testosterone treatment to assess any changes in the hypothalamic control of LH secretion. Supernatant and particulate fraction activities in female rats were depressed to male levels following injection on day 3; supernatant activity after injection on day 10 was also slightly decreased. These findings suggest that masculinization of the mechanisms controlling LH secretion in the hypothalamus, produced by neonatal testosterone, is caused by changes in LH-RF metabolism and that these peptidases in the rat hypothalamus are responsible for this metabolism.

THE EFFECTS OF ORCHIDECTOMY AND TESTOSTERONE PROPIONATE INJECTION ON PEPTIDASE ACTIVITY IN THE MALE RAT HYPOTHALAMUS

1973 ◽  
Vol 72 (1) ◽  
pp. 1-8 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper
Keyword(s):  
Luteinizing Hormone ◽  
Testosterone Propionate ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Peptidase Activity ◽  
Female Rat ◽  
Similar Relationship ◽  
Testosterone Treatment ◽  
Rat Hypothalamus

ABSTRACT It has previously been shown that the activity of certain peptidases in the female rat hypothalamus is related to the release of luteinizing hormone releasing factor from the tissue (Griffiths & Hooper 1972a). The activity of these enzymes was investigated after orchidectomy and testosterone propionate injection to determine if a similar relationship exists in male rats. The depression in supernatant activity following orchidectomy and the elevation after testosterone treatment are interpreted as confirming this, and it is proposed that alterations in peptidase activity may be used as an index of gonadotrophin release in male as well as in female rats.

scholarly journals Effect of androgen on Kiss1 expression and luteinizing hormone release in female rats

2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa
Keyword(s):  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Female Rats ◽  
Hormone Release ◽  
Lh Surge ◽  
Continuous Release ◽  
Ovulatory Dysfunction ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Hyperandrogenic women have various grades of ovulatory dysfunction, which lead to infertility. The purpose of this study was to determine whether chronic exposure to androgen affects the expression of kisspeptin (ovulation and follicle development regulator) or release of luteinizing hormone (LH) in female rats. Weaned females were subcutaneously implanted with 90-day continuous-release pellets of 5α-dihydrotestosterone (DHT) and studied after 10 weeks of age. Number of Kiss1-expressing cells in both the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) was significantly decreased in ovary-intact DHT rats. Further, an estradiol-induced LH surge was not detected in DHT rats, even though significant differences were not observed between DHT and non-DHT rats with regard to number of AVPV Kiss1-expressing cells or gonadotrophin-releasing hormone (GnRH)-immunoreactive (ir) cells in the presence of high estradiol. Kiss1-expressing and neurokinin B-ir cells were significantly decreased in the ARC of ovariectomized (OVX) DHT rats compared with OVX non-DHT rats; pulsatile LH secretion was also suppressed in these animals. Central injection of kisspeptin-10 or intravenous injection of a GnRH agonist did not affect the LH release in DHT rats. Notably, ARC Kiss1-expressing cells expressed androgen receptors (ARs) in female rats, whereas only a few Kiss1-expressing cells expressed ARs in the AVPV. Collectively, our results suggest excessive androgen suppresses LH surge and pulsatile LH secretion by inhibiting kisspeptin expression in the ARC and disruption at the pituitary level, whereas AVPV kisspeptin neurons appear to be directly unaffected by androgen. Hence, hyperandrogenemia may adversely affect ARC kisspeptin neurons, resulting in anovulation and menstrual irregularities.

FURTHER STUDIES ON ENZYMIC INACTIVATION OF LUTEINIZING HORMONE – RELEASING HORMONE (LH-RH) BY PEPTIDASES IN THE RAT HYPOTHALAMUS

1975 ◽  
Vol 79 (1) ◽  
pp. 7-15 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper ◽  
C. R. N. Hopkinson
Keyword(s):  
Enzyme Activity ◽  
Luteinizing Hormone ◽  
Assay System ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Lh Rh ◽  
A Site

ABSTRACT Luteinizing hormone-releasing hormone (LH-RH) is known to be inactivated by peptidases in the rat hypothalamus with consequent loss of LH-releasing ability. To make a further study of the peptidases' action on the decapeptide, synthetic LH-RH and its [1–9NH2] analogue were incubated with the supernatant hypothalamic fraction containing the enzyme activity. Using an assay system measuring gonadotrophin release in ovariectomized/steroid-primed rats, both LH-RH and the [1–9NH2] analogue were found to be inactivated to different extents after incubation with the fraction, the analogue completely losing both LH- and FSH-releasing activity, and the releasing hormone almost completely losing its LH- and totally losing its FSH-releasing activity. The findings extend the initial studies by showing that the peptidases can remove both the decapeptide's intrinsic LH- and FSH-releasing activity and that these enzymes act on LH-RH at a site other than the C-terminal glycinamide, since they are able to inactivate the [1–9NH2] analogue lacking this residue.

Oxytocin modulates the luteinizing hormone response of the rat anterior pituitary to gonadotrophin-releasing hormone in vitro

1995 ◽  
Vol 145 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J J Evans ◽  
S J Hurd ◽  
D R Mason
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
The Self ◽  
Female Rats ◽  
Hormone Response ◽  
Priming Process ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Abstract Although GnRH is believed to be the primary secretagogue for LH, oxytocin has also been shown to stimulate LH release from the anterior pituitary. We investigated the possibility that the two secretagogues interact in the modulation of LH release. Anterior pituitaries were removed from adult female rats at pro-oestrus, and tissue pieces were pre-incubated in oxytocin for 3 h prior to being stimulated with 15 min pulses of GnRH. LH output over the 1 h period from the beginning of the GnRH pulse was determined. Control incubations were carried out in the absence of oxytocin, and background secretory activities without GnRH stimulation were also determined. Tissue which was pre-exposed to oxytocin (0·012–1·25 μm) had an increased LH response to GnRH (1·25 nm). The increase was larger than the sum of the LH outputs obtained with oxytocin and GnRH separately, revealing that oxytocin synergistically enhanced LH secretion elicited by GnRH (P<0·05; ANOVA). If stimulation by GnRH was delayed for 2 h after incubation with oxytocin, an increase in LH secretion was still observed, indicating that oxytocin-induced modulation did not rapidly disappear. Oxytocin pre-incubation was observed to result in an increase of maximal GnRH-induced LH output (P<0·001; t-test), as well as an increase of intermediate responses. The LH response of the anterior pituitary to subsequent pulses of GnRH was modified by the self-priming process. The effect of oxytocin pretreatment on the response of primed tissue to GnRH was also investigated. It was found that pre-incubation in oxytocin also enhanced the LH response of primed tissue to GnRH. The study has revealed that oxytocin increases the LH output of anterior pituitary tissue in response to GnRH. The effect occurs on both GnRH-primed and unprimed tissues. The results suggest that oxytocin has the potential to regulate the dynamics of the pro-oestrous LH surge. Journal of Endocrinology (1995) 145, 113–119

scholarly journals Galanin Enhancement of Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Secretion in Female Rats Is Estrogen Dependent

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 484-490 ◽  
Author(s):  
Cynthia L. Splett ◽  
Joseph R. Scheffen ◽  
Joshua A. Desotelle ◽  
Vicky Plamann ◽  
Angela C. Bauer-Dantoin
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Luteinizing Hormone Secretion ◽  
Ovx Rats ◽  
Lh Secretion ◽  
Lines Of Evidence

The hypothalamic peptide GnRH is the primary neuroendocrine signal regulating pituitary LH in females. The neuropeptide galanin is cosecreted with GnRH from hypothalamic neurons, and in vitro studies have demonstrated that galanin can act at the level of the pituitary to directly stimulate LH secretion and also augment GnRH-stimulated LH secretion. Several lines of evidence have suggested that the hypophysiotropic effects of galanin are important for the generation of preovulatory LH surges. To determine whether the pituitary actions of galanin are enhanced by the preovulatory steroidal milieu, LH responses to galanin administration (with or without GnRH) were examined in: 1) ovariectomized (OVX); 2) OVX, estrogen (E)-primed; and 3) OVX, E- and progesterone-treated female rats. Results from the study indicate that galanin enhances GnRH-stimulated LH secretion only in the presence of E (in OVX, E-primed, or E- and progesterone-treated rats). Galanin alone does not directly stimulate LH secretion under any of the steroid conditions examined. In the absence of gonadal steroids (OVX rats), galanin inhibits GnRH-stimulated LH secretion. These findings suggest that the primary pituitary effect of galanin is to modulate GnRH-stimulated LH secretion, and that the potentiating effects of galanin occur only in the presence of E.

scholarly journals Erythropoietin-producing hepatocellular receptor A7 restrains estrogen negative feedback of luteinizing hormone via ephrin A5 in the hypothalamus of female rats

2020 ◽  
Vol 319 (1) ◽  
pp. E81-E90 ◽  
Author(s):  
Shang Li ◽  
Junyu Zhai ◽  
Bing Xu ◽  
Jiansheng Liu ◽  
Weiwei Chu ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Female Rats ◽  
Female Rat ◽  
Female Reproduction ◽  
Systemic Injection ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
17Β Estradiol ◽  
Lh Secretion

We have previously shown that systemic injection of erythropoietin-producing hepatocellular receptor A7 (EPHA7)-Fc raises serum luteinizing hormone (LH) levels before ovulation in female rats, indicating the induction of EPHA7 in ovulation. In this study, we aimed to identify the mechanism and hypothalamus-pituitary-ovary (HPO) axis level underlying the promotion of LH secretion by EPHA7. Using an ovariectomized (OVX) rat model, in conjunction with low-dose 17β-estradiol (E2) treatment, we investigated the association between EPHA7-ephrin (EFN)A5 signaling and E2 negative feedback. Various rat models (OVX, E2-treated OVX, and abarelix treated) were injected with the recombinant EPHA7-Fc protein through the caudal vein to investigate the molecular mechanism underlying the promotion of LH secretion by EPHA7. Efna5 was observed strongly expressed in the arcuate nucleus of the female rat by using RNAscope in situ hybridization. Our results indicated that E2, combined with estrogen receptor (ER)α, but not ERβ, inhibited Efna5 and gonadotropin-releasing hormone 1 ( Gnrh1) expressions in the hypothalamus. In addition, the systemic administration of EPHA7-Fc restrained the inhibition of Efna5 and Gnrh1 by E2, resulting in increased Efna5 and Gnrh1 expressions in the hypothalamus as well as increased serum LH levels. Collectively, our findings demonstrated the involvement of EPHA7-EFNA5 signaling in the regulation of LH and the E2 negative feedback pathway in the hypothalamus, highlighting the functional role of EPHA7 in female reproduction.

THE EFFECT OF OVARIECTOMY ON THE ACTIVITY OF CERTAIN ENZYMES IN THE FEMALE RAT HYPOTHALAMUS

1972 ◽  
Vol 69 (2) ◽  
pp. 249-256 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper
Keyword(s):  
Enzyme Activity ◽  
Luteinizing Hormone ◽  
Inverse Relationship ◽  
Supernatant Fraction ◽  
Female Rat ◽  
Hormone Release ◽  
Similar Relationship ◽  
Hormone Levels ◽  
Rat Hypothalamus ◽  
Detectable Difference

ABSTRACT Previous work in the rabbit has shown that the activity of certain peptidases in the hypothalamus which inactivate oxytocin, changes with stimuli known to release gonadotrophins, and may be used as an index of gonadotrophin hormone release (Hooper 1966a,b, 1968; Frith & Hooper 1971a,b). Using this approach, a study was made of the activities of similar peptidases in the rat hypothalamus following ovariectomy, a condition known to cause gonadotrophin release. Enzyme activity in the supernatant fraction was found to decrease progressively with time after ovariectomy, until 42 days after operation, thereafter maintaining a level not significantly different from that at 42 days; there was no detectable difference in particulate enzyme activity after ovariectomy. An inverse relationship between supernatant enzyme activity and luteinizing hormone levels is suggested. It is concluded that a similar relationship to that in the rabbit exists between enzyme activity in the rat hypothalamus and the release of luteinizing hormone-releasing factor from the tissue.

Effects of galanin-like peptide on luteinizing hormone secretion in the rat: sexually dimorphic responses and enhanced sensitivity at male puberty

2006 ◽  
Vol 291 (6) ◽  
pp. E1281-E1289 ◽  
Author(s):  
J. M. Castellano ◽  
V. M. Navarro ◽  
R. Fernández-Fernández ◽  
J. Roa ◽  
E. Vigo ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Metabolic Stress ◽  
Female Rats ◽  
Metabolic Status ◽  
Male Rats ◽  
Intracerebral Injection ◽  
Luteinizing Hormone Secretion ◽  
Male Puberty ◽  
Lh Secretion

Reproductive function is exquisitely sensitive to adequacy of nutrition and fuel reserves, through mechanisms that are yet to be completely elucidated. Galanin-like peptide (GALP) has recently emerged as another neuropeptide link that couples reproduction and metabolism. However, although the effects of GALP on luteinizing hormone (LH) secretion have been studied, no systematic investigation on how these responses might differ along sexual maturation and between sexes has been reported. Moreover, the influence of metabolic status and potential interplay with other relevant neurotransmitters controlling LH secretion remain ill defined. These facets of GALP physiology were addressed herein. Intracerebral injection of GALP to male rats induced a dose-dependent increase in serum LH levels, the magnitude of which was significantly greater in pubertal than in adult males. In contrast, negligible LH responses to GALP were detected in pubertal or adult female rats at diestrus. Neonatal androgen treatment to females failed to “masculinize” the pattern of LH response to GALP. In addition, metabolic stress by short-term fasting did not prevent but rather amplified LH responses to GALP in pubertal males, whereas these responses were abrogated by pharmacological inhibition of nitric oxide synthesis. We conclude that the ability of GALP to evoke LH secretion is sexually differentiated, with maximal responses at male puberty, a phenomenon which was not reverted by manipulation of sex steroid milieu during the critical neonatal period and was sensitive to metabolic stress. This state of LH hyperresponsiveness may prove relevant for the mechanisms relaying metabolic status to the reproductive axis in male puberty.

INFLUENCE OF AGE ON THE RELEASE OF LUTEINIZING HORMONE INDUCED BY OESTROGEN AND PROGESTERONE IN IMMATURE RATS

1972 ◽  
Vol 55 (1) ◽  
pp. 97-103 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK
Keyword(s):  
Luteinizing Hormone ◽  
Single Injection ◽  
Significant Rise ◽  
Female Rats ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Old Rats ◽  
Lh Secretion ◽  
Phasic Release

SUMMARY In immature female rats serum luteinizing hormone (LH) concentration, as measured by radioimmunoassay, was found to be higher at 10 or 15 days of age than thereafter. Animals ovariectomized soon after birth or at 5 days of age showed a significant rise in serum LH levels 10 days later. A positive feedback effect on LH secretion was observed on the day following a single injection of oestradiol benzoate (OB) in 28-day-old rats but not in younger animals. However, in animals primed with OB a second dose of OB 2 days later resulted in a significant rise in serum LH levels even in rats of 22 days of age. Progesterone (1 mg) injected 3 days after the injection of a single dose of OB induced, a few hours later, a significant rise in serum LH concentration. This effect was observed from the 22nd day of age but not in younger animals. The magnitude of the response to progesterone, as revealed by the serum LH levels, sharply decreased at the time of puberty. It is concluded that the mechanisms responsible for the tonic release of LH are ready to function at the time of birth or shortly thereafter, while those involved in the phasic release mature around 22 days of age.

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