Evidence of a photoinducible phase for the release of luteinizing hormone in the domestic hen

1982 ◽  
Vol 94 (3) ◽  
pp. 397-406 ◽  
Author(s):  
Susan C. Wilson

Hens raised on a schedule of 8 h light: 16 h darkness (8L : 16D) were exposed to changes in photoperiod at 17 or 18 weeks of age. These involved exposure to either an abrupt increase in photoperiod to 16 h per day or to skeleton photoperiods comprising a main period of 7·75 or 4 h light together with a pulse of 15 min or 4 h light provided at different times during the period of darkness. An increase in photoperiod to 16 h per day stimulated a two- to threefold increase in the plasma concentration of LH within 1–3 days. Interruption of a 7·75L : 16D schedule by 15 min light between 13·75 and 19·75 h after the beginning of the main photoperiod stimulated LH secretion in the immature and adult hen and a higher rate of lay than that of the 8L : 16D control group. There was a significant (P < 0·01) correlation between the concentration of LH in the plasma and the rate of lay. The photostimulated rise in the plasma concentration of LH in the immature hen was not associated with any increase in the responsiveness of the pituitary gland to LH releasing hormone. Of the treatments in which a 15-min pulse of light was provided, the schedules of 7·75L : 10D : 0·25L : 6D and 7·75L : 12D : 0·25L : 4D, which were most effective in stimulating LH release, appeared to be interpreted as 0·25L : 6D : 7·75L : 10D and 0·25L : 4D : 7·75L : 12D respectively. In hens given a 7·75-h main photoperiod, in which phase-reversal did not occur, 15 min light was most stimulatory when given 14–16 h after the begining of the main photoperiod, although not to the same extent as an increase in photoperiod to 16 h per day. In hens for which an 8-h complete photoperiod was changed to a 4-h main photoperiod, together with a further 4-h pulse of light provided at different times during the period of darkness, the period of maximum sensitivity to light occurred 11 h after the onset of the main photoperiod and at this time light stimulated LH release to the same extent as an increase in complete photoperiod from 8 to 16 h per day. Results of this study suggest that the period of maximum photosensitivity shifts its phase after a change in the form of photoperiod and is primarily entrained to dusk.

1982 ◽  
Vol 93 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Susan C. Wilson ◽  
T. R. Morris

Concentrations of LH and progesterone were measured in the plasma of ducks which were, from 3 weeks of age, raised on either a constant photoperiod of 16 h light: 8 h darkness or a lighting schedule which simulated natural changes in daylength. In ducks raised on a constant photoperiod of 16 h light: 8 h darkness the plasma concentration of LH increased steeply between 7 and 3·5 weeks before the onset of lay. Concentrations of LH then declined, gradually at first, but then rapidly during the 7 days before the first oviposition in association with a pronounced increase in the plasma concentration of progesterone. During the 18 days before the first egg was laid there was a significant (P < 0·01) negative correlation between the plasma concentrations of LH and progesterone. The patterns of LH release during sexual development of ducks raised on a schedule which simulated natural changes in daylength were variable but could be categorized according to the daylength at which each duck came into lay. In ducks coming into lay soon after the winter solstice when daylength was short (8·0–8·5 h light/day) there was a pronounced 15-fold prepubertal increase in the plasma concentration of LH although in some ducks high LH levels were not maintained until 3–4 weeks before the first oviposition and were not always followed by a rise in the plasma concentration of progesterone. In contrast, in ducks coming into lay when daylength had increased to 11·0–11·5 h light/day there were only minor fluctuations in the plasma concentration of LH until a small two- to threefold increase in LH was observed during the 2 weeks before the first oviposition.


1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.


1983 ◽  
Vol 98 (1) ◽  
pp. 137-145 ◽  
Author(s):  
S. C. Wilson ◽  
R. C. Jennings ◽  
F. J. Cunningham

The characteristics of the diurnal rhythm in the concentration of LH in plasma of the domestic hen varied according to age and duration of photoperiod. A pronounced increase in LH was observed at the onset of darkness in immature hens whether maintained on schedules of 16 h light:8 h darkness (16L:8D) or 8L:16D. During weeks 4·5–15 or −17·5 raised concentrations of LH were maintained until 6 and 12 h after the onset of darkness in hens held on 16L:8D and 8L:16D respectively. By 19 weeks of age the diurnal rhythm of LH secretion had changed to resemble more closely that observed in the laying hen. An increase in the concentration of LH in plasma at the onset of darkness was of comparatively short duration and gave way, within 2–3 h, to a steep decline before a further slight increase in LH, which tended to occur at 11–14 h after the onset of darkness. Superimposed on this diurnal rhythm of LH secretion in the laying hen were a one- to threefold increase in the concentration of LH during 8–4 h before ovulation and a much less pronounced increase in LH during 0–8 h after ovulation. The pattern of changes in the concentration of LH in plasma during the ovulatory cycle was not modified by the repeated withdrawal of blood at intervals of 2 h.


1983 ◽  
Vol 102 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. D. Schanbacher ◽  
J. E. Kinder

Abstract. The acute castrate ram (wether) was used as an experimental model to investigate the site(s) of feedback on luteinizing hormone (LH) by testosterone, dihydrotestosterone and oestradiol. At the time of castration, wethers were implanted subdermally with Silastic capsules containing either crystalline testosterone (three 30 cm capsules), dihydrotestosterone (five 30 cm capsules) or oestradiol (one 6.5 cm capsule). Blood samples were taken at 10 min intervals for 6 h 2 weeks after implantation to determine serum steroid concentrations and to characterize the patterns of LH secretion. Pituitary LH response to exogenous LRH (5 ng/kg body weight) were also determined at the same time. The steroid implants produced serum concentrations of the respective hormones which were either one-third (testosterone) or two-to-four times (dihydrotestosterone, oestradiol) the levels measured in rams at the time of castration. Non-implanted wethers showed rhythmic pulses of LH (pulse interval 40–60 min) and had elevated LH levels (16.1 ± 1.6 ng/ml; mean ± se) 2 weeks after castration. All three steroids suppressed pulsatile LH release and reduced mean LH levels (to below 3 ng/ml) and pituitary LH responses to LRH. Inhibition of pulsatile LH secretion by all three steroids indicated that testosterone as well as its androgenic and oestrogenic metabolites can inhibit the LRH pulse generator in the hypothalamus. Additional feedback on the pituitary was indicated by the dampened LH responses to exogenous LRH.


1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.


2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa

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.


1987 ◽  
Vol 253 (3) ◽  
pp. E233-E237
Author(s):  
R. S. Chuknyiska ◽  
M. R. Blackman ◽  
G. S. Roth

We measured in vitro release of luteinizing hormone (LH) in the presence of 1.5 mM extracellular calcium, with and without LH-releasing hormone (LHRH; 10(-10) to 10(-7) M) or the ionophore A23187 (10(-7) to 10(-4) M), in primary cultures of anterior pituitary cells from intact mature (6 mo) and old (24 mo) male and intact and ovariectomized mature and old female Wistar rats. Base-line as well as LHRH- and A23187-mediated LH secretion was decreased from cells of old rats. However, exposure to A23187 led to a nearly twofold greater augmentation of LH release from cells of old rats, thus decreasing the apparent age-related LH secretory deficit by approximately one-half. We then measured LHRH-mediated (10(-8) M) vs. A23187-mediated (10(-4) M) LH release with and without extracellular calcium (0.08-1.5 mM). For cells from both mature and old rats, there was a similar calcium dependency for A23187- and LHRH-mediated LH release, with optimal LH secretion at 1.0-1.5 mM extracellular calcium concentrations. Again, both LHRH- and A23187-stimulated LH release was significantly lower and exposure to A23187 led to a greater increase in LH release from cells of old rats. Taken together with similar findings in other systems, these data suggest that the in vitro LH secretory defect of pituitary cells from old rats results in part from one or more defects in calcium mobilization and that such alterations may be a widespread manifestation of aging.


1995 ◽  
Vol 145 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J J Evans ◽  
S J Hurd ◽  
D R Mason

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


Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4558-4564 ◽  
Author(s):  
Gregory A. Dissen ◽  
Robert K. Dearth ◽  
H. Morgan Scott ◽  
Sergio R. Ojeda ◽  
W. Les Dees

Abstract We determined whether the effect of alcohol (ALC) to suppress LH secretion in immature female monkeys is due to a hypothalamic or pituitary site of action. Beginning at 20 months of age, four monkeys received a single intragastric dose of ALC (2.4 g/kg), and four monkeys received an equal volume of a saline/sucrose solution daily until they were 36 months old. For the hypothalamic response test, two basal samples (3.5 ml) were collected at 15-min intervals via the saphenous vein, and then N-methyl-d-l-aspartic acid (NMA; 20 mg/kg) was given iv and four more blood samples collected. Three weeks later, this protocol was repeated except LH-releasing hormone (LHRH) (5 μg/kg) was used to test pituitary responsiveness. NMA or LHRH was administered 3 h after the ALC. After the pituitary challenge, each monkey was ovariectomized and 6 wk later, implanted with an indwelling subclavian vein catheter. Blood samples were drawn every 10 min for 8 h to assess effects of ALC on post-ovariectomy LH levels and the profile of LH pulsatile secretion. The hypothalamic challenge showed NMA stimulated LH release in control monkeys, an action that was blocked by ALC. The pituitary challenge revealed that LHRH stimulated LH release equally well in control and ALC-treated monkeys. A post-ovariectomy rise in LH was observed in both groups, but levels were 45% lower in ALC-treated monkeys. This reduction was attributed to an ALC-induced suppression of both baseline and amplitude of pulses. Results demonstrate that the ALC-induced suppression of LH in immature female rhesus monkeys is due to an inhibitory action of the drug at the hypothalamic level.


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