scholarly journals Median Eminence Dopaminergic Activation Is Critical for the Early Long-Day Inhibition of Luteinizing Hormone Secretion in the Ewe**Presented, in preliminary form, at the Congress “Bioclock’s 97: the photic system and time measurement in Vertebrates,” Poitiers, France, July 9–11, 1997.

Endocrinology ◽  
1998 ◽  
Vol 139 (12) ◽  
pp. 5094-5102 ◽  
Author(s):  
Fabrice Bertrand ◽  
Catherine Viguié ◽  
Sophie Picard ◽  
Benoît Malpaux

Abstract In ewes, photoperiod modulates LH release. The median eminence (ME) dopaminergic activity seems to be implicated in the inhibition of LH secretion by photoperiod. This study investigated the functional importance of ME dopaminergic activity for LH secretion inhibition in three inhibitory photoperiodic treatments: after 33 long days (LD) (LD1 treatment), after 72 LD (LD2 treatment), and after 34 short days. Using reverse microdialysis on three groups of seven ewes, a solution of α-methyl-paratyrosine [αMPT, an inhibitor of tyrosine hydroxylase (TH); 10 mm in Ringer’s lactate] was infused into the ME for 5 h, preceded by a 5-h control period during which only vehicle was infused, in each of the three photoperiodic treatments. αMPT dramatically decreased the 3,4-dihydroxyphenylacetic acid concentration, similarly in all three photoperiodic treatments, suggesting a similar inhibition of TH activity. In the LD1 treatment, αMPT significantly increased LH pulse frequency (+1.22 ± 0.46 pulse/5 h from control period, mean± sem, n = 9; P < 0.05) and mean concentration (+51 ± 28%; P < 0.001). In the other two photoperiodic treatments, αMPT had no significant effect on LH release. Thus, blockade of dopamine synthesis in the ME seems to stimulate LH secretion in early, but not long-term, inhibition by LD nor after the transition to short days. Therefore, dopaminergic activity of the ME seems to be critical for LH secretion inhibition in some photoperiodic inhibitory treatments but not in others.

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.


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.


1999 ◽  
Vol 163 (2) ◽  
pp. 243-254 ◽  
Author(s):  
F Bertrand ◽  
J Thiery ◽  
S Picard ◽  
B Malpaux

In ewes, photoperiod modulates LH release and dopaminergic terminals in the median eminence (ME) have a critical role in the establishment of long-day inhibition of LH secretion. This study was undertaken to determine the type of dopaminergic receptors, D1-like or D2-like, that mediate the action of dopamine on LH secretion at the ME level in this situation. This was assessed, in ovariectomized and estradiol-treated ewes, with the use of reverse microdialysis in the ME in three experiments: first, when LH secretion was stimulated by short days, by determining the response to three doses (0.01, 0.1 or 1 mg/ml) of a D1-like (SKF38393) and a D2-like (quinpirole) agonist; secondly, during early long-day inhibition of LH secretion, by determining the ability of SKF38393 and quinpirole (1 mg/ml) to mimic the inhibitory effects of dopamine, after a blockade of its synthesis with alpha-methyl-para-tyrosine (alphaMPT; 2 mg/ml); and thirdly, during early long-day inhibition of LH secretion, by determining the response to three doses (0.009, 0.09 or 0.9 mg/ml) of a D1-like (SCH23390) and a D2-like (sulpiride) antagonist. In none of the conditions was effect of the D1-like analogs on LH secretion found, compared with the control treatments. In contrast, the D2-like analogs caused changes in LH secretion. First, with short days, quinpirole in the highest dose significantly reduced mean LH concentration (P<0.05) and LH pulse frequency (P<0.01). Secondly, with long days, addition of quinpirole to alphaMPT caused a significant decrease in LH secretion relative to alphaMPT alone (P<0.05). Thirdly, with long days, sulpiride at the highest dose significantly increased mean LH concentration (during the first 3 h of treatment, P<0.05) and LH pulse frequency (P<0.05). Prolactin secretion was also determined in these experiments, and D2-like agonist and antagonist caused an inhibition and a stimulation of prolactin secretion, respectively. These results demonstrate that, in the ME, inhibitory action of dopamine on LH secretion, critical for the initiation of long-day-induced inhibition, is mediated by D2-like, not D1-like, dopaminergic receptors.


1977 ◽  
Vol 73 (3) ◽  
pp. 685-695 ◽  
Author(s):  
C R Hopkins

With the use of poly-L-lysine, a method has been developed which induces acutely dissociated rat anterior pituitary cells to attach to glass and polyacrylamide surfaces. In these attached cells the recovery of the secretory response, which is impaired in acutely dissociated cells, has been followed, and it has been established that, in terms of their ability to secrete luteinizing hormone (LH) in response to the specific secretogogue luteinizing-hormone-releasing hormone (LHRH), the cells become maximally responsive after 48 h. The attached cells also allow the short-term kinetics of LH secretion to be followed with great facility; and, when cells allowed to recover for 48 h are used, it is shown that in response to LHRH the pattern of LH release is biphasic.


1988 ◽  
Vol 66 (1) ◽  
pp. 38-42 ◽  
Author(s):  
E. V. YoungLai ◽  
M. Wilkinson ◽  
N. Thompson ◽  
A. Byrne

To examine the role of opioid neurons on luteinizing hormone (LH) secretion in the female rabbit, we determined LH release at timed intervals after naloxone administration to rabbits aged 25–150 days. The LH response to naloxone (10 mg/kg) was not significantly elevated until day 43 when LH rose 76–113% above basal levels at 40–80 min. In 56-day-old females the corresponding increase was 160% at 15 min and in 65- to 67-day-olds it was 154%. From 70 to 80 days of age the LH response was blunted and no significant elevations could be elicited. By contrast, naloxone-induced LH increases were again evident when rabbits were older than 100 days. At all ages no significant change in FSH concentrations was observed. In the adult females, naloxone at 2.5, 5, and 10 mg/kg caused increases in LH secretion which occasionally were high enough to induce ovulation as exemplified by elevated serum progesterone 4 days later. These data suggest that opioid peptides may be involved in the prepubertal rise in LH and in the normal inhibition of adult secretion in the female rabbit.


1986 ◽  
Vol 250 (1) ◽  
pp. E62-E68 ◽  
Author(s):  
J. L. Turgeon ◽  
D. W. Waring

Whether adenosine 3',5'-cyclic monophosphate (cAMP) acts as a mediator for luteinizing hormone-releasing hormone (LHRH) in either its immediate LH release action or in its self-priming action was investigated. Pituitary pieces from either proestrous or estrous rats were superfused in vitro in the presence of dibutyryl cAMP [(Bu)2cAMP], 8-bromo-cAMP (8BrcAMP), forskolin, or control for 2-3 h. For proestrous but not estrous pituitary pieces, a slight increase in base-line LH secretion rate occurred at approximately 70 min of exposure to elevated cAMP; in the same system LHRH caused an increase in LH secretory rate within 2 min in either proestrous or estrous tissue. In contrast to its ineffectiveness as a secretagogue, cAMP elevation resulted in a severalfold augmentation of both LHRH- and elevated K+-induced LH secretion from proestrous but not estrous pituitary pieces; for these experiments, superfusion with a cAMP analogue or forskolin for varying times preceded a 10-min pulse of either 8 nM LHRH or 47 mM K+. Augmentation was evident after 30 min of cAMP elevation; longer exposures were coincident with greater potentiation. Cycloheximide prevented (Bu)2cAMP augmentation of LHRH-induced secretion. These data show that cAMP does not mediate the immediate LH release action of LHRH, but cAMP does augment LHRH- or K+-induced LH secretion with characteristics in common with the self-priming action of LHRH.


Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4939-4945 ◽  
Author(s):  
F. J. Steyn ◽  
Y. Wan ◽  
J. Clarkson ◽  
J. D. Veldhuis ◽  
A. E. Herbison ◽  
...  

Current methodology to monitor pulsatile LH release in mice is limited by inadequate assay sensitivity, resulting in the need for collection of large blood volumes. Thus, assessment of pulsatile LH secretion in mice remains highly challenging, and observations are limited to adult mice. To address this, we developed a highly sensitive ELISA for assessment of mouse LH concentrations in small fractions of whole blood. We demonstrate that this assay is capable of reliably detecting LH down to a theoretical limit of 0.117 ng/mL in a 2-μL fraction of whole blood. Using an established frequent blood collection procedure, we validated the accuracy of this method by determining the pulsatile LH secretion in early-adult (10 weeks old) C57BL6/J male mice. Data demonstrate regular pulsatile release of LH, with peaks in LH secretion rarely exceeding 3 ng/mL. Moreover, assessment of LH release in Gpr54 knockout mice demonstrates the lack of pulsatile LH release after the loss of kisspeptin-mediated pubertal maturation. We next determined age-associated changes in pulsatile LH secretion by assessment of LH secretion in prepubertal (28 days old) C57BL6/J male mice and repeated assessment in the same mice in adulthood (120 days old). Data demonstrate that the rise in total LH secretion in mice after pubertal maturation occurs along with an overall rise in the pulsatile LH secretion rate. This was coupled with a significant increase in the number of LH secretory events (number of pulses). In addition, we observed a decrease in the clearance (increased half-life) and a decrease in the regularity (approximate entropy) of LH release. This method will be of wide general utility within the field of reproductive biology.


1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.


1996 ◽  
Vol 135 (3) ◽  
pp. 293-298 ◽  
Author(s):  
Joaquin Lado-Abeal ◽  
Jose L Liz ◽  
Carlos Rey ◽  
Manuel Febrero ◽  
Jose Cabezas-Cerrato

Lado-Abeal J, Liz JL, Rey C, Febrero M, Cabezas-Cerrato J. Effects of valproate-induced alteration of the GABAergic system on pulsatile luteinizing hormone secretion in ovariectomized women. Eur J Endocrinol 1996;135:293–8. ISSN 0804–4643 It is well established that valproate increases hypothalamic concentrations of γ-aminobutyric acid (GABA). Although little research has been done on the role of GABA in the control of pulsatile luteinizing hormone (LH) secretion in humans, our group recently found that administration of valproate had no significant effect on pulsatile LH secretion in late follicular and mid-late luteal phase normal women. However, the results of several studies of rats suggest that GABAergic regulation of LH secretion may depend on steroid levels. The objective of this work was to determine whether regular administration of sodium valproate inhibits pulsatile LH secretion in ovariectomized women. Twelve women who had undergone ovariectomy for causes other than malignant tumors were each studied in two 8 h sessions, in each of which blood samples were taken every 5 min. The first session was the control; for the second, 400 mg of sodium valproate was administered every 8 h during the seven preceding days and at 08.00 h and 14.00 h on the day of the study session. Serum valproate was determined by repolarization fluorescence spectrophotometry, and LH, estradiol and progesterone by radioimmunoassay. The serum LH series were subjected to a deconvolution procedure to reconstruct the pattern of pituitary LH secretion. Luteinizing hormone pulses were identified by the authors' nonparametric method. Control and post-valproate results were compared with regard to number of pulses, pulse duration, the quantity of LH secreted in each pulse, interpulse interval and mean serum LH level. There was no statistically significant difference between control and post-valproate results for any of the variables considered. It is concluded that sustained serum valproate levels do not alter pulsatile secretion of LH in ovariectomized women. This implies that, in humans, GABA is probably not a decisive factor in the regulation of the GnRH pulse generator. J Cabezas-Cerrato, Endocrinology and Nutrition Service, General Hospital of Galicia, c/Galeras s/n 15705, Santiago de Compostela, La Coruña, Spain


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.


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