scholarly journals Alcohol Alters Luteinizing Hormone Secretion in Immature Female Rhesus Monkeys by a Hypothalamic Action

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.

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.


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.


1981 ◽  
Vol 88 (3) ◽  
pp. 393-400 ◽  
Author(s):  
B. D. SCHANBACHER

An experiment was conducted to determine the importance of episodic LH secretion during pubertal development in beef bulls. Testicular growth, LH secretory patterns and serum testosterone concentrations were monitored in control bulls, and bulls implanted with one or two oestradiol-filled capsules from 26 to 38 weeks of age. Control but not oestradiol-treated bulls showed normal testicular growth and episodic LH secretory patterns. Serum LH and testosterone responses of 38-week-old control and oestradiol-treated bulls to an intravenous challenge of 5 μg LH releasing hormone indicated normal pituitary responsiveness, but steroidogenic responsiveness had not yet developed in oestradiol-treated bulls. Removal of the capsules at 38 weeks of age resulted in a normal episodic release pattern for LH, with concomitant growth of the underdeveloped testes up to 44 weeks of age. Serum concentrations of LH and testosterone were within the range of normal, adult values by 42 weeks of age. These results suggest that oestradiol can interfere with episodic LH secretion and normal pubertal development in beef bulls, and furthermore that episodic LH secretion is commensurate with the establishment of normal development of the bovine testis during puberty.


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.


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.


1983 ◽  
Vol 99 (2) ◽  
pp. 301-310 ◽  
Author(s):  
S. C. Wilson ◽  
P. G. Knight ◽  
F. J. Cunningham

Treatment of intact cockerels with the synthetic antioestrogen tamoxifen caused a significant increase in the plasma concentration of LH. In contrast, passive immunization with an antiserum raised against oestradiol-17β did not lead to an increase in plasma LH. A pronounced depressive effect of injections of 0·1 mg testosterone propionate (TP) or 0·1 mg oestradiol benzoate (OB) on plasma concentrations of LH was prevented by tamoxifen. Furthermore, a pronounced rise in the concentration of LH releasing hormone in the posterior hypothalamus after the injection of cockerels with OB was completely inhibited by tamoxifen. Neither 0·1 nor 0·5 mg androstenedione modified the concentration of LH in plasma. A dose of 0·05 mg TP, which failed to depress the concentration of LH in plasma of intact cockerels, caused a marked fall in plasma LH in castrated cockerels. Tamoxifen itself exhibited weak oestrogen agonist activity in castrated cockerels by causing a reduction in the concentration of LH in plasma. However, tamoxifen prevented any further depressive effect on LH resulting from the injection of TP. These findings suggest that testosterone exerts an inhibitory influence on LH secretion at the central neural level, partially at least, by means of the product of its aromatization, oestradiol-17β.


1977 ◽  
Vol 84 (1) ◽  
pp. 45-50 ◽  
Author(s):  
E. V. YoungLai

ABSTRACT Experiments were performed in the rabbit to determine whether 20α-hydroxy-4-pregnen-3-one (20-OHP) can maintain luteinizing hormone (LH) secretion after injections of LH-releasing hormone (LH-RH). Female rabbits were castrated at least 2 weeks prior to investigation. On the day before LH-RH injection they were cannulated and a dose of oestradiol benzoate (OeB), 100 μg/kg, given intramuscularly. LH-RH, 500 ng/kg, was injected as a bolus via the cannula and 20-OHP, 100 μg/kg and 2.5 mg/kg, injected intramuscularly immediately after. Blood was withdrawn at intervals for up to 5½ h after LH-RH injection. LH secretion dropped to pre-stimulation levels within 3 h after LH-RH alone or in combination with 20-OHP. Administration of LH-RH to oestrogen primed intact females also gave a peak of LH which returned to pre-stimulation levels within 3 h. However, mating seemed to maintain LH levels for a greater period of time.


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