GABA-ergic and dopaminergic mechanisms in gonadotrophin secretion in males – effects of baclofen and metoclopramide

1983 ◽  
Vol 103 (4) ◽  
pp. 451-456 ◽  
Author(s):  
Alan N. Elias ◽  
Agnes V. Szekeres ◽  
Sergio Stone ◽  
Lubomir J. Valenta ◽  
Tarek Haw ◽  
...  
Keyword(s):  
Normal Male ◽  
Dopamine Antagonist ◽  
Control Phase ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Dopaminergic Mechanisms ◽  
Lh Release ◽  
Normal Men ◽  
Opposing Effects ◽  
Lh Secretion

Abstract. The GABA analogue, baclofen, and the dopamine antagonist, metoclopramide, were studied with respect to their effects on basal and LRH-induced LH and FSH release in 6 normal male volunteers. Basal gonadotrophin secretion was unchanged following the administration of baclofen or metoclopramide given alone or in combination. LRH-stimulated LH release was significantly blunted after metoclopramide administration in the baclofen pre-treated volunteers. Serum LH concentration (mean ± sd) in the control phase was 30.1 ± 17.2 mIU/ml and was 19.4 ± 9.6 mIU/ml after baclofen plus metoclopramide (P < 0.02). LRH-stimulated values, however, were unaffected by baclofen or metoclopramide when the drugs were given alone. LRH-stimulated FSH release was not significantly influenced by baclofen or metoclopramide given alone or in combination. Basal Prl secretion increased significantly when baclofen and metoclopramide were given separately and in combination. Basal Prl concentration (mean ± sd) increased from 14 ± 2 ng/ml to 18.7 ± 4.8 ng/ml after baclofen and to 111.5 ± 31.9 ng/ml after metoclopramide (P<0.01). The rise in serum Prl concentration, however, was not significantly different when measured after metoclopramide alone (111 ± 31.9 ng/ml) or after metoclopramide and baclofen (112 ± 33.3 ng/ml). It is proposed that GABA and dopamine exert opposing effects on LH secretion in normal men.

scholarly journals Beta-endorphin/beta-lipotropin release and gonadotropin secretion after acute exercise in normal males

1986 ◽  
Vol 61 (6) ◽  
pp. 2045-2049 ◽  
Author(s):  
A. N. Elias ◽  
K. Iyer ◽  
M. R. Pandian ◽  
P. Weathersbee ◽  
S. Stone ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Acute Exercise ◽  
Suppressive Effect ◽  
Normal Male ◽  
Base Line ◽  
Gonadotropin Secretion ◽  
Beta Endorphin ◽  
Serum Lh ◽  
Normal Males ◽  
Lh Secretion

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response to acute exercise and the relationship of these opioid peptides to basal and luteinizing hormone-releasing hormone (LRH)-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion was studied in eight normal male volunteers. Acute exercise resulted in a rise in plasma beta-LPH levels that returned to base line when measured 60 min after exercise. Plasma beta-EP levels did not demonstrate any rise when measured immediately after 20 min of exercise or at 60 min after exercise. Serum LH concentrations in individual volunteers declined to nadir values 60–180 min after exercise after which they showed a rebound to levels higher than the preexercise values in three of five volunteers in whom nadir LH levels were attained before the final (180 min) measurement. Serum FSH concentrations were unaltered by exercise. Acute exercise similarly did not alter the LH/FSH response to exogenous LRH stimulation. Pretreatment of the volunteers with the narcotic antagonist, naloxone, failed to alter the postexercise or LRH-stimulated LH and FSH release. The data suggest that beta-EP does not exert a suppressive effect on LH secretion after acute exercise in normal human males. Whether the suppression of LH secretion after acute exercise in unconditioned males is due to factor(s) cosecreted with beta-LPH, an increase in brain beta-EP or to alternate mechanisms such as alteration in central dopaminergic or GABAergic tone remains to be established.

The role of oestrogens on gonadotrophin secretion in the testicular feminization syndrome1

1980 ◽  
Vol 95 (3) ◽  
pp. 314-318 ◽  
Author(s):  
Martha Medina ◽  
Alfredo Ulloa-Aguirre ◽  
Maria A. Fernández ◽  
Gregorio Pérez-palacios
Keyword(s):  
Clomiphene Citrate ◽  
Poor Response ◽  
Testicular Feminization ◽  
Normal Response ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Before And After ◽  
Complete Form ◽  
Lh Secretion

Abstract. The role of oestrogens on gonadotrophin secretion was assessed in three related patients with the complete form of testicular feminization syndrome. Serum LH and FSH levels were measured before and after I.RH stimulation as well as before, during and after chronic clomiphene citrate administration. Moderately elevated LH basal levels with a significant LH rise following I.RH were observed. Normal or even low FSH level with poor response to LRH were found in all subjects. Administration of clomiphene citrate resulted in a significant serum LH increase without any change of FSH. Following castration both LH and FSH rose and a normal response to LRH was observed. These results were interpreted as demonstrating that, while endogenous oestrogens modulate LH secretion in patients with androgen unresponsiveness, it plays no role in regulating FSH secretion and suggested that a factor of testicular origin without androgenic or oestrogenic activity is responsible for FSH regulation.

Alterations of the hypothalamic GnRH interpulse interval sequence over the normal menstrual cycle

1988 ◽  
Vol 255 (5) ◽  
pp. E696-E701 ◽  
Author(s):  
N. Santoro ◽  
J. P. Butler ◽  
M. Filicori ◽  
W. F. Crowley
Keyword(s):  
Menstrual Cycle ◽  
Renewal Process ◽  
Gnrh Secretion ◽  
Late Luteal Phase ◽  
Normal Menstrual Cycle ◽  
Lh Release ◽  
Interval Sequence ◽  
Normal Women ◽  
Normal Men ◽  
Lh Secretion

Luteinizing hormone (LH) is released in a pulsatile fashion from the anterior pituitary in response to hypothalamic gonadotropin-releasing hormone (GnRH) secretion. Previous autocorrelation analysis of the sequence of interpulse intervals of LH secretion in normal men has supported the hypothesis that the underlying hypothalamic mechanism of GnRH secretion governing episodic LH release is a renewal process, indicating that hypothalamic "memory," if present, does not extend back further in time than the preceding secretory pulse. A similar analysis of pulsatile LH secretion was undertaken in 45 studies of normal women, obtained throughout the menstrual cycle. Analysis of these studies revealed a process consistent with renewal throughout the follicular and early luteal phases. However, this relationship appears to break down in the mid-to-late luteal phase, indicating that alternative feedback pathways provide an overriding influence on the underlying renewal process of hypothalamic GnRH secretion. Pulsatile progesterone secretion by the corpus luteum, which first emerges at this stage of the menstrual cycle, may be the agent responsible for this feedback.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

ACUTE EFFECTS OF HYPOTHALAMIC LESIONS UPON GONADOTROPHIN SECRETION IN THE FERRET

1981 ◽  
Vol 89 (3) ◽  
pp. 329-336 ◽  
Author(s):  
B. T. DONOVAN ◽  
M. B. TER HAAR
Keyword(s):  
Platinum Electrodes ◽  
Acute Effects ◽  
Hypothalamic Lesions ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
High Concentrations ◽  
Lh Secretion ◽  
Steel Electrodes

The changes in FSH and LH secretion after placement of lesions in the hypothalamus were traced in ferrets serially bled at 15 min intervals. Passage of the lesioning current through platinum electrodes in anoestrous females was associated with an immediate surge in LH and FSH output. Damage to the hypothalamus of oestrous females also caused an immediate surge of LH secretion, but then a long-lasting second rise in blood LH content set in. High concentrations of LH were never sustained overnight. The response of long-term spayed females to the placement of hypothalamic lesions was similar to that of anoestrous ferrets, while that of anoestrous or oestrous ferrets was not altered by acute removal of the ovaries. Manipulation of the ovaries appeared to facilitate FSH and LH secretion. The response of males was similar to that of anoestrous females. Marked increases in FSH and LH release were also seen in females when lesions were made with steel electrodes, but had subsided on the following day.

EFFECTS OF NALOXONE ON LUTEINIZING HORMONE AND PROLACTIN IN SERUM OF RATS

1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Immature Female ◽  
Subcutaneous Injections ◽  
Serum Lh ◽  
Opiate Peptides ◽  
Lh Release ◽  
Lh Secretion

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.

Suppressive effect of prolactin on oestrogen-induced secretion of LH by sequentially perifused rat hypothalamus-pituitary

1985 ◽  
Vol 108 (2) ◽  
pp. 151-155 ◽  
Author(s):  
Jin-Woo Lee ◽  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Shirou Otsuka ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Experimental Period ◽  
Suppressive Effect ◽  
Control Group ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Hypothalamic Level ◽  
Experimental Group ◽  
Perifusion System

Abstract. The effect of prolactin (Prl) on oestrogeninduced gonadotrophin secretion was examined in vitro in a sequential double chamber perifusion system. As control groups, mediobasal hypothalamus (MBH)-pituitary pairs or pituitaries without the MBHs were perifused with Medium 199. As an experimental group, MBH-pituitary pairs were perifused with Medium 199 containing 1 μg/ml of rat Prl. These groups were stimulated with 10−7m oestradiol-17β (E2) for 30 min, and luteinizing hormone (LH) in the serial fractions of effluent was measured. In the control group of MBH-pituitary pairs perifused with medium without Prl, secretion of LH began to rise within 30 min after the beginning of stimulation, reached a peak 30 min after the end of stimulation and then remained at a plateau for the rest of the experimental period, whereas in the control group of pituitaries alone no significant response was observed. In the experimental group perifused with medium containing Prl, LH-secretion showed peaks 20 and 80 min after the end of E2-stimulation, respectively, and the first peak was significantly (P < 0.01) less than the level in the control group. These data demonstrate that Prl at this concentration suppressed the rapid LH release induced by E2. Its site of action is suggested to be at the hypothalamic level, and its possible mechanism of action is discussed.

The synthesis and release of gonadotropins in response to gonadotropin-releasing hormone of the rat anterior pituitary gland during weight reduction

1990 ◽  
Vol 122 (5) ◽  
pp. 628-632 ◽  
Author(s):  
Fumikazu Kotsuji ◽  
Takeshi Aso ◽  
Naoyuki Kamitani ◽  
Toshiro Tominaga
Keyword(s):  
Weight Loss ◽  
Pituitary Gland ◽  
Weight Reduction ◽  
Female Rats ◽  
Serum Lh ◽  
Female Wistar Rats ◽  
Progressive Weight Loss ◽  
Lh Release ◽  
Lh Secretion

Abstract. It is well recognized that weight reduction produces the suppression of serum LH but not FSH level in rodents. In order to clarify the mechanism by which the discrepancy between LH and FSH levels is brought about, the influence of weight loss on the pituitary function was explored using female rats. The changes of the pituitary response to GnRH and the basal secretion of gonadotropins with progressive weight loss were investigated by in vitro short-term incubation of the pituitary gland after prolonged weight loss in female Wistar rats. On the first day of diestrous and until day 14 of the diet, GnRH induced LH and FSH release from the pituitary and a decrease in pituitary content of them, but the total amount of gonadotropin in culture medium and pituitary tissue was not affected. On day 30 of the diet, the decrease in pituitary content disappeared. On day 60 LH release disappeared, whereas pituitary FSH and the total amount of gonadotropins were increased by GnRH. Non-stimulated FSH but not LH secretion per mg of pituitary was augmented during dieting. The data indicate that pituitary responsiveness to GnRH and non-stimulated FSH release were modified by weight loss: the LH-releasing action of GmRH was diminished, the gonadotropin-synthesizing action of GnRH was augmented, and non-stimulated FSH release was increased.

ABSENCE OF POSITIVE FEEDBACK EFFECT OF OESTROGEN ON LH RELEASE IN PATIENTS WITH TESTICULAR FEMINIZATION SYNDROME

1978 ◽  
Vol 87 (2) ◽  
pp. 259-267 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takayuki Kinugasa ◽  
Keiichi Kurachi ◽  
Keishi Matsumoto
Keyword(s):  
Sex Differentiation ◽  
Serum Testosterone ◽  
Normal Male ◽  
Testicular Feminization ◽  
Serum Lh ◽  
Exogenous Oestrogen ◽  
Lh Release ◽  
Normal Males ◽  
Lh Rh

ABSTRACT The response of serum LH to exogenous oestrogen administration was studied in 5 patients with testicular feminization syndrome (TFS). The serum LH levels were elevated in all the patients, while serum testosterone levels were within the normal male range. Serum FSH levels were elevated in 4 patients and normal in one patient. Intravenous administration of 100 μg of LH-RH provoked a further increase in both LH and FSH. Following intravenous injection of 20 mg of conjugated oestrogen (Premarin®), the LH levels were serially determined until 120 h in TFS patients, 5 normal males, and 10 normal females during the mid-follocular phase (D7-9). Both TFS patients and normal males showed no LH release following oestrogen injection in contrast to normal females who displayed a significant increase in LH with a peak at 48 to 56 h after the injection. These results seem to suggest that the insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. The possible role of oestradiol conversion from testosterone in the hypothalamus is discussed.

A comparison of the effects of gonadal steroids on naloxone-induced LH secretion in gonadectomized rats

1986 ◽  
Vol 110 (2) ◽  
pp. 327-334 ◽  
Author(s):  
G. M. Spencer ◽  
S. A. Whitehead
Keyword(s):  
Inhibitory Effect ◽  
Gonadal Steroids ◽  
Ovariectomized Rats ◽  
Endogenous Opioid ◽  
Feedback Effects ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Endogenous Opioid Systems ◽  
Hypothalamic Pituitary Axis ◽  
Lh Secretion

ABSTRACT The effects of the opiate antagonist naloxone on serum LH concentrations was investigated in gonadectomized rats given different regimes of steroid pretreatment. Two injections of testosterone given 48 and 24 h before naloxone treatment failed to reinstate LH responses to this drug in castrated rats while subcutaneous testosterone-filled silicone elastomer capsules implanted for a week were effective in this respect. Injections of oestrogen, oestrogen plus progesterone or progesterone alone all restored LH responses to naloxone in ovariectomized rats when given 48 and/or 24 h before drug treatment, although the magnitude of these responses varied according to the precise steroid treatments. The hypothalamic-pituitary axis was also responsive to naloxone just before the progesterone-induced LH surge in oestrogen-primed ovariectomized rats. Results show that gonadal steroids are permissive to the effects of opiate drugs, but they suggest that endogenous opioid systems do not necessarily mediate the negative feedback effects of steroids. Some other factor(s), as yet unidentified in the rat, may control the opioid modulation of gonadotrophin secretion or exert an independent inhibitory effect on gonadotrophin release. J. Endocr. (1986) 110, 327–334

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