Orchidectomy and NMDA increase GnRH secretion as measured by push-pull perfusion of rat anterior pituitary

1995 ◽  
Vol 268 (4) ◽  
pp. E685-E692 ◽  
Author(s):  
D. R. Grattan ◽  
S. K. Park ◽  
M. Selmanoff
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Anterior Pituitary ◽  
Extracellular Fluid ◽  
Gonadotropin Releasing Hormone ◽  
Male Rat ◽  
Acute Administration ◽  
Before And After ◽  
Gnrh Release ◽  
Lh Release

Using push-pull perfusion to measure concentrations of gonadotropin-releasing hormone (GnRH) in the extracellular fluid of the anterior pituitary gland of the male rat, we have measured GnRH release at specific times before and after castration and in response to acute administration of N-methyl-D-aspartate (NMDA). After castration (7 days), mean GnRH levels were substantially increased (4.3-fold) compared with intact controls (0.94 +/- 0.16 vs. 0.22 +/- 0.08 pg/10 min, respectively, P < 0.05) due to an increase in both the frequency and amplitude of GnRH pulses. Testosterone partially reduced GnRH release (0.62 +/- 0.10 pg/10 min). NMDA induced a rapid increase in plasma luteinizing hormone (LH) in both intact and castrated rats and increased GnRH concentrations in the perfusion samples (P < 0.05). There was no change in LH release induced by two doses of injected GnRH (5 and 25 ng/100 g body wt) 2 days after castration, but by 6 days after castration the response to both doses was significantly increased. These results demonstrate that GnRH release in the male rat is acutely increased by NMDA and is chronically increased after orchidectomy. Increased pituitary sensitivity to GnRH also contributes to the hypersecretion of LH after castration, particularly at longer times after removal of testosterone negative feedback.

scholarly journals Effects of Central Injection of Anti-LPS Antibody and Blockade of TLR4 on GnRH/LH Secretion during Immunological Stress in Anestrous Ewes

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Karolina Haziak ◽  
Andrzej Przemysław Herman ◽  
Dorota Tomaszewska-Zaremba
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Immune Stress ◽  
Immunological Stress ◽  
Lh Release ◽  
Lh Secretion ◽  
Tlr4 Receptor

The present study was designed to examine the effect of intracerebroventricular (icv) administration of antilipopolysaccharide (LPS) antibody and blockade of Toll-like receptor 4 (TLR4) during immune stress induced by intravenous (iv) LPS injection on the gonadotropin-releasing hormone/luteinizing hormone (GnRH/LH) secretion in anestrous ewes. Injection of anti-LPS antibody and TLR4 blockade significantly (P < 0.01) reduced the LPS dependent lowering amount ofGnRHmRNA in the median eminence (ME). Moreover, blockade of TLR4 caused restoration ofLH-βtranscription in the anterior pituitary decreased by the immune stress. However, there was no effect of this treatment on reduced LH release. The results of our study showed that the blockade of TLR4 receptor in the hypothalamus is not sufficient to unblock the release of LH suppressed by the immune/inflammatory challenges. This suggests that during inflammation the LH secretion could be inhibited directly at the pituitary level by peripheral factors such as proinflammatory cytokines and circulating endotoxin as well.

Synthesis and release of luteinizing hormone in vitro: manipulations of Ca2+ environment

1985 ◽  
Vol 249 (2) ◽  
pp. E165-E174
Author(s):  
T. C. Liu ◽  
G. L. Jackson
Keyword(s):  
Luteinizing Hormone ◽  
Total Protein ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Total Cell ◽  
Ionophore A23187 ◽  
Pituitary Cells ◽  
Free Medium ◽  
Lh Release

We determined if luteinizing hormone (LH) synthesis is Ca2+ dependent and coupled to LH release. We monitored LH synthesis when LH release was stimulated either by specific [gonadotropin-releasing hormone (GnRH)] or nonspecific stimuli (50 mM K+ and 2 or 20 microM Ca2+ ionophore A23187) and inhibited by Ca2+-reduced medium. LH synthesis was estimated by measuring incorporation of [3H]glucosamine (glycosylation) and [14C]alanine (translation) into total (cell and medium) immunoprecipitable LH by cultured rat anterior pituitary cells. Both GnRH (1 nM) and 50 mM K+ significantly stimulated LH release and glycosylation, but had no effect on LH translation. A23187 also stimulated LH release, but significantly depressed glycosylation of LH and total protein and [14C]alanine uptake. Deletion of Ca2+ from the medium depressed both GnRH-induced LH release and glycosylation. Addition of 0.1 mM EGTA to Ca2+-free medium not only inhibited GnRH-induced release and glycosylation of LH but also uptake of precursors and glycosylation and translation of total protein. Thus glycosylation and release of LH are Ca2+ dependent. Whether parallel changes in LH release and glycosylation reflect a cause and effect relationship remains to be determined.

EFFECT OF HYPOTHALAMIC DEAFFERENTATION ON THE CONTROL OF LUTEINIZING HORMONE SECRETION

1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Positive Feedback ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Luteinizing Hormone Secretion ◽  
Ovarian Steroids ◽  
Medial Hypothalamus ◽  
Lh Release ◽  
Positive Feedback Effect

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.

Melatonin inhibition of GnRH-induced LH release from neonatal rat gonadotroph: involvement of Ca2+ not cAMP

1995 ◽  
Vol 269 (1) ◽  
pp. E85-E90 ◽  
Author(s):  
J. Vanecek ◽  
D. C. Klein
Keyword(s):  
Luteinizing Hormone ◽  
Second Messenger ◽  
Gonadotropin Releasing Hormone ◽  
Neonatal Rat ◽  
Dibutyryl Camp ◽  
Releasing Hormone ◽  
Cyclic Monophosphate ◽  
Lh Release

Melatonin inhibits gonadotropin-releasing hormone-induced release of luteinizing hormone (LH) from the neonatal rat gonadotrophs. The second messenger involved is not known, although there are several candidates, including adenosine 3',5'-cyclic monophosphate (cAMP) and intracellular free Ca2+. The present study addresses the question of which second messenger mediates melatonin inhibition of LH release. We found that the effect of melatonin was not prevented by cAMP protagonists, including 8-bromo-cAMP, dibutyryl cAMP, 3-isobutyl-1-methylxanthine, and forskolin. However, treatments that enhanced Ca2+ influx masked the effects of melatonin, and treatments that blocked Ca2+ influx mimicked the effects of melatonin. Moreover, melatonin decreased K(+)-induced LH release, which is dependent on Ca2+ influx but did not block release of LH due to thapsigargin-induced mobilization of Ca2+ from intracellular stores. These findings indicate that melatonin inhibits gonadotropin-releasing hormone-induced LH release, primarily through an action involving inhibition of Ca2+ influx, and that cAMP does not seem to be involved in this effect of melatonin.

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

Differential effects of forskolin on LH and GH release

1985 ◽  
Vol 249 (4) ◽  
pp. E392-E397
Author(s):  
W. S. Evans ◽  
T. H. Brannagan ◽  
E. R. Limber ◽  
M. J. Cronin ◽  
A. D. Rogol ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Female Rats ◽  
Second Phase ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Lh Release ◽  
Biphasic Release

The effects of forskolin, an agent which increases intracellular levels of cAMP, on basal luteinizing hormone (LH) and growth hormone (GH) release and on gonadotropin-releasing hormone (GnRH)-stimulated LH release were documented. Continuously perifused dispersed anterior pituitary cells from female rats at random stages of the estrous cycle were used. Secretory rates of both LH and GH increased in a concentration-dependent manner in response to a 1-h challenge with 0.03, 0.1, 0.3, 1, or 3 microM forskolin. In response to 0.3 microM forskolin, maximum GH release was achieved within 15-20 min, after which secretion decreased. In contrast, LH release increased gradually, became maximal at 1.5-2 h, and remained constant until the forskolin was withdrawn. Cells exposed to 10 nM GnRH for 4 h exhibited a biphasic release of LH with the interphase nadir occurring at 30 min. The second phase of LH release was enhanced by simultaneous addition of forskolin with the GnRH. Whereas second phase release did not increase further, exposure of the cells to forskolin for 60 or 120 min before GnRH resulted in increased first-phase LH release. We suggest that, whereas our data are consistent with a role for cAMP in mediating the acute release of GH, cAMP may be involved in the process through which nonimmediately releasable LH becomes available for release.

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