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At least 271 records · Page 15Linked to original sources
PubMed1984

Developmental changes in luteinizing hormone secretion in the female guinea pig. I. Effects of ovariectomy, estrogen, and luteinizing hormone-releasing hormone.

Negative feedback regulation of LH release was studied by ovariectomy and estrogen treatment in female guinea pigs of four different ages (days 10, 30, 50, and 150). The average age at first ovulation in guinea pigs in our colony was 60.1 +/- 2.2 days (n = 33). Bilateral ovariectomy (OVX) on day 30, 50, or 150 of age resulted in a sharp increase in serum LH concentrations within 3 days, and this rise continued for 9 days, when LH values reached a plateau. In contrast, when OVX was performed on day 10 of age, only a slight elevation in LH levels was observed during the first 16 days after surgery. Twenty days after OVX (day 30 of age), LH concentrations started to increase rapidly and reached the maximum value on day 38 of age; this latter response was similar to that observed immediately after OVX in animals in the three older age groups. Serum LH concentrations after LHRH administration (2 micrograms/kg BW) were similar in ovariectomized females on days 23 and 43 of age, suggesting that the postcastration increase in LH secretion after day 26 of age was not due to a change in pituitary sensitivity. Daily injections of estradiol benzoate at doses of 0.5 and 2.0 micrograms/kg BW from 15-20 days after OVX suppressed LH levels in all four age groups. The present findings indicate that an increase in the capacity for LH release occurs around day 30 in the female guinea pig. Since this increased LH release is not due to an apparent change in pituitary sensitivity to LHRH, the endogenous release of LHRH may be inhibited before day 30 of age. These results suggest that an alteration in the regulation of LH release by the brain may occur before the onset of puberty in female guinea pigs.

Aging↗
PubMed1990

Interleukin-1 inhibits the ovarian steroid-induced luteinizing hormone surge and release of hypothalamic luteinizing hormone-releasing hormone in rats.

Interleukin-1 (IL-1), a polypeptide cytokine secreted by activated macrophages, has been postulated as a chemical messenger between the immune and endocrine systems. IL-1-immunopositive neurons and fibers have been visualized in the human and rat hypothalamus, and IL-1 receptors are present in the rat brain. We have examined the effects of human recombinant IL-1 (alpha- and beta-subtypes) on LH release in vivo and hypothalamic LHRH release in vitro. Ovariectomized rats were primed with estradiol benzoate, and progesterone was injected 48 h later to elicit a LH surge in the afternoon. IL-1 alpha and IL-1 beta were injected either intracerebroventricularly (icv) via a preimplanted cannula in the third ventricle of the brain or iv. Systemic injection of IL-1 alpha or IL-1 beta (58.8 pmol at 1300 and 1500 h) failed to influence the afternoon LH surge seen in saline-injected control rats. However, IL-1 beta (1.76 pmol) administered icv at 1300 and 1500 h or a single icv injection at 1300 h blocked the progesterone-induced LH surge. Similar icv injections of IL-1 alpha also significantly suppressed the afternoon LH surge compared to that in saline-injected control rats. However, IL-1 alpha was relatively less effective than the beta-subtype, since the LH surge was detected in some rats. To ascertain whether suppression of the LH surge was due to inhibition of LHRH release, the medial basal hypothalamus-preoptic area of estradiol benzoate-progesterone-treated ovariectomized rats was incubated with and without IL-1. Both IL-1 alpha and IL-1 beta, at concentrations of 0.1 nM and higher, significantly suppressed LHRH release in vitro from the medial basal hypothalamus-preoptic area. In contrast, IL-1 (10 nM) was completely ineffective in suppressing LHRH release from the microdissected median eminence. These results demonstrated an overall inhibitory effect of icv IL-1 on the LHRH-LH axis and suggest that suppression of the steroid-induced LH surge by IL-1 may primarily be due to inhibition of LHRH release at hypothalamic sites located within the blood-brain barrier.

Animals↗
PubMed1990

Progesterone enhances the surge of luteinizing hormone by increasing the activation of luteinizing hormone-releasing hormone neurons.

The ability of progesterone (P) to enhance the surge of LH in the rat is well documented, but whether its primary site of action is on the pituitary or brain is unclear. To determine whether P can alter the activation of LHRH neurons, 1) intact female rats were treated with the P antagonist RU486 (5 mg) at 1230 h on proestrus and killed at specified times during the afternoon and evening for comparison of plasma LH levels and cFos expression in LHRH neurons with untreated proestrous rats. RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus. 2) Ovariectomized (OVX) rats were primed with estradiol benzoate (EB, 1 microgram) and then were treated with EB alone (50 microgram) or EB plus P (5 mg). Treatment with EB without P resulted in significantly lower peak LH levels and a reduced cFos response in LHRH neurons than the EB-P treated rats. These data suggest that the actions of P eventuate in an enhanced activation of LHRH neurons that may be responsible for the increased magnitude of the LH surge.

Animals↗
PubMed1975

Blockage of estrogen-induced release of luteinizing hormone by reserpine and potentiation of synthetic gonadotropin-releasing hormone-induced release of luteinizing hormone by estrogen in the ovariectomized ewe.

These experiments tested the effects of reserpine on estrogen-induced LH release and the effects of estrogen on gonadotropin-releasing hormone-induced LH release in ovariectomized ewes. Injection of 50, 200, or 500 mug of estradiol benzoate (EB) into progesterone-treated ewes, or of 50 mug of EB into non-treated ewes induced a large surge in serum LH levels approximately 15 h later. Injection of 5 mg/ewe of reserpine 6 h prior to the EB, blocked the LH surge. Reserpine reduced, but did not block the release of LH induced by injection of 20 mug or 40 mug of synthetic gonadotropin-releasing hormone (GnRH). Injection of graded doses (5, 10, or 20 mug) of GnRH into progesterone-treated ewes that had been treated with reserpine, induced increases in serum LH levels that were proportional to the logarithm of the dose. In the final series of experiments both progesterone-treated and non-treated ewes were injected with reserpine and then with either EB or oil. Fifteen hours after receiving EB or oil they were injected with either GnRH or the diluent. GnRH elevated serum LH levels significantly higher in ewes given EB than in those given oil. LH levels in ewes given oil and diluent were not elevated. These data suggest that reserpine blocked EB-induced LH release by an action on the central nervous system and that EB acted directly on the anterior pituitary to increase the response to GnRH.

Animals↗
PubMed1976

Inhibition of luteinizing hormone release by analogs of luteinizing hormone-releasing hormone (LHRH) in vitro.

Sixteen synthetic analogs of LH-releasing hormone (LHRH) were tested for their ability to inhibit the stimulation of LH release induced by 3 X 10(-9)M LHRH in anterior pituitary cells in monolayer culture. Half-maximal inhibition of LHRH-induced LH release was obtained with 7 analogs at concentrations which ranged from 3 X 10(-6)M to 3 X 10(-5)M. None of these seven analogs had significant LH-releasing activity at concentrations up to 10-5M. Nine analogs had no detectable antagonistic activity when tested in up to a 3000-fold molar ratio of analog to LHRH.

Animals↗
PubMed1976

Reduced luteinizing hormone release by synthetic luteinizing hormone-releasing hormone (LHRH) in postpartum lactating rats.

The ability of the pituitary to release LH in response to synthetic LHRH was tested in lactating female rats on days 7 and 17 post partum, and compared with that of normal cycling female rats on diestrous day 2 (controls). Three consecutive injections of LHRH (100 ng/100 g BW, sc), each 50 min apart, were given to each rat and sequential blood samples were collected at 25-min intervals by cardiac puncture under light ether anesthesia. In all 3 groups, the 2nd and 3rd injections of LHRH produced much greater increases in serum concentrations of LH than the 1st injection. However, this self-priming effect of LHRH on LH response was markedly attenuated in the postpartum lactating rats (PPL), compared with the normal cycling female rats on diestrous day 2. Three consecutive injections of LHRH produced significantly less LH release in PPL rats than in normal cycling female rats on diestrous day 2. Both day 7 and day 17 PPL rats released equally small amounts of LH in response to LHRH administration. The total amount of LH released by anterior pituitaries (APs) during a 5 h incubation in medium-199, from day 7 or day 17 in PPL rats, was significantly less than that released by the APs from normal cycling female rats on diestrous day 2. APs from day 7 and day 17 PPL rats also released less LH in vitro in response to LHRH (50 ng) stimulation than APs from normal cycling female rats. When APs from normal cycling female rats on diestrous day 2 were incubated with LHRH, the increments in LH release were greater at the end of the 2nd and 3rd h than after the 1st h of incubation. However, such increments in LH release were relatively small when APs from day 7 or day 17 PPL rats were similarly incubated with LHRH.

Animals↗
PubMed2001

Stimulation effect of galanin-like peptide (GALP) on luteinizing hormone-releasing hormone-mediated luteinizing hormone (LH) secretion in male rats.

Galanin-like peptide (GALP) is a recently isolated hypothalamic peptide which has sequence homology to galanin and binds to galanin receptors with high affinity. It has been shown that GALP neurons are localized in the arcuate nucleus and that GALP-immunoreactive fibers are in close apposition with LHRH neurons in the medial preoptic area (MPA). In the present study, we found that intracerebroventricular (icv) administration of GALP increased the plasma LH level but did not change the levels of other hormones. Concomitantly, accumulation of c-Fos protein was dramatically increased in the nuclei of LHRH-positive cells in the MPA by icv GALP administration. Furthermore, the GALP-induced plasma LH response was completely abolished by pretreatment with Cetrorelix, a LHRH receptor antagonist. On the other hand, GALP did not affect the release of LH, FSH, TSH, ACTH, GH or PRL directly from dispersed rat pituitary cells in vitro. These results strongly suggest a role for GALP in the control of gonadotropin secretion through a hypothalamic mechanism involving the release of LHRH.

Animals↗