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At least 1,369 records · Page 76Linked to original sources
PubMed1975

Effects of progesterone and synthetic luteinizing hormone releasing hormone on the release of luteinizing hormone during sexual maturation in the hen (Gallus domesticus).

Single intramuscular injections of 0-5 mg progesterone/kg resulted in increased LH secretion in laying hens but not in pullets with completely undeveloped sexual organs. Injections of the steroid were first able to stimulate LH release 8-10 weeks before the onset of lay when the comb, ovary and oviduct had started to grow and basal plasma LH concentrations were beginning to rise. At this time, injecitons of 10 mug synthetic LH-RH/kg resulted in an incremental change in plasma LH levels of around 26 ng/ml. A similar incremental change was observed after giving the same dose of LH-RH to pullets with no signs of sexual development. Three to four weeks before the first eggs were laid, basal plasma LH levles started to fall, the pituitary became progressively more insensitive to synthetic LH-RH and injections of 0-5 mg progesterone/kg resulted in a reduced LH response. Ten mug LH-RH/kg caused incremental changes in blood levels of LH of less than 5 ng/ml. The final stage of sexual maturation occurred during the week before the onset of lay and was characterized by a rapid growth of large yolky ovarian follicles and a further fall in the sensitivity of the pituitary to synthetic LH-RH. However, injections of 0-5 mg progesterone/kg resulted in a prolonged release of LH. These observations are discussed in relation to the maturatio of the positive feedback mechanism by which progesterone stimulates the secretion of LH.

Animals↗
PubMed1976

Production of antisera against highly purified human follicle-stimulating hormone, luteinizing hormone and thyroid-stimulating hormone.

Antisera were produced in rabbits against highly purified preparations of human LH (2000 or 10,000 i.u./mg), human FSH (5500 i.u./mg), and human TSH (7-5 i.u./mg). Most rabbits produced antisera of high titre and high avidity. Cross-reactions were minimal between human TSH and human chorionic gonadotrophin (HCG) and between human FSH and HCG but marked between human LH and HCG. TSH and FSH also showed a constant but relatively weak cross-reaction. LH cross-reacted with FSH to a higher degree than did HCG. The avidity of the antisera was high. It was concluded that much of the lack of specificity recorded for glycoprotein antisera are effects of impure immunogens. Some of the true cross-reactions are probably explained by shared antigenic determinants of the beta-subunits. Unadsorbed antisera could be used for assay of FSH and TSH in plasma from pregnant women.

Animals↗
PubMed1981

Further studies on the effectiveness with which exogenous luteinizing hormone and follicle-stimulating hormone stimulate the release of endogenous follicle-stimulating hormone during the rat oestrous cycle.

The effects of exogenous rat LH or FSH on the release of endogenous FSH in the cyclic rat have been investigated. Rats were administered phenobarbitone to block the spontaneous increases in gonadotrophins in plasma during pro-oestrus and oestrus and then cannulated through the jugular vein or cannulated and hypophysectomized during the late morning or early afternoon of pro-oestrus. Comparison of patterns of plasma FSH in hypophysectomized and intact rats after i.v. injection of 0.5 micrograms FSH at 17.00 h suggested that exogenous FSH stimulated the release of endogenous FSH in less than 5 h. Intravenous LH (2 micrograms at 16.00 and at 18.00 h) raised the level of FSH in plasma between 2 and 6 h after the first injection of LH. Both gonadotrophins stimulated FSH release by the pituitary gland during the morning of oestrus. Comparison of patterns of plasma FSH in hypophysectomized and intact rats after i.v. injection of 0.25 or 0.05 micrograms FSH at 14.00 h suggested that the latency between FSH injection and stimulation of some FSH release by the pituitary gland is as short as 2 h. Intravenous LH (3, 4 or 9 micrograms) at 14.00 h did not increase the level of FSH in plasma within 2 h and was only minimally effective in raising the level within 4 h. Intravenous LH (2 micrograms at 16.00 and at 18.00 h) on the afternoon of dioestrus day 2 was nearly as effective in increasing the levels of FSH in plasma as it was when administered to pro-oestrous rats. This procedure did not raise the plasma levels of FSH in rats used on dioestrus day 1. The results suggest that in the phenobarbitone-blocked, pro-oestrous rat (1) a small increase (less than that observed spontaneously) in plasma rat FSH during pro-oestrus is effective in stimulating FSH release by the pituitary gland, (2) an increase in plasma rat FSH can exert positive feedback on its own secretion within 2 h and (3) a large increase in plasma rat LH is not very effective in increasing the plasma level of FSH over a period of 4 h. The results also suggest that the spontaneous increase in plasma levels of FSH and, to a lesser extent, of LH is involved in causing the selective phase of FSH release which occurs during late pro-oestrus and the morning of oestrus, and that LH and FSH act differently, but not necessarily by way of a different mechanism, to stimulate release of FSH by the pituitary gland.

Animals↗
PubMed1993

Influence of stage of lactation, exogenous luteinizing hormone-releasing hormone, and suckling on estrus, positive feedback of luteinizing hormone, and ovulation in sows treated with estrogen.

The overall objective of this study was to investigate the LH response and occurrence of estrus and ovulation in sows treated with estradiol benzoate (EB) at mid- (d 14) or late (d 28) lactation. Experiment 1 tested the hypothesis that hourly pulses of LHRH given to sows treated with EB would cause a greater proportion to exhibit LH surges. Sows (n = 32) at mid- or late lactation were given (i.m.) corn oil (CO) or EB (10 micrograms/kg BW) at 0 h and no pulses or hourly pulses (100 ng/pulse) of the LHRH agonist des-Gly10,[D-ALA6]-LHRH ethylamide (LHRH-A) from 54 to 96 h, the anticipated period of positive feedback of LH. Blood samples for determination of estradiol-17 beta (E2) and LH were collected every 6 h from -12 to 120 h from sows treated with EB. Estrus was checked daily with a mature boar, and ovulation was assessed by measuring progesterone in blood 1 wk after estrus induced by EB or 2 wk after weaning at 34 +/- 1.4 d postpartum. Lactational estrus occurred in 0 of 16 and 15 of 16 sows given CO and EB, respectively; however, no sow ovulated in response to EB. Concentrations of LH were lower (P < .01) during mid- than during late lactation, and LHRH-A pulses had no effect on secretion of LH and E2. The LH concentrations during the pretreatment (-12 to 0 h), negative feedback (6 to 54 h), and positive feedback (60 to 96 h) periods at mid-lactation (.32 +/- .03, .22 +/- .01, and .54 +/- .08 ng/mL, respectively) differed (P < .01) from values at late lactation (.80 +/- .06, .49 +/- .02, and 1.47 +/- .17, respectively). Preovulatory-like surges of LH occurred in one of eight (peak 2.1 ng/mL) and seven of eight (peak 2.9 +/- 1 ng/mL) sows given EB at mid- and late lactation, respectively. Experiment 2 tested the hypothesis that the hypothalamus and pituitary of sows weaned 96 h before they were given EB would show a greater responsiveness than those weaned and given EB simultaneously. Sows (n = 16) at mid- or late lactation were treated with EB (10 micrograms/kg BW; i.m.), and one-half of the sows were suckled until the moment of EB treatment, whereas the other half had their litters weaned 96 h before treatment with EB.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

A two-sample method for assessing growth hormone response to growth hormone-releasing hormone challenge: use as a predictor of gain in beef bulls.

In two experiments, Black Angus bulls were challenged at weaning with GHRH analog and evaluated for their GH response to determine whether GH response can predict subsequent growth characteristics. The GH response was determined by measuring GH in blood serum collected 0 and 10 min after GHRH injection (Exp. 1: 1.5 microg/100 kg BW human GHRH, n = 34; Exp. 2: 1.5 and 4.5 microg/100 kg BW bovine GHRH [treatments LGHRH and HGHRH, respectively] administered 3 h after a 4.5 microg/100 kg BW "clearance dose" of GHRH, n = 38]. In Exp. 1, GH response did not predict growth or carcass measurements. In Exp. 2, GH response to LGHRH was positively related to ADG (R2 = .18; P = .007) during a 112-d controlled feeding trial. In addition, there was a tendency for bulls with a greater GH response to HGHRH to exhibit greater ADG than animals with a low response. However, GH response to GHRH was not related to changes in hip height (HH) or carcass ultrasound measurements at d 112 of the growth performance trial. Response of GH to repeated GHRH challenges was consistent within animal over time (r = .47; P = .003). The use of a clearance dose 3 h prior to GHRH challenge improved the relationship between GH response and ADG. Results of this study suggest that GH response to GHRH challenge is a useful tool for identifying beef bulls with superior growth potential.

Animals↗
PubMed1997

Cross-talk signals in the CNS: role of neurotrophic and hormonal factors, adhesion molecules and intercellular signaling agents in luteinizing hormone-releasing hormone (LHRH)-astroglial interactive network.

Neuron-astrocyte interactions play a crucial role during development and in the adult brain. During development, glial cells are involved in the guidance of neuronal precursors and in extending neuronal fiber projections. Astrocytes can promote neurite outgrowth, both "in vitro" and "in vivo". In the central nervous system (CNS), they express receptors for a variety of growth factors (GFs), neurotransmitters and/or neuromodulators. In turn, neuronal cells can respond to astrocyte-derived growth factors and control astrocyte function via a common set of signaling molecules and intracellular transducing pathways. It is also well established that astrocytes are involved with regenerative failure within the CNS following injury. Increasing evidence support the viewpoint that soluble factors from lymphoid/mononuclear cells modulate the growth and function of cells found in the CNS, specifically macroglia and microglia cells. Furthermore, glial cells can secrete immunoregulatory molecules that influence immune cells, as well as the glial cells themselves. In recent years, a bi-directional flow of informational molecules between LHRH neurons, subserving the neuroendocrine control of reproductive function, and astroglia cells has been disclosed. During their maturation and differentiation in vitro, astroglial cells release peptide growth factors that markedly accelerate LHRH neuronal phenotypic differentiation . In addition, these peptides induce the acquisition of mature LHRH secretory potential, with a potency depending on both the "age" and the specific brain localization of the astroglia, as well as the degree of LHRH neuronal differentiation "in vitro". Different experimental paradigms such as co-culture and mixed culture models between the GT1-1 neurons and astroglial cells in primary culture, disclosed the presence of a bi-directional flow of informational molecules regulating both proliferative and secretory capacities of each cell type. Growth factors are key players in LHRH neuron-astroglia crosstalk. In particular, basic fibroblast growth factor (bFGF) was identified as a major differentiation factor for the immortalized hypothalamic LHRH neuronal cell line. A specific synergy/cooperation between bFGF and other growth factors was also revealed at specific stages of LHRH neuron differentiation, indicating that the sequential expression of specific growth factors may participate in the processes of LHRH neuron migration, differentiation and functional regulation. Since bFGF is expressed in GT1-1 neurons and glial cells a possible paracrine/autocrine regulatory loop is suggested. Indeed, neutralization experiments aimed at counteracting endogenous bFGF during neuron-glia interactions dramatically inhibited astroglia neurotrophic effects. On the other hand, the importance of adhesion molecules in cell-to-cell communication was underscored by the significant inhibition of GT1-1 LHRH production and cell proliferation following the counteraction of neuron-neuron/neuron-glia interactions through addition of neuronal cell adhesion molecule (N-CAM) antiserum. Other information came from pharmacological experiments manipulating the astroglial-derived cytokines and/or nitric oxide, which revealed a crosstalk between the neuronal and astroglial compartments. From the bulk of this information, it seems likely that interactions between astroglia and LHRH neurons play a major role in the integration of the multiplicity of brain signals converging on the LHRH neurons that govern reproduction.

Animals↗