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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pulsatile release of gonadotropin-releasing hormone and the consequent secretion of gonadotropins are regulated by a complex interplay of steroids, neuropeptides, catecholamines, and environmental factors. Estrogen and progesterone influence the amplitude and frequency of luteinizing hormone pulsatile secretion. These effects lead to both a diurnal variation in pulse frequency, with a lower frequency at night, and variation during the menstrual cycle, with a lower frequency and increased amplitude during the luteal phase. Opioid peptides inhibit the pulsatile discharge of gonadotropin-releasing hormone and luteinizing hormone. The opioid antagonist, naloxone, causes an increase in luteinizing hormone secretion, particularly during the luteal phase. The administration of opioid receptor agonists, such as beta-endorphin, results in a decline in serum luteinizing hormone during the early follicular phase. Corticotropin-releasing factor, which is increased during stress, inhibits pulsatile luteinizing hormone secretion, and this effect can be blocked by the simultaneous administration of naloxone. These observations suggest that corticotropin-releasing factor exerts its effects on luteinizing hormone through an opioidergic intermediary. Endogenous catecholamines such as dopamine inhibit pulsatile luteinizing hormone release; however, the mechanism involved is not clear.
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PMID:Neuromodulatory regulation of gonadotropin-releasing hormone pulsatile discharge in women. 224 Jan 30

The ability of hormones to bind to their functional receptors on turtle (Pseudemys scripta) endocrine target tissues in the cold was tested by treating tissues with secretagogues at low temperatures (5-15 degrees) and then following subsequent target stimulation in the absence of secretagogue at a warm temperature (28 degrees). Administration of thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone, and growth hormone-releasing hormone to pituitaries at low temperatures (20 degrees or below) suppressed responses in growth hormone (GH) and thyrotropin (TSH) secretion and there was little or no response in pituitaries subsequent to warming. In contrast, gonadotropin-releasing hormone treatment of pituitaries, TSH treatment of thyroid glands, and gonadotropin (FSH and LH) treatment of testes in the cold (down to 5 degrees) was followed by a large response in the target glands (secretion of LH, thyroxine, and testosterone (T), respectively) following warming. Additional studies with FSH and LH showed that these hormones can bind to testes rapidly (within 5 min) at low temperatures where no acute response is observed, although the dose sensitivity and the extent of this priming in the cold are less than at warm temperatures. Thus, postreceptor events may be more important than binding per se for temperature effects on hormone responses of tissues, but even this component of cell function varies among tissues. The effects of a receptor-independent secretagogue (tetraethylammonium chloride), which causes cell depolarization by blocking K+ efflux, were also blocked at low temperatures in thyrotropes and somatotropes but not in gonadotropes. Rapid depressions in TSH and GH secretions following cooling of TRH-stimulated pituitaries and of T secretion in LH-stimulated testes provide further evidence for cold sensitivity of postreceptor processes in these tissues.
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PMID:The role of hormone binding in the cold suppression of hormone stimulation of the pituitary, thyroid, and testis of the turtle. 228 80

Stress-related activation of the hypothalamic-pituitary-adrenal axis (HPA) is associated with suppression of the reproductive axis. This effect has been explained by findings indicating that corticotropin-releasing hormone suppresses hypothalamic gonadotropin-releasing hormone (GnRH) secretion via an opioid peptide-mediated mechanism, and that glucocorticoids suppress both GnRH and gonadotropin secretion and inhibit testosterone and estradiol production by the testis and ovary, respectively. To evaluate whether glucocorticoids suppress the effects of estradiol on its target tissues, we examined the ability of dexamethasone to inhibit estradiol-stimulated uterine and thymic growth in ovariectomized rats. Estradiol alone, given daily for 5 days, caused dose-dependent uterine and thymic growth. Dexamethasone alone, given daily for 5 days, caused a dose-dependent decrease in body weight gain and in thymic growth. When estradiol and dexamethasone were administered simultaneously, however, body weight gain and thymic growth were also inhibited (p less than 0.05). Dexamethasone decreased estradiol-induced uterine cytosolic and nuclear estrogen receptor concentrations (E2 R0, p less than 0.05; E2nR0, respectively), but had no effect on estradiol-induced progesterone receptor concentrations (P4R0, p greater than 0.05). Levels of uterine glucocorticoid receptors were not affected by estrogen and/or dexamethasone treatment. These findings suggest that stress levels of glucocorticoids, administered over a 5-day interval, block the estradiol-stimulated growth of female sex hormone target tissues. This effect may be partially mediated by a glucocorticoid-induced decrease of the estradiol receptor concentration. Thus, another mechanism by which the HPA may influence reproductive function during stress is by a direct effect of glucocorticoids on the target tissues of sex steroids.
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PMID:Glucocorticoids inhibit estradiol-mediated uterine growth: possible role of the uterine estradiol receptor. 231 Aug 19

Sexual differentiation of the rat brain is affected by certain compounds administered during the neonatal period. We evaluated the effects of exposure to THC during the critical period of sexual differentiation of the female rat brain on postpubertal estrous cycles and brain neurotransmitter levels. Newborn female rats were injected either with vehicle (oil) or with different doses of THC (0.38; 1.9 or 3.8 mg/100 g) subcutaneously during the first 5 days after birth. The rats were examined daily by vaginal lavage smears from 3 to 10 months of life for phases of estrous cyclicity. The animals were then sacrificed and the anterior hypothalamus preoptic area (AHPOA) and medial basal hypothalami (MBH) were collected, processed and the methionine-enkephalin (met-enkephalin), beta-endorphin-like immunoreactivity (beta-end LI), LHRH and substance-P were measured by radioimmunoassays. In addition, serum LH and prolactin levels were measured by radioimmunoassay. Compared with the control rats, the rats perinatally exposed to THC exhibited either constant metestrus diestrus type vaginal smears or irregular estrous cycles. In the THC-treated animals, the met-enkephalin and beta-end LI levels were lower in the AHPOA and higher in the MBH. The LHRH levels of THC-treated rats were significantly lower in the MBH. The substance-P levels were significantly lower in the AHPOA of THC treated animals. In the THC-treated rats, serum LH was low but, the prolactin levels were not significantly different from the control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early exposure to delta 9-tetrahydrocannabinol influences neuroendocrine and reproductive functions in female rats. 243 39

Light microscopic double immunocytochemical stainings, performed on sea bass hypothalamo-hypophysial sections, revealed the projection of different neuropeptide-immunoreactive neurons innervating the hormone-producing cell populations in the pituitary gland. In the rostral pars distalis (PD) the ACTH cells were found in close proximity to fibers immunoreactive for somatostatin (SRIF), growth hormone-releasing hormone (GRF), corticotropin-releasing hormone (CRF), vasotocin (VT), isotocin (IT), substance P (SP), neurotensin, and galanin (GAL), while the PRL cell zone seemed only innervated by nerve fibers immunopositive for GAL. In the proximal PD, fibers immunoreactive for SRIF, GRF, VT, IT, cholecystokinin, SP, neuropeptide Y, and GAL formed a close relationship with the growth hormone cells. The gonadotrophs were observed near nerve fibers immunostained for gonadotropin-releasing hormone, IT, and less obviously GRF and VT, while fibers positive for GRF, CRF, VT, IT, SP, and GAL penetrated between and formed a close association with the thyrotrophs. In the pars intermedia the MSH cells and the PAS-positive (PAS+) cells seemed both innervated by separate nerve fibers immunoreactive for GRF, CRF, melanin concentrating hormone, VT, IT, and SP. All these results suggest a functional role of the neuropeptides in the adenohypophysis of the sea bass, possibly in the synthesis and/or release of hypophysial hormones from the different cell types.
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PMID:Immunocytochemical demonstration of close relationships between neuropeptidergic nerve fibers and hormone-producing cell types in the adenohypophysis of the sea bass (Dicentrarchus labrax). 246 54

The roles of corticotrophin-releasing factor (CRF) and beta-endorphin in the suppression of LH and FSH secretion during lactation were investigated using ovariectomized lactating rats separated from their litters overnight. Within 1 h of returning the pups to their mothers a marked fall in plasma LH concentration and a large increase in plasma prolactin were noted. However, resuckling caused no significant change in plasma concentration of FSH until 12 h after the return of the litter but a significant decline occurred thereafter. Twenty-four hours after removal of the litter, a single i.v. injection of 200 microliters anti-LHRH serum caused similar changes in plasma concentrations of LH and FSH observed in nursing rats during suckling. These results suggest that the suckling stimulus itself is responsible for the suppression of LH as well as FSH, via inhibition of the secretion of LHRH. Twenty-four hours after removal of the litter, a single intracerebroventricular (i.c.v.) injection of either 10 micrograms CRF or beta-endorphin resulted in a rapid decrease in plasma LH. Only beta-endorphin caused a marked increase in plasma levels of prolactin within 1 h whereas FSH was less affected by either hormone. Repeated i.c.v. administration of 10 micrograms CRF or beta-endorphin at 6-h intervals caused a prolonged inhibition of LH as well as FSH secretion during 48 h, with beta-endorphin being less effective than CRF. These results demonstrate that the suckling stimulus alone suppressed the secretion of both LH and FSH, and suggest that this effect may be mediated by the inhibition of LHRH secretion from the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibitory effects of corticotrophin-releasing factor and beta-endorphin on LH and FSH secretion in the lactating rat. 252 94

The application of immunogold techniques to localize pituitary hormones produces label that can be quantified and correlated with different secretory states. This report focuses on three major applications of the technology. In the first set of studies, immunogold labels for adrenocorticotropin (ACTH) or luteinizing hormone (LH beta) and follicle-stimulating hormone (FSH beta) were applied to ultrathin sections of pituitaries from adrenalectomized rats or from rats in different stages of the estrous cycle. During the first week after adrenalectomy, ACTH cell area increased. The concentration of immunoperoxidase label (amount of label/area of the corticotropes) decreased. Counts of gold markers showed that there were no changes in the concentration of antigens per granule. Three weeks after adrenalectomy, the amount of immunoperoxidase label increased along with the concentration of that label. The concentration of gold label for ACTH on granules also increased. All changes correlated well with increases in serum ACTH stimulated by adrenalectomy. In the studies of cycling rats, gonadotropes showed increases in the number of gold markers for LH beta or FSH beta per granule area just before an elevation in serum levels. There were also increases in the proportion of granules that contained only LH beta or FSH beta (monohormonal) before the rise in secretion. Thus, nonparallel release of gonadotropins might be attributed to changes in the ratio of gonadotropins packaged per granule. In the second series of studies, avidin-gold labels were used to identify sites of binding of biotinylated ligands. These studies illustrate and quantify binding by biotinylated gonadotropin-releasing hormone (GnRH) to ovarian or pituitary target cells. Triple-labeling protocols (avidin-peroxidase followed by immunogold) show that the target cells in the pituitary contain gonadotropins. In the third set of studies, avidin gold or avidin peroxidase was used to label sites of hybridization of a biotinylated cRNA probe to gonadotropin beta subunit mRNA. The sites of hybridization appear on rough endoplasmic reticulum; however, further work is needed to improve cell ultrastructure and perserve antigens. Triple-labeling protocols (avidin-peroxidase followed by immunogold) show the feasibility of the technique as well as the need for further refinement. To summarize, these studies describe multiple applications of gold labels for the localization of antigens, ligands, and mRNA. The labels are sensitive for detection of antigens and ligands and easily quantified. Quantitative analyses show changes in concentration of gold label that correlate well with secretory states.
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PMID:Localization and quantification of hormones, ligands, and mRNA with affinity-gold probes. 254 76

Seven cases with uremia (6 men, 1 woman, mean age = 55.6 +/- 2.2 years) were studied with four combined hypothalamic releasing hormones (corticotropin-releasing hormone, CRH; luteinizing hormone-releasing hormone, LHRH; thyrotropin-releasing hormone, TRH; and growth hormone-releasing hormone, GHRH) for assessment of anterior pituitary functions. The mean basal levels of corticotropin (ACTH, 22.4 +/- 5.2 pg/ml), thyrotropin (TSH, 2.4 +/- 0.6 microU/ml), and follicle stimulating hormone (FSH, 26.0 +/- 3.4 mIU/ml) in uremic patients were not significantly different from those (34.0 +/- 3.5 pg/ml, 2.0 +/- 0.4 microU/ml, and 23.2 +/- 6.4 mIU/ml) of controls (5 men, 1 woman, mean age = 54 +/- 2.5 years), but the ACTH and TSH responses to the releasing hormones were significantly lower than those of the controls. The mean basal levels of luteinizing hormone (LH, 70.7 +/- 16.3 mIU/ml), cortisol (9.8 +/- 1.2 micrograms/dl) and prolactin (109.3 +/- 23.2 ng/ml) in uremic patients were significantly higher than those of normals (27.3 +/- 6.6 mIU/ml, 6.5 +/- 0.7 micrograms/dl and 15.7 +/- 3.4 ng/ml), while suppressed LH, cortisol and prolactin responses to the releasing hormones were observed in the uremic group. The mean basal growth hormone (GH) level in uremic patients (3.1 +/- 0.4 ng/ml) was not significantly different from that (2.8 +/- 0.7 ng/ml) of normals, but the GH response to the releasing hormones was significantly higher than that of controls. These results show pituitary dysfunction, such as blunted ACTH, TSH, LH and prolactin response, exists in uremic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anterior pituitary functions in patients with uremia tested by stimulation with four combined hypothalamic releasing hormones. 256 85

On the basis of their properties of noradrenergic and/or thromboxane inhibition, or on their activation of the dopaminergic reward system and/or beta-endorphin, the following substances or treatments are predicted to be effective in treating alcohol or drug addiction: ginger; carbon dioxide; dietary sulfur; methionine; calcium; LHRH; high intensity light; interferon; negative ions; serotonin antagonists such as methysergide and cyproheptadine; guanabenz and guenfacine; antihistamines; head-out water immersion; X-irradiation; and forced unilateral left nostril breathing.
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PMID:Predicting new effective treatments of alcohol addiction on the basis of their properties of inhibition of noradrenergic activity and/or thromboxane or on the activation of the dopamine reward system and/or beta-endorphin. 257 15

Over many years a large number of studies have demonstrated that nicotine and exposure to cigarette smoke produce marked neuroendocrine changes in animals and in man. The initial effects of nicotine are characterized by a marked hypersecretion of ACTH, vasopressin, beta-endorphin, prolactin and LH. Many of these very acute stimulatory effects of nicotine rapidly disappear, probably due to a desensitization of the central nicotinic cholinergic receptors involved. Instead, upon acute intermittent treatment with nicotine or exposure to cigarette smoke, an inhibition of prolactin, LH and TSH secretion occurs, which is associated with maintained hypersecretion of corticosterone. These effects are probably mediated via activation of central cholinergic receptors of the ganglionic type. Evidence indicates that the inhibitory effects of nicotine on LH and prolactin secretion are produced via an activation by these nicotinic receptors of the tubero-infundibular dopamine neurons, releasing dopamine as a prolactin inhibitory factor. Dopamine inhibits LHRH release via an axonic interaction involving D1-like dopamine receptors in the median eminence. It therefore seems possible that the reduced fertility found in heavy smokers may be counteracted by D1 receptor antagonists. The symptoms associated with glucocorticoid hypersecretion induced by nicotine is discussed considering not only the peripheral side effects but also permanent deficits in hippocampal glucocorticoid receptors and loss of hippocampal neurons. In view of the important influence of hormones on immune functions, it seems likely that smoking will cause disturbances in immune responsiveness. Finally, the nicotine-induced alterations of neuroendocrine function, especially in the pituitary-adrenal axis and in vasopressin release, may also lead to behavioural consequences in smokers, especially in the withdrawal phase.
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PMID:Neuroendocrine actions of nicotine and of exposure to cigarette smoke: medical implications. 266 Jan 82


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