UNIPROT:P01189 - FACTA Search

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

The effects of estrogen on the response of hypothalamic arcuate neurons to mu-opioid and GABAB agonists were investigated. Intracellular recordings were made from arcuate neurons in slices prepared from ovariectomized guinea pigs that were pretreated with estrogen or vehicle. Estrogen shifted the dose-response curve to the mu-opioid agonist DAMGO (Tyr-D-Ala-Gly-MePhe-Gly-ol) by 3.4-fold; the EC50 for DAMGO was 240 +/- 25 nM in estrogen-treated females versus 70 +/- 12 nM in the controls. The maximal hyperpolarization induced by DAMGO was equivalent in neurons from both groups. The Ke for the naloxone antagonism of the DAMGO response was similar in both groups, which would indicate that the affinity of the mu-receptor was unchanged. To explore where in the receptor/G-protein/K+ channel cascade estrogen may be acting to attenuate the mu-opioid-mediated hyperpolarization, the response to the GABAB agonist baclofen was also tested. Estrogen treatment also shifted the dose-response curve for the baclofen-induced hyperpolarization by 3.3-fold without altering the maximum hyperpolarization; the EC50 shifted from 11.0 +/- 4.0 microM to 36.0 +/- 5.0 microM. All of the neurons were identified after linking the intracellular biocytin with streptavidin-FITC, and a subpopulation of cells in both groups were immunoreactive for beta-endorphin. We conclude that estrogen decreases the functional coupling of the mu-opioid and GABAB receptors to the inwardly rectifying K+ channel possibly through an action on the G-protein.
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PMID:Estrogen suppresses mu-opioid- and GABAB-mediated hyperpolarization of hypothalamic arcuate neurons. 131 80

The effects of ovariectomy and estrogen on prolactin secretion and/or the activity of tuberoinfundibular dopamine (TIDA) neurons were examined by either concurrently measuring concentrations of prolactin in plasma and 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence of female rats or by determining the rate of DA synthesis (accumulation of 3,4-dihydroxyphenylalanine (DOPA) after the administration of a decarboxylase inhibitor) in the median eminence. For comparison, concentrations of alpha-melanocyte-stimulating hormone (alpha MSH) in plasma and DOPAC in the intermediate lobe of the pituitary (an index of the activity of tuberohypophysial DA neurons) were also determined. Ovariectomy produced a time-dependent decrease in the accumulation of DOPA and the concentrations of DOPAC in the median eminence and prolactin in plasma with maximal effects occurring by 7 days. Estrogen administration to ovariectomized rats increased plasma prolactin and median eminence DOPAC concentrations to levels comparable to those in diestrous controls. In contrast, neither ovariectomy nor estrogen replacement altered the concentrations of alpha MSH in plasma or DOPAC in the intermediate lobe. Administration of the DA agonist bromocriptine blocked the ability of estrogen to increase plasma prolactin and median eminence DOPAC concentrations. Also, administration of antiserum to rat prolactin blocked the stimulatory action of estrogen on median eminence DOPAC concentrations. Taken together, these results indicate that the stimulatory effect of estrogen on the activity of TIDA neurons is mediated by prolactin.
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PMID:Evidence that prolactin mediates the stimulatory effects of estrogen on tuberoinfundibular dopamine neurons in female rats. 132 1

The expression of kidney androgen-regulated protein (KAP) gene in mouse kidney is regulated in a multihormonal fashion. As determined by in situ hybridization analysis, epithelial cells of proximal convoluted tubules of cortical nephrons express KAP mRNA in response to androgenic stimulation while similar cells in the juxtamedullary S3 segment of the tubules express KAP mRNA under estrogenic and pituitary hormonal control. In situ hybridization analysis of kidney sections using hypophysectomized (hypox) mice resulted in a total absence of KAP mRNA suggesting the participation of a pituitary hormone(s) in the constitutive expression of KAP mRNA in S3 cells. Treatment of hypox mice with steroid hormones showed that androgens restored the ability of cortical tubule cells to synthesize KAP mRNA. Estrogen treatment, on the other hand, partially induced KAP gene expression only in S3 cells. These results indicated that the androgenic response of the gene is independent of pituitary function, while expression in S3 cells, although partially induced by the direct action of estrogens, is primarily regulated by a pituitary factor. In order to elucidate which hormone(s) is responsible for KAP gene expression in S3 cells, individual pituitary hormones were administered to hypox normal animals and to strains of mice genetically deficient in certain pituitary hormones. Surgically treated C57BL/6 female and male mice were implanted for 7 days with osmotic pumps containing individual pituitary hormones, after which the kidneys were analyzed by in situ hybridization. Mice injected with growth hormone (GH), corticotropin (ACTH), prolactin (PRL), or vehicle failed to express KAP mRNA. Mice treated with thyrotropin (TSH), follitropin (FSH), and lutropin (LH) exhibited high levels of KAP mRNA in S3 cells of females as well as in the renal cortex of male animals. Expression in the cortex in response to LH and FSH may be due to their gonadotropic effect on testosterone production. Similarly, contamination of TSH samples with small amounts of the gonadotropins may explain the cortical response to TSH. TSH produced the strongest response in S3 cells suggesting that it is responsible for the permissive effect of the pituitary on KAP gene expression. This conclusion was supported by studies performed with the dwarf mouse (dw/dw) which lacks PRL, GH, and TSH due to a mutation in the pit-1 gene. In situ hybridization analysis of dwarf mice kidney sections showed a complete lack of KAP gene expression. The possible participation of GH and PRL was eliminated on the basis of the hormone replacement studies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of pituitary hormones on the cell-specific expression of the KAP gene. 133 21

Progestin receptor-containing cells in the hypothalamus of the adult female green monkey (Cercopithecus aethiops) were examined by double-label immunocytochemical methods to determine their anatomical location, neurotransmitter content and afferent connections. Animals were ovariectomized and administered either estradiol valerate or the oil injection vehicle, and were sacrificed after 10 days of treatment. Using a monoclonal antibody raised against rabbit uterine progestin receptor (PR), the distribution of PR-immunoreactive cells in the mediobasal hypothalamus and the effect of estrogen treatment on this distribution was determined. PR-immunoreactive cells were found throughout the ventromedial nucleus (VMN), in the area between the VMN and fornix, and in the medial portion of the infundibular nucleus. Estrogen treatment dramatically increased both the number of labeled cells and the intensity of immunoreaction product in these regions. In double-immunostained sections, boutons immunoreactive for antigens indicative of serotonin, pro-opiomelanocortin derived peptides, GABA, catecholamine, neuropeptide Y, substance P, cholecystokinin, and somatostatin were demonstrated to establish synaptic contact with the soma of PR-immunoreactive hypothalamic neurons. In colchicine-pretreated animals, all PR-containing neurons in the mediobasal hypothalamus were found to contain immunoreactivity for glutamic acid decarboxylase, the enzyme required for synthesis of GABA. No evidence of colocalization with other antigens, including LHRH, was observed. Because LHRH neurons are known to receive a rich GABAergic innervation PR-containing GABAergic cells may represent steroid-sensitive sites of integration for inputs from other neural systems involved in the control of gonadotropin secretion.
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PMID:Transmitter content and afferent connections of estrogen-sensitive progestin receptor-containing neurons in the primate hypothalamus. 135 61

Estrogen stimulates expression of proenkephalin mRNA in neurons of the hypothalamic ventromedial nucleus, and evidence is accumulating that synaptic release of one of the peptide end products, met-enkephalin, influences events that regulate reproductive behavior. To address the question of whether estrogen acts directly on neurons that synthesize met-enkephalin or indirectly through a separate neuronal population, we combined estrogen autoradiography with endogenous opioid peptide (EOP) immunohistochemistry. In agreement with previous studies, the ventrolateral subdivision of the hypothalamic ventromedial nucleus was densely packed with EOP-immunoreactive cells. In males, 48% of the estrogen-concentrating cells of the ventrolateral subdivision of the hypothalamic ventromedial nucleus contained EOP, and, in females, 27% of the estrogen-concentrating cells contained EOP. These findings indicate that estrogen acts directly on neurons that express EOP and suggest a mechanism that underlies sexually differentiated reproductive behavior.
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PMID:Endogenous opioid-immunoreactive neurons of the ventromedial hypothalamic nucleus concentrate estrogen in male and female rats. 185 83

A new transplantable rat pituitary tumor was induced in F344 female rats with dimethylbenz(a)anthracene and estrogen (MtT/F-DMBA) and studied for 20 serial transplant generations. The tumor grew without estrogen supplements in female rats by the second transplant generation. Sensitivity to estrogens, as indicated by a prolonged latency period for tumor development, was seen at the 20th, but not the 5th transplant generation. MtT/F-DMBA tumors expressed prolactin (PRL), growth hormone (GH), and adrenocorticotropin (ACTH) mRNAs. A decrease in the percentage of cells expressing PRL mRNA, PRL protein, and in the number of secretory granules per cell occurred with serial transplantation. S-100 protein-positive folliculostellate cells were present in the hyperplastic pituitary but not in the transplantable tumors. Estrogen treatment at the 20th transplant generation prolonged the tumor latency period, increased the number of cells expressing PRL mRNA greater than 5-fold by in situ hybridization analysis (14 +/- 2% versus 77 +/- 5%), increased PRL secretion (132 +/- 40 ng/ml versus 3762 +/- 890 ng/ml), and increased the number of cytoplasmic secretory granules per cell. These results indicate that hyperplastic pituitary and true pituitary neoplasms differ in their ability to grow readily after transplantation. The presence of S-100 protein-positive folliculostellate cells, which are present in hyperplastic but not in neoplastic pituitary tissues, may serve as a morphologic marker to separate hyperplastic and neoplastic rat pituitary tissues. Transplantable tumors remained responsive to estrogen with expression of a more differentiated phenotype, including an increased number of cells expressing PRL mRNA and increased numbers of PRL secretory granules.
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PMID:Regulation of prolactin gene expression in a DMBA-estrogen-induced transplantable rat pituitary tumor. 212 15

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

This study was designed to explore the hormonal regulation of CNS opioid peptide levels in female Sprague Dawley rats. Forty-eight animals were divided into 2 equal groups for acute and chronic studies. Each group was further divided into 4 subgroups, each containing 6 animals. Each rat in the control group received an inert pill (in 0.25 ml corn oil daily by gavage); the second group, 15 micrograms norethindrone (NE, a potent progestin present in the oral contraceptive Micronor); the third group, 15 micrograms NE and 1 microgram ethinyl estradiol, EE2 (present in the oral contraceptive Modicon) and the fourth group, 10 times the dose of the third group. Rats were treated either acutely for 5 days or chronically for 7 weeks. Opioid peptides were estimated by radioimmunoassay. Acute administration of 150 micrograms NE + 10 micrograms EE2 decreased the levels of methionine-enkephalin (ME), leucine-enkephalin (LE), dynorphin (DYN) and beta-endorphin like immunoreactivity (beta-EI) by about 50% in the pituitary. The same dose on chronic administration also decreased DYN, but increased the levels of ME and LE in the pituitary by 331 and 69%, respectively. In the hypothalamus, chronic administration of NE + EE2 increased the level of ME (155%) and LE (87%) as well as of DYN (97%). In the striatum, the levels of LE (33%) and DYN (115%) were elevated during chronic administration. It is concluded that the acute administration of NE + EE2, in general, reduces the levels of ME, LE, DYN and beta-EI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oral contraceptives on the rat brain and pituitary opioid peptides. 286 95

Membranes prepared from the adrenal gland of mice and rats possess high affinity binding sites that recognize 125I-labeled human low density lipoprotein (LDL). These binding sites resemble the functional LDL receptors that mediate the uptake of LDL by cultured mouse and bovine adrenal cells. The number of LDL binding sites per mg of membrane protein increased 2- to 5-fold over 24 h when mice or rats were treated with adrenocorticotropin (ACTH). In rats, this increase was accompanied by a similar ACTH-induced increase in the adrenal uptake of intravenously administered 125I-LDL, suggesting that the LDL binding sites mediate the uptake of LDL by the adrenal in the intact animal. The number of LDL binding sites on adrenal membranes rose by 5-fold when animals were rendered lipoprotein-deficient, either by treatment of mice with 4-aminopyrazolopyrimidine or by treatment of rats with 17 alpha-ethinyl estradiol. This increase was prevented when endogenous ACTH secretion was blocked by administration of dexamethasone, suggesting that ACTH was required. The current experiments suggest that LDL receptors provide one source of cholesterol for the mouse and rat adrenal in vivo and that the number of LDL receptors of this organ is regulated by ACTH.
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PMID:Regulation of low density lipoprotein receptors by adrenocorticotropin in the adrenal gland of mice and rats in vivo. 624 39

The purpose of this study was to investigate the effect of oral administration of progesterone (15 micrograms norethindrone, NE) in presence and absence of estradiol (1 microgram ethinyl estradiol, EE2) on the CNS levels of beta-endorphin like immunoreactivity (beta-EI) in female rats. In acute study (5 days), NE alone did not change beta-EI significantly in pituitary. NE and EE2 together decreased beta-EI by 37% (47% at 10X dose). In chronic study (7 weeks), 2NE had no significant effect on pituitary beta-EI, however, NE and EE2 together at 10X dose decreased it by 14%. In the hypothalamus, NE alone or in presence of EE2 had no significant effect on beta-EI, but 10X dose of NE+ EE2 caused 50 and 76% decrease in beta-EI in acute and chronic study. Striatum was the only tissue where NE alone caused a decrease of 82% in beta-EI when given acutely and 52% when given chronically. EE2 had some protective effect on this decrease since when given together (NE+EE2) the decrease in beta-EI was 21% in acute and 43% in chronic study. Thus our results, along with other studies on the regulation of gonadotropin levels by opioids, suggest that oral contraceptives alter the level of beta-EI and in turn may regulate the release of gonadotropins. Morphine and endogenous opioids have been shown to decrease gonadotropin secretion in various species including humans, apparently by suppressing the release of LH-RH from the hypothalamus (1-5). The opiate antagonist naloxone not only causes up to 10-fold increase in the secretion of gonadotropins (1,3, 6-9) but also opposes the negative feedback effect of steroids on the hypothalamic-pituitary-gonadotropin axis (8), suggesting a regulatory interaction between the endogenous opioids, gonadotropins and gonadal steroids. Like ACTH, the secretion of beta-endorphin is inhibited by glucocorticoids (10). Naloxone induced release of LH is facilitated by estradiol in humans (11) suggesting an antagonistic effect of estradiol on the endogenous opioids. beta-endorphin may play a significant role in neurochemical mechanisms of gonadotropin release in the human menstrual cycle. A preovulatory increase of beta-endorphin in serum occurs 2 days prior to LH surge and a postovulatory decrease in beta-endorphin occurs 5 days later.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of oral contraceptives on the rat brain and pituitary beta-endorphin. 631 7

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