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 neurointermediate lobes of dark-adapted toads Xenopus laevis were incubated for 30 min in [3H]arginine and then "chased" for various time periods. By use of this pulse-chase paradigm there were detected 10 trichloroacetic acid (TCA)-precipitable peptides separated on acid-urea polyacrylamide gels and one TCA-soluble peptide separated by high-voltage electrophoresis (pH 4.9) with melanotropic activity. Each of these peptides had a different degree of melanocyte stimulating hormone (MSH) activity as revealed by the Anolis skin bioassay. Three of these TCA-precipitable peptides comigrated with ACTH, beta-lipotrophin, and alpha-MSH on acid-urea gels. Evidence suggesting a precursor-product mode of biosynthesis of the melanotropic peptides is presented. 7 of the 10 TCA-precipitable peptides and the one TCA-soluble peptide with melanotropic activity were released into the medium. The half-time of release of the TCA-precipitable peptides was about 2 h, whereas the half-time of TCA-soluble peptide release was about 30 min. The release of these peptides was inhibited by 5 X 10(-5) M dopamine. Dopamine inhibition of release did not appear to affect the biosynthesis of the melanotropic peptides, but did appear to enhance the degradation of the newly synthesized TCA-soluble peptide in the tissue. White adaptation of the toads greatly decreased the biosynthesis of all of the TCA-precipitable melanotropic peptides.
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PMID:Biosynthesis, processing, and control of release of melanotropic peptides in the neurointermediate lobe of Xenopus laevis. 89 50

An important factor in regulating secretion from endocrine cells is the cytoplasmic concentration of cyclic-AMP. Many regulatory substances are known to either stimulate or inhibit the production of this second messenger through activation of their receptors. In the present study, we have monitored changes in cyclic-AMP efflux from melanotrope cells of Xenopus laevis in response to established neurochemical regulators of alpha-MSH secretion. In vitro superfusion of neurointermediate lobes allows for a dynamic recording of cyclic-AMP production in relation to hormone secretion. Unlike alpha-MSH secretion, the efflux of cyclic-AMP was not dependent on the concentration of extracellular calcium, indicating that hormone release and cyclic-AMP efflux are mediated by different mechanisms. The phosphodiesterase inhibitor IBMX and the adenylate cyclase activator forskolin stimulated cyclic-AMP efflux, but had no stimulatory effect on alpha-MSH release. This indicates that an increase in cyclic-AMP production in melanotrope cells is not necessarily accompanied by an increase in the rate of alpha-MSH release. Corticotropin-releasing factor stimulated cyclic-AMP efflux with dynamics similar to that induced by the amphibian peptide sauvagine. Dopamine and the GABAB receptor agonist baclofen both inhibited cyclic-AMP efflux and alpha-MSH release, with similar dynamics of inhibition and similar dose-response relationships. It is proposed that an inhibition of cyclic-AMP efflux is coupled to an inhibition of alpha-MSH secretion.
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PMID:Dynamics of cyclic-AMP efflux in relation to alpha-MSH secretion from melanotrope cells of Xenopus laevis. 127 39

Dopamine and gamma-aminobutyric acid (GABA) inhibit POMC peptide release from the pituitary intermediate lobe, via interaction with D2 or GABA-A/benzodiazepine receptors. Here, we examined the effects of an antianxiety triazolobenzodiazepine, adinazolam, on corticotropin-releasing factor (CRF)-stimulated POMC peptide secretion from the rat neurointermediate pituitary. Neurointermediate lobes (NILS) were incubated with CRF (10(-7) M), then adinazolam (10(-8) or (10(-9) M) was added, with CRF remaining in the medium. Aliquots were removed at 15-min intervals and frozen for radioimmunoassay of beta-endorphin. Adinazolam alone did not significantly affect secretion as compared to controls or CRF alone. Adinazolam incubated with CRF led to significant inhibition of beta-endorphin secretion, as compared to CRF alone. In addition, adinazolam was as effective as dopamine or the CRF antagonist, alpha-helical CRF, in preventing CRF-induced beta-endorphin release. Adinazolam appears to act directly on the pituitary to suppress hormone release induced by a stress-related hypothalamic peptide.
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PMID:Benzodiazepine suppression of corticotropin-releasing factor (CRF)-induced beta-endorphin release from rat neurointermediate pituitary. 148 May 15

Various drugs and hormones influence the light microscopic and especially the electron microscopic structure of the anterior pituitary and its tumors. Many structural effects are known only from animal experiments since specimens from human pituitaries are mostly not available. The structure of growth hormone (GH) cells is relatively stable. A massive GH cell hyperplasia is known only in rare cases with growth hormone releasing factor (GRF) excess from tumors. Prolactin cells can be stimulated by drugs, neurotransmitters, and hormones which decrease the dopamine inhibition. Adrenocorticotropic hormone (ACTH) cells are stimulated by stress, some hormones, loss of adrenals, and drugs which activate the alpha 1- and beta-receptors or inhibit the alpha 2-receptors. They are suppressed and changed into Crooke's cells by treatment with glucocorticoids. Thyroid-stimulating hormone (TSH) cells increase in number and size in states for overstimulation especially by thyrotropin releasing hormone (TRH). A decrease results from hyperthyroidism and possibly from somatostatin, L-dopa, and dopamine. Gonadotroph cells transform into castration cells in strongly hyperactive states (gonadectomy, antiandrogens, gonadotropin releasing hormone [Gn-RH]agonists, aminoglutethimide). Special types of pituitary adenomas can be treated with drugs which suppress hormone production and proliferation. Dopamine agonists and somatostatin reduce the tumor size of varying proportions of GH secreting adenomas in acromegaly. Ultrastructurally, a decrease of cytoplasmic and nuclear volume and an increase of lysosomes are found. Bromocriptine and other dopamine agonists are established in the treatment of prolactin secreting adenomas. They induce a shrinkage in many cases. Ultrastructurally, a reduction of cellular and nuclear size, an increase in number of secretory granules and of lysosomes, and a reduction of rough endoplasmic reticulum can be demonstrated.
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PMID:Effect of drugs on pituitary ultrastructure. 154 57

Dopamine (DA) neurons participate in tonic inhibition of prolactin (PRL), whereas beta-endorphin (beta-End) and serotonin (5-HT) neurons appear to be important stimulatory links for nocturnal PRL surges that occur throughout the first half of pregnancy in the rat. The purpose of this study was to determine how these neuronal components might be organized within the pathway controlling PRL release during gestation. Maximal stimulation of DA receptors with the agonist bromocriptine mesylate (Bromo) completely blocked the PRL response to beta-End (100 ng/microliters/min for 15 min) given intracerebroventricularly (i.c.v.) on day 8 of pregnancy. DA receptor blockade, produced by implanting a 25 mg pellet of haloperidol (Hal) on day 7 of pregnancy, resulted in PRL levels of 500-600 ng/ml by the following morning. beta-End i.c.v. or 250 mg/ml/kg BW of the DA synthesis inhibitor, alpha-methyl-p-tyrosine (alpha-MPT), given during the intersurge period, were equally effective in significantly increasing PRL (p less than 0.01) above pretreatment levels. beta-End and alpha-MPT evoked similar increases in rats pretreated with Hal, suggesting the stimulatory effect of beta-End on nocturnal PRL surges may primarily be due to DA inhibition. The next objective was to determine how beta-End and 5-HT might interact to stimulate the nocturnal surge. Day 8 pregnant rats were infused continuously with the opioid receptor blocker, naloxone hydrochloride (Nal), at a rate of 2.0 mg/10 min from 1000-1300 h. The PRL response to an injection of 20 mg/kg BW 5-hydroxytryptophan (5-HTP) at 1200 h was greatly attenuated, compared to controls infused with saline instead of Nal. This suggests that 5-HT stimulates PRL, at least in part, by an action at opioid receptors. Distilled H2O or 10 mg/kg BW of the selective S2 receptor blocker, ketanserin tartrate (Ket), was given intraperitoneally (i.p.) during the intersurge period on day 8 of pregnancy. All animals demonstrated an identical response to beta-End given 2 hours later, regardless of the type of pretreatment. It appears that beta-End does not stimulate PRL by way of an S2 receptor. Although beta-End induced a significant increase in PRL on day 16 of pregnancy, the response was attenuated by more than 60% compared to the response on day 8 of pregnancy. This attenuation may involve placental lactogens, shown to be secreted during this time and to inhibit PRL secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanisms for the stimulatory effects of opioidergic and serotonergic input signals on prolactin in pregnant rats. 157 43

Using high-performance liquid chromatography (HPLC) in combination with radioimmunoassay, three forms of alpha-MSH (des-acetyl, mono-acetyl and di-acetyl alpha-MSH) were separated and identified in tilapia neurointermediate lobes and plasma, and in medium from lobes superfused in vitro. The presence of acetylated forms in lobe extracts indicated that the peptides are acetylated intracellularly. Di-acetyl alpha-MSH was, especially in comparison with monoacetyl alpha-MSH, relatively more abundant in lobe extracts than in plasma. This suggests that the three forms of alpha-MSH are not released according to their relative intracellular abundances. The possibility of regulation of this differential release by dopamine and TRH was investigated, using a microsuperfusion system. Dopamine was a potent inhibitor of alpha-MSH release, but did not modulate the relative abundance of the different forms of alpha-MSH released from the MSH cells. TRH was a potent stimulator of alpha-MSH release. It enhanced in vitro the release of di-acetyl alpha-MSH more than the release of mono-acetyl alpha-MSH. Thus tilapia may be able to modulate not only the quantitative but also the qualitative signal from the MSH cells. This might enhance the flexibility of the animals to respond to environmental challenges.
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PMID:Regulation of differential release of alpha-melanocyte-stimulating hormone forms from the pituitary of a teleost fish, Oreochromis mossambicus. 164 62

The influence of adrenocorticotropic hormone (ACTH) in the adaptive changes on central dopamine (DA) autoreceptors following chronic administration of desipramine (DMI) has been examined in rats. Dopamine had an inhibitory effect on basal and K(+)-induced release of [3H]DA from slices of striatum and n. accumbens of rats treated chronically (10 days) with ACTH (50 IU/kg, s.c.), DMI (10 mg/kg, i.p.) or the combination of ACTH and DMI. In slices of n. accumbens, but not in slices of striatum of rats exposed to the combined treatment of ACTH and DMI, a significant decrease in the inhibitory effect of exogenous DA on stimulated release of [3H]DA was observed. Chronic administration of ACTH or DMI alone had no effect. The effect of the combined treatment with both agents, on the reactivity of these DA receptors was evaluated by means of apomorphine-induced hypoactivity. The administration of ACTH and DMI (5 mg/kg, i.p.) reduced the hypoactivity induced by apomorphine, as compared to hypoactivity in rats treated with ACTH or DMI alone. Experiments with ACTH4-10 revealed that the peptide modified biochemical and behavioural parameters of dopaminergic function, which may implicate a direct action of the peptide on the brain, rather than on the release of adrenal hormones. These findings suggest that ACTH accelerates the onset of DMI-induced adaptive changes on dopamine in the mesolimbic area. However, because the effect of ACTH4-10 on release of adrenocortical hormone was not investigated, the possibility cannot be disregarded that the effect of the peptide was secondary to an enhancement of release of adrenal hormone.
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PMID:Adrenocorticotropic hormone influences the development of adaptive changes in dopamine autoreceptors induced by chronic administration of desipramine. 165 7

Apomorphine (Apo), a D1/D2 Dopamine (DA) agonist, at high doses (500 micrograms/kg) induces a short-lasting insomnia, antagonized by a secondary injection of corticotropin-like intermediate lobe peptide (CLIP, 10 ng); these effects are also observed with hypophysectomized (hypoX) rats. The administration of the serotonin (5-HT) agonist 8-hydroxy-2-di-n-propylamino-tetralin (8-OHDPAT, 0.3 mg/kg) induces also an insomnia which, unlike Apo, is followed by a significant PS rebound. CLIP, again, antagonizes the 8-OHDPAT-induced insomnia. Finally, Bromocriptine (5 mg/kg), an agonist for both DA and 5-HT, induces first an insomnia (antagonized by CLIP), followed by a PS rebound; these effects persist in hypoX rats.
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PMID:Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 2--Aminergic regulatory processes. 196 3

In a group of adult Soay rams housed indoors under an artificial light cycle of alternating 16-week periods of long and short days, there was a conspicuous long-term cycle in the peripheral plasma concentrations of beta-endorphin and prolactin. The levels of beta-endorphin were highest under short days and lowest under long days (15-fold change), and inversely related to the changes in the plasma levels of prolactin (120-fold change). The role of dopamine in the control of beta-endorphin and prolactin was investigated in a series of experiments, conducted under both long and short days, in which rams were treated with dopamine receptor agonists (dopamine and bromocriptine) and antagonists (pimozide and sulpiride). Naloxone (opioid antagonist) was also administered to assess the additional involvement of endogenous opioids. Dopamine injected i.v. (6.6 mg/kg every 10 min) did not significantly affect the mean plasma concentrations of beta-endorphin and prolactin under either long or short days. Pimozide (0.08 mg/kg i.m. every 2 h) caused a large increase in the mean plasma concentrations of beta-endorphin and prolactin under long days but not short days. Naloxone (1.6 mg/kg, i.v.), administered alone or in combination with dopamine or pimozide, had no effect on the mean plasma concentrations of beta-endorphin and prolactin, except under short days when, combined with pimozide, it induced an increase in the plasma concentrations of the two polypeptides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the photoperiod-induced cycle in the peripheral blood concentrations of beta-endorphin and prolactin in the ram: role of dopamine and endogenous opioids. 228 Feb 12

G protein-mediated effects on cAMP production were evaluated in the corpus striatum of diabetic rats 5 and 14 weeks after alloxan injection by measuring both D1-receptor-induced stimulation and D2-receptor-mediated inhibition of adenylate-cyclase activity. At 5 weeks of diabetes, no obvious alterations of G protein functions were detected. Both dopamine-stimulated adenylate cyclase and bromocriptine-induced inhibition of enzyme activity were indeed similar in control and diabetic animals. Fourteen weeks after alloxan injection, profound alterations were observed. Dopamine-stimulated cAMP production was markedly increased in diabetic rats, whereas bromocriptine ability to reduce cAMP formation was almost abolished at this late stage of diabetes. Hypoactivity of Gi/Go proteins was also confirmed by the reduced ability of the GTP non-hydrolyzable analog GTP-gamma-S to inhibit forskolin-stimulation of adenylate cyclase. These results show an apparent functional imbalance between Gs and Gi/Go-mediated transduction mechanisms, with an increased efficacy of Gs activity likely due to the loss of Gi/Go inhibitory functions. Concomitantly with such transductional alteration detected in chronic diabetes, we observed a marked increase of the striatal content of met-enkephalin, which is known to utilize Gi/Go proteins for inhibition of adenylate cyclase. The measurement of other transmitters (vaso-active intestinal peptide, substance P, serotonin, noradrenaline, and dopamine) did not reveal any difference with respect to controls. The observed transductional defect in diabetic animals and the increased content and/or hyperinnervation by the metenkephalinergic system could be correlated as mutual compensatory mechanisms.
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PMID:Denervation and hyperinnervation in the nervous system of diabetic animals: III. Functional alterations of G proteins in diabetic encephalopathy. 251 14

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