Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of opioid peptides isolated from brain and peripheral tissue have been identified, and several types of opiate receptor postulated for these endogenous substances. In this study the effects of pharmacological manipulation of 5-hydroxytryptamine (5-HT) on the antinociceptive activity of morphine and two synthetic enkephalin analogus (D-ala2-leu-enkephalin and D-ala2-met-enkephalin) were investigated in mice and rats. Centrally injected 5-HT and peripheral clomipramine pretreatment potentiated both morphine and synthetic enkephalin analgesia whilst peripheral doses of cyproheptidine, lesions in the dorsal medial raphe (DMR) and reserpine pretreatment attenuated opioid analgesia. In the reserpine-pretreated group, centrally injected 5-HT restored the antinociceptive activity of morphine and D-ala2-leu-enkephalin. These results are discussed with respect to clomipramine therapy.
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PMID:Opiate receptors, endorphins and drug therapy. 624 44

Platelets of healthy human subjects were incubated with 5-hydroxytryptamine (5-HT) followed by a second incubation with either beta-endorphin (beta-end) or the combination of beta-end and naloxone. beta-End (300 pg/ml) reduced the levels of 5-HT to 50% of initial values within 15-40 min. After 40-80 min incubation, the levels of 5-HT decreased to approximately zero. Addition of increasing amounts of beta-end (up to 300 pg/ml) produced increasing releases of 5-HT with increasing doses of beta-end. The response was dose-related, however variable, across subjects. Addition of either 28.7 or 57.4 pg naloxone to 300 pg beta-end did not antagonize the effects of beta-end on 5-HT.
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PMID:beta-Endorphin-induced release of 5-hydroxytryptamine from human platelets. 626 49

The influence of opioid substances on the secretion in vivo and in vitro of corticosterone, corticotrophin (ACTH) and corticotrophin releasing factor (CRF) in the rat was studied. Rats given a single injection of morphine exhibited a marked hypersecretion of ACTH and an exaggeration of the hypothalamo-pituitary-adrenocortical (HPA) response to stress. In contrast, animals rendered tolerant to morphine failed to release ACTH or corticosterone in response either to a subsequent injection of the opiate or to stress. The development of the inhibitory effect paralleled the development of tolerance to the analgesic actions of the drug. The production of ACTH by pituitary segments removed from control animals was not affected by the addition of opioid substances to the incubation medium. However, morphine, met-enkephalin and leu-enkephalin stimulated the secretion of CRF by hypothalami and their effects were competitively antagonized by naloxone. The secretory activity of hypothalami removed from rats treated acutely with morphine was enhanced. In contrast hypothalami from morphine-tolerant rats failed to secrete CRF in response to morphine, met-enkephalin, acetylcholine or 5-hydroxytryptamine. Neither the density nor the affinity of 3H-naloxone binding sites in the hypothalamus was influenced by the morphine treatment. The results suggest the opioid peptides and their receptors play a major role in the regulation of HPA function.
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PMID:Differences in hypothalamo-pituitary-adrenocortical activity in the rat after acute and prolonged treatment with morphine. 632 47

In thirty patients with common migraine the platelet concentrations of met-enkephalin immunoreactivity (ME) (76 +/- 9 pg/mg protein) were similar to those in 23 healthy volunteers (77 +/- 5), suggesting that there is no alteration in the ME pool in this biochemical compartment in migraine. Chronic treatment (4 weeks) with drugs that interfere with 5-hydroxytryptamine (5-HT) synthesis or uptake induced the expected changes in platelet 5-HT levels, i.e. a rise following administration of the 5-HT precursor 5-hydroxytryptophan (daily dose: 300-500 mg, n = 9) and a decrease after amine uptake inhibition by amitryptyline (30-75 mg, n = 7) and even more by chlorimipramine (30-50 mg, n = 9). Platelet ME concentrations rose by up to approximately 90% over the basal values after either 5-hydroxytryptophan (significantly from week 2) or amitriptyline (at week 2) and were unchanged after chlorimipramine, indicating that 5-HT and ME concentrations in platelets can vary independently. The high platelet ME levels following 5-hydroxytryptophan and amitriptyline cannot be explained at present. They might be due either to increased ME synthesis, possibly in the megakaryocyte, or to decreased utilization by platelets or both.
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PMID:Platelet met-enkephalin immunoreactivity and 5-hydroxytryptamine concentrations in migraine patients: effects of 5-hydroxytryptophan, amitriptyline and chlorimipramine treatment. 661 Apr 76

In a histopathological and immunocytochemical study of biopsy and/or operation specimens from 27 patients with endocrine tumors of the colon and rectum ("hind-gut carcinoids") enkephalin-immunoreactive tumor cells were observed in two cases. Both patients were obese women, about 50 years of age, with a history of constipation. The tumors were situated near the anus in the dorsal wall of the rectum. One tumor had metastasized to a lymph node, and the other showed vascular invasion. The tumor cells were non-argentaffin; some were argyrophil. One tumor contained only few enkephalin-immunoreactive cells but had numerous beta-endorphin-immunoreactive cells, which were distinct from the former. The other contained large numbers of enkephalin-immunoreactive cells but no beta-endorphin cells. Both tumors also harboured glucagon-immunoreactive cells; in one there were also cells containing immunoreactive pancreatic polypeptide. These cells were distinct from the enkephalin-storing ones. No 5-hydroxytryptamine could be detected in the two tumors.
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PMID:Immunocytochemical demonstration of enkephalin and beta-endorphin in endocrine tumors of the rectum. A survey of 27 colo-rectal carcinoids. 698 63

Picogram amounts (50-150 pg/mg protein) of immunoreactive met-enkephalin material (met-enkephalin IR) were detected by radioimmunoassay in human, rat and rabbit platelets. Characterization of this material by thin-layer chromatography, gel filtration chromatography and high-pressure liquid chromatography indicated that it behaves identically with synthetic met-enkephalin. No high molecular weight met-enkephalin IR could be detected in the platelet extracts, even after trypsin hydrolysis, using two antisera which are able to recognize some of the putative met-enkephalin precursors present in the adrenal gland or striatum. In vitro, thrombin released platelet-met-enkephalin IR concomitantly with 5-hydroxytryptamine (5-HT), suggesting a common subcellular localization, i.e. the 5-HT storing organelles, for met-enkephalin IR and the amine. In vivo, platelet met-enkephalin IR in the Sprague-Dawley rat was affected neither by adrenalectomy nor by hypophysectomy. Thirteen-and 18-week-old spontaneous hypertensive rats (SHR) had lower platelet concentrations of met-enkephalin IR than age matched normotensive Wistar-Kyoto rats.
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PMID:Met-enkephalin immunoreactivity in blood platelets. 709 67

Two types of inhibition of basic peptide-induced rat mast cell secretion are reported. Pretreatment of rat peritoneal mast cells with Vibrio comma neuraminidase, an enzyme which cleaves sialic acid from oligosaccharides, led to inhibition of 5-hydroxytryptamine release induced by the basic peptides polylysine, corticotropin 1-24 and a decapeptide sequence of human IgE. Inhibition was similarly observed when mast cells were challenged in the presence of the cationic cell membrane-active substance benzalkonium chloride. It is postulated that both of these experimental procedures inhibit basic peptide-induced secretion by depletion of cell surface negative charge. Sialic acid itself does not act as a specific receptor for basic peptides, since a molar excess of sialic acid in free solution failed to inhibit secretion by binding to basic peptides in the fluid phase.
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PMID:Neuraminidase- and benzalkonium chloride-dependent inhibition of basic peptide-induced rat mast cell secretion. 717 80

A synthetic basic decapeptide from the C4 domain of human immunoglobulin E, corticotropin-(1-24)-peptide, polyarginine and polylysine stimulated up to 90% net release of 5-hydroxytryptamine from mast cells in rat peritoneal-cell suspensions. Concentration-response curves to all four polypeptides were parallel. Polyarginine and polylysine (EC50 congruent to 0.05 microM) were approximately 100-fold more potent than immunoglobulin E decapeptide and corticotropin-(1-24)-peptide (EC50 congruent to 5 microM). Polypeptide-induced release was complete within 5-10s. Immunoglobulin-E-decapeptide-induced 5-hydroxytryptamine release was additive to that induced by low concentrations of polyarginine, but non-additive to that induced by high concentrations of polyarginine. In contrast, release induced by antigen was additive along the whole length of the concentration-response curve to polyarginine. Benzalkonium chloride inhibited immunoglobulin-E-decapeptide- and polyarginine-induced 5-hydroxytryptamine release but enhanced release induced by immunological stimulation.
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PMID:Immunoglobulin E decapeptide-induced 5-hydroxytryptamine release from rat peritoneal mast cells. Comparison with corticotropin-(1-24)-peptide, polyarginine, polylysine and antigen. 732 27

Effects of intraventricular (third ventricle) injection of morphine and beta-endorphin on the release of serotonin (5-HT; 5-hydroxytryptamine) and 5-HIAA (5-hydroxy indolacetic acid) from the spinal cord were studied using urethane anesthetized spinally perfused rats. Intraventricular injection of morphine (25 micrograms) increased the 5-HT level in the perfusate about threefold. The increase of 5-HT release reached at peak between 30 and 60 min after the first injection of morphine. However, the levels of 5-HIAA, a metabolite of 5-HT, was not significantly altered by intraventricular injection of morphine. Furthermore, second intraventricular injection of morphine at the same dose did not increase 5-HT level in the spinal perfusate. In contrast to the results with morphine, beta-endorphin (10 micrograms) administered intraventricularly did not alter the release of 5-HT and 5-HIAA from the spinal cord. In addition, acute antinociceptive tolerance to intraventricular morphine induced by a prior intraventricular injection of morphine was studied in pentobarbital anesthetized rats. Acute tolerance was induced by intraventricular pretreatment with morphine (20 micrograms) for 120 min and the same dose of morphine was injected intraventricularly. The tail-flick test was used as an antinociceptive test. Pretreatment of rats with morphine intraventricularly reduced inhibition of the tail-flick response to intraventricularly injected morphine. The results support our previous hypothesis that beta-endorphin and morphine administered supraspinally activate separate descending systems. Spinopetal serotonergic descending pathway is selectively activated by intraventricularly injected morphine but not beta-endorphin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intraventricular injection of morphine and beta-endorphin on serotonin release from the spinal cord in rats. 753 10

The present study examined the effects of gamma-aminobutyric acid (GABA) agonists and antagonists on basal periventricular-hypophysial dopaminergic (PHDA) neuronal activity with a focus on the role of endogenous GABA in mediating 5-hydroxytryptamine- and stress-induced decreases in PHDA neuronal activity. PHDA neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in terminals of these neurons in the intermediate lobe of the pituitary. Plasma concentrations of alpha-melanocyte-stimulating hormone (alpha MSH) also were determined to provide a further index of PHDA neuronal activity. Administration of the GABAB agonist baclofen, but not the GABAA agonist isoguvacine, produced dose- and time-related decreases in intermediate lobe DOPAC concentrations and corresponding increases in plasma alpha MSH concentrations. Administration of either the GABAA antagonist SR-95,531 [2-(3-carboxypropyl)-3-amino-6-(4-methoxyphenyl)-pyridazinium bromide] or GABAB antagonists 2-hydroxysaclofen and CGP-35,348 [P-(3-aminopropyl)-P-diethoxymethyl-phosphinic acid; SR-95-531 did not alter basal intermediate lobe DOPAC concentrations or plasma alpha MSH concentrations per se, indicating that endogenous GABA does not tonically inhibit PHDA neuronal activity or alpha MSH secretion. 2-Hydroxysaclofen and CGP-35,348 did, however, reverse the baclofen-induced decrease in intermediate lobe DOPAC concentrations and increase in plasma alpha MSH concentrations. In a similar fashion, 2-hydroxysaclofen blocked the inhibitory effects of stress and the 5-hydroxytryptamine2/1c receptor agonist DOI [1-(2,5-dimethoxy-4-iodophenyl-2-aminopropane] on PHDA neuronal activity. These results indicate that GABAB and not GABAA receptor activation inhibits basal PHDA neuronal activity, and that GABAB receptor activation mediates the inhibitory effects of 5-hydroxytryptamine and stress on PHDA neurons.
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PMID:gamma-Aminobutyric acid receptor-mediated regulation of periventricular-hypophysial dopaminergic neurons: possible role in mediating stress- and 5-hydroxytryptamine-induced decreases in neuronal activity. 796 62


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