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)

The influence of amygdaloid kindling on brain and pituitary content of immunoreactive dynorphin (IR-DYN) and other opioid peptides was studied in rabbits. The kindling was very effective in increasing the hippocampal levels of IR-DYN, alpha-neoendorphin and Leu-enkephalin, but remained without any significant effect on the levels of IR-DYN and beta-endorphin in the majority of brain structures studied. The concentration of IR-DYN in the hippocampus remained at the control level throughout the development but was increased dramatically after completion of kindling. Biochemical alterations persisted for at least one month following the completion of kindling. The obtained results suggest that the hippocampal IR-DYN and related peptides may play some role in the maintenance of amygdaloid-kindled seizures.
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PMID:Opioid peptides, particularly dynorphin, after amygdaloid-kindled seizures. 613 21

Previous studies have shown that morphiceptin is a highly selective mu-receptor agonist. Recently we have obtained a more potent and stable analog, Tyr-Pro-NMePhe-D-Pro-NH2 (PL017). This peptide retains mu-receptor selectivity. beta-Endorphin is known to be a potent but non-selective opioid peptide for mu-, delta- and benzomorphan binding sites. Dynorphin is a putative kappa-agonist with significant affinity to mu-, delta- and benzomorphan binding sites in rat brain membranes. To understand the structural requirement for receptor type selectivity the enkephalin sequence of beta-endorphin and dynorphin was replaced by that of morphiceptin analog. Replacing the Met-enkephalin sequence of beta h-endorphin by PL017 yields a peptide highly selective for mu-binding sites. Substituting the Leu-enkephalin sequence of dynorphin-17 produces a peptide [PL017-dynorphin(6-17)] that retains high affinities for mu- and kappa-binding sites and has very low affinities for delta- and benzomorphan binding sites. These results suggest that a morphiceptin sequence at the amino-terminus of large opioid peptides can dictate mu-receptor selectivity. An enkephalin sequence at the amino-terminus of large opioid peptides seems to be required to retain high affinity for delta- and benzomorphan binding sites. The high affinity of PL017-dynorphin(6-17) for kappa-binding sites but not for benzomorphan binding sites suggests that benzomorphan sites of rat brain are not kappa-sites.
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PMID:The role of amino-terminal sequence of beta-endorphin and dynorphin in the determination of opiate receptor type selectivity. 614 89

Gamma-aminobutyric acid (GABA) blocked concentration of the pigments in melanophores and erythrophores of intact crabs. GABA blocked the release of pigment concentrating hormones from the isolated eyestalk. Octopamine (OA) blocked black pigment dispersion in intact crabs, but did not affect red pigment dispersion or concentration. OA blocked the release of black pigment dispersing hormone from isolated eyestalks. Met-enkephalin, but not Leu-enkephalin, stimulated black and red pigment concentration in intact crabs. Met-enkephalin, but not Leu-enkephalin, stimulated the release of pigment concentrating hormones from isolated eyestalks. Naloxone blocked the effects of Met-enkephalin in intact crabs and on isolated eyestalks. Beta-endorphin induced black pigment dispersion in intact crabs and in isolated legs.
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PMID:Regulation of neurohormone release in the fiddler crab, Uca pugilator: effects of gamma-aminobutyric acid, octopamine, Met-enkephalin, and beta-endorphin. 614 82

A simple, rapid method is described for separating neuropeptides. Samples were injected on Sep-Pak disposable reverse phase cartridges and eluted with a step gradient of n-propanol in formate-pyridine buffer. Enkephalins are separated from metabolic products. Separation alpha, beta and gamma-endorphin demonstrated, and Met- and Leu-enkephalin are also separated. This inexpensive, reproducible method a useful in studies of neuropeptide metabolism, purification of synthesized peptides, separation prior to RIA, or concentration of neuropeptides.
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PMID:Rapid separation of enkephalins and endorphins on Sep-Pak reverse phase cartridges. 617 36

When bovine chromaffin cells are dissociated from the adult adrenal gland and placed in culture, they begin to synthesize vasoactive intestinal polypeptide (VIP); they also contain high levels of enkephalin peptides. The regulation of expression of VIP and enkephalin in these cells by cyclic nucleotides was examined. Exposure of cultured chromaffin cells to cholera toxin (CT), forskolin (F), isobutylmethylxanthine (IBMX), 8-bromo-cyclic AMP (8-Br-cAMP) or dibutyryl cyclic AMP (dbcAMP) increases VIP and met-enkephalin biosynthesis as measured by an increase in total (cellular + secreted) VIP and met-enkephalin in treated versus untreated cells. Enkephalin levels increase 1.5 to 3.0 -fold while VIP levels increase 10 to 20 -fold after 48 hours of exposure to the compounds above. Increased enkephalin levels are maximum by 48 hours of exposure; VIP levels are elevated by forskolin or cholera toxin already at 17 hours of exposure. Neither forskolin nor cholera toxin alter catecholamine levels in cultured cells even after 72 hours of exposure. Thus, VIP and ME expression in cultured chromaffin cells can be regulated by intracellular cAMP. Measurement of preproenkephalin messenger RNA (mRNAenk) by quantitative Northern blot hybridization with a preproenkephalin complementary DNA probe revealed that exposure of chromaffin cells to forskolin elicits a greater than two-fold increase in mRNAenk, suggesting that the regulation of neuropeptide expression by elevated intracellular cAMP occurs at a transcriptional locus.
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PMID:Cyclic adenosine monophosphate regulates vasoactive intestinal polypeptide and enkephalin biosynthesis in cultured bovine chromaffin cells. 619 86

Opioid peptides are present in peripheral blood, and may bind to human lymphocytes. In order to determine their influence on human lymphocytes we studied the effect of endogenous opioid peptides on human lymphocyte natural killer function. Beta-endorphin and several analogues (i.e., gamma-endorphin) are shown to enhance human peripheral blood natural killer function. The enhancement of natural killing by these opioid peptides was dose-dependent and naloxone (an opiate antagonist) reversible. In studying various analogues of beta-endorphin, beta-lipotropin and gamma-endorphin were approximately 3-5 times more effective at enhancing peripheral blood NK function than Leu-enkephalin and -endorphin. In addition, we observed that naloxone reversed human fibroblast interferon mediated enhancement of human blood lymphocyte natural killer function. These observations suggest that circulating endogenous opioid peptides may have a physiologic role in regulating human blood lymphocyte natural killing.
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PMID:Endorphins stimulate normal human peripheral blood lymphocyte natural killer activity. 620 82

The effects of intracerebroventricular injections of synthetic ovine beta-endorphin were tested in conscious rats with gastric and pancreatic fistulas. In the range of 0.8 to 25 microgram injected in the third ventricle of the brain, basal gastric and pancreatic secretions were strongly inhibited in a dose-dependent manner. Pancreatic volume, bicarbonate output, and total protein output were similarly inhibited, while the bicarbonate concentration was only slightly changed. Similar effects were noted after the administration of morphine. In the present model system, morphine was 20-30 times less active than beta-endorphin on a molar basis. Beta-Endorphin inhibition of pancreatic secretion was reversed by naloxone, suggesting that opiate receptors are involved in this phenomenon. Gastric acid secretion participated in the pancreatic effects of beta-endorphin to only a slight extent, since pancreatic inhibition by the endorphin was decreased only slightly in rats with gastic fistula in which gastric juice was diverted and did not reach the duodenum. The comparison of intravenous and intraventricular injections of beta-endorphin and morphine suggested that the observed inhibitions originated in the central nervous system. No effects were detected after the administration of alpha-endorphin, Met-enkephalin or Leu-enkephalin, although pancreatic secretion was measurably inhibited by long-acting synthetic enkephalin analogues.
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PMID:Central inhibition of basal pancreatic and gastric secretions by beta-endorphin in rats. 625 Sep 35

1. In homogenates of guinea-pig brain, the characteristics of the binding of [3H]-ethylketazocine, an agonist for the putative kappa-receptor, were determined by estimation of the affinity and capacity of binding, by competitive inhibition for the binding site by unlabelled ligands and by selective protection of the binding site from alkylation by phenoxybenzamine. 2. At 25 degrees C the maximum number of binding sites for [3H]-ethylketazocine was about 14 pmol/g fresh brain, of which about 50% were high affinity sites. 3. In competition experiments, the high affinity binding of [3H]-ethylketazocine to the kappa-binding site was readily displaced by several kappa-agonists but not by the selective mu-ligand, D-Ala2, MePhe4, Gly-ol5-enkephalin or the selective delta ligand, D-Ala2, D-Leu5-enkephalin. In contrast, the kappa-agonists tested so far exhibit a high degree of cross-reactivity with the mu-binding site but somewhat less with the sigma-binding site. Similar specificities were observed in protection experiments. 4. The approximate proportions of the three subtypes of opiate receptor in the guinea-pig brain are 25% mu-binding sites, 45% delta-binding sites and 30% kappa-binding sites. 5. The endogenous opioids, Met-enkephalin, Leu-enkephalin and porcine beta-endorphin have only a low affinity for the kappa-binding site.
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PMID:Characterization of the kappa-subtype of the opiate receptor in the guinea-pig brain. 626 35

The binding characteristics of two highly potent analgesic enkephalin analogs, [D-Thr2, Thz5]-and [D-Met2, Thz5]-enkephalinamide, to the rat brain membrane preparation have been investigated using tritiated Leu-enkephalin, human beta-endorphin or dihydromorphine as the primary ligand. Concentrations for 50% inhibiting activity of the enkephalin analogs are much lower in displacing tritiated dihydromorphine in comparison with that for the other two tritiated ligands. In addition, a correlation between analgesic potency and capacity to displace tritiated dihydromorphine is observed. These data may explain the high antinociceptive activity of the enkephalin analogs and support the hypothesis that the mu-receptor is involved with analgesia.
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PMID:Opiate receptor-binding activity of [D-Thr2,Thz5]-and [D-Met2,Thz5]-enkephalinamides. 627 45

The effects of opioid peptides on th response to stimulation of adrenergic or non-adrenergic inhibitory nerve were investigated in the guinea-pig taenia coli. Leu-enkephalin, met-enkephalin, (D-ala2) met-enkephalin and beta-endorphin inhibited non-adrenergic inhibitory response, in a dose-dependent manner. (D-ala2) metenkephalin and beta-endorphin were the most potent compounds in inhibiting the elicited relaxation, having ID50 values of 1 micro M. The inhibitory actions of these opioid peptides were reversed by naloxone (1 micro M). Naloxone itself potentiated the non-adrenergic inhibitory response. On the contrary, the adrenergic inhibitory response was not affected by application of leu-enkephalin, beta-endorphin or naloxone. Using an immunohistochemical method, met-enkephalin immunoreactive nerve fibers were observed in the longitudinal muscle layer, Auerbach plexus and circular muscle layer of the taenia. From these observations, it is concluded that endogenous opioid peptides may play a regulatory role in non-adrenergic inhibitory neurotransmission but endogenous opioid peptides may play a regulatory role in non-adrenergic inhibitory neurotransmission but not in adrenergic neurotransmission.
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PMID:[Modulation by endogenous opioid peptides of non-adrenergic neurotransmission in the guinea-pig taenia coli (author's transl)]. 627 76


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