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 concentrations of beta-endorphin have been shown to change in the rat brain during pregnancy and lactation. This study has been performed in order to analyze whether also brain opioid receptors might undergo significant modifications during these two physiological situations. The maximal binding capacity (Bmax) and the constant of affinity (Ka) of the mu-subpopulation of opioid receptors have been evaluated in the hypothalami of female rats at different stages of pregnancy (7, 15 and 22 days), on the day of parturition (12-18 h after delivery) and 6-8 days postpartum (both in lactating and in nonlactating animals). Female rats killed on the day of estrus served as controls. The receptor binding assay has been performed utilizing [3H]-dihydromorphine [( 3H]-DHM) as the ligand for the mu-opioid receptors. Hypothalamic concentrations of beta-endorphin as well as serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin have also been evaluated by radioimmunoassay. The results showed that the concentration of hypothalamic mu-opioid receptors increased during pregnancy, being significantly higher than in the controls at days 15 and 22 of gestation. After delivery, the concentration of these receptors returned towards control values, regardless on whether the animals were lactating or not. The Ka values of [3H]-DHM for the mu-receptors did not change significantly in the different groups of experimental animals. Hypothalamic beta-endorphin content showed a modest though not significant increase at the end of gestation (day 22) and returned to control values 12-18 h after delivery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic opiatergic tone during pregnancy, parturition and lactation in the rat. 165 58

The involvement of delta opioid receptors in supraspinal analgesia was investigated. With this aim, opioids that produced analgesia in the tail immersion test were administered i.c.v. to mice a few minutes before the irreversible antagonist, beta-funaltrexamine (beta-FNA). Protection of the respective analgesic effects from beta-FNA blockade was obtained when evaluated 24 h later. Moreover, mu ligands protected the analgesia evoked by ED50s of morphine, [D-Ala2,N-Me-Phe4,Met-(o)5-ol]enkephalin (FK 33-824), [D-Ala2,N-Me-Phe4,Gly-ol5]enkephalin (DAGO) and human beta-endorphin at doses (ED50s) lower than those required for delta ligands (approximately ED90s) to reach a similar protection. delta Preferential ligands effectively protected the analgesia induced by ED50s of [D-Ala2,D-Leu5]enkephalin (DADLE), [D-Thr2,Leu5]enkephalin-Thr6 (DTLET) and [D-Pen2,D-Pen5]enkephalin (DPDPE) from the beta-FNA-deteriorating effect. FK 33-824 and DAGO also provided good protection of the analgesia elicited by these delta ligands whereas morphine protected much less. Binding studies after i.c.v. injection of beta-FNA showed that its alkylating effect on opioid receptors was restricted to periventricular areas. In PAG, where the mu/delta receptor ratio is about 10, [3H]DADLE specific binding was still present after ED50s of DPDPE, DAGO, morphine and DADLE as protecting agents. [3H]Dihydromorphine [( 3H]DHM) binding was well protected by ED90s of morphine and DAGO, and to a lesser extent by DPDPE and DADLE. These results suggest that delta ligands, after binding to delta receptors, also need to act upon mu receptors to produce high levels of supraspinal analgesia in the tail immersion test.
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PMID:Evaluation of delta receptor mediation of supraspinal opioid analgesia by in vivo protection against the beta-funaltrexamine antagonist effect. 256 40

Interleukin 1 (IL1) is a macrophage-derived polypeptide which signals neurons in the preoptic-anterior hypothalamus to initiate fever and the acute-phase glycoprotein response. Recently, increases in cerebrospinal fluid and hypothalamic levels of beta-endorphin have been reported during endotoxin (LPS)- and IL1-induced fevers, suggesting that this opioid may participate in the modulation of IL1 effects in the CNS. In this study, we investigated whether purified (human) IL1 influences the specific binding of three prototypic opioid agonists (2-D-alanine-5-L-methionineamide, DAME; (-)-ethylketocyclazocine, EKC; dihydromorphine, DHM) and one antagonist (naloxone) to opioid receptor-enriched membrane preparations in cerebral cortex, hypothalamus, midbrain, pons, medulla, and cerebellum of guinea pig brain. IL1 reduced the binding of these ligands to their receptors during a 30-min incubation. The extent of IL1 inhibition of a given ligand for its binding sites varied according to the brain region; within some regions, the extent of this inhibition also varied with the four ligands tested. But in cortex the effect of IL1 on the specific binding of DHM is dose-dependent. Similar results were obtained with crude homologous IL1. S. enteritidis endotoxin, suspended in pyrogen-free saline at concentrations from 4 to 36 micrograms/ml, did not inhibit the binding of these opioid ligands to their receptors in any brain region. These results indicate that IL1 interacts with the opiate receptors in guinea pig brain. This interaction, moreover, is not limited to the hypothalamus alone, the primary site of the pyrogenic action of IL1, but also occurs in other brain regions.
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PMID:Interleukin 1 reduces opioid binding in guinea pig brain. 301 Feb 57

Using prototypic ligands for each type of opioid receptors (mu, delta, kappa, and sigma) as well as compounds derived from each class of endogenous opioid peptides (beta-endorphin, enkephalins, and dynorphins), we have undertaken the characterization of adrenomedullary opioid binding sites. The specific binding of [3H]etorphine ([3H]ET) to a membrane preparation of bovine adrenal medulla was greatly increased when the incubation temperature was raised from 22 to 37 degrees C. Characterization of the opioid binding sites was obtained at 37 degrees C with [3H]ET (nonspecific opioid ligand), [3H]ethylketocyclazocine ([3H]EKC; kappa), [3H]dihydromorphine ([3H]DHM; mu), [3H]-[D-Ala2,D-Leu5]enkephalin ([3H]DADLE: delta), and N-[3H]allylnormetazocine ([3H]SKF-10047; sigma) in the absence or presence of blocking agents for cross-reacting receptors. [3H]ET had a high affinity binding site (KD = 0.98 nM) with a Bmax of 119 pmol/g protein. All the other opioid compounds showed biphasic saturation curves with KD ranging from 0.6 to 1.29 nM for the high affinity binding site and from 2.49 to 12.1 nM for the low affinity binding site. The opioid mu-receptor was characterized by the high affinity binding site for [3H]DHM (KD = 1.29 nM; Bmax = 38 pmol/g protein). Blockade of the cross-reacting receptor sites for [3H]EKC, [3H]DADLE, and [3H]SKF-10047 revealed the presence of kappa (KD = 0.66 nM; Bmax = 12 pmol/g protein), kappa 2 (benzomorphan site; KD = 11.1 nM; Bmax = 56 pmol/g protein), delta (KD = 0.67 nM; Bmax = 4.7 pmol/g protein), and sigma (KD = 4.54 nM; Bmax = 32 pmol/g protein) opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Opioid receptors in bovine adrenal medulla. 609 79

C57 BL/6J (C57) mice display a particular pattern of responses following morphine administration, such as a rapid development of tolerance to the pharmacological action of the opiate and an increase in locomotor activity after a single injection of the drug. We have measured met-enkephalin content and the responsiveness of different opiate receptors after repeated administration of morphine and naloxone. Prolonged morphine administration changes neither met-enkephalin levels, nor the density of the opiate receptors in mice brain. In contrast repeated administration of the opiate antagonist naloxone, produced a marked increase in the number of 3H- DHM and 3H- DADLE binding sites in striatum and brainstem without modifying met-enkephalin concentrations. Behavioral studies have indicated that the morphine-induced increase in locomotor activity is enhanced in naloxone pretreated mice, thus suggesting a possible correlation between the behavioral response to morphine in C57 mice and the higher number of opiate receptors in the striatum.
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PMID:Modulation of opioid system in C57 mice after repeated treatment with morphine and naloxone: biochemical and behavioral correlates. 632 41