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 analgesic effect of intracerebroventricular administration of morphine, ketocyclazocine, [D-ala2]-methionine enkephalinamide (DAM), [D-ala2-D-leu5]-enkephalin (DADLE), leuenkephalin, metenkephalin, and beta-endorphin on acetic acid-induced abdominal writhing (AAW) was investigated in naive and morphine-tolerant mice. It was found that the relative potencies of a series of opioids are different in naive and morphine-tolerant groups. In naive animals, the order of potency (ED50, nmol) was beta-endorphin greater than morphine = DAM greater than DADLE greater than ketocyclazocine = leuenkephalin = metenkephalin. The morphine-tolerant animals were cross-tolerant to ketocyclazocine and to all the peptides studied; DAM and beta-endorphin exhibited the highest degree of tolerance. In morphine-tolerant animals, the order of potency was morphine = DADLE = beta-endorphin greater than DAM = ketocyclazocine = metenkephalin greater than leuenkephalin. The results indicate that endogenous opioid systems may be affected by tolerance development to morphine.
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PMID:Analgesic cross-tolerance between morphine and opioid peptides. 609 81

In previous studies, we observed that dynorphin- (1-13), but not dynorphin-(1-9), can significantly inhibit morphine- or beta-endorphin-induced analgesia despite not having any appreciable analgesic activity itself. Dynorphin-(1-13) showed no inhibitory effect on Sandoz FK33824-induced analgesia. In the present study, we examined the effect of dynorphin on morphine-, beta-endorphin-, D-ala2-D-leu5-enkephalin- or Sandoz FK33824-induced analgesia in both naive, morphine-tolerant and morphine-dependent mice. It was found that although dynorphin may inhibit morphine- or beta-endorphin-induced analgesia in naive animals, the peptide is not effective in inhibiting D-ala2-D-leu5-enkephalin- or Sandoz FK33824-induced analgesia. Dynorphin is also effective in blocking spontaneous withdrawal jumping in morphine-dependent animals. It is suggested that dynorphin-(1-13) may play a modulatory role in regulating analgesia due to morphine or beta-endorphin, but not that due to enkephalin. The action of peptides on morphine- or beta-endorphin-induced analgesia in the naive state is different from that of the tolerant state, suggesting that dynorphin may be involved in the development of morphine tolerance and physical dependence.
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PMID:Possible regulatory role of dynorphin on morphine- and beta-endorphin-induced analgesia. 611 98

The ability of several opioids in potentiating the synaptic activation of CA1 pyramidal cells in the rat hippocampal slice were compared. Morphine and the opioid peptides, (D-ala2, D-leu5)-enkephalin (DADL), morphiceptin, beta-endorphin, and Tyr-D-Ser-Gly-Phe-Leu-Thr (DSThr) caused a concentration-dependent, naloxone-reversible shift to the left in the input-output (IO) curve constructed by plotting the population spike as a function of the field EPSP. These opioids then produced an increase in the size of the population spike while leaving the EPSP unaffected. In contrast, the kappa agonist prototype, ethylketazocine, had no effect on the IO curve when perfused in concentrations up to 10 microM. The rank order of potency for the opioids in the CA1 region of the hippocampus was DADL greater than DSThr greater than beta-endorphin greater than morphiceptin greater than morphine much greater than ethylketazocine. Thus, opioids that are more specific for delta opiate receptors were the most potent and mu receptor agonists, the least potent in this action. Taken together with previous studies suggesting that morphine and DADL may interact with a common opiate receptor in the CA1 region, the results are consistent with the notion that these epileptiform effects may be primarily mediated by delta opiate receptors in this area although the potency of morphiceptin indicates that mu receptors play some role in this effect.
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PMID:Opioid pharmacology in the rat hippocampal slice. 613 61

Treatment with the enzyme arylsulfatase in vivo selectively attenuated the effect of analgesia induced by morphine, beta-endorphin or ethylketocyclazocine but not that induced by Sandoz FK33824 or D-ala2-D-leu5-enkephalin. The effect on morphine analgesia was indicated both by an increased morphine ED50 in the presence of a fixed dose of naloxone and by a decreased naloxone ED50 in the presence of a fixed dose of morphine. Arylsulfatase treatment in vivo also selectively affected in vitro ligand binding; Bmax values of the low affinity binding site of dihydromorphine, naloxone, D-ala2-D-leu5-enkephalin, D-ala2-met5-enkephalinamide and ethylketocyclazocine were decreased significantly while the Bmax values of the high affinity sites as well as the KD values of both the high and low affinity sites were affected little or not at all. The data suggest that the change induced by the enzyme may have been due to the alteration of certain constituents of the low affinity opiate binding site.
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PMID:Differential modification of opiate receptor activity by arylsulfatase treatment. 613 34

Tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) activities, dopamine (DA), noradrenaline (NA), adrenaline (A), met 5-enkephalin (Met-Enk), leu5-enkephalin (Leu-Enk), dynorphin (Dyn) and beta-endorphin (beta-end) were measured simultaneously in ten human pheochromocytomas = 1 - TH activity was highly variable, from 22 to 2220 U/g tissue. 2 - DBH activity, in contrast, was rather constant, from 96 to 582 U/g. 3 - Catecholamines (A and NA) concentrations showed only small variations. 4 - The four opioid peptides were detected in all cases and exhibited a wide range of tissue concentrations (Enk much greater than Dyn greater than beta-end). 5 - Met-Enk and Leu-Enk concentrations were highly correlated; no correlation was observed with the other opioid peptides. 6 - A very strong correlation was observed between enkephalins concentrations and both catecholamines concentrations and DBH activities. These results are discussed in term of the significance of the co-localization of these various biologically active substances, principally with regard to the possible regulation of catecholamine synthesis by opioid peptides and conversely.
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PMID:Simultaneous evaluation of the catecholamine pathway and three opioid peptide-producing systems in human pheochromocytomas. 614 74

The binding of 3H-beta-endorphin to rat brain homogenates, reported by several other laboratories, has suggested unique selective beta-endorphin binding sites. We now present additional evidence supporting the concept of distinct beta-endorphin binding (epsilon) sites in rat brain. In competitive displacement studies, 3H-beta-endorphin was inhibited far better by unlabeled beta-endorphin than a variety of opiates and enkephalins. Conversely, beta-endorphin inhibited the binding of a series of 3H-labeled ligands, including dihydromorphine, ethylketocyclazocine, SKF 10,047, naloxone and D-ala2-D-leu5-enkephalin, far less potently than their corresponding unlabeled drug. Other differences were also found. Compared to 3H-dihydromorphine and 3H-D-ala2-D-leu5-enkephalin binding, 3H-beta-endorphin binding was far less sensitive to the reagent N-ethylmaleimide and more sensitive to the proteolytic enzyme trypsin. The regional distribution for 3H-beta-endorphin binding was also distinct from other 3H-ligands tested. This evidence supports the concept of a distinct binding site for beta-endorphin which does not correspond to the previously defined opioid binding sites.
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PMID:Binding of 3H-beta-endorphin in rat brain. 629 32

The intrathecal administration of several mu (morphine), delta (d-ala2-d-leu5-enkephalin, dimeric leu-enkephalin) and mixed mu/delta (beta-endorphin) agonists produced a dose-dependent inhibition of all cutaneous thermal (Tail Flick/Hot Plate) nociceptive responses in the rat. The kappa agonist U50488H had no analgesic potency in thermal nociceptive tests. On a visceral chemical test (writhing) and agonists exerted a powerful suppression of the response. In contrast at doses 10 to 50 times the ED50 on cutaneous thermal tests, delta agonists had no effect on the writhing response. At higher intrathecal doses, delta ligands produced flaccidity. These observations suggest the existence of three discriminable populations of opioid receptors in the spinal cord whose activation has different effects on the animals response to noxious stimuli.
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PMID:Differential association of spinal mu, delta and kappa opioid receptors with cutaneous thermal and visceral chemical nociceptive stimuli in the rat. 631 19

Opiate binding sites in five brain regions were labeled with the mu and delta markers, 3H-morphine and 3H-[D-Ala2,D-leu5]enkephalin, respectively. The highest densities of both 3H-morphine and 3H-DADLE labeled sites are found in striatum and frontal cortex. Hypothalamus and midbrain contain predominantly 3H-morphine labeled sites. The selectivity of the opioid peptides [D-Ala2,D-leu5]enkephalin, beta-endorphin and dynorphin(1-13) for the two opiate sites was investigated by comparing the potency of these unlabeled compounds against the mu and delta markers in different brain regions. This determination has the effect of controlling for the breakdown of peptides within each region. While the enkephalin analogue shows a preference for the delta binding site and beta-endorphin is more nearly equipotent towards the two binding sites, dynorphin(1-13) shows a high affinity and selective preference for the mu binding site over the delta site. The potency of the opioid peptides in displacing the mu and delta markers varies from region to region according to the relative densities of the two opiate binding site populations.
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PMID:Regional interactions of opioid peptides at mu and delta sites in rat brain. 632 40

In pentobarbital-anesthetized rabbits, iv injection of 9 nmol (31 micrograms) human beta-endorphin (beta h-endorphin)/kg BW caused a significant (P less than 0.05) increase in serum glucose and a significant decline in serum insulin during the subsequent 60 min. When 9 nmol/kg BW beta h-endorphin were injected simultaneously with 0.7 g glucose/kg BW, the clearance of serum glucose and the expected glucose-stimulated rise in serum insulin were both inhibited. The threshold dose for the insulinopenic effect of beta h-endorphin in the anesthetized, glucose-loaded rabbit was 0.09 nmol/kg BW. Threshold doses/kg BW were determined for six structurally related peptides found to possess insulinopenic activity: camel beta-endorphin, 0.09 nmol; N-arg-beta h-endorphin, 0.09 nmol; D-ala2-beta h-endorphin, 0.09 nmol; leu5-beta h-endorphin, 0.09 nmol; met-(O)5-beta h-endorphin, 0.9 nmol; and beta h-endorphin1-27, 0.9 nmol. Threshold dose/kg BW for somatostatin was 9 nmol. The following compounds were inactive at 9 nmol/kg BW: N-acetyl-beta h-endorphin; N-acetyl-arg-beta h-endorphin; beta h-endorphin2-31; beta h-endorphin6-31; beta h-endorphin(((1-5 + 6-31))); beta h-endorphin1-18 (gamma-endorphin); beta h-endorphin1-17 (alpha-endorphin); beta h-endorphin1-5 (met-enkephalin); leu5-beta h-endorphin (leu-enkephalin); met-NH2(5)-beta h-endorphin1-5 (met-enkephalinamide); D-ala2-leu5-beta h-endorphin1-5; D-ala2-N-me-phe4, met-(O)5-ol-beta h-endorphin1-5; and D-ala2-D-leu5-beta h-endorphin1-5. Ninety nmoles per kg BW of naloxone did not alter the insulinopenic effect of 0.9 nmol/kg BW beta h-endorphin. As little as 2.9 X 10(-10) molar beta h-endorphin inhibited glucose-stimulated release of insulin by rabbit pancreas slices in vitro. The capacities of the peptides and alkaloids to inhibit insulin secretion in vitro followed the same general order as the in vivo insulinopenic capacities. Naloxone at 2.9 X 10(-6) M did not reduce the antisecretagogue effect of 2.9 X 10(-8) M beta h-endorphin. These findings, when compared with previously described structure-activity relationships for opioid receptors, indicate the presence of a novel receptor for beta-endorphin in rabbit pancreas, the activation of which inhibits glucose-stimulated secretion of insulin.
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PMID:Effects of opioid peptides and opiate alkaloids on insulin secretion in the rabbit. 633 12

Opioids and opioid peptides influence the threshold to a seizure which is a model of petit mal epilepsy (Cowan, Geller and Adler, 1979). The present authors investigated representative opioid compounds in a model of a grand mal seizure, maximal electroshock (MES). Although all of the opioids and opioid peptides tested blocked tonic hindlimb extension, they divided into two groups, based on their ability to decrease the total length of the tonic component of the maximal electroshock seizure and their sensitivity to blockade by naloxone. The first group contained morphine, meperidine, methadone, ethylketocyclazocine (EK), D-ala2-met-enkephalinamide, D-ala2-leu5-enkephalin and beta-endorphin. The compounds in this group caused a decrease in the length of the tonic component that was dose-related, with the maximum decrease amounting to approx. 40%. The effect was blocked by the prior administration of 1 mg/kg of naloxone. The second group contained the partial agonists, pentazocine and cyclazocine. These opioids also caused a dose-related decrease in the length of the tonic component and, in the largest doses, the tonic component of the convulsion was completely blocked. Naloxone, in doses as large as 10 mg/kg, did not appreciably reverse the action of either drug.
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PMID:The anticonvulsant effect of opioids and opioid peptides against maximal electroshock seizures in rats. 672 28


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