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)

Using a rat tail-flick analgesic assay that uses a cold water-ethylene glycol mixture (-10 degrees C) as the noxious stimulus, we have been able to demonstrate a dose-related, naloxone-reversible analgesic effect for dynorphin A (1-17), the proposed endogenous ligand for the kappa receptor. Male Sprague-Dawley rats were implanted surgically with cannulas in the right lateral ventricle at least 1 week before testing. Five microliters of either drug or saline, followed by a 3-microliter saline flush, were administered. Nociceptive threshold was measured as the latency for the rat to flick or remove its tail from the bath solution after immersion. Dynorphin produced a dose-related analgesia at doses of 1 to 50 micrograms i.c.v., reaching 100% maximum possible analgesia (compared to predrug base line) at the highest dose. We found similar dose-related analgesia when we tested the selective mu agonist [Try-D-Ala-Gly-NMe-Phe-Gly-ol] (0.01-1 microgram), the selective kappa receptor ligand U-50,488H (100-500 micrograms), the selective delta agonist [D-Pen2,5]-enkephalin (50-200 micrograms) and beta-endorphin (0.1-10 micrograms). Naloxone (1.0 mg/kg) was able to block the antinociceptive effect of all but the highest doses of dynorphin, which required 10.0 mg/kg of naloxone. When we compared the same dosages of dynorphin using hot water (55 degrees C) as the noxious stimulus, no antinociception was observed. Although we do not known the mechanisms responsible for the differences between the hot and cold water tests, it may be that the cold water tail-flick test, which is able to assess the antinociceptive activity of both opioid agonists and mixed agonist-antagonists, is a more sensitive measure of the type of analgesia mediated by kappa receptors.
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PMID:Antinociceptive action of intracerebroventricularly administered dynorphin and other opioid peptides in the rat. 290 Mar 24

The level of opioid peptides: beta-endorphin and dynorphin, binding to the mu and kappa opioid receptors and the analgesic response of those endogenous opioid systems to stress were investigated in two strains of mice: C57BL/6 (C57) and DBA/2 (DBA). The nociceptive threshold of DBA mice was higher than that of C57 mice. KD values for spinal mu receptors were lower in C57, while KD for cerebral kappa receptors were higher in this strain. DBA mice have significantly higher concentrations of dynorphin in the hypothalamus and neurointermediate lobe of the pituitary. Stress-induced analgesia was much greater in C57 than in DBA mice. In the hypothalamus both stress procedures depressed the concentrations of beta-endorphin in C57, and dynorphin in DBA mice. The level of beta-endorphin increased in the neurointermediate lobe in C57 and in anterior lobe of the pituitary in DBA mice. In the spinal cord both stress procedures depressed the dynorphin level. The above data indicate that C57 and DBA mice differ in the endogenous opioid peptide content, stress-induced alteration and opioid receptor affinity, the effects which might correlate with their different responses to environmental factors and pharmacological agents.
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PMID:The difference in stress-induced analgesia in C57BL/6 and DBA/2 mice: a search for biochemical correlates. 290 36

Mechanisms of hypnotic analgesia are still poorly understood and conflicting data are reported regarding the underlying neurochemical correlates. The present study was designed to investigate the effects of hypnotically induced analgesia and hypnotizability on experimental ischemic pain, taking into account pain and distress tolerance as well as the neurochemical correlates. 11 high hypnotizable Ss and 10 low hypnotizable Ss, as determined by scores on the Stanford Hypnotic Susceptibility Scale, Form C (Weitzenhoffer & E. R. Hilgard, 1962), were administered an ischemic pain test in both waking and hypnotic conditions. The following variables were measured: (a) pain and distress tolerance, (b) anxiety levels, and (c) plasma concentrations of beta-endorphin and adrenocorticotropic hormone (ACTH). Results confirmed significant increases of pain and distress tolerance during hypnosis as compared to the waking state, with positive correlations between pain and distress relief and hypnotizability. Moreover, a hypnotically induced dissociation between the sensory-discriminative and the affective-motivational dimensions of pain experience was found, but only in high hypnotizable Ss. Hypnotic analgesia was unrelated to anxiety reduction and was not mediated either by endorphins or by ACTH.
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PMID:Effects of hypnotic analgesia and hypnotizability on experimental ischemic pain. 292 94

The need for better analgesia during burn dressing changes (BDCs) in acutely burned children led us to assess pain during BDC with a large 0-10 thermometer-like scale which was well accepted and appeared to reflect the varying degrees of pain that patients experienced. Pain scores were obtained at least once each minute throughout 33 BDCs in 15 patients of 8-17 years. Plasma levels of beta-endorphin immunoactivity (iB-EP) were measured at 5 intervals before and after BDC; mean values (+/- S.E.M.) ranged from 30.5 +/- 4.63 pg/ml (before BDC and analgesic) to 19.2 +/- 3.02 pg/ml (immediately following BDC). The mean pain score (MPS) for each BDC was inversely related to the iB-EP levels of that day (P less than 0.001 with 4 of the 5 iB-EP determinations). The MPS varied directly with the extent of burn injury and inversely with weight; the 2 variables together predicted MPS as well as the iB-EP alone (r2 = 43 and 36% respectively).
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PMID:The assessment of pain and plasma beta-endorphin immunoactivity in burned children. 293 62

Neonatal administration of monosodium glutamate (MSG) produces necrosis of circumventricular structures, including perikarya in the medial-basal hypothalamus that contain beta-endorphin (BEND) and met-enkephalin. Since neonatal MSG treatment alters morphine analgesia, the present study examined neonatal MSG effects upon opioid analgesia observed following either BEND or d-ala d-leu enkephalin (DADL). Rats treated with either MSG or vehicle over the first ten post-natal days, were surgically prepared with a lateral ventricle cannula at 100 days of age. Respective groups received central injections of either BEND (0, 0.1, 0.5 or 1.0 microgram) or DADL (0, 4, 20 or 40 micrograms), and jump thresholds were assessed 15, 30, 45 and 60 min thereafter. Following testing, selected MSG-treated and control animals were prepared for BEND immunocytochemistry. While the magnitude, duration and sensitivity of BEND analgesia on the jump test failed to differ between groups, MSG-treated rats displayed a 10-fold leftward shift in sensitivity and a 200-300% increase in the magnitude of DADL analgesia. Immunocytochemical analysis indicated that MSG treatment depleted perikarya in the medial-basal hypothalamus, periventricular thalamic fibers and periaqueductal gray terminal fields that contained BEND. The differential effects of MSG treatment upon opiate and opioid analgesia are discussed in terms of possible alterations in opiate receptor subpopulations.
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PMID:Differential alterations in opioid analgesia following neonatal monosodium glutamate treatment. 293 2

Effects of electroacupuncture (EA) on pain threshold and beta-endorphin (beta-End) contents in plasma, pituitary (Pit), hypothalamus (Hyp) and cerebrospinal fluid (CSF) were studied in nontreated, dexamethasone (Dex) treated and adrenalectomized (Adrex) male SD rats by the use of specific determination of rat beta-End (combination of HPLC and RIA). EA increased pain threshold and plasma beta-End with no effect on beta-End contents in Pit, Hyp and CSF. Dex did not affect control pain threshold, but tended to reduce EA-induced increase in pain threshold (EA-analgesia, EAA) and EA-induced increase in plasma beta-End. Adrex increased plasma beta-End without change in control pain threshold. Adrex tended to reduce EAA, but a tendency of further increase in plasma beta-End was observed after addition of EA. Adrex increased Pit beta-End, but no further change in Pit beta-End was observed after addition of EA. A positive correlation between plasma beta-End and plasma ACTH was observed in nontreated, Dex treated and Adrex rats. No correlation between plasma beta-End and potency of EAA was observed in nontreated, Dex treated and Adrex rats. The hind-paw pressure test without EA increased plasma beta-End to the same degree as that produced by EA, and it produced no analgesia. These results suggest that Pit beta-End may not be mainly involved in the development of EAA.
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PMID:[Effects of electroacupuncture on beta-endorphin contents in rats]. 293 79

D-phenylalanine, bacitracin and puromycin produce long-lasting, naloxone-reversible analgesia in mice. Analgesic potency parallels potency of these compounds as inhibitors of met-enkephalin degradation by mouse brain enzymes. D-phenylalanine potentiates acupuncture analgesia in mice and humans and has been used to ameliorate a variety of human chronic pain conditions.
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PMID:Analgesic properties of enkephalinase inhibitors: animal and human studies. 293 46

Nineteen women were studied before, during and after labour by assessment of their mood using a variety of psychological tests and by measurement of their plasma concentrations of beta-endorphin and cortisol. Beta-endorphin and cortisol concentrations rose markedly during labour and were influenced by the type of analgesia used. A deterioration in cognitive performance between days 2 and 4 postpartum correlated positively with the fall in beta-endorphin concentrations from those in labour to those on the fourth day postpartum. The women were more anxious and depressed at 38 weeks' gestation than on days 1-4 postpartum and the elevation of mood on day 2 postpartum correlated with a measure of depression 8 weeks later. It is postulated that the phenomenon of postpartum blues is a reaction to the euphoria of delivery which in turn is a response to endorphin release during labour. Whilst these changes may have a role in promoting maternal-infant attachment it is at the expense of maternal depression some weeks later.
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PMID:Peripartum concentrations of beta endorphin and cortisol and maternal mood states. 293 37

Eleven male and 15 female sheep were subjected to electroacupuncture (EA) treatment, using 2 needle loci described in the Chinese veterinary literature as Yao Pang (lumbar region) and San Yang Lu (1 thoracic limb). Noninjurious cutaneous stimuli were applied, using a calibrated pin-prick probe, a clamp, and a contact heat (75 to 95 C) probe. Cutaneous pain thresholds (PT) were quantified in 7 body areas during control (no acupuncture needles and no electrostimulation) and EA experiments, before and after IV injection of naloxone. Using each animal as its own control, each EA experiment was classified as inducing either good or poor anagelsia on the basis of whole-body PT values. Plasma concentrations of immunoreactive beta-endorphin (beta E) and prolactin were quantified in sequential plasma samples collected at 9-minute intervals throughout all experiments. Electroacupuncture at each locus increased (P less than 0.01) PT (ie, caused cutaneous analgesia) in 6 of 7 body areas, and increased (P less than 0.05) plasma concentrations of immunoreactive beta E and prolactin. In EA experiments in which good analgesia was induced, plasma beta E was increased more (P less than 0.05) than in EA experiments in which poor analgesia was induced. This difference was more evident for the Yao Pang locus. Generally, plasma prolactin concentrations were increased more with good analgesia than with poor analgesia for the Yao Pang locus. Electroacupuncture stimulation of the San Yang Lu locus was associated with higher plasma beta E concentrations than that associated with the Yao Pang locus. Increases in plasma prolactin concentrations were comparable between loci.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electroacupuncture-induced analgesia in sheep: measurement of cutaneous pain thresholds and plasma concentrations of prolactin and beta-endorphin immunoreactivity. 293 27

The effect of intraventricular beta-endorphin-(1-27) on the spinal release of Met-enkephalin induced by intraventricular beta-endorphin was studied using the intrathecal superfusion technique in urethane anesthetized rats. Intraventricular injection of beta-endorphin at a dose of 15 micrograms released Met-enkephalin from the spinal cord. This release of Met-enkephalin induced by beta-endorphin was significantly reduced by beta-endorphin-(1-27), 60 micrograms, injected intraventricularly. Injection of beta-endorphin (1-27) itself did not cause any release of Met-enkephalin. The finding is in line with the previous report that beta-endorphin (1-27) inhibited the analgesia induced by beta-endorphin.
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PMID:beta-Endorphin-(1-27) inhibits the spinal beta-endorphin-induced release of Met-enkephalin. 294 Jan 95


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