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 blood-brain barrier is capable of transporting peptides with anti-opiate (Tyr-MIF-1) and opiate (enkephalins) activity out of the central nervous system. The relationship of this transport system to the various actions of opiates remains unexplored. This study examined the relationship between the rate of transport and opiate-induced analgesia. Both restraint, a stress that provokes an opiate-mediated analgesia, and the administration of morphine (12 mg/kg, i.p.) each induced an inhibition in the rate of transport. Such inhibition exhibited specificity, since the saturable, brain to blood transport of iodide remained unaltered. However, it was possible to dissociate analgesia and inhibition of transport. The onset and peak of analgesia, as measured by tail-flick latency induced by morphine, preceded the onset and peak of the inhibition of transport. Naltrexone, which blocks opiate-mediated analgesia, also induced inhibition of transport without any significant effect on tail-flick latency. (-) Naloxone but not (+) naloxone also weakly inhibited transport. Deprivation of food and water, associated with analgesia possibly mediated by the opiate, beta-endorphin, which is not transported out of the brain by this system, did not alter transport. These results suggest that while inhibition of transport and analgesia may occur together, these events probably represent two separate aspects of the action of opiates, that may even be mediated by separate receptor sites or peptides in the opiate family.
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PMID:Analgesia and the blood-brain barrier transport system for Tyr-MIF-1/enkephalins: evidence for a dissociation. 289 31

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 bandwidths of several polypeptides related to human beta-endorphin have been investigated with different n-alkylsilica stationary phases and different elution gradients of 0.1% trifluoroacetic acid-water-acetonitrile mobile phases. In particular, we have examined the influence of changes in the gradient steepness parameter, b, on peakwidth with five different octadecylphases, chemically bonded to porous spherical silica particles of nominally 4 micron and 6 micron average particle diameter, respectively. The effect on the zone dispersion of these polypeptide solutes as the average pore diameter of the silica matrix was increased from 7.3 nm to 30 nm with stationary phases of similar ligand densities packed into columns of identical configuration has been further documented. The experimental data on solute bandwidths and peak capacities are comparable with the corresponding bandwidth and peak capacity values calculated from analytical equations, derived from the general plate height theory and from gradient elution theory. These comparisons clearly demonstrate that anomalous bandbroadening phenomena may occur when polypeptides are eluted with steep gradients, i.e. with gradients of large b values. Moreover, as the relative chromatographic residence times of beta-endorphin peptides capable of forming a C-terminal amphiphilic secondary structures is increased, i.e. as the dwell times and median capacity factors, k, for such peptides are increased, significant divergencies arise between the observed peakwidth behaviour and the behaviour predicted by analytical relationships which describe either the dependency of peak bandwidth (as 4 sigma v) on the gradient steepness parameter, b, or the dependency of peak capacity on gradient time, tG, median capacity factor, k, and the Knox parameter, C, respectively. The importance of these divergences from the predicted bandwidth and peak capacity behaviour for polypeptides separated on reversed phases, and for resolution optimisation in particular, is evaluated. These investigations thus enable further assessment of the quantitative relevance of current models that describe polypeptide zone migration under gradient elution reversed-phase chromatographic conditions in which solute-dependent slow equilibria, mediated by conformational or solvation effects, may still occur.
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PMID:High-performance liquid chromatography of amino acids, peptides and proteins. LXVII. Evaluation of bandwidth relationships of peptides related to human beta-endorphin, separated by gradient-elution reversed-phase high-performance liquid chromatography. 293 99

To study the physiological roles of endogenous opioid peptides in drinking and feeding behaviors, the effects of water deprivation and fasting on plasma immunoreactive (IR) beta-endorphin (beta-end), IR-Antidiuretic hormone (ADH) and IR-Prolactin (Prl), pituitary IR-beta-end and IR-methionine-enkephalin (IR-Met-enk) and IR-ADH, and hypothalamic IR-beta-end and IR-Met-enk were observed in rats. The effects of water deprivation on hypothalamic dopaminergic system was also studied. In water deprived rats, plasma IR-beta-end and Prl were decreased significantly. In the neurointermediate lobe, IR-Met-enk, but not IR-beta-end, was decreased, although these peptides did not change in the anterior lobe and hypothalamus. Intraperitoneal injection of haloperidol reversed the decrease in plasma IR-beta-end in water deprived rats but did not change it in control rats. Subcutaneous injection of CB-154, on the other hand, decreased the plasma IR-beta-end in control rats but not in water deprived rats. The dopamine (DA) turnover rate in hypothalamus, in addition, was increased in water deprived rats as compared with controls. In fasted rats, IR-beta-end in plasma, but not in pituitary lobes and hypothalamus, was increased. The present results suggest that the increase of hypothalamic dopaminergic activity, in part, is related to the suppressed secretions of pituitary IR-beta-end and Prl in water deprivation, and plasma IR-beta-end play some roles in feeding behavior in rats.
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PMID:Influences of water deprivation and fasting on hypothalamic, pituitary and plasma opioid peptides and prolactin in rats. 294 40

The neurobehavioral responsiveness of two strains of rats, Fischer-344 (CDF) and Sprague-Dawley (CD), to a repeated foot-shock-induced analgesia (FSIA) stress was compared in this study. Rats were either restrained or freely moving during shock presentation (sham controls were exposed to the shock environment only). The foot-shock (15-s, 1.5-mA scrambled electric shock) was observed to induce analgesia in the CDF, but not the CD strain following acute presentation; analgesia was evaluated using time for tail-withdrawal from hot water (55 degrees C). Both strains exhibited an analgesic response when latency to tail withdrawal was evaluated just prior to daily FSIA presentations over 15 total sessions indicating that these rat strains were behaviorally conditioned to this repeated stressor. However, the levels of conditioned analgesic responses to foot-shock were: greater in the CDF and most evident when rats were restrained on the shock-grid while being administered the foot-shock. All rats were quickly sacrificed following the 15th conditioning session to determine the effects of this stressor on neurotransmitter and neuroendocrine function in both strains of rat. Experimental subjects were exposed to the shock grid but not shocked during this last session. The following was found: plasma corticosterone (CORT) and prolactin levels and adrenal CORT levels were significantly increased by repeated stress in the CDF strain; only plasma CORT levels were elevated in the CD rat; pituitary immunoreactive beta-endorphin levels were significantly higher (+46%) amongst all experimental groups in the CDF strain, but stress was not observed to alter peptide steady-state levels in either strain; dopamine (DA), 5-hydroxytryptamine and metabolites (5-hydroxyindoleacetic acid and dihydroxyphenylacetic acid) levels were generally higher in the hypothalamus and frontal cortex of the CDF rat but turnover rates (implied from metabolite/amine ratios) indicated that these systems were more sluggish in this rat strain; hypothalamic DA turnover was significantly attenuated by repeated FSIA + restraint in both strains, but the dynamics of this effect appeared to be different between rat strains; and frontal cortex 5-HT turnover was significantly elevated by repeated FSIA + restraint in only the CDF rat. This research indicates that the CDF rat is extremely sensitive to an acute FSIA stress and it is less able than the CD rat to adapt to repeated presentation of this stress.
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PMID:Neuroendocrine, biogenic amine and behavioral responsiveness to a repeated foot-shock-induced analgesia (FSIA) stressor in Sprague-Dawley (CD) and Fischer-344 (CDF) rats. 294 19

In children with burn injuries we found, in earlier studies, an inverse association of plasma beta-endorphin immunoactivity (iB-EP) and pain levels. To further explore the effects of burn trauma on the peripheral release of beta-endorphin and the occurrence of centrally mediated stress analgesia, plasma iB-EP levels and tail flick latency (TFL) were measured in rats subjected (while anesthetized) to scald injury. In comparison to sham burn (dip in tepid water), burn injury increased plasma iB-EP and TFL; both the duration and magnitude of these effects were directly proportional to the extent of burns. In rats receiving no treatment, TFLs were unchanged throughout the time of the burn experiments. At 2 days post-burn TFLs were invariably back to pre-burn levels. Administration of the long-acting opioid antagonist naltrexone prior to burn injury prevented the rise in TFL. Thus the trauma of burns appeared to bring about a stress-induced analgesia (SIA). The marked increase in iB-EP during this SIA and its antagonism by naltrexone suggest that it was opioid and hormonal in character.
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PMID:Increases in plasma beta-endorphin and tail flick latency in the rat following burn injury. 294 29

This research was carried out to define the effects on men of head-out water immersion in a bath at 38.41 +/- 0.04 degrees C (mean +/- S.E.) with a method similar to that used for therapeutical rehabilitation and time of immersion of 30 minutes. Beta-endorphin, renin activity, aldosterone, cortisol, HGH, FSH, LH, TSH, T3, T4 and prolactin haematic levels were analysed. Seventeen healthy subjects (fourteen males and three females), aged 21-65 years (mean age 29.8 +/- 2.6) were studied. Water immersion caused a decrease in FSH and LH haematic concentrations; no significant changes occurred in beta-endorphin, renin activity, aldosterone, prolactin, cortisol, HGH, TSH, T3, T4 and FTI values. Thirty minutes after the end of immersion, FSH and LH levels returned to pre-immersion values. The probable pathogenesis of these observations is suggested.
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PMID:[Hormonal, beta-endorphin and renin activity changes in man during partial immersion, as a therapeutic method, in water at 38 degrees C]. 295 Mar 39

Rats were trained and tested in an open field for habituation of rearing responses, for a water-finding task, or for both tasks simultaneously. Training-test interval was 24 hr. The water-finding task consisted of locating a metal tube in one of the walls of the box, which was attached to a water bottle on the outside; animals were water deprived between training and testing. Retention was estimated by measuring the latency to lick from the tube on the test session. Rats learned this task either with or without water deprivation, also prior to training. Habituation learning (reduction of the number of rearings between the training and test session) occurred either simultaneously with the water-finding task or in animals trained without the water tube, so that they could not learn the water-finding task. As happens with many other tasks, training in the open field was followed by a large decrease of hypothalamic beta-endorphin immunoreactivity, attributable to a release of this substance. Posttraining IP naloxone (1.6 mg/kg) administration facilitated, and posttraining beta-endorphin (2.0 micrograms/kg), leu-enkephalin (5.0 micrograms/kg), or electroconvulsive shock (15 mA, 60 Hz, 2 sec) depressed the retention of habituation; this occurred regardless of whether the animals were trained and/or tested with or without water deprivation, and whether the task was acquired alone or simultaneously with the water-finding task. By contrast, none of these treatments had any effect on retention of the water finding task, acquired either with or without prior water deprivation. Thus, habituation was, and water-finding was not, sensitive to posttraining treatments known to affect endogenous opioids: the opioids themselves, their antagonist, naloxone, and electroconvulsive shock which releases brain opioids and causes naloxone-reversible retrograde amnesia. Learning of the water-finding task was merely incidental to exploration of the open field; it took place even when the animals were trained without the water tube. This suggests that the posttraining treatments that affect endogenous opioid function affect memory only of the task(s) that actually cause the release of brain beta-endorphin (in this case, probably habituation), and not of others that may occur simultaneously but are merely incidental (water-finding). A feature apparently common to the former is that they must directly involve either the recognition of novelty, or the initiation of an interaction with a new environment, or perhaps the habituation of such interaction.
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PMID:Differential effect of posttraining naloxone, beta-endorphin, leu-enkephalin and electroconvulsive shock administration upon memory of an open-field habituation and of a water-finding task. 295 61

Plasma beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and cortisol concentrations were measured by perimenstrual period in 11 patients affected by premenstrual syndrome (PMS) and in 8 asymptomatic healthy volunteers. Blood samples were collected every 2 to 3 days, for 1 month, starting from midcycle. The Menstrual Distress Questionnaire (MDQ) was administered during the testing period. Plasma beta-LPH and cortisol levels remain stable during the perimenstrual period, in both controls and PMS patients. On the contrary, PMS patients showed a decrease of plasma beta-EP in the week preceding menses and during the first days of menstrual flow. Beta-EP values of PMS patients regain normal levels during the next follicular phase. No changes of beta-EP levels were recorded in asymptomatic women. MDQ scores revealed that PMS patients complained of water retention, pain discomfort, and mood swings. The transient and reversible decrease of plasma beta-EP in PMS patients near to and at menses remains to be clarified.
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PMID:Premenstrual fall of plasma beta-endorphin in patients with premenstrual syndrome. 295 25

Mice were trained and tested in a step-through inhibitory avoidance task with a 24-h interval between training and testing. At one of several intervals prior to the test session (9 h, 6 h, 3 h, or 6 min), they were given one of the following novel experiences: 4 min in a small Plexiglas box containing an empty water bottle, or 4 min hanging from the wire mesh ceiling of a large Plexiglas box. When given 3 h or 6 min before testing, both novel experiences enhanced retention test performance. The effect was antagonized by naltrexone and mimicked by an administration of beta-endorphin 6 min prior to testing. Thus, the findings are consistent with previous evidence suggesting that the effects of novel experiences on retention test performance are due to an activation of the brain beta-endorphin system. When one of the novel experiences given 3 h or 6 min prior to testing was preceded by the same experience given 6 h earlier retention test performance was not enhanced. Thus, the enhancing effect is obtained only if the experience is novel. Further, an experience given prior to retention testing did not affect performance if either the same or a different experience was given 3 h earlier. This finding is consistent with previous evidence indicating that following a novel experience, the brain beta-endorphin remains unresponsive for several hours. These results provide additional evidence that novel experiences prior to retention testing affect retention performance and provide additional support for the view that the effect may involve the release of beta-endorphin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of novel experiences on retention of inhibitory avoidance behavior in mice: the influence of previous exposure to the same or another experience. 295 35


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