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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy sportive men before, during, and after progressively more strenuous physical exercise. In a double-blind study conducted on two different days, 20 mg of the opioid-antagonist naloxone or placebo was administered prior to exercise. A significant pain threshold elevation was found during exercise for finger (ANOVA, P less than 0.004) and dental pulp stimulation (P less than 0.01). Pain threshold elevation was most pronounced during maximal exertion, at which time the subjects reported the greatest subjective fatigue. Thresholds remained elevated 10-15 min after the end of exercise, and, 60 min after exercise, thresholds returned to baseline values. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (P less than 0.0001) 5-10 min after exercise. Plasma beta-endorphin, cortisol, and catecholamines increased significantly (P less than 0.0005, all values) during exercise. Plasma beta-endorphin levels did not correlate significantly with pain thresholds (r = -0.37, NS). Naloxone failed to affect pain thresholds, although beta-endorphin and cortisol increased significantly more (P less than 0.02) during exercise after naloxone. It is concluded that short-term, exhaustive physical exercise can evoke a transient elevation in pain thresholds. This exercise-induced elevation in pain threshold does not, however, appear to be directly related to plasma endorphin levels.
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PMID:Experimental pain thresholds and plasma beta-endorphin levels during exercise. 202 Feb 72

We have previously shown that central administration of beta-endorphin results in a reduction of ornithine decarboxylase activity. Ornithine decarboxylase catalyses the rate-limiting step in the biosynthesis of the polyamines putrescine, spermidine and spermine, thought to modulate nucleic acid synthesis. The present study examines the effects of intracisternal injection of beta-endorphin on brain and liver DNA synthesis in preweanling rats. In six-day-old rats, beta-endorphin (0.75 micrograms/g brain wt) produced approximately a 70% inhibition in brain and liver DNA synthesis 1 h after injection, and values were still subnormal in both tissues 10 h later. Subcutaneous administration of beta-endorphin did not alter liver DNA synthesis. Thus, it is most likely that the suppressed liver DNA synthesis observed in animals given beta-endorphin intracisternally is mediated by central mechanisms. Co-administration of naloxone plus beta-endorphin intracisternally prevented the response, indicating an opioid receptor-mediated phenomenon. Naloxone alone caused small but significant increases in brain and liver DNA synthesis, suggesting a tonic influence on tissue DNA by endogenous opioids in the CNS. Acute inhibition of ornithine decarboxylase activity by alpha-difluoromethylornithine did not alter DNA synthesis, indicating that the decreases in DNA synthesis induced by beta-endorphin are unrelated to the ornithine decarboxylase/polyamine system. The effect appears to be restricted to early development as no significant changes in DNA synthesis were obtained in 20-day-old animals. The results from these studies indicate that CNS beta-endorphin has the ability to influence DNA synthesis in central as well as in peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of central administration of beta-endorphin on brain and liver DNA synthesis in preweanling rats. 205 54

Opioid peptides and catecholamines play an important role in the control of appetite, behaviour and hormonal secretion. To evaluate the role of the opioid and adrenergic systems in the hormonal dysfunction of anorexia nervosa (AN), we investigated the effects of naloxone and clonidine on serum GH, LH, FSH, beta-endorphin, TSH, prolactin and cortisol concentrations in 35 women with AN. Basal plasma beta-endorphin concentrations were significantly lower than those in healthy controls. The response of beta-endorphin to clonidine in the AN patients was increased, whereas the response of beta-endorphin to naloxone was decreased. Basal serum cortisol concentrations were significantly higher in the AN patients than that in the controls. There was a significant increase in the cortisol response to naloxone in the controls but a lack of cortisol response to naloxone in the patients with AN. Naloxone produced a significant increase in LH release in the controls during the luteal phase of the menstrual cycle, as well as in the majority of AN patients. Clonidine caused a diminution of LH in the controls and did not alter LH in the patients. After clonidine injection, a significant increase in GH release was observed in both groups of subjects. If these disturbances persist after normalization of body weight, it might suggest that altered opioid and adrenergic activity is an aetiological factor in the pathogenesis of anorexia nervosa.
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PMID:Are disturbances in opioid and adrenergic systems involved in the hormonal dysfunction of anorexia nervosa? 212 11

Naloxone-resistant binding sites for beta-endorphin have previously been observed on transformed peripheral blood mononuclear cells and on the EL4-thymoma cell line. These sites may be related to the naloxone-insensitive immunomodulatory effects of beta-endorphin. The present study was performed 1) to determine whether these sites are present on normal splenocytes and 2) to characterize them. Ficoll-hypaque-purified murine splenocytes were used in a RRA with [125I]beta-endorphin. Neither fresh intact cells obtained from viral antibody-free mice nor membrane preparations showed evidence of binding. However, splenocytes cultured in 5% fetal bovine serum for 24-96 h showed sites on intact cells or membranes (after 3 h in culture no sites were present). Intact cultured splenocytes demonstrated a saturable binding isotherm, and Scatchard analysis showed a single site (Kd = 4.1 X 10(-9) M). Competition studies showed that N-acetyl-beta-endorphin (N-Ac-beta-endorphin)-(1-31) was equipotent to beta-endorphin-(1-31). beta-Endorphin-(6-31) and beta-endorphin-(28-31) were approximately 10- and 1000-fold less potent, respectively, whereas beta-endorphin-(1-27) and naloxone were completely ineffective. Covalent cross-linking of [125I]beta-endorphin to splenocytes and resolution by gel electrophoresis showed bands at 66K and 57K which were displaced equipotently by increasing amounts of beta-endorphin and N-Ac-beta-endorphin. beta-Endorphin-(18-31) or (28-31) were less potent, and naloxone or other opioid ligands selective for receptor subtypes were ineffective. Thus, high affinity, naloxone-insensitive binding sites for beta-endorphin, which show competition characteristics distinctively different from brain opiate receptors, are inducible on normal mouse splenocytes. N-Ac-beta-endorphin, presumed to be an inactivation product of beta-endorphin because it fails to bind brain opiate receptors, may be functional at this naloxone-insensitive binding site.
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PMID:Murine splenocytes express a naloxone-insensitive binding site for beta-endorphin. 213 72

Cumulus enclosed or denuded oocytes obtained from ovaries of 25- to 27-day Sprague-Dawley rats underwent spontaneous germinal vesicle breakdown (GVBD) when cultured for 6 h in Krebs-Ringer's buffered solution (KRBS). This spontaneous division was found to be inhibited by adding beta-endorphin to the culture system and the inhibition was dose dependent, ranging from 200 to 800 pg/ml KRBS. Naloxone, a potent opioid antagonist without any agonistic action, did not stimulate spontaneous GVBD when added to the KRBS at doses ranging from 80 to 120 pg/ml. However, by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin, the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely.
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PMID:The effect of beta-endorphin on rat oocyte maturation in vitro. 213

To characterize the effect of beta-endorphin on T-lymphocyte activation, we examined its influence on membrane currents, intracellular calcium flux, and c-myc mRNA levels during mitogenic stimulation of Jurkat cells. While beta-endorphin weakly enhanced voltage-activated K+ currents of Jurkat cells by itself, it suppressed these currents in the presence of mitogen. Naloxone, by itself, also enhanced K+ current amplitude, but in the presence of mitogen partially reversed the suppressive effect of beta-endorphin. A 5-30 min exposure to beta-endorphin resulted in an increase in the rate of mitogen-stimulated intracellular calcium release and an increase in c-myc mRNA levels relative to controls. Longer exposure (1-2 h) to beta-endorphin retarded intracellular calcium release, and suppressed c-myc expression. The suppressive effects were reversed by naloxone and mimicked by the K+ channel blocker, tetraethylammonium ion. These data suggest that opiate receptors and K+ channels of Jurkat cells are functionally coupled in a way that modulates intracellular calcium release and c-myc expression - two key processes in T-cell mitogenesis.
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PMID:Beta-endorphin modulates T-cell intracellular calcium flux and c-myc expression via a potassium channel. 213 66

1. Intraventricular administration of human beta-endorphin and elephant beta-endorphin significantly prolonged the tail flick response tested 30 min later. However, elephant beta-endorphin was about 7-8 times more potent than human beta-endorphin in the tail flick test. 2. beta-Endorphin antagonized the antinociceptive effect of both human beta-endorphin and elephant beta-endorphin by the same extent. Naloxone also antagonized the antinociceptive effects of the beta-endorphins but it was less effective than beta-endorphin. 3. Human beta-endorphin and elephant beta-endorphin were of equal potency in inhibiting the abdominal constriction response induced by intraperitoneal (i.p.) acetic acid. Both beta-endorphin and naloxone antagonized these effects of the beta-endorphins with naloxone being more effective. 4. The present study showed that different opioid receptor subtypes may be involved in the tail flick test and the abdominal constriction test. Furthermore, elephant beta-endorphin was a better antinociceptive agent than human beta-endorphin in the tail flick test.
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PMID:Preliminary study on the antinociceptive effect of elephant beta-endorphin. 214 Sep 62

The relationship between morphine tolerance and pituitary-adrenocortical activity was examined. In rats made tolerant to morphine by implantation of morphine-containing pellets, there was a significant reduction in plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI), whereas no significant changes in cortisol levels were seen. Naloxone treatment induced an increase in plasma beta-END-LI and cortisol levels in morphine-tolerant animals. Additionally, acute morphine administration induced an increase in plasma levels of beta-END-LI and cortisol, an effect which was prevented by naloxone. These results are consistent with an increased release of pro-opiomelanocortin-derived peptides after acute morphine and with a decreased release of these peptides in tolerant rats, and suggest that opioid peptides play an important role in the regulation of pituitary-adrenocortical function.
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PMID:Plasma beta-endorphin and cortisol levels in morphine-tolerant rats and in naloxone-induced withdrawal. 214 20

Naloxone administered at a dose of 0.2 mg/kg post-training antagonizes the deleterious effect of post-training beta-endorphin administration and prevents the enhancing effect of pretest beta-endorphin administration, on retention of a step-down inhibitory avoidance task in rats. Given at a higher dose (0.4 mg/kg), naloxone caused, in addition to these effects, a pronounced retrograde facilitation which was additive with that caused by post-training ACTH or epinephrine administration. These findings show that post-training naloxone has two different effects or sets of effects, each with a different dose threshold: An interference with beta-endorphin induced state dependency and a true modulatory effect.
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PMID:Dual action of post-training naloxone on memory. 215 76

The studies were done to determine whether inhibition of the tail-flick response induced by beta-endorphin and morphine microinjected into periaqueductal central gray (CG) was mediated by stimulating different types of opioid receptors and by activating different descending pain modulatory systems in rats. beta-Endorphin (0.3-20 micrograms) or morphine (0.3-20 micrograms) microinjected bilaterally into CG produced a dose-dependent inhibition of the tail-flick response. Naloxone (0.3-3 micrograms) injected into CG was more effective in antagonizing inhibition of the tail-flick response induced by CG administered morphine than by beta-endorphin. beta-Endorphin-(1-27) (3 micrograms) injected CG effectively antagonized CG beta-endorphin-induced inhibition of the tail-flick response but slightly potentiated CG morphine-induced inhibition. Intrathecal injection of naloxone (0.3-30 micrograms) dose-dependently reversed inhibition of the tail-flick response induced by beta-endorphin (2 micrograms) but not by morphine (4 micrograms) injected into CG. On the other hand, yohimbine (0.3-30 micrograms) injected intrathecally dose-dependently antagonized inhibition of the tail-flick response induced by morphine (4 micrograms) but not by beta-endorphin (2 micrograms) given into CG. It was concluded that beta-endorphin and morphine produce inhibitions of the tail-flick response by stimulating epsilon and mu opioid receptors, respectively, and the descending pain modulatory system activated by beta-endorphin from CG involves spinal opioid receptors but not alpha-2 adrenoceptors whereas the descending system activated by morphine from CG involves spinal alpha-2 adrenoceptors but not opioid receptors.
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PMID:Different mechanisms mediate beta-endorphin- and morphine-induced inhibition of the tail-flick response in rats. 215 50


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