Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven women undergoing abdominal hysterectomy under halothane and nitrous oxide analgesia had plasma samples taken before, during and after surgery for assay of adrenocorticotrophin (ACTH), beta-endorphin, beta-lipotrophin and methionine (Met)-enkephalin immunoreactivity. Plasma ACTH, beta-endorphin and beta-lipotrophin all rose in parallel from the start of surgery and were unaffected by postoperative opiate analgesia. Plasma Met-enkephalin concentrations did not change significantly during the course of the surgery and immediate post-operative period, although the variance of the samples increased at the time of the first skin incision. These data indicate that the stress of surgery and post-operative pain, while producing marked elevations of proopiomelanocortin-derived peptides, are not associated with changes in plasma Met-enkephalin. These data exclude a role for circulating Met-enkephalin in the modulation of surgical pain but do not exclude such a role for beta-endorphin.
 ...
PMID:The effect of surgery on plasma beta-endorphin and methionine-enkephalin. 285 64

Rats were trained in a two-lever food-reinforced procedure to discriminate between the effects of saline and the opioid kappa receptor agonist ethylketocyclazocine. After acquisition of this discrimination, generalization tests with opioid peptides such as beta-endorphin, alpha-neoendorphin, dynorphin A and some dynorphin-derived peptides were conducted. The rats dose-dependently generalized the effects of intracerebroventricularly injected ethylketocyclazocine but not beta-endorphin, alpha-neoendorphin, dynorphin A1-8, dynorphin A1-13, D-Cys2-L-Cys5-dynorphin A1-13 or dynorphin A. D-Cys2-L-Cys5-dynorphin A1-13, in contrast to dynorphin A itself, dose-dependently caused analgesia and catatonia that was reversible with naloxone. Studies into the receptor preference of this derivative, using the technique of "selective tolerance", revealed that this dynorphin derivative is almost devoid of kappa-receptor activity.
 ...
PMID:Generalization tests with intraventricularly applied pro-enkephalin B-derived peptides in rats trained to discriminate the opioid kappa receptor agonist ethylketocyclazocine. 286 51

We evaluated the development of naloxone-reversible and naloxone-non-reversible analgesia induced by footshock in rats of different ages and correlated it with the concentrations of beta-endorphin and dynorphin in brain areas and the spinal cord. We observed that naloxone-non-reversible shock-induced analgesia appeared first and its appearance might be related to the early presence of high dynorphin concentrations in the spinal cord. Naloxone-reversible analgesia appeared later together with the reaching of adult concentrations of cerebral beta-endorphin.
 ...
PMID:Naloxone-reversible and non-reversible shock-induced analgesia during development. 286 71

We have shown that a number of compounds which inhibit the degradation of met-enkephalin can produce naloxone-reversible analgesia in mice. These compounds also potentiate the analgesia produced by acupuncture, foot shock, and transcutaneous nerve stimulation in animals and humans. The potency of their effectiveness as analgesics or potentiators parallels their potency as inhibitors of mouse brain enkephalinase. D-Phenylalanine (DPA), one of these enkephalinase inhibitors, has been used successfully for the management of chronic intractable pain in humans and to potentiate the treatment of many painful conditions by acupuncture. Other aspects of pharmacology of DPA will be discussed, including its effects on the cardio-vascular system, behavior, and lack of development of tolerance and dependence when used chronically in animals and humans.
 ...
PMID:Pharmacology of enkephalinase inhibitors: animal and human studies. 286 74

Circular dichroism was used as a probe for competitive binding of two opioid peptides, dynorphin-(1-13) and beta-endorphin, with cerebroside sulfate, a membrane lipid thought to be part of the morphine receptor complex. The rationale was that bound beta-endorphin is partially helical but bound dynorphin-(1-13) remains unordered, thus making it possible to detect the degree of binding of beta-endorphin. The addition of dynorphin-(1-13) to a cerebroside sulfate solution of beta-endorphin invariably displaced beta-endorphin from the peptide-lipid complex, but the addition of beta-endorphin had little effect on dynorphin-(1-13) bound to the lipid. Similar results were obtained for competitive binding of the two peptides with two other amphiphiles, sodium dodecyl and decyl sulfate. The maximum number of binding sites on dynorphin-(1-13) and beta-endorphin was between five and six, which coincides with the five positively charged side chains plus an alpha NH+3 group at the NH2 terminus on both peptide molecules. The results support our working hypothesis that dynorphin-(1-13) may displace beta-endorphin bound to the receptor, which in turn can account for the inhibition of beta-endorphin-induced analgesia by dynorphin-(1-13).
 ...
PMID:Competitive binding of dynorphin-(1-13) and beta-endorphin to cerebroside sulfate in solution. 286 34

Certain neuropeptides previously linked to stress and implicated in CNS control of analgesia/algesia were tested using a recently developed analgesiometric model, the rabbit ear-withdrawal test. The latency to ear withdrawal increased in a dose-related manner after beta-endorphin was injected intracerebroventricularly (IVC). Intermediate doses (0.5 and 1.0 micrograms) of adrenocorticotropic hormone (ACTH) caused hyperalgesia as indicated by decreases in latency. Corticotropin-releasing factor (CRF, 0.5 and 1.0 micrograms) also caused significant hyperalgesia late in the testing period. alpha-Melanocyte stimulating hormone (alpha-MSH, 0.25-2.0 micrograms), a molecule that shares the first 13 amino acid sequence with ACTH, and somatostatin (0.25-2.0 micrograms), caused no significant change in latency. However, 1.0 microgram doses of each peptide antagonized the analgesic effect of beta-endorphin (1.0 microgram) in the following order of potency: ACTH = alpha-MSH greater than CRF greater than somatostatin. The results support the idea that CNS peptides that are released during stress can exert opposing actions on acute pain, even though they may cause little effect alone.
 ...
PMID:Influence of centrally administered peptides on ear withdrawal from heat in the rabbit. 288 94

Electrical stimulation of the ventral midbrain periaqueductal grey (PAG) elicited an antinociception (analgesia) in freely moving rats. Stimulated animals displayed a pronounced decrease in levels of immunoreactive (ir)-beta-endorphin (beta-EP) in the midbrain PAG. This depletion was selective in that: animals placed in the chamber and not stimulated revealed neither an analgesia nor an alteration in levels of ir-beta-EP. No change in levels of ir-beta-EP was detectable in other brain regions. Both stimulated rats and rats placed in the chamber and not stimulated revealed a rise in circulating ir-beta-EP: the magnitude of this rise did not, however, differ between these groups. Levels of ir-Met-enkephalin, ir-Leu-enkephalin and ir-dynorphin A were modified neither in the PAG nor in other CNS tissues. The data demonstrate that electrical stimulation of the midbrain PAG selectively influences (presumably activates) pools of beta-EP therein. Together with our finding that destruction of PAG-localized beta-EP neurones to block stimulation-analgesia, the data suggest that an activation of intrinsic pools of beta-EP underlies stimulation-produced analgesia elicited from the PAG in the rat.
 ...
PMID:Activation of periaqueductal grey pools of beta-endorphin by analgetic electrical stimulation in freely moving rats. 288 14

Male rats were injected s.c. once daily during the first week of life with beta-endorphin (BE), morphiceptin, the antiopiate Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), or one of the two opiate peptides in combination Tyr-MIF-1. Pups treated with neonatal BE removed their tails from a series of increasingly hot water baths significantly faster than controls on day 9, confirming our earlier studies. In addition, we found that Tyr-MIF-1 blocked this effect of BE. At 4.5 months, latency to lick a hindpaw in the hot-plate test was significantly faster in groups given BE alone, morphiceptin alone, or the control vehicle than in any of the 3 groups given Tyr-MIF-1. At 6 months the two groups given opiate peptides alone showed faster tail-flick latencies than the controls and the groups given Tyr-MIF-1. These results indicated that the long-term nociceptive changes induced by the opiate peptides were opposite to those induced by Tyr-MIF-1. Mean tail-flick latencies of the groups on day 9 correlated well with hot-plate and tail-flick scores in adulthood, indicating that the effects of the peptides were persistent. The neonatal peptide treatments did not differentially affect the analgesia induced by the stress of footshock or warm-water swim. Rats given either of the opiate peptides alone tended to fall off a rotorod faster than those in the other groups. These results support the role of Tyr-MIF-1 as an antiopiate and further illustrate the long-term effects of neonatally administered peptides.
 ...
PMID:Long-term hyperalgesia induced by neonatal beta-endorphin and morphiceptin is blocked by neonatal Tyr-MIF-1. 288 15

The hyperphagia and obesity induced by ventromedial hypothalamic (VMH) electrolytic lesions in female rats were associated with a 70-94% decrease in the level of beta-endorphin (beta-E) in the hypothalamus and other regions of brain, but not in the pituitary. Dynorphin (Dyn) and methionine-enkephalin (ME) levels were also decreased. Rats with VMH lesions were less sensitive to the inhibitory effect of naloxone on their food-intake. Mice injected with gold thioglucose (GTG) also showed a decrease in the hypothalamic content of beta-E and Dyn and exhibited 30% less analgesia compared to control mice after cold swim stress.
 ...
PMID:Effect of electrolytic and chemical ventromedial hypothalamic lesions on food intake, body weight, analgesia and the CNS opioid peptides in rats and mice. 289 79

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.
 ...
PMID:Analgesia and the blood-brain barrier transport system for Tyr-MIF-1/enkephalins: evidence for a dissociation. 289 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>