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)

Earlier studies from this laboratory indicated that intracerebroventricular administration of physostigmine and clonidine activated both a spinal descending analgesic and antianalgesic system. It was proposed that the latter was mediated spinally by dynorphin A (1-17), because small intrathecal doses (fmol) of dynorphin A (1-17) antagonized analgesia, while intrathecal administration of naloxone and nor-binaltorphimine (at doses which had no effect on spinal mu and kappa receptors) enhanced analgesia by attenuating the antianalgesic component. In the present studies in mice, using the tail-flick response, intrathecal administration of dynorphin antibody (antiserum to dynorphin) enhanced the analgesic effect of (10 min) physostigmine and clonidine given intraventricularly. Peak effect for the antiserum was at 1 hr. Inhibition of the tail-flick response, induced by DAMGO (Tyr-D-Ala2-Gly-NMePhe4-Gly-ol5, a mu agonist), U50, 488 H (trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate hydrate, a kappa agonist) and morphine was also enhanced by intrathecal administration of dynorphin antiserum. Thus, a variety of analgesic agonists appear to activate a dynorphin-mediated antianalgesic system. Such a system appears not to be activated by intraventricular administration of beta-endorphin and DPDPE (D-Pen2-D-Pen5-enkephalin, a delta agonist) because neither beta-endorphin- nor DPDPE-induced analgesia was enhanced by intrathecal administration of antiserum. The results of the experiments with the antibody provide further evidence to support the role of dynorphin A (1-17), as a putative endogenous opioid, which mediates an antianalgesic descending system in the spinal cord.
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PMID:Spinal dynorphin A (1-17): possible mediator of antianalgesic action. 197 11

The effects of intracerebroventricular (i.c.v.) administration of D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 (CTOP), a selective mu-opioid receptor antagonist, (Allyl)2-Tyr-Aib-Aib-Phe-Leu-OH (ICI 174864) and (N,N-Bisallyl-Tyr-Gly-Gly-psi-(CH2S)-Phe-Leu-OH (ICI 154129), selective delta-opioid receptor antagonists on blocking analgesia induced by beta-endorphin, morphine, D-Ala2-NMePhe4-Gly-ol-enkephalin (DAMGO), D-Ala2-D-Leu5-enkephalin (DADLE) and D-Pen2-enkephalin (DPDPE) administered i.c.v. were studied in male ICR mice. The analgesia was assessed by the tail-flick and paw-licking (hot-plate) tests. The potencies of opioid agonists injected i.c.v. for producing analgesia were DAMGO greater than DADLE greater than beta-endorphin greater than morphine greater than DPDPE. Intracerebroventricular administration of CTOP (0.05 micrograms) selectively antagonized inhibition of the tail-flick and paw-licking response induced by morphine, DAMGO or DADLE but not beta-endorphin or DPDPE. ICI 174864 (5 micrograms) and ICI 154129 (5 micrograms) injected i.c.v. selectively antagonized analgesia induced by DPDPE or DADLE but not beta-endorphin, morphine or DAMGO injected i.c.v. These results indicate that analgesia induced by morphine and DAMGO is mediated by the stimulation of mu-opioid receptors while analgesia induced by DPDPE is mediated by the stimulation of delta-opioid receptors. DADLE-induced analgesia is mediated by the stimulation of both mu- and delta-opioid receptors. Analgesia induced by beta-endorphin is mediated by neither mu- nor delta-opioid receptors.
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PMID:Different types of opioid receptors mediating analgesia induced by morphine, DAMGO, DPDPE, DADLE and beta-endorphin in mice. 197 34

Previous studies have shown that 2 Hz but not 100 Hz electroacupuncture (EA) stimulation released beta-endorphin in PAG of the rat to induce analgesia. The present study was undertaken to see whether dynorphin plays a role in PAG in mediating analgesia induced by low and high frequency EA. Injection of affinity purified dynorphin antibody (1:350,000 in RIA titer) 1 microliter into PAG blocked 2 Hz EA analgesia almost completely, and 15 Hz EA analgesia partly, leaving 100 Hz EA analgesia intact. This blocking effect was totally disappeared when the antibody was diluted to 1/10 of its original concentration (1:35,000). Besides, injection of dynorphin into PAG through chronically implanted cannula showed no analgesic effect. The results suggest that the blockade of 2 Hz EA analgesia by high titer dynorphin antibody injected into PAG may have been the result of cross reactivity of the antibody to other opioid peptides (such as beta-endorphin, enkephalin, etc) released in the PAG area. The data also stress the importance of using antibodies of proper titer and concentration to exclude false positive or false negative conclusions in adopting the antibody microinjection techniques, as was repeatedly shown in the immunohistochemical studies.
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PMID:[Influence of microinjection of dynorphin antibody into periaqueductal gray (PAG) on analgesia induced by electroacupuncture of different frequencies in rats]. 198 Apr 31

Analgesia and anaesthesia produced by fentanyl, urethane and ether, but not pentobarbital, occurred concomitantly with an increase in the concentration of plasma beta-endorphin like immunoreactivity (BEIR), probably of pituitary origin. This increase was not associated with significant changes in pituitary or brainstem beta-endorphin content. Pretreatment with naloxone caused a reduction in plasma BEIR increase following Hypnorm, ether and urethane; and in the analgesia following Hypnorm and urethane. Pentobarbital, alone or in combination with naloxone, did not increase the concentration of plasma beta-endorphin. These results may indicate participation of endogenous opioids in the mechanism of action of urethane.
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PMID:Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma. 200 54

alpha N-acetyl human beta-endorphin-(1-31) injected icv to mice antagonized the analgesic activity of beta-endorphin-(1-31) and morphine whereas the analgesia evoked by DADLE and DAGO was enhanced by this treatment. The modulatory activity of alpha N-acetyl beta-endorphin-(1-31) was exhibited at remarkable low doses (fmols) reaching a maximum that persisted even though the dose was increased 100,000 times. The regulatory effect of a single dose of the acetylated neuropeptide lasted for 24h. The activity of alpha N-acetyl human beta-endorphin-(1-31) was partially retained by the shorter peptide alpha N-acetyl human beta-endorphin-(1-27) and to a lesser extent by beta-endorphin-(1-27), beta-endorphin-(1-31) lacked this regulatory activity on opioid analgesia. Acetylated beta-endorphin-(1-31) displayed a biphasic curve when competing with 5 pM [125I]-Tyr27 human beta-endorphin-(1-31) specific binding, the first step (20 to 30% of the binding) was abolished with an apparent IC50 of 0.35 nM, and the rest with an IC50 of 200 nM. It is suggested that alpha N-acetyl beta-endorphin-(1-31) changed the efficiency of the opioid analgesics by acting upon a specific substrate that is functionally coupled to the opioid receptor, presumably the guanine nucleotide binding regulatory proteins Gi/Go.
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PMID:alpha N-acetyl derivatives of beta-endorphin-(1-31) and -(1-27) regulate the supraspinal antinociceptive activity of different opioids in mice. 200 58

The purpose of this study was to explore possible neural connections between the nucleus accumbens and amygdala involved in analgesia. The latency of the escape response elicited by radiant heat applied on snout of the rabbit was taken as an index for nociception. It was found that: (1) the analgesic effect elicited by intra-accumbens injection of morphine was attenuated dose-dependently by intra-amygdala administration of opioid antagonist naloxone, or antisera against met-enkephalin (ME) or beta-endorphin (beta-EP), suggesting the involvement of ME and beta-EP in the accumbens-amygdala connection; (2) the analgesia produced by intra-amygdaloid injection of morphine was not affected by naloxone administered to nucleus accumbens, suggesting a one-way connection between the two nuclei; (3) the analgesia of intra-accumbens injection of morphine was significantly attenuated by muscimol, the GABA receptor agonist, and enhanced by bicuculline methochloride, the GABA receptor antagonist injected into the same site where morphine was administered. The results suggest that the analgesic effect of morphine administered to the nucleus accumbens is mediated by the suppression of the GABAergic inhibitory neurons located within the nucleus.
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PMID:[The neural pathway from nucleus accumbens to amygdala in morphine analgesia of the rabbit]. 208 73

The effect of acute and repeated exposure to ethanol on endogenous opioid peptides level in rats was studied. Acute ethanol administration decreased beta-endorphin level in hypothalamus and anterior lobe of pituitary as well as alpha-neoendorphin in the spinal cord. In contrast, repeated ethanol treatment increased hypothalamic beta-endorphin content and did not affect the peptide level in the pituitary. No changes in alpha-neoendorphin and dynorphin level after repeated ethanol administration were observed. Exposure of rats to long-term noxious stimuli by means of induction of monoarthritis prevented the increase in hypothalamic beta-endorphin level by repeated ethanol treatment. As measured by tail-flick test only the first two administrations of ethanol resulted in analgesia. Further administration of increasing doses of ethanol did not affect the pain threshold. Altered response of endogenous opioid systems to repeated ethanol treatment as compared with effects of its acute administration may suggest involvement of these systems in development of tolerance to ethanol.
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PMID:The effects of ethanol treatment on endogenous opioid peptides level and analgesia in monoarthritic rats. 209 95

RIA and HPLC-ECD were used respectively to detect beta-endorphin-like immunoreactive substances (beta-EPIS), noradrenaline and 3-methoxy-4-hydroxyphenyloglycol (MHPG), a noradrenaline metabolite, in the perfusate from the rabbit's preoptic area before and after 10 min of electroacupuncture (EA). It was found that, the content of beta-EPIS in the perfusate increased during acupuncture analgesia, while those of noradrenaline and MHPG decreased. A negative correlation (r = -0.831; P less than 0.05) was shown between the changes of beta-EPIS and MHPG contents during acupuncture analgesia, indicating that beta-endorphin may be related to the inhibition of noradrenaline release during acupuncture analgesia.
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PMID:[Changes of releases of beta-endorphin-like immunoreactive substances and noradrenaline in rabbit's preoptic area during acupuncture analgesia]. 214 11

In 66 patients who had to undergo radical abdominal hysterectomy because of cancer of the cervix uteri, the plasma concentrations of beta-endorphin were observed intra- and postoperatively. Two anaesthetic techniques were used: neuroleptanalgesia and thoracolumbar epidural analgesia with sedation and controlled inhalation of a mixture of oxygen and nitrous oxide. While the higher dosage of analgesics administered intraoperatively resulted in markedly lower plasma concentrations of beta-endorphin, there was no such effect in the postoperative phase. Patients with epidural analgesia who were absolutely painless postoperatively had, during that stage, higher concentrations of beta-endorphin in the plasma than those patients who had been given neuroleptanalgesia. They had received no analgetic treatment during the postoperative observation period. These differences are attributed to an increased adaptability of patients subsequent to neuroleptanalgesia. The neuronal block can result in a decrease in functional activity of the suprarenal medulla and impair adaptability. The stress-induced opioid analgesia can be suppressed by circulating enkephalin from the suprarenal medulla.
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PMID:[The quality of analgesia in relation to the plasma concentration of beta-endorphin during neuroleptanalgesia and epidural analgesia]. 214 17

Rats placed in a cold environment (4 degrees C) for 2 h had a sustained increase in tail flick latency (TFL) as well as an increase in tail pinch latency (TPch) that was often biphasic with an early peak response at 15 min and a later, often higher, peak at 2 h. Plasma beta-endorphin levels after a modest increase at 5 min (24%) declined throughout the remaining time in the cold. The long-acting opioid antagonist naltrexone had no effect on TFL increases but led to greater increases in TPch (P less than 0.04). In morphine-tolerant rats TFL response was the same as in controls but TPch increases were greater (P less than 0.04). Rats exposed to 2 h of cold for 17 or 18 consecutive days generally developed tolerance to the analgesia of cold, i.e. TFL and TPch increases were diminished; however, the response to morphine on day 18 was the same as in rats never exposed to cold. Adrenalectomy and hypophysectomy led to significantly smaller increases in TFL (P less than 0.02 and P less than 0.001, respectively). The TPch response in contrast, was greater in adrenalectomized (P less than 0.001) and the same in hypophysectomized rats compared to sham controls. An opioid kappa receptor antagonist (Mr 1452) given prior to cold reduced both TFL and TPch response during the first hour. Thus the analgesia induced by cold appeared to shift from an early possibly kappa opioid to a later non-opioid form. The TFL effects seemed to be under hormonal influence while the TPch were not.
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PMID:Antinociception in the rat induced by a cold environment. 215 95


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