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 effects of D-Ala2-beta-endorphin administered either intravenously (IV) or intracisternally (IC) in squirrel monkeys were tested using a number of behavioral measures: general activity, eating, social behavior, aggression/distress, analgesia, and startle/escape. There were 10 groups (N = 5) consisting of 4 dose levels administered IC (0.4, 40, 400 microgram/kg) and 6 dose levels injected IV (0, 4, 40, 80, 400, 800 microgram/kg). Every monkey was tested with all tasks on each of 5 identical repeated trials, one pre-injection baseline trial and 4 post-injection trials. After IC administration, the 2 largest doses exerted toxic effects, which were partially reversed with naloxone, producing in 2 cases muscular rigidity and profound sedation. The smaller 4 microgram/kg dose produced significant decreases in activity over trials but increased reactivity to noxious stimulation after the initial post-injection trial. With IV injection reliable changes in activity and approach to food were found. The results demonstrate significant behavioral effects of an endorphin analog in the squirrel monkeys after both central and peripheral injection.
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PMID:Behavioral effects of D-Ala2-beta-endorphin in squirrel monkeys. 10 11

Both C-terminal fragments of lipotropin (beta-LPH) (endorphins) and N-terminal fragments (e.g., ACTH 4-10) delayed extinction of pole-jumping avoidance behavior in rats. After subcutaneous injection Met5-enkephalin appeared to be as active as ACTH 4-10 whereas beta-LPH 61-69, alpha- and beta-endorphin were more potent in delaying extinction of pole-jumping avoidance behavior (approximate ED50 of alpha-endorphin 4 x 10(-11) M rat.) However, the potency of beta-LPH 61-69 and alpha-endorphin appeared to be approximately the same whereas that of beta-endorphin was less than that of ACTH 4-10 after intraventricular administration (approximate ED50 of alpha-endorphin 0.2 x 10(-11) M rat). alpha-Endorphin and ACTH 4-10, administered subcutaneously in a dose which markedly delayed extinction of pole-jumping avoidance behavior, had only slight effects on open field behavior and on responsiveness to electric footshock. A 5 times higher dose of both peptides facilitated passive avoidance behavior. Morphine in two doses significantly delayed extinction of pole-jumping avoidance behavior but the effect was not dose dependent. The specific opiate antagonist naltrexone, however, markedly facilitated extinction of the avoidance response. ACTH 4-10, alpha- and beta-endorphin and a behaviorally potent ACTH 4-9 analog (Org 2766) restored pole-jumping avoidance behavior of rats pretreated with naltrexone. Treatment with a similar dose of naltrexone blocked beta-endorphin-induced analgesia. These results suggest that the influence of peptides related to C-terminal and N-terminal fragments of lipotropin on extinction of avoidance behavior may be dissociated from those exerted on opiate receptor sites. Subcutaneously injected beta-LPH 61-69 or intraventricularly administered beta-endorphin induced a shift from lower to higher frequencies of hippocampal theta rhythm during paradoxical sleep in the same way as that found after ACTH 4-10. This effect is interpreted as indicating an increased arousal state in certain midbrain limbic structures. This may, as has been postulated for ACTH 4-10, alter the motivational value of environmental stimuli (e.g., aversive stimulation).
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PMID:Behavioral and electrophysiological effects of peptides related to lipotropin (beta-LPH). 20 66

Three analogs of human beta-endorphin (beta h-EP) have been synthesized: [Gly31]beta h-EP, [Gly31]beta h-endorphinamide, and [Gly31]beta h-endorphinylglycine. All are more active than beta h-EP in both the guinea pig ileum bioassay and the opiate receptor binding assay. The last two analogs are about twice as active as beta h-EP in an assay for analgesia. Modification at position 31 and extension at the COOH terminus may afford a route toward analogs with even greater biological activity.
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PMID:beta-Endorphin: synthesis of analogs modified at the carboxyl terminus with increased activites. 22 65

Hypophysectomized rats are supersensitive to the hypothermic effects of morphine and beta-endorphin injected intraventricularly as early as 1 week after surgery. At 2 weeks after surgery, there is a significant increase in the antinociceptive potency for these opiates. The route of opiate injection must be considered in interpretations of these results. The enhanced opiate potency following subcutaneous morphine injection in hypophysectomized rats may be partially explained by adrenal dysfunction, as demonstrated by a similar sensitization to subcutaneous morphine following adrenalectomy. By contrast, no enhancement of opiate potency was observed upon direct intraventricular injection of morphine or beta-endorphin in adrenalectomized rats. Furthermore, the potency of intravenous beta-endorphin is profoundly enhanced in adrenalectomized mice; five out of nine animals died when injected with a dose of the peptide that produced only mild analgesia in sham controls. The complete reversal of this intravenous beta-endorphin supersensitivity by dexamethasone implies a possible physiological interplay between the peptide and adrenal function.
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PMID:beta-Endorphin: pituitary and adrenal glands modulate its action. 27 Jul 3

The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.
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PMID:Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. 29 52

Intraventricular administration of a peptide from ovine pituitaries whose structure is identical to the 61-91 C-terminal portion of beta-lipotropic hormone (61-91 beta-LPH) induced catalepsy, muscular hypertonus and analgesia in rats. Naloxone inhibited both the analgesic and cataleptic effects. 1-dihydroxyphenylalanine (1-DOPA) completely prevented the cataleptic effect. The cataleptic effect of 61-91 beta-LPH was potentiated by 1-5-hydroxytryptophan (5-HTP).
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PMID:Cataleptic effect of 61-91 beta-lipotropic hormone in rat. 30 38

In chicks with cannulae chronically implanted into the III cerebral ventricle, the effects of a single dose (10 micrograms) of beta-endorphin on GABA and free glutamic acid content, GAD and GABA-T activities in the diencephalon, brain-stem and brain hemispheres were studied at the time of maximal behavioural stuporous state and analgesia. A significant decrease in GABA concentration both in the diencephalon and brain-stem, accompanied by a significant increase in GABA-T activity in the same areas, was shown to occur. No changes were observed in GAD activity and in glutamic acid content in the studied areas of the brain. In conclusion, present experiments suggest that some central effects of a beta-endorphin may be due to an interference with GABA-ergic transmission.
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PMID:Effects of intraventricular beta-endorphin on GABA system in some areas of chick brain. 52 83

Several analogues of Met-enkephalin and beta-endorphin were tested for their analgesic properties after systemic injection. The latencies of mice to flick their tails away from a source of heat revealed that analogues of the opiate peptides can cause analgesia when injected by this route. In particular, compounds specifically designed to be more lipophilic or to possess additional binding sites were shown to be potent analgesic after peripheral administration.
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PMID:Analgesia after peripheral administration of enkephalin and endorphin analogues. 53 61

Rats chronically implanted with intrathecal catheters displayed a dose-dependent increase in the hot-plate and tail-flick response latencies following the injection of human beta-endorphin into the lumbar spinal subarachnoid space through the indwelling catheter. beta-Endorphin was approximately 25 times more potent than morphine on a molar basis. Matching morphine and beta-endorphin doses such that approximately equal submaximal submaximal effects occurred, it was observed that the antinociception produced by beta-endorphin lasted approximately three times longer than that produced by morphine. Experiments with intrathecal injection of beta-endorphin into the spinal subarachnoid space of cats fitted with intrathecal catheters also revealed a potent antinociceptive effect which was completely antagonized by naloxone. In the rats, naloxone administered systemically in doses of 10--100 microgram/kg produced a parallel shift in the dose-response curves of both nociceptive measures suggesting a competitive antagonism. Using a dose ratio analysis, an in vivo pA2 of 7.1 for naloxone was obtained. These data and those derived from previous work based on the pA2 suggest that the interaction of morphine, certain pentapeptides, and beta-endorphin is the same with regard to the spinal opiate receptor population mediating behaviorally defined analgesia.
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PMID:Antinociceptive effects of intrathecally administered human beta-endorphin in the rat and cat. 58 58

Microinjected directly into the preoptic anterior hypothalamus (POAH), beta-endorphin (0.74--7.4 nmol) induced an increase in rectal temperature (RT) in the free-moving rat. Whereas the initial phase of the endorphin-induced rise in RT was partially attenuated by naloxone (5 or 20 mg/kg i.p.) or naltrexone (3 mg/kg i.p.), the late phase was completely blocked by the prostaglandin synthetase inhibitor, indomethacin (15 mg/kg i.p.). Pretreatment with a combination of indomethacin and naloxone resulted in an almost total block of the endorphin-induced increase in RT. Furthermore, the central serotonin antagonist, methergoline (1 mg/kg i.p.) antagonized the endorphin-evoked fever indicating serotonin may mediate the rise in RT. In contrast to the fever evoked in the POAH, beta-endorphin (7.4 nmol), given into the lateral cerebral ventricle (LCV), elicited a marked drop in RT, catalepsy, and analgesia which were completely blocked by naloxone (5 mg/kg). Similar to morphine, beta-endorphin elicited a naloxone-reversible hyperthermia when administered into the subarachnoid space surrounding the spinal cord. The similarities between beta-endorphin and morphine in their actions on RT as well as the possible role of serotonin or prostaglandins in beta-endorphin's thermogenic action are discussed.
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PMID:Action of intracerebrally injected beta-endorphin on the rat's core temperature. 58 33


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