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)

Acute intraventricular administration of human beta-endorphin (15 microgram) produced analgesia, hypothermia and catalepsy in male Sprague-Dawley rats. Injections of beta-endorphin given every 8 hr for 3 days resulted in the development of tolerance to all of the above mentioned pharmacological effects. Tolerance developed rapidly to the hypothermic effect and less rapidly to the analgesic and cataleptic effects. After the third or the fourth injection of beta-endorphin, pronounced hyperthermia, rather than hypothermia, was observed. After seven or eight injections of beta-endorphin, tolerance to the analgesic effect was complete and the cataleptic effect was reduced to 50% of the original. Daily s.c. administration of Pro-Leu-Gly-NH2 (MIF) or cyclo(Leu-Gly) (2 mg/kg each) blocked the development of tolerance to the analgesic and cataleptic effects of beta-endorphin. The hyperthermic effect of beta-endorphin in beta-endorphin-tolerant rats was partially blocked by both MIF and cyclo(Leu-Gly). Multiple injections of MIF or cyclo(Leu-Gly) did not alter beta-endorphin-induced analgesia, catalepsy and hypothermia in rats which were given repeated intraventricular injections of saline. Since MIF is a naturally occurring peptide of hypothalamic origin, these studies suggest that the hypothalamus may be an important site in regulating the pharmacological effects of chronically administered endogenous opiates.
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PMID:Inhibition of tolerance to the pharmacological effects of human beta-endorphin by prolyl-leucyl-glycinamide and cyclo(leucylglycine) in the rat. 611 70

Light microscopic immunocytochemistry was employed to investigate possible sites of interaction between the endogenous opioid peptides and monoamines in the rat central nervous system. The opioid and related peptides examined included beta-endorphin (beta-END), alpha-MSH (alpha-MSH) and leucine-enkephalin (Leu-ENK). The monoamines were examined using antisera generated against tyrosine hydroxylase, dopamine-beta-hydroxylase as well as serotonin. Due to the long-tract nature of the central monoamine projections as well as beta-END/alpha-MSH fiber systems, serial section analyses were performed utilizing parasagittal brain sections. Many areas rich in both the monoamines as well as opioid peptides were investigated. These included several thalamic and hypothalamic nuclei, several limbic structures, mesencephalic periaqueductal gray, brain stem noradrenergic cell groups and their rostral projections, the dopaminergic nigrostriatal system, and the serotonergic raphe nuclei and their projections. The results suggest a more intimate linkage between the monoamines and the opioid peptides than previously realized. Some of the intricacies of monoamine-opioid peptide interaction, in particular those pertaining to their possible role in pain and analgesia, catalepsy, and neuroendocrine effects are also discussed.
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PMID:Some perspectives on monoamine-opioid peptide interaction in rat central nervous system. 612 45

The interactions of thyrotropin releasing hormone, its metabolites and synthetic analogues with acute and chronic effects of endogenous and exogenous opiates have been described. The endogenous and exogenous opiates are represented by beta-endorphin and morphine, respectively. The pharmacological effects of opiates include analgesia, temperature effects, respiratory depression, catalepsy, locomotor activity, opiate receptor binding, tolerance, and physical dependence. Thyrotropin releasing hormone and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents. Thyrotropin releasing hormone does not interact with the opiate receptors in the brain. Potential therapeutic applications of thyrotropin releasing hormone and its synthetic analogues in counteracting some of the undesirable effects of opiates are discussed.
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PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

New data on tachykinins and bombesins are displayed and the present situation of research on the novel amphibian skin peptides sauvagine and dermorphin is illustrated. The potent stimulant effect of sauvagine on ACTH and beta-endorphin release has been confirmed both in vivo and on columns of isolated and dispersed rat pituitary cells, and similarly the potent inhibitory effect on PRL and GH release, both in the rat and man. Particular emphasis is laid on the occurrence of sauvagine-like immunoreactivity in fish urophysis and in amphibian nervous structures, including the retina. It is suggested that the long-searched corticotropin releasing factor and PRL release-inhibiting factor may be a sauvagine-like peptide. Dermorphin, in its turn, has been found to cause, by intracerebroventricular injection, not only analgesia and catalepsy, but also conspicuous EEG and behavioral changes in the rabbit and chick, as well as a sharp reduction in gastric emptying time and gastric acid output in the rat, together with marked stimulation of PRL release.
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PMID:The brain-gut-skin triangle: new peptides. 617 95

beta-Endorphin was microinjected into rat brain in order to localize central sites associated with some of its pharmacologic effects: namely, analgesia (inhibition of the tail-flick response), catalepsy and changes in body temperature. Microinjections (1 microliter) were made bilaterally under halothane anesthesia and the effects of beta-endorphin were repeatedly assessed at 15- or 30-min intervals for 2 hr. beta-Endorphin produced analgesia and catalepsy when it was injected at low doses (ED50, 1.3 to 2.7 micrograms) into the medial preoptic area, nucleus accumbens, anterior hypothalamus and the periaqueductal gray-4th ventricular spaces. Brain areas of intermediate sensitivities (ED50, 3.7 to 16 micrograms) were the medial thalamus, posterior hypothalamus and areas around the fasciculus retroflexus. The frontal cortex, striatum and lateral areas of the brain were relatively insensitive (ED50 greater than 17 micrograms) to the effects of beta-endorphin on analgesia and catalepsy. beta-Endorphin had complex effects on body temperature. For example, when beta-endorphin was injected into the nucleus accumbens or preoptic area, low doses (1.1--2.1 micrograms) produced hyperthermia; higher doses (8.5 micrograms) produced hypothermia. The brain regions in which low doses of beta-endorphin elicit pharmacologic effects correspond to the anatomic areas in which the endogenous beta-endorphin system is distributed. Similar correspondence to the endogenous enkephalin system was not obtained.
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PMID:beta-Endorphin: central sites of analgesia, catalepsy and body temperature changes in rats. 624 33

ACTH1-24 and beta-endorphin simultaneously injected at 5-10 microgram dose into the lateral ventricle, reciprocally suppress most of their respective behavioural effects (stretching-yawning syndrome, sexual excitement and hyperalgesia for ACTH1-24 and catalepsy and analgesia for beta-endorphin). The results obtained support the hypothesis that ACTH1-24 and beta-endorphin might interact antagonistically at CNS level.
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PMID:Reciprocal antagonism between ACTH1-24 and beta-endorphin in rats. 626 26

The effects of the C-terminal octapeptide of cholecystokinin (CCK-8) and its related peptides on the onset and duration of beta-endorphin-induced catalepsy on injection of the peptides into the lateral ventricle were investigated in male rats. The onset of catalepsy was delayed to some extent by nonsulfated CCK-8 and CCK-7 but CCK-8 and caerulein were ineffective. Naltrexone and caerulein significantly shortened the duration of catalepsy, but CCKs were less effective to shorten it. Pentagastrin had no effect on either parameter.
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PMID:Suppressive effect of cholecystokinin and its related peptides on beta-endorphin-induced catalepsy in rats. 627 61

A variety of behavioral tests were used to characterize the cataleptic state induced by various treatments. Besides catalepsy, posture, locomotion, rigidity and the presence of reflexive responses were assessed. Measures of analgesia and body temperature were taken. The behavioral profiles of beta-endorphin, morphine, etonitazene, haloperidol, arecoline and GABA were compared at the time maximal catalepsy scores were obtained. Results indicated that, for an equivalent degree of catalepsy, the profile of beta-endorphin was similar to that of opiates, except for changes in body temperature; beta-endorphin's profile differed markedly from that of haloperidol, arecoline and GABA. Catalepsy was less pronounced with the latter two drugs. There were similarities in the behavioral profile of haloperidol and arecoline.
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PMID:Similarities of the cataleptic state induced by beta-endorphin and morphine. 629 79

Evidence from a variety of experimental models has suggested the existence of mu 1, mu 2 and delta binding sites for morphine and the enkephalins in the central nervous system. Additional biochemical experiments now support this concept of a common high affinity site for opiates and opioid peptides. Mu sites have now been implicated in a number of pharmacological actions, including supraspinal analgesia, prolactin release, and catalepsy, but not in others (spinal analgesia, respiratory depression, and the guinea pig ileum). The hypothesis of mu 1 sites was supported by the unique opioid meptazinol, which selectively bound to mu 1 sites. As expected from its mu 1 binding selectivity, its analgesic actions in the mouse, localized supraspinally, were antagonized by the selective mu 1 antagonist naloxonazine and it had no respiratory depressant actions. Other binding studies suggested the presence of discrete SKF10,047-selective (KD approximately 5 nM) binding sites in rat brain which differed from both kappa sites and the previously reported PCP-binding sigma sites. Additional binding and autoradiographical studies have also implied the presence of beta-endorphin, or epsilon, sites in the CNS.
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PMID:Biochemical and pharmacological evidence for opioid receptor multiplicity in the central nervous system. 631 56

Naloxone injected intrathecally had a different effect on the inhibition of the inhibition of the tail flick response produced by beta-endorphin and morphine injected intraventricularly. The intrathecal naloxone completely antagonized the effect of beta-endorphin but had only a very weak effect on morphine. In the same rats the cataleptic response to beta-endorphin was antagonized as well; however no definitive conclusion could be made regarding the antagonism of the morphine-induced catalepsy. The results indicate that spinal endorphin is involved in the production of intraventricular beta-endorphin-induced spinal tail flick inhibition and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological action via the activation of different descending inhibitory systems.
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PMID:Evidence that spinal endorphin mediates intraventricular beta-endorphin-induced tail flick inhibition and catalepsy. 632 57


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