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 behavioral effects of beta-endorphin, [D-Ala2, D-Leu5]-enkephalin and morphine were investigated in golden hamsters and in rats. In golden hamsters, beta-endorphin and [D-Ala2, D-Leu5]-enkephalin induced loss of righting reflex, whereas morphine caused no such effect. Both opiate peptides and morphine caused the inhibition of tail-flick response and catalepsy in rats. beta-Endorphin was the most potent, followed by [D-Ala2, D-Leu5]-enkephalin and then by morphine. The catalepsy induced in rats by [D-Ala2, D-Leu5]-enkephalin was different from that of beta-endorphin and morphine in that it produced catalepsy without muscular rigidity. beta-Endorphin and [D-Ala2, D-Leu5]-enkephalin caused hypothermia in golden hamsters; morphine was less active in altering the body temperature. beta-Endorphin caused hypothermia at high doses and hyperthermia at low doses in rats. These heterogenous behavioral responses indicate that multiple types of receptors mediate the effects of opiates in the central nervous system.
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PMID:Behavioral activities of opioid peptides and morphine sulfate in golden hamsters and rats. 11 44

Microinjection of the C-fragment (also called beta-endorphin), which is amino acid sequence 61-91 of the endogenous pituitary hormone, beta-lipotropin (beta-LPH), in the periaqueductal gray of the rat resulted in profound sedation and catalepsy, while microinjection of smaller fragments-that is, methionine-enkephalin [sequence beta-LPH-(61-65)] and its related pentapeptide, leucine enkephalin, and alpha-endorphin [sequence beta-LPH-(61-76)] resulted in attenuated forms of this behavior. This indicates that the C-fragment is an important neuromodulator of the central nervous system. The similarity of this behavior to that seen after systemic administration to experimental animals of exogenous neuroleptics suggests that a disturbance in the bioavailability of this neuropeptide to receptor sites in brain-perhaps due to lack of enzymatic cleavage from the circulating parent hormone, beta-lipotropin--may be an etiological factor in those psychopathological states for which the exogenous neuroleptics exert an ameliorative influence.
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PMID:The C-fragment of beta-lipotropin: an endogenous neuroleptic or antipsychotogen? 18 95

The injection of various doses of morphine, subcutaneously, or of beta-endorphin, intraventricularly, changes the turnover rate of gamma-aminobutyric acid (TRGABA) in the substantia nigra, globus pallidus and nucleus caudatus. The TRGABA decreases in N. caudatus but increases in globus pallidus and substantia nigra. These changes are dose related and can be inhibited by naltrexone. The increased TRGABA in globus pallidus elicited by these opioid receptor agonists may be associated with catalepsy since muscimol, a specific GABA receptor agonist, injected into the globus pallidus causes a dose-related catalepsy. Since this GABA receptor agonist injected into the substantia nigra fails to cause catalepsy, one can exclude that the increase in the TRGABA of substantia nigra elicited by opiate receptor agonists is operative in mediating the catalepsy elicited by opioids.
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PMID:Opiate receptor agonists as modulators of gamma-aminobutyric acid turnover in the nucleus caudatus, globus pallidus and substantia nigra of the rat. 21 44

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

Acute intracisternal administration of human beta-endorphin produced catalepsy and increased striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPA) and homovanillic acid (HVA). All of these effects were blocked by naloxone. Apomorphine, a dopamine receptor antagonist, also prevented beta-endorphin-induced catalepsy and the increase in striatal DOPAC and HVA. The combination of subcataleptic doses of haloperidol and beta-endorphin produced catalepsy and large increases in striatal DOPAC and HVA. These data provide evidence for a role for nigrostriatal dopamine neurons in beta-endorphin-induced catalepsy. The apparent increase in striatal dopamine turnover following beta-endorphin administration may be compensatory.
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PMID:Dopaminergic mediation of beta-endorphin-induced catalepsy. 56 67

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

Repeated intracisternal injections of human beta-endorphin lead to development of tolerance with respect to the catalepsy, analgesia, and hypothermia which are seen following a single injection. The initial injection of beta-endorphin results in increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in neostriatum, as well as increases in the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in hypothalamus and brainstem and a decrease in 5-HIAA in hippocampus. In the present study, we report changes in metabolism of dopamine and serotonin in specific brain areas during the development of tolerance to beta-endorphin. Thus, the development of tolerance to beta-endorphin with respect to catalepsy, analgesia, and hypothermia may be mediated by development of tolerance to the effects of beta-endorphin on brain dopamine and serotonin release.
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PMID:Alterations in brain dopamine and serotonin metabolism during the development of tolerance to human beta-endorphin in rats. 74 24

The objective of this study was to evaluate histologically the toxicity of human beta-endorphin on the rat central nervous system after intrathecal administration. Animals received a single injection of 5 micrograms (n = 9) or 50 micrograms (n = 10) on each of four consecutive days, while others received 50 micrograms (n = 8) as a single dose. The control groups received either physiologic saline (n = 10) during each of four consecutive days or had sham operations (n = 4). Tests for nociception (tail-flick latency), motor function, and reflexes (righting reflex, eye-blink reflex, and inclined plane) were performed 5, 15, 30, 60, and 120 min after injection. Both dosages produced a dose-dependent impact on these parameters. In the 50-micrograms group, there were no significant differences in analgesia between the first and the fourth doses injected. The 50-micrograms dose produced catalepsy in some animals. All changes returned to baseline within 24 h. One animal in the 50-micrograms group developed hind limb paralysis after a single injection. Histologic sections from brain, brain stem, and spinal cord were prepared. No changes in histology were found except for that in the paretic animal, which had anoxic changes in the hippocampus and other cortical areas. Human beta-endorphin produced no neurotoxicity. The effect on nociception, reflexes, and motor function confirmed the results of previous studies.
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PMID:Histologic examination of the rat central nervous system after intrathecal administration of human beta-endorphin. 144 53

Pentobarbital anesthesia causes about a 10-fold increase in the antinociceptive potency of beta-endorphin microinjected into the periaqueductal gray (PAG) region of the rat brain. The antinociceptive response to PAG morphine was markedly attenuated during anesthesia, but returned as the rats regained consciousness. As they recovered from anesthesia, muscular rigidity and body stiffness (catalepsy) also occurred in the pentobarbital treated animals receiving morphine. These results are consistent with the activation of separate and distinct descending pain inhibitory neuronal systems by these two opioid agonists, and the differential modulation of the systems by pentobarbital. They also suggest that the mechanism underlying muscular responses to morphine is sensitive to pentobarbital, and is not shared by beta-endorphin.
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PMID:Antinociception from the administration of beta-endorphin into the periaqueductal gray of rat is enhanced while that of morphine is inhibited by barbiturate anesthesia. 149 80

The effects of novel opioid antagonists on the behavioural syndrome induced by electroconvulsive shock (ECS) in rats have been examined and compared with those of the established agent naloxone. A single ECS produced catalepsy and significantly increased tail immersion response times during the 15 min following the seizure. These responses were inhibited by a low dose of naloxone (1 mg kg-1, i.p.) and also by RX8008M (16-methylcyprenorphine; 1 mg kg-1, i.p.) which blocks mu- and delta- but not kappa-opioid receptor function. In comparison, the antinociception and catalepsy induced by ECS was not attenuated by the selective delta-receptor antagonist naltrindole (1 mg kg-1, i.p.). These results suggest that ECS-induced antinociception and catalepsy may be mediated by endogenous opioids acting at mu-opioid receptors and are consistent with biochemical studies showing the release of beta-endorphin in both animals and man following this procedure.
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PMID:Investigation of the different types of opioid receptor involved in electroconvulsive shock-induced antinociception and catalepsy in the rat. 168 23


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