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 review, based largely on our own results describes the present state of knowledge of some aspects of opioid peptides and their physiological role. Studies on the effect of opioid peptides and opiates on brain function and the changes of brain level of endogenous opioids under various conditions have demonstrated, among others, the role of opioids in stress and stress-induced analgesia, the involvement of various opioid receptors in spinal mechanisms of analgesia, the inhibitory role of dynorphin in seizures in contrast to proconvulsant action of beta-endorphin system and mu receptor, and led to postulation of the role of beta-endorphin interaction with serotonin for ingestive behavior and a possible involvement of beta-endorphin system in the mechanism of action of antidepressant treatments.
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PMID:Some aspects of physiology and pharmacology of endogenous opioid peptides. 614 28

Experiments were designed to test the hypothesis that pituitary hormones may be delivered directly to the brain. Concentrations of adrenocorticotropic hormone (ACTH) in the plasma were determined in blood samles obtained simultaneously from the carotid artery, the sagittal sinus, and the jugular vein of three awake sheep. Seizures were induced electrically to stimulate ACTH secretion, and at precise intervals thereafter several simultaneous comparisons were made in each animal. In many of the post-seizure comparisons, the ACTH plasma concentrations within the sagital sinus exceeded those within the carotid artery as well as those within the jugular vein, indicating that this hormone was released from the pituitary and carried directly through capillary beds of brain to the venous blood within the sagittal sinus. The experiment was repeated in one hypophysectomized sheep and, in this animal, ACTH concentration in the plasma was reduced, but that in the sagittal sinus still was elevated after the seizure, an indication that some ACTH (or ACTH-like material) was released from the brain itself.
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PMID:Adrenocorticotropic hormone may be transported directly from the pituitary to the brain. 625 7

A controlled study of 5 patients with infantile spasms was performed to determine the effectiveness of corticotropin (ACTH) treatment. Patients were monitored serially, using a time-synchronized polygraphic and video system. Serum cortisol levels were determined by radioimmunoassay. Four patients showed total cessation of seizures and normalization of the EEG on low-dose ACTH therapy. Two of these patients became hypertensive, requiring discontinuance of ACTH. Serum cortisol levels increased markedly in all patients after initiation of ACTh therapy. There appeared to be no consistent difference in serum cortisol levels between patients receiving 20 units/day of ACTH and those receiving 30 or 40 units/day, and there was no difference in cortisol levels in those patients who became hypertensive and those who did not.
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PMID:A controlled study of ACTH therapy in infantile spasms. 625 55

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
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PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

Intraventricular injection of beta-endorphin (0.1-3 micrograms) into gerbils from the UCLA seizure sensitive strain reduced the incidence and severity of spontaneous epileptiform seizures, both the motor manifestations and the preceding high voltage focal spiking and accompanying seizure activity in the cortical EEG. This "'anticonvulsant" effect of beta-endorphin was prevented by prior administration of naloxone (1 mg . kg-1 IP). These findings suggest that the endogenous opioid peptide may be involved in the normal suppression of the epileptic diathesis in these animals during the interictal periods.
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PMID:Modulation of spontaneous seizures in the mongolian gerbil: effects of beta-endorphin. 628 49

The proconvulsant actions of high doses of systemic morphine are probably mediated by 3 different systems. One of them produces non-convulsant electrographic seizures and can be activated separately from the others both by intracerebroventricular injections as well as microinjections into discrete subcortical areas. The enkephalins and beta-endorphin, when administered to the same loci, produce similar effects. Pharmacological evidence suggests that specific opiate receptors of the delta-subtype mediate the epileptiform effects produced by this system. The second system mediating proconvulsant effects of systemic morphine is not mediated by stereo-specific opiate receptors. It produces behavioral convulsions, and the GABA-ergic system has been implicated in its action. A third proconvulsant action of systemic morphine can be activated separately from the other two systems by administering this compound with other convulsive agents or manipulations. Specific mu-type opiate receptors are implicated in this effect. In addition to potent proconvulsant effects, systemic morphine also has anticonvulsant properties which are mediated by specific opiate mu-receptors. The conditions under which morphine acts as a proconvulsant rather than an anticonvulsant agent are, as yet, not understood.
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PMID:Pro- and anticonvulsant actions of morphine and the endogenous opioids: involvement and interactions of multiple opiate and non-opiate systems. 631 87

The effects of various opiate receptor agonists on the seizure threshold after an intravenous infusion of pentylenetetrazol were investigated in rats. The mu- and epsilon-receptor agonists, morphine (20-40 micrograms) and beta-endorphin (5-10 micrograms) show proconvulsant properties towards clonic and tonic seizures. The delta-receptor agonist (D-Ala2,D-Leu5-enkephalin, DADL 5-40 micrograms) and alpha-neoendorphin (20-40 micrograms) show pro- and anticonvulsant properties towards clonic and tonic seizures, respectively. Anticonvulsant properties of DADL are possibly due to its action on the spinal cord, since after the intrathecal injection this effect is still observed. Similarities between DADL and alpha-neoendorphin suggest that they may act through the same receptor. The kappa-receptor agonist dynorphin A (5-20 micrograms) and its degradation-resistant analogue D-Arg-dynorphin1-13 (10 micrograms) show significant anticonvulsant properties. Our present results suggest that the kappa-receptor agonist dynorphin may act physiologically as an endogenous anticonvulsant, in contrast to other opioid peptides.
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PMID:The effect of various opiate receptor agonists on the seizure threshold in the rat. Is dynorphin an endogenous anticonvulsant? 631 15

The effects of repeated infusion of small, initially subconvulsive amounts of beta-endorphin, met-enkephalin or morphine sulfate into the amygdala and hippocampus were investigated. beta-endorphin and met-enkephalin evoked epileptiform spiking when infused into the posterior amygdala or ventral hippocampus. Morphine evoked epileptiform spiking when infused into the anterior amygdala. Naloxone blocked or terminated the spiking. Repetition of the infusions led to the gradual development of bilateral generalized convulsions by beta-endorphin and met-enkephalin and to the development of tolerance to morphine. An unexpected observation was that handling, immobilization or conspecific threat potentiated the epileptiform effects of beta-endorphin and morphine in many cases. These results suggest that endogenous opiate mechanisms might play a role in convulsive seizures and that stressful stimuli can exacerbate opiate seizures.
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PMID:Intracerebral beta-endorphin, met-enkephalin and morphine: kindling of seizures and handling-induced potentiation of epileptiform effects. 632 69

Opioid agonists were used to investigate the modulation of seizures mediated by mu, kappa and delta opiate receptors in the seizure-sensitive Mongolian gerbil. Morphine (1.0-25 mg/kg, s.c.) were used as prototypic agonists for mu, kappa and delta opiate receptors. Each opioid decreased the incidence and severity of the seizure as compared to control values. The anticonvulsant effects of morphine (10 mg/kg, s.c.) and ketocyclazocine (0.5 mg/kg, s.c.) were reversed by naloxone (1.0 mg/kg, s.c.), while the anticonvulsant effects of N-allylnormetazocine (2 mg/kg, s.c.) were not significantly changed by naloxone. Additionally, abnormal behavior was observed following administration of the opioids. Morphine (10 mg/kg, s.c.) produced excitation and hyperresponsiveness with intermittent cataleptic-like states. Ketocyclazocine (10 mg/kg, s.c.) predominantly produced a stuporous, immobile state, accompanied by some loss of posture. N-allylnormetazocine (10 mg/kg, s.c.) produced ataxia and stereotypic side-to-side head nodding . Naloxone was able to reverse the behavioral effects produced by morphine and ketocyclazocine but not those produced by N-allylnormetazocine. The data presented are consistent with earlier studies which demonstrated the anticonvulsant effects of beta-endorphin in the gerbil. This study further suggests that opioids have a protective role against seizure activity in the gerbil and the opioid anticonvulsant effect is not specific to one type of opioid agonist.
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PMID:Similar anticonvulsant, but unique, behavioural effects of opioid agonists in the seizure-sensitive Mongolian gerbil. 633 Jun 6

Morphine, beta-endorphin and [D-Ala2, D-Leu5] enkephalin administered intracerebroventricularly exerted a protective effect on electroconvulsive shock (ECS)-induced seizures in mice. This effect was reversed by intraperitoneal injections of naltrexone. The role of mu and delta receptors in ECS-induced convulsions is discussed.
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PMID:Opioid antagonism of electroshock-induced seizures. 633 Jul 66


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