Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kyotorphin is an analgesic neuropeptide isolated from the bovine brain in 1979. Further studies showed that kyotorphin produces an analgesia through an increased release of met-enkephalin in the brain and the spinal cord. We showed that it is also found in the human cerebrospinal fluid and the concentrations of kyotorphin in normal human CSF is 1.19 +/- 0.51 pmol.ml-1. We also found that it is lower in patients with persistent pain (0.24 +/- 0.04 pmol.ml-1). Above results suggest that kyotorphin acts as a putative neuromediator and/or an endogenous pain modulator in the human brain.
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PMID:[Kyotorphin like substance in human cerebrospinal fluid of patients with persistent pain]. 176 21

Tiapride icv 400 micrograms/rabbit exhibited analgesic and synergistic effects on electroacupuncture analgesia (EAA) in rabbits. Both electroacupuncture (EA) and tiapride (icv 400 micrograms/rabbit) enhanced the beta-endorphin-like immunoreactive substance (beta-EPIS) level in cerebrospinal fluid (CSF) measured by radioimmunoassay (RIA). When EA and tiapride were used in combination, a further increase of beta-EPIS content was found. The results suggested that promotion of beta-EPIS release by tiapride may be one of the mechanisms of synergistic effect of tiapride on EAA.
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PMID:Effect of tiapride on electroacupuncture analgesia. 178 Dec 81

Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule, proopiomelanocortin, beta-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body. The peptide produces analgesia by inhibiting the firing of peripheral somatosensory fibers. It also affects other senses, such as vision, hearing, and smell. Whereas the ability to increase beta-endorphin secretion during times of surgical stress is positively correlated with amelioration of pain, the administration of exogenous opioids, such as fentanyl, reduces plasma beta-endorphin. Decreased beta-endorphin concentrations may play a role in trigeminal neuralgia, migraine headache, and rheumatoid arthritis.
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PMID:Peripheral beta-endorphin and pain modulation. 181 47

Acupuncture analgesia (AA) caused by low frequency stimulation of the acupuncture point (AP) was abolished by hypophysectomy and adrenalectomy. Termination of the AA producing pathway from the AP to the pituitary gland was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with AA was in the posterior HARN (P-HARN). AA in the hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during acupuncture stimulation, were both restored by intraperitoneal microinjection of 0.5 mg/kg morphine or 0.1 micrograms beta-endorphin into the P-HARN during acupuncture stimulation. Of the analgesia produced by dopamine or beta-endorphin injected into the P-HARN, that caused by beta-endorphin disappeared after denervation of the M-HARN. The P-HARN neurons that responded to acupuncture stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-endorphin. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-endorphin might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy.
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PMID:Dopaminergic transmission in the hypothalamic arcuate nucleus to produce acupuncture analgesia in correlation with the pituitary gland. 184 81

Cholera toxin, an agent that impairs the function of Gs transducer proteins, was injected (0.5 microgram/mouse, icv) and the antinociceptive activity of opioids and clonidine was studied 24h later in the tail-flick test. In these animals, an enhancement of the analgesic potency of morphine, beta-endorphin and clonidine could be observed. Cholera toxin did not modify the antinociception evoked by the enkephalin derivatives DAGO and DADLE. Pertussis toxin that catalyses the ADP ribosylation of alpha subunits of Gi/Go regulatory proteins was given icv (0.5 microgram/mouse). This treatment reduced the analgesic effect of opioids and clonidine. However, while the analgesia elicited by DAGO, DADLE and clonidine was greatly decreased, the effect of morphine and beta-endorphin was reduced to a moderate extent. It is concluded that Gi/Go regulatory proteins functionally coupled to opioid and alpha 2 receptors are implicated in the efficacy displayed by opioids and clonidine to produce supraspinal analgesia. Moreover, these two receptors are susceptible to regulation by a process that might involve a Gs protein.
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PMID:Cholera toxin and pertussis toxin on opioid- and alpha 2-mediated supraspinal analgesia in mice. 185 Apr 93

Analgesia produced by systemic cocaine (20 mg/kg intraperitoneally) was not attenuated by dexamethasone (0.25-2.5 mg/kg) in the formalin or tail pinch test in rats. The result suggests that the activation of the corticotropin releasing factor-adrenocorticotropin/beta-endorphin axis does not explain cocaine-induced analgesia.
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PMID:An attempted reversal of cocaine-induced analgesia by dexamethasone. 185 23

The present experiment was designed to study whether or not prior exposure to inescapable shock is accompanied by sex-dependent changes in pituitary and central levels of immunoreactive beta-endorphin, which is proposed to play an important role in opioid analgesia induced by aversive stimulation. Further, the effects of brief reexposure (5 min) to the chamber where inescapable shock was experienced earlier, were established in both sexes. Elevated levels of beta-endorphin were found 24 hours after inescapable shock, in the anterior pituitary of males and in the midbrain periaqueductal gray of both males and females. Reexposure to the experimental chamber only affected beta-endorphin levels if shock had been experienced in this chamber. Reexposure after inescapable shock reduced beta-endorphin content of the arcuate nucleus of males and beta-endorphin content of the periaqueductal gray of males and females. The present results are related to previous findings of sensitization and conditioning of analgesic reactions. The sex differences found in the present experiment are discussed with respect to sex-dependent behavioral consequences of inescapable shock.
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PMID:Pituitary and brain beta-endorphin in male and female rats: effects of shock and cues associated with shock. 187 Nov 93

Dose-response curves of three receptor-selective opioids were established in a group of nonburned and a group of burned rats. Morphine (mu-agonist), biphalin (mu- and delta-agonist), and U50488H (kappa-agonist) were administered to each group, and analgesia was measured by tail flick latency testing. Each opioid had a significant increase in potency (i.e., a decrease in ED50 values) in the burned (15% body surface area) compared with the nonburned groups. Moderate doses of each drug (i.e., ED50 doses estimated from nonburned group data) in each case augmented stress-induced analgesia in the burned group. Analgesic doses failed to prevent a significant increase in plasma beta-endorphin and corticosterone after larger surface area (25%) burns. Regardless of receptor specificity, opioid analgesic potency is increased acutely after burn injuries.
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PMID:Enhanced potency of receptor-selective opioids after acute burn injury. 189 68

One of the central issues in present experimental pain research is to establish the identity, location, and mechanism of action of various opioids (opioid peptides and alkaloids) and multiple opioid receptors in the modulation of nociceptive processes. At the cerebral level, studies employing several experimental approaches point to an essential role of beta-endorphin in analgesia, induced by electrical stimulation of the periaqueductal grey of the midbrain. Tolerance and cross-tolerance studies suggest that mu-opioid receptors mediate this effect. The significance of delta- and, in particular, chi-opioid receptors in cerebral pain modulation is less well documented. At the spinal level, nociception is relayed in the dorsal horn, where opioid peptides as well as all types of opioid receptors are abundant. mu-opioid receptor-mediated antinociceptive processes appear to be most important in this region, but delta-opioid receptors may also be involved. In addition, a role of chi-opioid receptors can be demonstrated under certain conditions. Recent experiments indicate that opioids may also modulate nociception in the periphery, in particular in inflamed tissue. The identification of opioid receptors and their endogenous ligands, the opioid peptides, marked the beginning of a new era in pain research. The differentiation of several types of opioid receptors and the subsequent characterization of a series of opioid peptides illustrate the striking complexity of opioid systems. The implications of this multiplicity for neurobiology in general and for the understanding of pain mechanisms in particular are presently not fully understood. In this presentation some aspects of opioidergic pain control at various levels of the neuraxis will be discussed.
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PMID:Opioids and opioid receptors mediating antinociception at various levels of the neuraxis. 196 32

The situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.
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PMID:Influence of opiate systems in pain transmission during angina pectoris. 196 35


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