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)

Endogenous opioids (EO) probably do not modulate endotoxin (LPS)- or interleukin 1 (IL1)-induced fever because naloxone does not prevent its development. Yet, increases in CSF and hypothalamic levels of beta-endorphin have been reported during LPS-and IL1-induced fevers. Since IL1 also reduces the specific binding of opioids to their receptors in guinea pig brain, the opioids could be involved in modulating nonfebrile effects of IL1. To determine whether EO might have a role in the IL1-induced acute-phase glycoprotein response of guinea pigs, (1) naloxone (5 and 10 mg/kg, SC) was injected prior to LPS (S. enteritidis 2 micrograms/kg, IV; N = 5), and (2) morphine (MOR, 10 micrograms/microliter), [D-ala2]-met-enkephalinamide (DAME, 5 micrograms/microliter), or dynorphin A (DYN, 5 micrograms/microliter) was injected into the preoptic area (1 microliter, bilaterally; N = 8/treatment) or into the 3rd ventricle (N = 4/treatment); pyrogen-free saline was the control injection. Measurements were: core temperature (Tco) and, as indices of acute-phase glycoproteins, plasma levels of copper (Cu) and N-acetylneuraminic acid (NANA). Naloxone did not prevent the fever or the increases in plasma Cu and NANA levels evoked by LPS. The intracerebral administration of opioid agonists by either route induced variable rises in Tco, each with a different pattern, but no increases in plasma Cu and NANA levels. Thus, EO do not participate in the central modulation of acute-phase glycoprotein synthesis, but may have a role in influencing other nonthermal IL1 effects in the CNS.
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PMID:Hypothalamic opioids and the acute-phase glycoprotein response in guinea pigs. 241 70

A seventeen year old boy presented with destructive arthropathy of the lower limbs and discovertebral spaces. Past history yielded recurrent episodes of indolent fractures and progressive knee and ankle deterioration. The patient denied any pain sensation in the past and at examination. Other neurological tests were normal. Beta-endorphin level was elevated in the CSF. Response to the cold pressor test was modified after injection of Naloxone. The nosology and physiopathology of congenital insensitivity to pain are discussed.
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PMID:[A case of congenital insensitivity to pain with destructive arthropathies of the limbs and spine. Discussion on nosology and physiopathology of the disease]. 242 25

Spontaneously elevated nociceptive threshold levels were markedly diminished after Naloxone injections in 4 patients with congenital insensitivity to pain. This finding suggested the hypothesis of a relation between congenital insensitivity to pain and permanent hyperfunction of an endomorphinic system. Radio-immunoassay of CSF beta-endorphin was performed in all 4 cases. The normal or only slightly elevated levels cannot explain electrophysiologic findings, but as a function of the multiplicity of endogenous opioid systems, hyperactivity of another endomorphinic system cannot be excluded. Other hypotheses may also be proposed.
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PMID:[Cerebrospinal fluid beta-endorphin in congenital insensitivity to pain]. 243 47

There are indications to suggest a relationship between low levels of 5-hydroxy-indoleacetic acid (5HIAA) in the cerebrospinal fluid and suicidal behavior. Many depressed patients show an elevated cortisol secretion. As beta-endorphin is derived from the same precursor as ACTH, it is expected that plasma beta-endorphin levels will also rise in depressed patients. We report here a case of severe depression with diurnal variation who showed low CSF 5HIAA prior to his suicide. In contrast, his catecholamine metabolites were 50% above the mean values of other depressed patients. Hormonal measurements, however, showed low cortisol, prolactin and beta-endorphin levels.
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PMID:Diurnal rhythms of plasma cortisol, beta-endorphin and prolactin, and cerebrospinal fluid amine metabolite levels before suicide. Case report. 243 87

Metabolites of selected neurotransmitters (5-HIAA, HVA and DOPAC) and beta-endorphin were measured in the CSF of 39 chronic pain patients and compared to controls. Twelve of the pain patients also fulfilled criteria for major depression. The concentration of 5-HIAA was increased in female but not male pain patients; there was no significant difference in the CSF concentrations of HVA and DOPAC. The presence of depression did not influence the concentrations of neurotransmitters. No correlation was found between the concentrations of monoamine metabolites and beta-endorphin. However, there was a positive correlation between 5-HIAA and HVA in controls and chronic pain patients without depression but not in depressed patients. It is concluded: chronic pain states are associated with elevation of CSF 5-HIAA in female patients; depression abolishes a positive correlation between 5-HIAA and HVA.
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PMID:CSF monoamine metabolites in chronic pain. 244 27

A recent neuropathological study has reported decreased levels of dynorphin A immunoreactivity in striato-pallidal fibers in the brain of a patient with severe Gilles de la Tourette's syndrome (TS). This observation, taken with the neuroanatomic distribution of dynorphin and its broad range of motor and behavioral effects, has led to speculation concerning its role in the pathobiology of TS. We report on the presence of elevated concentrations of dynorphin A [1-8] in the CSF of 7 TS patients, aged 20 to 45 years. The increase in CSF dynorphin was found to be associated with the severity of the obsessive compulsive symptoms but not with tic severity in these patients. Although CSF studies lack the precision necessary to address questions of selective involvement of neuronal system in specific CNS locations, these findings suggest that endogenous opioids are involved in the pathobiology of TS and related disorders. Tourette's syndrome (TS) is a chronic neuropsychiatric disorder of childhood onset that is characterized by multiple motor and phonic tics that wax and wane in severity and an array of behavioral problems including some forms of obsessive compulsive disorder (OCD) (1). Once thought to be a rare condition, the prevalence of TS is now estimated to be one case per 1,000 boys and one case per 10,000 girls, and milder variants of the syndrome are likely to occur in a sizeable percentage of the population (2). Although the etiology of TS remains unknown, the vertical transmission of TS within families follows a pattern consistent with an autosomal dominant form of inheritance (3,4). Neurobiologic and pharmacological data have implicated central monoaminergic and neuropeptidergic systems in the pathophysiology of TS, and basal ganglia structures remain the prime candidates as the neuroanatomical origin for TS and related conditions (1). Endogenous opioids, including dynorphin and met-enkephalin are concentrated in structures of the basal ganglia (5), are known to interact with central dopaminergic neurons (6, 7), and may play an important role in the control of motor functions (8). Post-mortem brain studies have directly implicated opioids in the pathophysiology of Parkinson's disease (9), Huntington's disease (10), and most recently in TS (11). The neuropathological study of Haber et al. (11) reported decreased levels of dynorphin A [1-17] immunoreactivity in striatal fibers projecting to the globus pallidus in the brain of a patient with severe TS. This ovservation, taken with the neuroanatomic distribution of dynorphin and its broad range of motor and behavioral effects, has led to speculation concerning its role in the pathobiology of TS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Elevated CSF dynorphin A [1-8] in Tourette's syndrome. 246 50

Cerebrospinal fluid beta-endorphin-like immunoreactivity (CSF BLI) was determined for 69 patients who met DSM-III criteria for delirium and for 8 controls. The CSF BLI was significantly lower in the delirious patient group than in the controls (12.5 +/- 3.0 pg/ml versus 15.0 +/- 3.4 pg/ml, p less than 0.05). CSF BLI had no correlation with age or neuroleptic drug dosage, but did have a significant positive correlation with cognitive functioning as evaluated by the Mini-Mental State. Our findings suggest a role for beta-endorphinergic dysfunction in the development of delirium.
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PMID:CSF beta-endorphin-like immunoreactivity in delirium. 252 20

The etiology of the SAS is unknown. To test whether endogenous opioids could be pathologically active in SAS, markers of opioid systems were measured in the CSF of 15 patients with SAS and in control subjects. Measured by receptor assay, the concentration of so-called fraction 1 opioid was higher in patients with SAS (3.0 +/- 1.5 pmol/ml; mean +/- SD) than in control subjects (1.1 +/- 0.5 pmol/ml) (p less than 0.01), whereas that of fraction 2 opioid was similar in the two groups. Beta-endorphin-like activity, measured by radioimmunoassay, was somewhat lower in patients with SAS (14.0 +/- 2.8 pmol/ml) than in control subjects (21.8 +/- 7.6 pmol/ml) (p less than 0.05). Six months after surgical treatment of the soft palate, new measurements were made in eight patients. Fraction 2 endorphin and beta-endorphin showed no consistent changes. A decrease in the level of fraction 1 from 4.1 +/- 1.5 pmol/ml to 2.3 +/- 1.0 pmol/ml (p less than 0.02) was noted in those six patients showing a successful clinical course. The data support the hypothesis that in SAS the opioid activity is increased.
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PMID:Increased CSF opioid activity in sleep apnea syndrome. Regression after successful treatment. 252 20

Significantly lower met-enkephalin levels were found in CSF from cluster headache sufferers as compared to age-matched healthy volunteers, whereas it was not possible to demonstrate any clear-cut difference for beta-endorphin. CSF opioid levels may rise following manual or electroacupuncture. It was studied whether traditional Chinese (manual) acupuncture affected CSF levels of met-enkephalin or beta-endorphin in these patients, and to what extent this treatment would be beneficial for the headache. A significant rise in lumbar CSF met-enkephalin levels was found, whereas no clear change in beta-endorphin levels was obtained. The treatment was, however, of little value in preventing the headache.
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PMID:Low CSF met-enkephalin levels in cluster headache are elevated by acupuncture. 252 27

Migraine is a psychobiological disorder in which a recurrent failure of opioid and adrenergic systems might occur, as plasma and CSF studies suggest. In order to elucidate the relationship between noradrenergic and opioidergic functions, the plasma beta-endorphin (beta-EP) response to clonidine and the cortisol response to dexamethasone were evaluated together in 25 patients suffering from migraine without aura, and with chronic tension headache (MTH). Baseline beta-EP plasma levels and beta-EP response to clonidine were significantly lower in MTH subjects than in controls, suggesting a postsynaptic hypothalamo-pituitary impairment. Forty-four percent of the MTH subjects showed either a lack of suppression of plasma cortisol following dexamethasone administration, or basal cortisol concentrations higher than controls and suppressors, suggesting a disinhibition of the hypothalamopituitary-adrenal (HPA) axis. An inverse correlation was found between pain severity and beta-EP secretion induced by clonidine (delta max), and no relationship was found between beta-EP and mood. These data suggest a failure of central noradrenergic activity, or perhaps an impaired secretion of beta-EP not related to HPA axis hyperactivity or to affective state.
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PMID:Neuroendocrine evidence of deranged noradrenergic activity in chronic migraine. 255 58


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