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)

Dopaminergic neuron controls CNS functions such as meso-limbic, striato-nigral and tubero-infundibular systems. The purpose of the present study is the evaluation of the hypothalamic dopaminergic neuron activity in neuro-degenerative disorders. alpha-melanocyte-stimulating hormone (alpha-MSH) is synthesized in the arcuate nucleus and lateral part of the hypothalamus, and its secretion is under the inhibitory control of the dopaminergic neuron both in the hypothalamus and pituitary. alpha-MSH-like-immunoreactivity (alpha-MSH-LI) in CSF is thought to be representative to the dopaminergic neuron activity in the hypothalamus. We therefore evaluated CSF levels of alpha-MSH-LI in spinocerebellar degenerations and extrapyramidal diseases. The subjects are 11 patients with Parkinson's disease, 16 with Shy-Drager syndrome (SDS), 16 with cerebellar cortical atrophy, 3 with Machado-Joseph disease, 3 with dentato-rubro-pallido-luysian atrophy and 2 with Huntington's disease as well as 24 controls. All patients with Parkinson's disease were administered levodopa and carbidopa. CSF was sampled through lumbar puncture in the morning. After the centrifugation, supernatant of CSF was stored at -40 degrees C until used. alpha-MSH in CSF was extracted by Rainero's method and measured by RIA. alpha-MSH-LI levels in control was 23.9 +/- 2.6 pg/ml (mean +/- SD). The significant elevation was observed in Parkinson's disease (40.3 +/- 7.5, p less than 0.001) and SDS (42.3 +/- 9.4, p less than 0.001). The levels showed not significant correlation with age, duration of illness or severity of autonomic disorder. Most of other diseases demonstrated the levels within normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abnormality of hypothalamic dopaminergic system in neuro-degenerative diseases--evaluation of alpha-melanocyte-stimulating hormone-like immunoreactivity in cerebrospinal fluid]. 176 56

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

Beta-endorphin/beta-lipotropin immunoreactivity (BE/BLPH-IR) content was evaluated in the CSF of patients suffering by deafferentation pain syndromes. BE/BLPH-IR CSF concentrations of these patients were compared with those obtained in a group of patients affected by low back pain and in a control group without pain problems. No statistically significant variation in BE/BLPH-IR levels were found between controls and subjects with different types of chronic pain.
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PMID:Evaluation of beta-endorphin/beta-lipotropin immunoreactivity content in the CSF of patients affected by deafferentation pain syndromes. 182 20

By means of RIA, the contents of Leu-enkephalin, Met-enkephalin, and Beta-endorphin in CSF of 32 epileptic patients and 24 controls were determined. It was found that the mean Leu-enkephalin content in CSF of the epileptic patient group was significantly higher than that of the control group (P less than 0.01), whereas the mean contents of Met-enkephalin and Beta-endorphin in CSF showed no significant change as compared with those of the control group. The increase of Leu-enkephalin was not related to such factors as type of seizure, age of onset, length of time after the last seizure, taking of antiepileptic drugs, and abnormality in cranial CT manifestation. This suggested that endogenous opioid peptides might take part in the neurochemical mechanism of human epilepsy, and leu-enkephalin could play an important role in the development of epileptic episodes.
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PMID:[Opioid peptides in cerebrospinal fluids of epileptic patients]. 190 3

Precursors to beta-endorphin (BE) and methionine enkephalin (ME), and proteolytic enzymes that cleave those BE and ME precursors to BE and ME, were determined in several milliliters of human cerebrospinal fluid. Endogenous peptides were purified by reversed-phase high-performance liquid chromatography (HPLC), and were detected with radioreceptor assay (RRA), radioimmunoassay, and mass spectrometry (MS). Total opioid receptor activity measurements and the profile of HPLC-receptor activity of human CSF samples were both used to monitor neuropeptide metabolism. MS data linked the molecular ion of ME to a unique fragment ion. A later-eluting fraction (84 min) in a 90-min HPLC gradient appeared in all HPLC-RRA profiles, contained opioid receptor activity that displaced [3H]etorphine, and the quantitative and qualitative patterns of opioid receptor activity in those profiles both changed within the few minutes that elapsed between acquiring the first and second cerebrospinal fluid samples. That 84-min fraction contained precursors to opioid peptides and was fractionated further with a more shallow 120-min HPLC gradient into three sections that displayed delta-opioid receptor-preferring activity, using [3H]ME as ligand. These three sections were hydrolyzed separately with human cerebrospinal fluid as the source for endogenous neuropeptides to yield products that correlated to immunoreactive BE in section I and immunoreactive ME in section III.
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PMID:Proenkephalin A and proopiomelanocortin peptides in human cerebrospinal fluid. 196 61

Concentrations of beta-endorphin in the cerebrospinal fluid were measured in 21 painless subjects and 37 patients with chronic pain. Statistical analysis of the results showed no significant difference between the two groups. This lack of correlation between beta-endorphin concentrations in the CSF and the presence of chronic pain highlights the difficulties and limitations encountered when trying to determine the role of endogenous opioid systems with this method.
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PMID:[Cerebrospinal fluid beta-endorphin in chronic pain in man]. 213 10

Twenty-five patients with chronic progressing multiple sclerosis were examined for the content of beta-endorphin in blood serum, supernatants of activated lymphocytes and CSF by RIA. At the same time the parameters of cellular immunity were appraised. Different relations were discovered between cellular immunity and the content of beta-endorphin in biological fluids which may play a material part in the pathogenesis of multiple sclerosis.
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PMID:[Study of cellular immunity and the opioid peptide system in patients with multiple sclerosis]. 216 Jan 62

Cerebrospinal fluid beta-endorphin-like immunoreactivity (CSF BLI) was determined on 3 occasions for elderly delirious patients and the BLI levels were compared with age-equivalent controls. Delirious patients showed a significant reduction in the BLI values in the first sample and a declining trend was seen in the follow-up. The results suggest a role for beta-endorphinergic dysfunction in the genesis of some symptoms of delirium, and this dysfunction may be a common phenomenon in various forms of delirium and dementia.
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PMID:A longitudinal study of cerebrospinal fluid beta-endorphin-like immunoreactivity in delirium: changes at the acute stage and at one-year follow-up. 226 Apr 89

The authors investigated the relationship between items on the Beck Depression Inventory and CSF levels of corticotropin-releasing hormone (CRH) in 17 depressed patients. Linear regression analysis showed that self-accusation, expectation of punishment, and crying accounted for 82% of CRH variance.
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PMID:Relationship of cognitive factors to CSF corticotropin-releasing hormone in depression. 230 55

Baseline concentrations of beta-endorphin (beta-EP) and monoamine metabolites (MHPG: 3-methoxy-4-hydroxy-phenylglycol, HVA: homovanillic acid, 5-HIAA: 5-hydroxyindoleacetic acid) in lumbar CSF (LCSF) and ventricular CSF (VCSF) were measured in 18 patients with intractable pain; 10 with deafferented pain and 8 with peripheral pain. Control values were obtained from 37 individuals of various ages. Changes in the concentrations of these substances were determined before and after giving stimulations (2-5 V, 0.2-0.5 msec, 40-50 Hz, 20-sec duration) to 6 patients through electrodes implanted in deep brain structures (DBS; posterior limb of the internal capsule in 5 patients and rostral mesencephalic lemniscus medialis in one patient), and to 2 other patients through electrodes implanted in the spinal dorsal column (DCS). The control value of beta-EP in LCSF was 57.6 +/- 24.7 pg/ml, which was not significantly different from that of VCSF. Great variation in the individual control LCSF beta-EP concentrations was found, but it was not related to differences in age. The mean baseline LCSF beta-EP concentration was significantly higher (p less than 0.05) than the control in the patients with deaffernted pain before stimulation. One of the monoamine-metabolites, MHPG, showed higher level in the patients with peripheral pain (p less than 0.01). The LCSF beta-EP concentration was not affected by deep brain stimulation, but was increased by dorsal column stimulation. In one patient with excellent pain relief by stimulation of the posterior limb of the internal capsule, the LCSF HVA and 5-HIAA concentrations were conspicuously increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[beta-Endorphin and monoamine metabolite concentrations in patients with intractable pain--changes before and after deep brain or spinal dorsal column stimulation]. 241 30


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