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 influence of the hippocampus upon pituitary release of adrenocorticotropic hormone (ACTH) was studied in male Sprague-Dawley rats which had concentric bipolar stainless stell electrodes chemically implanted in the dorsal and ventral hippocampus. Blood samples were withdrawn at half-hour intervals from a cannula in the right atrium. Plasma corticosterone levels reflected ACTH release. 30 min of 25 or 250-cps electrical stimulation of the hippocampus in the freely-behaving, non-stressed rat resulted in significant increases in basal plasma corticosterone levels evident at the end of stimulation. In afternoon experiments, after stimulation at either hippocampal site with 25 cps only, the increase was followed by a delayed inhibitroy phase and temporary inhibition of the circadian rise in corticosterone levels. The inhibitory effect was more pronounced with ventral than with dorsal hippocampal stimulation. The basis for these differential effects is discussed in terms of the anatomical organization of the hippocampus.
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PMID:Effect of electrical stimulation of the hippocampus upon corticosteroid levels in the freely-behaving, non-stressed rat. 93 26

We compared the nocturnal plasma prolactin (PRL) and beta-endorphin (B-E) concentrations prior to and after sleep deprivation (SD) in eight epileptic patients with complex partial seizures. After the period of SD (1) the mean number of interictal epileptiform discharges and the mean plasma PRL levels showed a significant rise during light non-REM stages of sleep, and (2) mean nocturnal plasma PRL and B-E concentrations showed a moderate rise during the first few hours of sleep, significant only for plasma PRL. In a patient with multiple complex partial seizures during sleep, the levels of plasma PRL and B-E concentrations were closely related to ictal discharges. The data obtained in this stress-free environment suggest a centrally mediated interaction between the release of PRL and B-E, in relation to epileptic discharges.
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PMID:The effect of epileptiform discharges on neurohormonal release in epileptic patients with complex partial seizures. 296 4

We measured lumbar cerebrospinal fluid (CSF) levels of somatostatin, cholecystokinin, neurotensin, atrial natriuretic factor, vasoactive inhibitory peptide, neuropeptide Y, adrenocorticotrophic hormone, corticotropin releasing hormone, beta-endorphin, metenkephalin, cortisol, alanine, glycine, aspartate, glutamate, taurine, and gamma-aminobutyric acid in 25 inpatients with epilepsy at known interictal and postictal times and in 11 neurologically normal volunteers. There were no significant differences between interictal or postictal complex partial seizures (CPS), postictal generalized tonic-clonic seizures (GTC), and control CSF neuropeptide, cortisol, and amino acid (AA) levels. However, there were nonsignificant trends for CSF levels of several neuropeptides to be increased after CPS and GTC as compared with interictal baseline levels. There were significant correlations between levels of certain CSF neuropeptides or (AAs) and serum antiepileptic drug (AED) levels. Several correlations were noted between CSF levels of AAs, including a correlation between the excitatory neurotransmitters aspartate and glutamate identified only after CPS.
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PMID:Cerebrospinal fluid levels of neuropeptides, cortisol, and amino acids in patients with epilepsy. 809 91