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)

Synaptosomal preparations from rat hippocampus were incubated with methylprednisolone or adrenocorticotropin. High affinity choline uptake was not affected by either hormones. Methylprednisolone however enhanced newly synthesized acetylcholine release in the presence of high potassium or acetylcholine concentrations, while adrenocorticotropin had no effect. Dopamine uptake was inhibited when synaptosomes from septum or striatum were incubated with methylprednisolone. We conclude: a) high glucocorticoid concentrations and not adrenocorticotropin can directly enhance acetylcholine release but only from stimulated cholinergic synaptosomes, and b) high glucocorticoids can reduce dopamine uptake by dopaminergic synaptosomes. The results imply that increased glucocorticoid levels during stress or disease, can directly modulate the neuronal activity of specific cholinergic and dopaminergic systems in the brain.
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PMID:Presynaptic effects of glucocorticoids on dopaminergic and cholinergic synaptosomes. Implications for rapid endocrine-neural interactions in stress. 303 12

Release of beta-endorphin is modulated by physiologic stress and a variety of hormonal and pharmacologic factors. Prostaglandin E2 inhibits release of beta-endorphin and corticotropin from pituitary corticotroph cells, suggesting that suppression of prostaglandin levels should increase beta-endorphin release. This hypothesis was tested by administration of 600 mg ibuprofen before surgical stress in humans in comparison to placebo and methylprednisolone. Plasma samples were analyzed for immunoreactive beta-endorphin with concurrent measurement of pain and apprehension. Levels of immunoreactive beta-endorphin increased during surgery in the placebo group but were significantly greater in the group of patients pretreated with ibuprofen. Methylprednisolone suppressed intraoperative immunoreactive beta-endorphin, compared with both placebo and ibuprofen. Parallel in vivo and in vitro studies indicate that nonsteroidal anti-inflammatory drug potentiation of endorphin release is mediated at the level of the pituitary corticotroph cell. These results show that ibuprofen enhances pituitary release of beta-endorphin by corticotroph cells in response to stress.
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PMID:Ibuprofen elevates immunoreactive beta-endorphin levels in humans during surgical stress. 924 21