INT6128
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Electrical stimulation-induced release of beta-endorphin from genetically modified neuro-2a cells. | |||||||||||||||
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Using electrical field stimulation we were able to identify a stimulation pattern that significantly increased the release of beta-endorphin-immunoreactive material, although to a limited extent. | |||||||||||||||
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In this article we address the question of whether the release of beta-endorphin, an opioid with a potent analgesic effect, could be induced by electrically stimulating stably transfected Neuro-2a cells. | |||||||||||||||
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Physical exercise stimulates marked concomitant release of beta-endorphin and adrenocorticotropic hormone (ACTH) in peripheral blood in man. | |||||||||||||||
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Six normal men were treated with oral metyrapone to stimulate the secretion of ACTH, beta-lipotropin, and beta-endorphin. | |||||||||||||||
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The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. | |||||||||||||||
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Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. | |||||||||||||||
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Suppression of electroacupuncture(EA)-induced beta-endorphin and ACTH release by hydrocortisone in man. | |||||||||||||||
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BACKGROUND: In the pituitary of lower species, pro-opiomelanocortin is expressed in corticotroph cells of the anterior and in melanotroph cells of the neurointermediate lobe; enzymatic processing in the corticotrophs results in the release of adrenocorticotropic hormone, beta-lipotropin, or beta-endorphin. | |||||||||||||||
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Therefore, any contribution of the endorphin system to the production of general anesthesia does not appear to require the release of beta-endorphin. | |||||||||||||||
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Two different signalling pathways for the induction of immunoreactive beta-endorphin secretion by human peripheral blood mononuclear cells. | |||||||||||||||
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Naloxone-induced ACTH release in man is inhibited by clonidine. | |||||||||||||||
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This suggests that naloxone causes ACTH release through these same central noradrenergic pathways. | |||||||||||||||
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We used the alpha 2-adrenergic agonist, clonidine, as a central nervous system inhibitor of ACTH release to see if it would alter naloxone-induced ACTH secretion in normal human volunteers. 2. | |||||||||||||||
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We conclude that clonidine, by blocking central noradrenergic pathways, which stimulate corticotropin-releasing hormone secretion, inhibits naloxone-induced ACTH secretion. | |||||||||||||||
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In dispersed monolayer culture, CRF failed to elicit ACTH release from the tumor cells, but dexamethasone caused a paradoxical increase in ACTH secretion in vitro. | |||||||||||||||
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Inhibition of serotonin-induced ACTH release in man by clonidine. | |||||||||||||||
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Fenfluramine, a serotonin releasing agent and uptake inhibitor, causes ACTH release in normal man. 2. | |||||||||||||||
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Central serotonergic pathways are hypothesized to be involved in the stimulation of hypothalamic adrenocorticotropic hormone (ACTH) secretagogue release by both circadian- and stress-induced mechanisms. | |||||||||||||||
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Fluoxetine produced a small but non-significant increase in Nal-stimulated ACTH and cortisol release in both morning and afternoon studies. | |||||||||||||||
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General Comments
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