INT916
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In order to evaluate the interaction between the opiate-like peptidergic pathways and the dopaminergic system in modulating prolactin (PRL) secretion, ten normal volunteers were studied according to a double-blind, cross-over, randomized experimental design. | |||||||||||||||
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The Authors, for testing the opiate receptors role in human PRL secretion, performed the following experiment: they administered: 1) to 24 women during day 2 and 4 of the puerperium, divided into 3 groups of 8 subjects, respectively 5, 10, 20 mg naloxone. 2) to 16 women during day 3 and 4 of the puerperium, divided into 2 groups of 8 subjects, during mechanical breast stimulation with a breast pump (10 min for each breast), respectively 5, 10 mg naloxone. 3) to 12 women in physiological menopause, in basal condition and after administration of oestradiol 17-n-valerate 4 mg/die over ten days, 10 mg naloxone. 4) to 7 women in physiological menopause, in basal condition and after administration of ethinyl-oestradiol 50 micrograms/die over ten days, 5 mg morphine hydrochloride. | |||||||||||||||
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The aim of this study was to ascertain whether there is a correlation between gonadal steroids and opioid control of prolactin (PRL) secretion. | |||||||||||||||
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These results suggest that gonadal steroid deficiency seems to cause a change in the opioid system and/or dopaminergic control of prolactin secretion. | |||||||||||||||
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Fluoxetine hydrochloride, a specific inhibitor of serotonin reuptake, was given orally to five adult males to study its effect on fasting and insulin-stimulated release of PRL. | |||||||||||||||
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Opioids regulate prolactin secretion through unknown mechanisms, perhaps acting on the synchronization of pulsatile pattern of prolactin (Lafuente 1994) and may have a role in stress-induced hyperprolactinemic response (Van Vugt and Meites 1980; Benker et al 1990). | |||||||||||||||
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A recent study showed that lithium affects variably prolactin secretion, in relation to duration of the therapy: a treatment of less than six months was found to increase prolactin levels as compared to controls, while bipolar patients on long term treatments (<six months) showed a decrease in prolactin levels (Basturk et al 2001). | |||||||||||||||
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The effects of lithium on prolactin secretion are controversial. | |||||||||||||||
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Only a few data concerning the effect of antidepressant drugs on prolactin secretion are currently available. | |||||||||||||||
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A plenty of mediators, of central, pituitary and peripheral origin (Freeman et al 2000, Figure 1), take part in regulating prolactin secretion, through a direct or indirect effect on lactotroph cells. | |||||||||||||||
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This pathway, referred to as “tuberoinfundibular-GABA (TI-GABA) system”, has been shown to modulate prolactin secretion in humans, possibly through serotoninergic stimulation of GABA interneurons (that express the 5HT1A membrane receptor) resulting in inhibition of TIDA cells and prolactin secretion (Emiliano and Fudge 2004). | |||||||||||||||
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Regulation of prolactin secretion | |||||||||||||||
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The main physiologic control of prolactin secretion is exerted by the inhibiting action of dopamine. | |||||||||||||||
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Estrogens modulate prolactin secretion in response to reproductive events through different mechanisms: amplification of mitotic activity of the lactotrophs, enhancement of prolactin gene transcription and translation through ER? | |||||||||||||||
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In a study by Bonuccelli et al (1985), on normal and epileptic subjects, no appreciable change in prolactin spontaneous secretion or in prolactin secretory circadian rhythm was observed, though a small increase in early sleep values was reported. | |||||||||||||||
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Sleep has a stimulatory effect on prolactin secretion. | |||||||||||||||
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It can also not be ruled out that melatonin might act via the opioid system, which then could affect prolactin secretion. | |||||||||||||||
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These data indicate a probable role for PGE2 or other prostanoids as well in the regulation of human PRL release but not in gonadotrophin secretion. | |||||||||||||||
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These data allow us to conclude that D may affect PRL release in humans; however, further investigation is necessary before any physiological significance might be attributed to D in man. | |||||||||||||||
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However, the limited neuroendocrine data available does shed some light on the mechanism of action of these agents and raises some important questions, particularly about the regulation of PRL secretion and the interaction between various neurotransmitter systems. | |||||||||||||||
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