INT8089
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In conclusion, LHRH may interact with central opioid systems causing an increased sensitivity to nociceptive stimulation (hyperalgesia) and reduction of the antinociceptive effect of morphine. | |||||||||||||||
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This facilitatory, modulating effect at the pituitary level involves an allosteric increase in LHRH binding to its receptor leading to augmented influx of Ca2+ from the extracellular space. | |||||||||||||||
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Whether the inhibition of Na channels is one of the several effects of LHRH-receptor interaction remains to be determined. | |||||||||||||||
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We conclude that an opiate delta receptor subtype is endogenously activated in the pituitary of castrated male rats to prevent masking of GnRH binding. | |||||||||||||||
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Under control incubation conditions, gonadotropin-releasing hormone (GnRH) binds only a fraction of its receptors in rat-cultivated pituitary cells. | |||||||||||||||
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In an attempt to characterize the pharmacology of opiate effects, naloxone (10 microM), a poorly selective opiate antagonist, restored masking of GnRH binding in cells from castrates. | |||||||||||||||
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Spontaneous unmasking of GnRH binding was found reversed by pertussis toxin (PTX), an inhibitor of alphai and alphao subunits of heterotrimeric G proteins, and by U73122, a phospholipase C (PLC) inhibitor. | |||||||||||||||
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Our data show that the concomitant administration of the pure antiandrogen flutamide in association with the luteinizing hormone-releasing hormone agonist (D-Trp6) luteinizing hormone-releasing hormone ethylamide caused a 64 to 78 per cent decrease in serum prostatic acid phosphatase on days 3 and 7 after the start of treatment in 70 patients with previously untreated stage D2 prostatic cancer. | |||||||||||||||
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We have examined the pharmacology of the voltage-sensitive Ca2+ channels (VSCCs) that mediate gonadotropin secretion from primary cultures of rat pituitary cells, stimulated by either cell depolarization or by binding of gonadotropin-releasing hormone (GnRH). | |||||||||||||||
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Thus, the novel model enables detection of interactions of administered hormones with endogenous GnRH. | |||||||||||||||
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Pentobarbital stimulates the activity of the GnRH pulse generator interacting with opioid neurons in rats in proestrus. | |||||||||||||||
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Abundant evidence suggests that opiatergic neurons play an important intermediary role in the regulation of LHRH release by ovarian steroids; however, it is unclear whether opiates communicate directly or indirectly with LHRH neurons. | |||||||||||||||
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Since we observed no competition between LHRH and naloxone for their binding sites in pituitary or brain, the only viable interpretation of our results is that naloxone increases LH by inducing the release of LHRH. | |||||||||||||||
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Stimulation of CRH neurones in the paraventricular nucleus also activates gamma-aminobenzoic acid and opioid neurones in the medial preoptic area and reduces GnRH cell recruitment, thereby decreasing GnRH pulse frequency. | |||||||||||||||
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Physiological and pharmacological evidence has suggested that both endogenous opiates and gonadotropin-releasing hormone (GnRH) itself can act centrally to exert a tonic inhibition on gonadotropin secretion via an inhibition of the neurosecretion of GnRH. | |||||||||||||||
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Therefore, interaction between oxytocin and GnRH in the control of LH may be postulated. | |||||||||||||||
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The overlapping distribution patterns of iron and gamma-aminobutyric acid, enkephalin, and luteinizing hormone-releasing hormone suggest that the distribution of iron is related to its association with the metabolism of one or more neurotransmitters or neuroactive compounds. | |||||||||||||||
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The initial stage in activation of gonadotrophs by GnRH appears to be binding to and clustering--probably dimerization--of GnRH receptors. | |||||||||||||||
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The role of endogenous opiate peptides in the mesencephalic central gray (MCG) and their possible interactions with gonadotropin-releasing hormone (GnRH) in the regulation of lordosis behavior was assessed in ovariectomized, estrogen-treated and estrogen-progesterone-treated female rats. | |||||||||||||||
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We studied whether Na+ and Ca2+ channels are involved in the neural mechanism responsible for the surge of gonadotropin-releasing hormone (GnRH) in proestrous rats. | |||||||||||||||
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General Comments
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