INT5916
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
This in turn activates 5-HT1A and 5-HT1B receptors resulting in inhibition of serotonin release into the synaptic cleft. | |||||||||||||||
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The onset of antidepressant action of Serotonin (5HT) selective reuptake inhibitors (SSRIs) was attributed in part to the decrease in firing activity of serotonin neurons produced by the activation of raphe 5HT1A autoreceptors at the time of treatment initiation. | |||||||||||||||
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The differential regulation of 5-HT1A and 5-HT1B/D agonist responses by GDP suggests that different G-protein subtypes are involved upon 5-HT1A receptor activation by 5-HT1A and 5-HT1B/D agonists. | |||||||||||||||
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The data support the hypothesis that activation of the 5-HT1A receptor may be relevant to the mechanism of action of serotonin reuptake inhibitors. | |||||||||||||||
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In the course of that study, we found that such treatment also alleviated the pain associated with cold sensations in the legs, insomnia, anorexia, and depression, all of which are thought to be mediated through activation of the 5-HT1A receptor. | |||||||||||||||
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Activation of 5-HT1A receptors potentiates the clonidine inhibitory effect in the locus coeruleus. | |||||||||||||||
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The excess 5-HT produced by these antidepressant drugs in the interstitial space of the midbrain raphe activates somatodendritic 5-HT1A autoreceptors, thereby attenuating terminal 5-HT release. | |||||||||||||||
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Stimulation of 5-HT1A, 5-HT1B, 5-HT2A/2C, 5-HT3 and 5-HT4 receptors or 5-HT uptake inhibition: short- and long-term memory. | |||||||||||||||
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Maternally deprived animals also showed a decrease in corticosteroid receptors and an increase in 5-HT 1A and 1B receptors restricted to the CA1 region of the hippocampus. | |||||||||||||||
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Although activation of the 5-HT1a receptor exhibits proejaculatory effects, activation of the 5-HT1b and 5-HT2c receptors are involved in the process of delaying ejaculation.16,17 It has been hypothesized that altered levels of serotonin or serotonin receptor sensitivity in the ejaculatory modulating centers of the central nervous system are the pathophysiologic basis of ejaculatory disorders.17
Current treatments for PE | |||||||||||||||
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No differences in magnitude of the effect of the two receptor subtypes were found, indicating that stimulation of either 5-HT1A or 5-HT1B receptors was equipotent in producing the antinociceptive tail-flick response. | |||||||||||||||
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Selective activation of 5-HT1A receptors seems to cause anxiolytic and possibly antidepressive effects. | |||||||||||||||
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Stimulation of 5-HT1A receptors causes central sympathoinhibition and an increase in cardiac vagal drive, which results in a profound fall in blood pressure. | |||||||||||||||
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The use of agonists and antagonists known to discriminate among different subtypes of serotonin receptors indicated that the hyperpolarizations were produced by activation of 5-HT1A receptors and the depolarizations were generated by activation of 5-HT2 and/or 5-HT1C receptors. | |||||||||||||||
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The observations suggest that the sumatriptan-induced contraction of the dural artery is mediated via activation of 5-HT1D or 5-HT1-like receptors, whereas it does not appear to activate the 5-HT2 receptors. | |||||||||||||||
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CONCLUSIONS: This study suggests that buspirone, but not sumatriptan, the selective agonist of 5-HT1-like receptors, causes miosis in humans by activation of 5-HT1A receptors, possibly located in the central nervous system where they inhibit iris sympathetic pathways. | |||||||||||||||
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Opioid or 5-HT1A receptor stimulation in the RVLM, but not in the CVLM, attenuates cardiovascular responses to muscle contraction. | |||||||||||||||
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Anandamide (AEA) potentiates 5-HT1A and inhibits 5-HT2A receptors supporting therapeutic efficacy in acute and preventive migraine treatment. | |||||||||||||||
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The effect of 5-HT on ERK activation appeared to be mediated through the activation of 5-HT1A receptors since similar results were obtained with R-+-8-hydroxy-DPAT, a selective 5-HT1A receptor agonist and WAY100635, a selective 5-HT1A receptor antagonist, reversed the 5-HT and the R-+-8-hydroxy-DPAT effects. | |||||||||||||||
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Building on a set-point model described previously for the hypothermic effect of 5-HT agonists, we have developed a model based on the concept of homeostatic control mechanisms, in which SSRIs exert their antidepressant effect by increasing the transduction set-point of the postsynaptic 5-HT1A receptor, and pindolol exerts its effect by increasing the rate of feedback mechanisms. | |||||||||||||||
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General Comments
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