INT6228
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Fluoxetine-induced changes in body weight and 5-HT1A receptor-mediated hormone secretion in rats on a tryptophan-deficient diet. | |||||||||||||||
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We have found that the distribution of 5-HT1A receptors in monkey brain, labelled with the agonist 3H-8-OH-DPAT and the antagonist 3H-WAY 100635 was very similar at the levels examined, and corresponded well with that observed for the cells containing mRNA coding for this receptor, confirming the somatodendritic localization of 5-HT1A receptors in monkey brain. | |||||||||||||||
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These data suggest that hindlimb scratching induced by 5-HT agonists may not be centrally mediated but rather may be mediated by a neuronal 5-HT1A receptor localized outside the blood-brain barrier. | |||||||||||||||
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Because 5-HT1A receptors located on the soma dendrites of serotonin (5-HT) neurons normally mediate an inhibition of 5-HT firing and release, the desensitization of these autoreceptors is essential for obtaining an enhancement of 5-HT transmission after treatment with 5-HT reuptake inhibitors (SSRIs). | |||||||||||||||
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Repeated administration of milnacipran induces rapid desensitization of somatodendritic 5-HT1A autoreceptors but not postsynaptic 5-HT1A receptors. | |||||||||||||||
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Repeated administration of milnacipran induces rapid desensitization of somatodendritic 5-HT1A autoreceptors but not postsynaptic 5-HT1A receptors. | |||||||||||||||
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To further assess the desensitization of alpha2C-autoreceptors, alpha2A-heteroreceptors and 5-HT1A autoreceptors regulating the synthesis of dopa/NA or 5-HTP/5-HT after chronic desipramine and fluoxetine, the effects of clonidine (agonist at alpha2-auto/heteroreceptors) and 8-OH-DPAT (agonist at 5-HT1A-autoreceptors) were tested. | |||||||||||||||
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In the present study, we investigated whether a link might exist between these effects, i.e., whether glucocorticoid receptor activation could be responsible for the fluoxetine-induced desensitization of 5-HT1A autoreceptors. | |||||||||||||||
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Fluoxetine-induced desensitization of somatodendritic 5-HT1A autoreceptors is independent of glucocorticoid(s). | |||||||||||||||
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In conclusion, the data demonstrate that 5-HT1A, 5-HT2, and 5-HT3 receptor subtypes are functionally present on NTS neurones receiving excitatory vagal afferent input. | |||||||||||||||
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Long-term treatment with 5-HT-uptake inhibitors and noradrenaline-uptake inhibitor produces desensitization of 5-HT1A autoreceptors and alpha 2-heteroreceptors, respectively, which may be related therapeutically to the delayed onset of the effects of antidepressants. | |||||||||||||||
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Extracellular levels of serotonin (5-HT) and the regulation of 5-HT release by the 5-HT1A receptor were examined after single and repeated treatment with different types of antidepressant drugs: the selective 5-HT uptake inhibitor fluoxetine, the selective norepinephrine uptake inhibitor desipramine and the 5-HT2A/2C/alpha 2 receptor antagonist mianserin (each at 15.0 mg/kg). | |||||||||||||||
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One, the 5-HT1a receptor, releases a growth factor from astroglial cells. | |||||||||||||||
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It has also been reported that the firing activity of almost one-half of DRN 5-HT neurons can be reduced by stimulating some postsynaptic 5-HT1A receptors, localized within the medial prefrontal cortex (mPFC) and that trigger a negative long-loop feedback [17], [27]. | |||||||||||||||
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