INT79822
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Our results indicate that in rat striatal axon terminals the K(+)-evoked release of dopamine is regulated by the presynaptic 5-HT1B heteroreceptors. | |||||||||||||||
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The 5-HT1B selective agonist CP93129 (3 ? | |||||||||||||||
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M) did not produce a significant reduction in evoked IPSC amplitude in the presence of the 5-HT1B antagonist NAS181 (10 ? | |||||||||||||||
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Clinical data suggest that coadministration of pindolol, a 5-HT1A/5-HT1B/beta-adrenoceptor antagonist, and selective serotonin reuptake inhibitors (SSRIs) may shorten the time of onset of a clinical action and may increase beneficial effects of the therapy of drug-resistant depression. | |||||||||||||||
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However, when constructed in the presence of WAY 100635 (10 nM) the selective and silent 5-HT1A antagonist, there was a significant (P < 0.001) rightward shift of the CP 93129 concentration-response curve in the paroxetine-treated rats but not in the controls, implying a desensitisation of the 5-HT1B autoreceptor by paroxetine. | |||||||||||||||
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The PAG contains a dense plexus of serotonergic nerve terminals [20], and varying levels of 5-HT1A, 5-HT1B, 5-HT1D and 5-HT1F receptor mRNA and protein has been found in different species [21-25]. | |||||||||||||||
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It is also consistent with prior studies which have reported that 5-HT1A levels within the PAG are relatively low compared to the adjacent dorsal raphe nucleus, and that 5-HT1A and 5-HT1B receptors are largely expressed within postsynaptic and presynaptic elements within the midbrain, respectively [43,44]. | |||||||||||||||
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In this regard, the extant evidence tends to support the novel concept of an adjunctive polypharmacy approach for the prevention and treatment of ADHD rather than single neurochemical and/or neurogenetic targets (eg, D1-D5, DAT1, DBH, COMT, 5HT1B, NR4A2, SLC1A3, BDNF, as well as loci at 4q13.2, 5q33.3, 11q22 and 17p11 [see above]). | |||||||||||||||
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Approximately 46% of the 5-HT1B-positive and 43% of the 5-HT1D-positive trigeminal ganglion neurons were also NF200 positive, indicating that many A-fibre trigeminal neurons express 5-HT1B or 5-HT1D receptors. | |||||||||||||||
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These genetic differences could be explained by various genes, the HTR1B, encoding the 5-HT(1) receptor subtype, MAOA gene that encodes the monoamino-oxidase, the main metabolic enzyme of this triptan, SLC6A4 (gene encoding the serotonin transporter) and DRD(2) (gene encoding the D(2) receptor), both involved in the pathogenesis of migraine. | |||||||||||||||
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General Comments
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