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Título : Autoradiographic characterisation of [35S]GTPgammaS binding stimulation mediated by 5-HT1B receptor in postmortem human brain
Autor : Mostany, Ricardo; Pazos, Ángel ; Castro, Elena
Palabras clave : [35S]GTPγS autoradiography
G-proteins
5-HT1B
Serotonin
Putamen
Substantia nigra
Globus pallidus
Fecha de publicación : ene-2005
Editor: Elsevier
Citación : Neuropharmacology 48(1): 25-33 (2005).
Resumen: G-protein activation mediated by 5-HT1B receptors was studied in human brain by [35S]GTPγS autoradiographic methods. 5-HT (10 μM) increased [35S]GTPγS binding in caudate–putamen nucleus, globus pallidus, dentate gyrus, CA1, entorhinal cortex and substantia nigra. In basal ganglia and midbrain, this effect was blocked by GR 127935 (5-HT1B/1D antagonist). In contrast, WAY 100635 (selective 5-HT1A antagonist) reversed the effect of 5-HT in hippocampus and entorhinal cortex. Therefore, a detailed pharmacological study was carried out in basal ganglia and substantia nigra using 5-HT and the 5-HT1B/1D agonists GTI and CP 93129. In these areas, these agonists stimulated [35S]GTPγS binding in a concentration-dependent manner, with no significant differences in the potency for a given structure. Furthermore, GTI was more potent in the putamen than in globus pallidus. In caudate–putamen, the three agonists showed the same efficacy, while in globus pallidus and substantia nigra the efficacy of 5-HT was higher than GTI and CP 93129. The selective 5-HT1B antagonist SB-224289 inhibited GTI- and CP 93129-stimulated [35S]GTPγS binding in basal ganglia and substantia nigra, while coincubation with BRL 15572 (selective 5-HT1D antagonist) did not result in any significant change. Here we report the anatomical pattern of distribution of 5-HT1B-dependent functionality by using specific pharmacological tools in human brain sections.
Descripción : Publisher full-text version of the paper available at Neuropharmacology journal site: http://www.sciencedirect.com/science/journal/00283908
Versión del editor: http://dx.doi.org/10.1016/j.neuropharm.2004.08.013
URI : http://hdl.handle.net/10261/4175
DOI: 10.1016/j.neuropharm.2004.08.013
ISSN: 0028-3908
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