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- W2095061873 abstract "(R)-N-(4,4-Bis(3-methyl-2-thienyl)but-3-en-1-yl)nipecotic acid (tiagabine) is a potent inhibitor of γ-aminobutyric acid (GABA) uptake, which maintains its initial anticonvulsant effects when administered to mice for a prolonged period (21 days). In the present study, mice received chronic (21 days) p.o. administration of tiagabine (15 mg/kg, twice daily) or vehicle alone and the densities of GABAA and GABAB receptors and of [3H]tiagabine recognition sites were measured in several brain regions. The following changes were observed following chronic administration of tiagabine as compared to vehicle: significant reduction (18–37%) in [3H]tiagabine binding in the temporal and entorhinal cortex and in the molecular and granular layer of the cerebellar cortex; increases in the number of GABAA sites (22–44%) in various regions of the frontal cortex, in caudate putamen and in the lateral septum; decreases in the numbers of GABAB sites (18–42%) in the motor cortex, the more dorsal parts of cortex, the anteroventral thalamic nucleus, medial geniculate, superior colliculus and the molecular layer of the cerebellar cortex. Such data suggest that the GABAergic system is differentially modulated in a regional specific manner in response to chronic elevation of the extracellular levels of GABA. The significance of these findings in relation to the reported lack of development of tolerance to the anticonvulsant effects of tiagabine is discussed." @default.
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- W2095061873 date "1995-06-01" @default.
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- W2095061873 title "Effects of chronic tiagabine treatment on [3H]GABAA, [3H]GABAB and [3H]tiagabine binding to sections from mice brain" @default.
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- W2095061873 doi "https://doi.org/10.1016/0920-1211(95)00010-8" @default.
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