PMID: 9182238Feb 1, 1996Paper

Comparative effects of the GABA uptake inhibitors, tiagabine and NNC-711, on extracellular GABA levels in the rat ventrolateral thalamus

Neurochemical Research
D A Richards, N G Bowery

Abstract

The primary mechanism by which the action of synaptically released GABA is thought to be terminated is by re-uptake into neurones and glial cells, and the pharmacological inhibition of this uptake may be beneficial in conditions where decreased GABAergic transmission has been implicated, such as epilepsy. We have compared the effects of two of these uptake inhibitors, tiagabine and NNC-711, on extracellular GABA levels in the thalamus of the rat, after both systemic and local administration. Both compounds produced dose-dependent increases in GABA concentration irrespective of the route of administration, but the concentrations required to produce increased extracellular GABA levels were considerably higher than those known to be effective for anticonvulsant purposes. These data suggest that, initially at least, alternative GABA transporters, not susceptible to inhibition by the compounds used, may still be able to remove synaptically released GABA from the extracellular space.

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Citations

May 14, 1998·British Journal of Pharmacology·M LancelR A Deisz
Sep 25, 2009·PloS One·László HéjaJulianna Kardos
Mar 13, 2012·Brain Research·Ben D RichardsonDonald M Caspary
Jan 26, 2010·Brain Research Reviews·Volker Eulenburg, Jesús Gomeza
May 26, 2004·Pharmacology, Biochemistry, and Behavior·S M RawlsMartin W Adler
Apr 4, 2014·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·Conny F WaschkiesBasil Künnecke
Feb 22, 2003·The Journal of Biological Chemistry·Richard D WhitlowSepehr Eskandari
Feb 13, 2001·Endocrine Reviews·E Terasawa, D L Fernandez

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