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1 concise synthesis of the epilepsy medication tiagabine.
2 h kinetic analysis and blocking studies with tiagabine.
3 on 10 mg of the oral GABA reuptake inhibitor tiagabine.
4 measured before and after administration of tiagabine (0.2 mg/kg of body weight), a GABA membrane tr
5 suppressed by the GABA transport inhibitors tiagabine (10 microM) and SKF89976-A (100 microM), but w
6 thyl-2-thienyl)but-3-enl-yl] nipecotic acid (tiagabine) (10 microM, n = 12) significantly prolonged t
7 thyl-2-thienyl)but-3-enl-yl] nipecotic acid (tiagabine) (10 microM, n = 12) significantly prolonged t
10 ar memories, as supported by the efficacy of tiagabine, a GABA reuptake inhibitor, to rescue fear res
11 hancement of extracellular GABA levels, thus tiagabine, a GABA transporter inhibitor, was evaluated a
17 nce over (18)F-GATT-31, with more consistent tiagabine blocking results (65%-71%) and with nondisplac
18 cortico-cortical pyramidal neurons following tiagabine, but not placebo, was a function of GABA conce
19 gabapentin, lamotrigine, oxcarbazepine, and tiagabine, compared with the use of topiramate, may be a
22 oxcarbazepine (HR, 2.07; 95% CI, 1.52-2.80), tiagabine (HR, 2.41; 95% CI, 1.65-3.52), and valproate (
23 the gamma-aminobutyric acid uptake inhibitor tiagabine hydrochloride was studied on electrical respon
26 docking of derivatives of the GAT1 inhibitor tiagabine into a protein homology model of GAT1 allowed
28 oth drug sessions, we identify the effect of tiagabine on GABAergic modulation of deep pyramidal and
29 n came from confirmation that the effects of tiagabine on local circuits depended not only on partici
30 ect of a test drug (GABA-reuptake inhibitor, tiagabine) on neuronal function (GABA-ergic dynamics), o
33 Enhancement of GABAergic transmission with tiagabine plus clonazepam partially rescues the effects
34 nhibitor vigabatrin and blocking uptake with tiagabine reduced the power of gamma oscillations more i
35 ially phenocopy the clinical side effects of tiagabine, suggesting that these side effects are inhere
36 perimental data, suggests initial binding of tiagabine to the substrate-binding site in the outward-o
37 AEDs gabapentin, lamotrigine, levetiracetam, tiagabine, topiramate, vigabatrin, and zonisamide do not
38 hich are substrates of the same enzymes (eg, tiagabine, valproic acid, lamotrigine, and topiramate).
40 ologically manipulated the GABA system using tiagabine, which blocks the synaptic GABA transporter 1,
41 ts into the mixed-type inhibition of GAT1 by tiagabine, which is an important anticonvulsant medicati