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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
8 n complex with its clinically used inhibitor tiagabine(3), with an ordered part of only 60 kDa.
9                                 Perfusion of tiagabine (50 microM) for 15 min, evoked large, slow dep
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
12                   GABA transport inhibitors (tiagabine and NO-711) prolonged evoked IPSC decay kineti
13                                  Two others, tiagabine and vigabatrin, are likely to be approved in t
14 l efficacy findings for baclofen, modafinil, tiagabine, and topiramate.
15 clinical trials, namely baclofen, modafinil, tiagabine, and topiramate.
16 lian cells and studied with [3H]GABA and [3H]tiagabine binding.
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
20            Each monkey received 0.5 mg/kg of tiagabine given approximately 20 min before radiotracer
21                                              Tiagabine had antinociceptive activity in both phase 1 (
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
24                     It is concluded that the tiagabine-induced depolarizations in this in vitro prepa
25  grating stimulus, before, 1, 3 and 5 h post tiagabine ingestion.
26 docking of derivatives of the GAT1 inhibitor tiagabine into a protein homology model of GAT1 allowed
27                   Our structure reveals that tiagabine locks GAT1 in the inward-open conformation, by
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
31 articipants, we administered either 15 mg of tiagabine or a placebo.
32 ministration of the GABA reuptake inhibitor, tiagabine (oral, 10 mg) in healthy older adults.
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).
39                                              Tiagabine, which blocks GABA reuptake, does not prolong
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