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1 s were blocked in the presence of a specific GABA(B) receptor antagonist.
2 g, a synthetic fluorophore and a fluorescent GABA(B) receptor antagonist.
3  selectively and respectively by GABA(A) and GABA(B) receptor antagonists.
4 te in the presence of AMPA, NMDA, mGluR, and GABA(B) receptor antagonists.
5 c and heterospecific vocalizations), whereas GABAB receptor antagonists [10 mum saclofen; 10-50 mum C
6                                          The GABAB receptor antagonist 2-hydroxy-saclofen appeared to
7                           Coinjection of the GABAB receptor antagonist 2-hydroxysaclofen 100 or 200 p
8 B-induced respiratory depression, a specific GABA(B) receptor antagonist, (2S)-(+)-5,5-dimethyl-2-mor
9                 Application of the selective GABA(B) receptor antagonist 3-[[(3,4-dichlorophenyl)-met
10                            Additionally, the GABA(B) receptor antagonist (3-aminopropyl)(diethoxymeth
11       The sensitivity of the GABA-IPSCs to a GABA(B) receptor antagonist and an agonist was decreased
12 a GABAA receptor antagonist, or CGP 35348, a GABAB receptor antagonist, blocked the antinociceptive a
13 assium currents that could be blocked by the GABA(B) receptor antagonist CGP 35348 and the G protein
14                                          The GABA(B) receptor antagonist CGP 35348 blocked the slow I
15 2 s, and were fully blocked by the selective GABA(B) receptor antagonist CGP 52432.
16 sion of excitatory events was blocked by the GABA(B) receptor antagonist CGP 54626.
17          This enhancement was blocked by the GABA(B) receptor antagonist CGP 55845 and intracellular
18                                The selective GABA(B) receptor antagonist CGP 55845A (1 microM) fully
19 r extent in the presence of the GABA type B (GABA(B)) receptor antagonist CGP 55845A, suggesting that
20 s PBI, were largely reversed by the specific GABAB receptor antagonist CGP 35348 (0.5 mM).
21  whereas intervention with vigabatrin or the GABAB receptor antagonist CGP 35348 prevented tonic-clon
22 cts in the spinal cord, either saline or the GABAB receptor antagonist CGP 35348 was injected intrath
23 ked by the K+ channel blocker barium and the GABAB receptor antagonist CGP 35348.
24                                          The GABAB receptor antagonist CGP 55,845A (CGP) blocked the
25 n was reversed or prevented by the selective GABAB receptor antagonist CGP 55845A (1 microM).
26                                          The GABAB receptor antagonist CGP 55845A (5 microM) decrease
27             Spinal pre-administration of the GABA(B) receptor antagonist, CGP-35348 (30 microg/50 mic
28                                            A GABA(B)receptor antagonist, CGP 35348, reversed the effe
29 local glutamate release, while the selective GABA(B) receptor antagonist CGP35348 (100 microM, 140 mi
30                           Application of the GABA(B) receptor antagonist CGP35348 reduced PPD, sugges
31 The effects of baclofen were reversed by the GABAB receptor antagonist CGP35348.
32 s, which was reversed to potentiation by the GABA(B) receptor antagonist CGP52432.
33 re no longer detectable in the presence of a GABAb receptor antagonist CGP52432.
34 lu2/3 receptor antagonist, LY341495, and the GABA(B) receptor antagonist, CGP52432, which was shown t
35                           Interestingly, the GABA(B) receptor antagonist CGP55845 potentiated the sti
36                           Treatment with the GABA(B) receptor antagonist CGP55845 restored memory of
37 utamate receptor antagonist LY341495 and the GABA(B) receptor antagonist CGP55845, suggesting that th
38    In hippocampal slices, treatment with the GABA(B) receptor antagonists CGP55845 or CGP52432 enhanc
39 CK+ basket cells even in the presence of the GABAB receptor antagonist CGP55845 (2 mum).
40                                          The GABAB receptor antagonist CGP55845 (3 mum) increased the
41 mined through pretreatment with the specific GABA(B) receptor antagonist, CGP55845, or its vehicle.
42                                          The GABAB-receptor antagonist CGP55845A abolished this effec
43 he specific gamma-aminobutyric acid, type B (GABAB), receptor antagonist CGP56999A (20 mg/kg, intrape
44 was rescued by intra-VTA administration of a GABAB receptor antagonist, demonstrating that reversal o
45                                              GABA(B) receptor antagonists, more so than an agonist, a
46 performance through treatment with selective GABA(B) receptor antagonists motivates studies to furthe
47  kainate receptor agonists were sensitive to GABAB receptor antagonists, nor was there any postsynapt
48 ts in DS by defining the effect of selective GABA(B) receptor antagonists on behavior and synaptic pl
49 owever, application of phaclofen (100 microM GABAB receptor antagonist or SCH 50911, a more potent GA
50                                          The GABA(B) receptor antagonist phaclofen decreased consumpt
51            CNQX, APV, bicuculline, CGP35348 (GABAB receptor antagonist), promethazine, atropine, d-tu
52                 In the indirect pathway, the GABA(B) receptor antagonist reduces EPSC amplitude in an
53                   In the direct pathway, the GABA(B) receptor antagonist reduces EPSC amplitude, indi
54                                          The GABAB receptor antagonist saclofen (200 mum) occluded ef
55  IPSC was reduced, but not abolished, by the GABA(B) receptor antagonist SCH 50911, suggesting that t
56                                  CGP55845, a GABA(B) receptor antagonist, significantly attenuated th
57              In the presence of GABA(A)- and GABA(B)-receptor antagonists, the burst discharges of im
58                           CGP55845, a potent GABA(B) receptor antagonist, was employed to determine t
59 sent experiments used CGP 35348, a selective GABAB receptor antagonist with a significantly higher af

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