ライフサイエンスコーパス: GABA(A) antagonist

1 d the response was reduced by bicuculline (a GABA(A) antagonist).

2 induction of active sleep by bicuculline (a GABA(A) antagonist).

3 f cholinergic antagonists and bicuculline, a GABAA antagonist.

4 erentially by furosemide, a subtype-specific GABAA antagonist.

5 ion were rescued by a subthreshold dose of a GABA(A) antagonist.

6 oride reversal potential and were blocked by GABA(A) antagonists.

7 a5beta3gamma2 (alpha5) subtype selective BzR/GABA(A) antagonist 7 is described.

8 s of decreased fluorescence are abolished by GABA(A) antagonists and reflect the activity of molecula

9 hronic systemic treatment of these mice with GABAA antagonists at non-epileptic doses causes a persis

10 ked by picrotoxin but not the more selective GABAA antagonist biccuculine.

11 The GABA(A) antagonist bicuculline (0, 5, and 10 ng) produce

12 Efflux increased by a further 30% when the GABA(A) antagonist bicuculline (50 microM) was added to

13 The GABA(A) antagonist bicuculline blocked only early enhanc

14 NST neurons extracellularly and to apply the GABA(A) antagonist bicuculline methiodide (BICM) into th

15 ication of the glutamate agonist AMPA or the GABA(A) antagonist bicuculline raised RF and the frequen

16 Intra-DRN and intra-MRN injections of the GABA(A) antagonist bicuculline significantly stimulated

17 hypothesis was tested first by applying the GABA(A) antagonist bicuculline to the dendritic zone of

18 ting a single barrel by iontophoresis of the GABA(A) antagonist bicuculline while the rest of the cor

19 were TTX-sensitive and mostly blocked by the GABA(A) antagonist bicuculline, indicating increased imp

20 However, in the presence of the GABA(A) antagonist bicuculline, p35 knock-out slices, bu

21 crease is blocked by comicroinjection of the GABA(A) antagonist bicuculline.

22 sensitization and resistance to the specific GABA(A) antagonist bicuculline.

23 D2-NMDA interaction was also blocked by the GABA(A) antagonists bicuculline and picrotoxin, suggesti

24 naptic inhibition was blocked by competitive GABA(A) antagonists bicuculline-methiodide (Bic) or GABA

25 tamate receptor antagonist kynurenate or the GABAA antagonist bicuculline (P > 0.05).

26 onse was partly or completely blocked by the GABAA antagonist bicuculline in all neurons tested.

27 In contrast, the GABAA antagonist bicuculline increased eating behavior a

28 Alternatively, application of the GABAA antagonist bicuculline methiodide (BIC) shortened

29 njections of CRH and fluoxetine, whereas the GABAA antagonist bicuculline methiodide potentiated the

30 The effects of GABA were reversed by the GABAA antagonist bicuculline, and the effects of baclofe

31 synaptic EPSCs evoked in the presence of the GABAA antagonist bicuculline, but resembled asynchronous

32 n could be overcome with the addition of the GABAA antagonist bicuculline, indicating that APs are su

33 ces, but not inhibition, were blocked by the GABAA antagonist bicuculline, suggesting that NPY-mediat

34 al neurons discharges was examined using the GABAA antagonists bicuculline and picrotoxin.

35 In contrast, microinjection of a GABA(A) antagonist (bicuculline or gabazine) into the CV

36 or 1-3 d in vitro with 10 microM GABA and/or GABAA antagonist (bicuculline or the pesticide dieldrin)

37 In contrast, microinjection of a GABA(A) antagonist, bicuculline, but not a GABA(B) antag

38 The application of GABA(A) antagonist, bicuculline, lowered all MTs but the

39 e it is blocked by both tetrodotoxin and the GABA(A) antagonist, bicuculline.

40 both normal and ETX rats were blocked by the GABA(A) antagonist, bicuculline.

41 al cerebrospinal fluid (aCSF; 100 nl) or the GABAA antagonist, bicuculline methiodide (BMI; 50 pmol i

42 BAB antagonist, 2-hydroxysaclofen, while the GABAA antagonist, bicuculline was ineffective.

43 zepam and secobarbital, and inhibited by the GabaA antagonist, bicuculline, by ligands for D2 or musc

44 Spinal administration of the GABAA antagonist, bicuculline, disrupted A3AR-mediated a

45 tality and bacterial load were reversed by a GABAA antagonist, bicuculline, indicating dependence on

46 preoptic area (POA) or microinjection of the GABAA antagonists, bicuculline or SR95531 (60 pmol in 60

47 Third, by applying GABA(A) antagonists during field-potential and optical r

48 induces patch-like activation of Crus II and GABAA antagonists fail to convert this patch-like activi

49 ight and slope, and this was reversed by the GABA(A) antagonist gabazine.

50 (IPSCs) that were reversibly blocked by the GABA(A) antagonist gabazine.

51 GABAA antagonist gabazine infusions into the PVN facilit

52 ayed pause in pause neurons treated with the GABA(A) antagonist, gabazine.

53 istration of bicuculline (1.5 mg/kg, n=8), a GABA(A) antagonist, increased Morris water maze goal lat

54 action potential probability and reversed by GABA(A) antagonists, indicating that GABA-mediated excit

55 ities associated with Down syndrome and that GABAA antagonists may be useful therapeutic agents for t

56 ions in afferent innervation of DGCs because GABA(A) antagonists normalized developmental differences

57 n prevent NAN, we proceeded to study whether GABA(A) antagonists (or agents capable of reversing EtOH

58 aluate this possibility, we administered the GABAA antagonist pentylenetetrazole (PTZ; 0.3 or 1.0 mg/

59 he D2-class agonist quinpirole (500 ng), the GABA(A) antagonist picrotoxin (0.25, 0.5 or 1 microg) or

60 ty was unaffected by bath application of the GABA(A) antagonist picrotoxin (50 microM, n = 9) or the

61 The RuBi-GABA effect was blocked by the GABA(A) antagonist picrotoxin, but not duplicated by dir

62 Using epidural application of the GABA(A) antagonist picrotoxin, which produces a topograp

63 iments were performed in the presence of the GABA(A) antagonists picrotoxin or bicuculline.

64 Infusion of the GABAA antagonist picrotoxin into the VM reduced both hig

65 ibition of spike firing was prevented by the GABAA antagonist picrotoxin, but EtOH had no effect on e

66 Prior NTS microinjection of bicuculline (GABA(A) antagonist) prevented the mGluR-mediated attenua

67 Localized microinjections of GABA(A) antagonist produced a reorganization of the geom

68 l-trained animals that injecting the IN with GABA(A) antagonists produces short-latency conditioned r

69 f single Put stimulation induced gabazine (a GABA(A) antagonist)-sensitive responses differed greatly

70 GABA(A) antagonists showed greater inhibition of myopic

71 The GABA(A) antagonist SR-95531 (gabazine) is known to block

72 (200 nm) of the highly specific competitive GABA(A) antagonist SR95531 (gabazine) reduces phasic inh

73 hed the tonic current to a similar extent as GABA(A) antagonists, suggesting a synaptic origin of the

74 the GABAd response to pentobarbital and the GABAA antagonists, this could not account for the greate

75 SR 95531, the competitive high-affinity GABAA antagonist was used as a reference compound.

76 picrotoxin self-infusion, but bicuculline, a GABA(A) antagonist, was self-infused into the VTA.