ライフサイエンスコーパス: gabazine

1 n(2+), akin to the GABAA receptor antagonist gabazine.

2 r the application of (+)-tubocurarine and/or gabazine.

3 ed with high and low doses of picrotoxin and gabazine.

4 neurons treated with the GABA(A) antagonist, gabazine.

5 this was reversed by the GABA(A) antagonist gabazine.

6 reversibly blocked by the GABA(A) antagonist gabazine.

7 to ketamine, by contrast, was unaffected by gabazine.

8 on model of epileptiform activity (10 microM gabazine + 10 microM CGP55845) was occluded by the SK ch

9 y abolished by the GABAA receptor antagonist gabazine (5 muM).

10 e duration of single Put stimulation induced gabazine (a GABA(A) antagonist)-sensitive responses diff

11 MT neurons and contrast them with effects of gabazine, a GABA(A) receptor blocker.

12 In line with this, we show that gabazine, a GABA-A receptor antagonist, is antihyperalge

13 Specific blockade of synaptic IPSCs with gabazine also reduced ISI variability, but only in OT ne

14 etrazol or combined application of 10 microM gabazine and 10 microM CGP55845.

15 ta are consistent with a model in which both gabazine and bicuculline act as allosteric inhibitors of

16 unds are based on the competitive antagonist gabazine and incorporate a variety of photoactive groups

17 endent tonic currents that were resistant to gabazine and inhibited by bicuculline.

18 chloride conductance that is insensitive to gabazine and to picrotoxin and thus not mediated by conv

19 A(A)-R antagonists bicuculline and SR-95531 (gabazine) and increased in frequency and duration by GAB

20 duced than with the non-selective antagonist gabazine, and both were blocked by atropine.

21 e blocked by the GABA(A) receptor antagonist gabazine, and exhibit short-term depression when tested

22 In all cases, decreases in the CSI during gabazine application were accompanied by an increase in

23 nt with a role for GABAA receptors; however, gabazine, at a concentration that abolished miniature GA

24 ether the injected (intraperitoneal) dose of gabazine blocked GABAergic inhibitory transmission, we e

25 onversely, the high affinity GABA(A) blocker gabazine blocked I(phasic) without affecting I(tonic).

26 Both types of events were blocked by gabazine, but only outward currents were significantly a

27 , GABA(A)R agonist (muscimol) or antagonist (gabazine), cell proliferation and differentiation into a

28 rtion of IPSPs and EPSPs between control and gabazine conditions.

29 These currents were blocked by gabazine, confirming that they were GABA(A) receptor-med

30 ron firing with the use of GABA-A antagonist gabazine decimated its occurrence.

31 ity by intraocular injections of muscimol or gabazine during this period did not alter the developmen

32 Gabazine equally increased neuronal activity, but it wid

33 fferent conditions: control, after gabazine, gabazine followed by strychnine, and strychnine alone.

34 ss four different conditions: control, after gabazine, gabazine followed by strychnine, and strychnin

35 Focal application of gabazine (GBZ) (50 microM) revealed the presence of a 20

36 antagonists bicuculline-methiodide (Bic) or GABAZINE (GBZ) and the chloride channel blocker picrotox

37 that partial blockage of GABAA receptors by gabazine (GBZ) application (10 mum, a concentration that

38 born cells survived up to 1 month in the UVN-gabazine group whereas the astroglial population increas

39 left IN and the left MCP, were injected with gabazine (GZ) into the IN to produce SLRs followed by an

40 Although gabazine had negligible efficacy as an inhibitor of prop

41 hereas blockade of muscle GABAA receptors by gabazine had opposite effects.

42 PeF stimulation with gabazine increased blood pressure, phrenic nerve dischar

43 Finally, gabazine increased noise correlation of simultaneously r

44 GABAA antagonist gabazine infusions into the PVN facilitate meningeal-evo

45 cited by 50 microM taurine were abolished by gabazine, insensitive to midazolam, and partially blocke

46 Gabazine insensitivity of the rho1 GABACR was highly dep

47 tion of a GABA(A) antagonist (bicuculline or gabazine) into the CVLM dramatically attenuated the symp

48 Thus, gabazine is a competitive antagonist with negligible neg

49 The GABA(A) antagonist SR-95531 (gabazine) is known to block glycine receptors, albeit wi

50 t gabazine or by an injection of an NBQX/CPP/gabazine mixture into the GPe.

51 Furthermore, neither gabazine nor bicuculline competes for binding at the ste

52 s were recorded after adding strychnine with gabazine or administering strychnine alone, suggesting a

53 application of the GABAA receptor antagonist gabazine or by an injection of an NBQX/CPP/gabazine mixt

54 han that in the presence of pentobarbital or gabazine or in resting receptors.

55 demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many

56 d depolarization persists in the presence of gabazine or tetrodotoxin, indicating a direct action.

57 ry postsynaptic currents, and are blocked by gabazine or tetrodotoxin, indicating an indirect action.

58 Gabazine produced an approximately parallel upward shift

59 tal from wild-type GABAA receptors; however, gabazine produced only a partial block of response pento

60 ific competitive GABA(A) antagonist SR95531 (gabazine) reduces phasic inhibition in hippocampal granu

61 spontaneously active GABAA receptors mediate gabazine-resistant tonic currents in pyramidal neurons.

62 Propofol activated gabazine-resistant, bicuculline-sensitive currents when

63 ductance as GABA-activated channels and were gabazine-resistant.

64 In contrast, GABA(A)R blockade using gabazine resulted in a significant decrease in SSA.

65 ted GABAA receptors in pyramidal neurons are gabazine-sensitive, it follows that tonic currents are n

66 57S) gamma 2L subunits, both bicuculline and gabazine showed weak agonist activity and actually poten

67 c IPSPs could be recorded in the presence of gabazine, showing the efficacy of gabazine treatment.

68 Although gabazine significantly reduced response reliability, ACh

69 on of alpha(1)H101C located at the BZD-site, gabazine (SR-95531, a GABA binding site antagonist) decr

70 o report opposing effects of bicuculline and gabazine, such that bicuculline surprisingly activated n

71 ic GABA(A)R with intracellular picrotoxin or gabazine, suggesting that Nxph1 is able to recruit or st

72 ining (beta3gamma2) GABAA receptors, whereas gabazine suppressed spontaneous activity in these recept

73 ttenuated by the GABA(A) receptor antagonist gabazine (systemically administered).

74 GABA, mediate tonic current; the failure of gabazine to block tonic current reflects a lack of negat

75 Treatment with bicuculline or gabazine to enhance neuronal activity promotes recruitme

76 resence of gabazine, showing the efficacy of gabazine treatment.

77 Bicuculline or gabazine (two competitive antagonists of GABA binding) r

78 d the negative efficacies of bicuculline and gabazine using the general anesthetic propofol to direct

79 for the tuberomammillary nucleus (TMN): when gabazine was microinjected directly into the TMN, it att

80 of neurons, GABA(A)R blockers bicuculline or gabazine were applied in addition to iGluR blockers.

81 the competitive GABA(A)R antagonist SR95531 (gabazine), which at high concentrations acts as a partia

82 they affected by the GABAA receptor blocker gabazine, which would be expected if they were polysynap

83 oapplication of GABA or muscimol, but not of gabazine, with MTSES prevented the effect, suggesting th

84 modulation of ccRTN neurons persisted after gabazine without a change in pattern.