ライフサイエンスコーパス: GABA(A) receptor antagonist

1 ulation by dopamine was reestablished with a GABAA receptor antagonist.

2 rgic transmission using local application of GABAA receptor antagonists.

3 eurons that were blockable by bicuculline, a GABA(A) receptor antagonist.

4 interictal bursts recorded in bicuculline, a GABA(A) receptor antagonist.

5 Ps, also detected at E16, were eliminated by GABA(A) receptor antagonist.

6 iontophoretic application of bicuculline, a GABA(A) receptor antagonist.

7 roxysteroids are also direct, noncompetitive GABA(A) receptor antagonists.

8 cell input resistance, which was reduced by GABA(A) receptor antagonists.

9 t still evident when IPSPs were prevented by GABA(A) receptor antagonists.

10 increased by exogenous GABA and inhibited by GABA(A) receptor antagonists.

11 tained increase in [Cl-]i was not blocked by GABA(A) receptor antagonists.

12 icrotoxin, a gamma-aminobutyric acid type A (GABA(A)) receptor antagonist.

13 wo groups of animals were assessed using the GABAA receptor antagonist [3H]SR 95531.

14 We then microinjected a GABAA receptor antagonist, an inhibitor of lactate trans

15 Local applications of GABA(A) receptor antagonists and agonists increase REM s

16 The autaptic current was abolished by GABA(A) receptor antagonists and substantially inhibited

17 ne-induced oxytocin release was inhibited by GABAA receptor antagonists as well as by an oxytocin rec

18 Bicuculline, a GABA(A) receptor antagonist at a dose of 0.1 pg, did not

19 Intracortical perfusion with the selective GABA(A) receptor antagonist bicuculline (0.1 microM, 140

20 tor antagonist strychnine (4 microM) and the GABA(A) receptor antagonist bicuculline (10 microM) dimi

21 abolished by co-application of GABA with the GABA(A) receptor antagonist bicuculline (40 microM).

22 method for study of small brain regions, the GABA(A) receptor antagonist bicuculline (50 muM) was inf

23 Intrathecal administration of the GABA(A) receptor antagonist bicuculline blocked inductio

24 Nigral application of the GABA(A) receptor antagonist bicuculline by reverse dialy

25 Low concentrations of the GABA(A) receptor antagonist bicuculline increase the amp

26 Local infusion of the GABA(A) receptor antagonist bicuculline increased seroto

27 eptor agonist muscimol (1 nmol/side), or the GABA(A) receptor antagonist bicuculline methiodide (12.5

28 The GABA(A) receptor antagonist bicuculline methiodide (8 mi

29 onist muscimol, or 5) glybenclamide plus the GABA(A) receptor antagonist bicuculline methiodide (BIC)

30 The GABA(A) receptor antagonist bicuculline methiodide (BMI)

31 Microinjection of the GABA(A) receptor antagonist bicuculline methiodide (BMI)

32 iovascular response to microinjection of the GABA(A) receptor antagonist bicuculline methiodide (BMI)

33 Local administration of the GABA(A) receptor antagonist bicuculline methiodide (BMI)

34 -anesthetized rats, passive diffusion of the GABA(A) receptor antagonist bicuculline methiodide from

35 potential near -70 mV and was blocked by the GABA(A) receptor antagonist bicuculline methiodide.

36 st concentrations used (1.0-2.5 microM), the GABA(A) receptor antagonist bicuculline produced an incr

37 Treatment of PKCepsilon-null mice with the GABA(A) receptor antagonist bicuculline restored cortico

38 receptor agonist muscimol, muscimol with the GABA(A) receptor antagonist bicuculline, and bicuculline

39 (3)H]NA release was partially blocked by the GABA(A) receptor antagonist bicuculline, and coapplicati

40 ctrical activity induced by injection of the GABA(A) receptor antagonist bicuculline, and the glutama

41 ng synaptic activity, via treatment with the GABA(A) receptor antagonist bicuculline, rapidly and rob

42 ng WIN55,212,2 actions were abolished by the GABA(A) receptor antagonist bicuculline, suggesting that

43 he interneuronal network, was blocked by the GABA(A) receptor antagonist bicuculline.

44 uction was insensitive to application of the GABA(A) receptor antagonist bicuculline.

45 ic currents (IPSCs) that were blocked by the GABA(A) receptor antagonist bicuculline.

46 or antagonist picrotoxin and the competitive GABA(A) receptor antagonist bicuculline.

47 contingent stimulations were reversed by the GABA(A) receptor antagonist bicuculline.

48 became broader after the application of the GABA(A) receptor antagonist bicuculline.

49 ation of the gamma-aminobutyric acid type A (GABA(A)) receptor antagonist bicuculline methiodide with

50 icroM CNQX, or 5 mM kynurenic acid) plus the GABA(A)-receptor antagonist bicuculline (BIC, 20 microM)

51 Perfusion of the GABAA receptor antagonist bicuculline (10 microM) into t

52 n (200 mum) occluded effects of CTOP but the GABAA receptor antagonist bicuculline (10 mum) did not.

53 , 0.25, 0.1 and 0.0625 microM doses) and the GABAA receptor antagonist bicuculline (3.0 and 1.0 micro

54 Bath application of the GABAA receptor antagonist bicuculline and glycine recept

55 AM251 was rescued by coadministration of the GABAA receptor antagonist bicuculline at reactivation, i

56 tion of PSCs at ECl or by treatment with the GABAA receptor antagonist bicuculline confirmed that PSC

57 g the GABAA receptor agonist muscimol or the GABAA receptor antagonist bicuculline into the IC or NBM

58 DCN inhibition by DCN administration of the GABAA receptor antagonist bicuculline methiodide (BMI) a

59 Microinjection of the GABAA receptor antagonist bicuculline methiodide (BMI) o

60 The GABAA receptor antagonist bicuculline methiodide had lit

61 t, tonic GABA currents, assessed either by a GABAA receptor antagonist bicuculline or a selective ext

62 The GABAA receptor antagonist bicuculline released glutamate

63 itro, the potassium channel blocker 4-AP and GABAA receptor antagonist bicuculline together induced s

64 MePhe4,Gly-(ol)5]-enkephalin (DAMGO) and the GABAA receptor antagonist bicuculline were greatly depre

65 nociception induced by microinjection of the GABAA receptor antagonist bicuculline, further demonstra

66 ropic glutamate receptor antagonists and the GABAA receptor antagonist bicuculline, granule cells sho

67 a (GABAa) receptor agonist muscimol, and the GABAa receptor antagonist bicuculline, respectively, on

68 ant path stimulation, in the presence of the GABAA receptor antagonist bicuculline.

69 ffects were blocked by pretreatment with the GABAA receptor antagonist bicuculline.

70 ociated interneurons), were abolished by the GABAA receptor antagonist bicuculline.

71 reversed near -70 mV and were blocked by the GABAA receptor antagonist bicuculline.

72 GABAA receptor antagonists bicuculline (10(-5) M) or pic

73 was blocked by the gamma-aminobutyric acidA (GABAA) receptor antagonist bicuculline (5 microM).

74 These effects were blocked by the GABA(A) receptor antagonist, bicuculline (10 microM) and

75 The mIPSCs were abolished by the GABA(A) receptor antagonist, bicuculline (10 microM).

76 In 26 animals, microinjection of the GABA(A) receptor antagonist, bicuculline (2 mM, 30 nl),

77 Microinjections of the GABA(A) receptor antagonist, bicuculline (20 nl, 1 mm),

78 irected injections to LS were made using the GABA(A) receptor antagonist, bicuculline (3-30 ng), or t

79 The PVN was disinhibited by microinjecting a GABA(A) receptor antagonist, bicuculline (BIC, 0.1 nmol)

80 by unilateral intracerebral infusions of the GABA(A) receptor antagonist, bicuculline methiodide (BIC

81 OXT (0.5 mug) and selective GABA(A) receptor antagonist, bicuculline methiodide (BMI

82 entration (in the presence or absence of the GABA(A) receptor antagonist, bicuculline).

83 However, 7 ng of the GABA(A) receptor antagonist, bicuculline, in LS signific

84 cardiovascular effects of microinjecting the GABA(A) receptor antagonist, bicuculline, into the rostr

85 The GABA(A) receptor antagonist, bicuculline, was unilateral

86 holineacetic acid (SCH50911), and a specific GABA(A) receptor antagonist, bicuculline, were administe

87 rate, and these effects were blocked by the GABA(A) receptor antagonist, bicuculline.

88 The GABA(A) receptor antagonists, bicuculline (10 microM) an

89 Then, administration of the GABAA receptor antagonist, bicuculline (10-60 pmol), int

90 The GABAA receptor antagonist, bicuculline, itself had no ef

91 ternatively, bilateral RMTg infusions of the GABAA receptor antagonist, bicuculline, suppress robust

92 Then, the GABAA receptor antagonist, bicuculline, was microinjecte

93 The GABAA receptor antagonist, bicuculline, was tested on 19

94 scimol or 5 microM muscimol+20 microM of the GABAA receptor antagonist, bicuculline.

95 lsatility were blocked by co-exposure to the GABAA receptor antagonist, bicuculline.

96 was largely resistant to bath application of GABAA receptor antagonists but was sensitive to manipula

97 Bicuculline, a GABAA receptor antagonist, completely reversed the effec

98 Treatment with bicuculline, a GABAA receptor antagonist, decreased DHHC9 expression in

99 GABA(A) receptor antagonists did not block retinal waves

100 These findings were consistent with GABAA receptor antagonists disinhibiting acetylcholine r

101 inic acetylcholine, AMPA, NMDA, glycine, and GABA(A) receptor antagonists does not alter the velocity

102 To determine whether this GABA(A) receptor antagonist effect is specific to the LH

103 epilepsy following repeated exposure to the GABAA receptor antagonist, flurothyl, in which mice deve

104 tered GABAergic agents was attenuated by the GABA(A) receptor antagonist gabazine (systemically admin

105 s have low failure rates, are blocked by the GABA(A) receptor antagonist gabazine, and exhibit short-

106 IPSCs, an effect completely abolished by the GABAA receptor antagonist gabazine (5 muM).

107 blocked either by a local application of the GABAA receptor antagonist gabazine or by an injection of

108 ent was fully blocked by Zn(2+), akin to the GABAA receptor antagonist gabazine.

109 ociception produced by the microinjection of GABA(A) receptor antagonists in the VMM.

110 For example, GABAA receptor antagonists, including furosemide, blocke

111 ChR-mediated inhibition, which is blocked by GABAA receptor antagonists, indicating the engagement of

112 ioid receptor agonist, and of bicuculline, a GABAA receptor antagonist, induced Fos in ipsilateral st

113 GABA(A) receptor antagonists inhibited half the recorded

114 has been reported that non-subtype-selective GABAA receptor antagonists injected into the nucleus pon

115 Microinjection of GABA(A) receptor antagonists into PnO induces a long las

116 Microdialysis of GABAA receptor antagonists into the PnO resulted in incr

117 cerebrospinal fluid (aCSF) or bicuculline, a GABAA receptor antagonist, into the PF-LHA in spontaneou

118 In the presence of GABA(A) receptor antagonists, kainate lowered the thresh

119 These findings suggest that GABAA receptor antagonists may offer a possible therapeu

120 th these findings, it has been reported that GABA(A) receptor antagonists microdialyzed into PnO resu

121 The GABA(A) receptor antagonist N-methyl-bicuculline (50 mic

122 er suppressing inhibition with picrotoxin, a GABA(A) receptor antagonist, NMDA receptor-mediated curr

123 Treatment of control mice with a GABAA receptor antagonist or deletion of the chloride-ac

124 -like state following local application of a GABAA receptor antagonist or kainate, glutamate receptor

125 Administration of either bicuculline, a GABAA receptor antagonist, or CGP 35348, a GABAB recepto

126 ession of Thy-1 and by administration of the GABA(A) receptor antagonist pentylenetetrazole.

127 monstrated a robust behavioral response to a GABA(A) receptor antagonist, pentylenetetrazole.

128 The GABA(A) receptor antagonist picrotoxin abolished this re

129 ents were blocked by both the noncompetitive GABA(A) receptor antagonist picrotoxin and the competiti

130 apparent in the absence and presence of the GABA(A) receptor antagonist picrotoxin and was abolished

131 Conversely, the GABA(A) receptor antagonist picrotoxin blocked spindle f

132 n be mimicked by single microinfusion of the GABA(A) receptor antagonist picrotoxin into the normal a

133 diated IPSCs recorded in the presence of the GABA(A) receptor antagonist picrotoxin.

134 SCs reversed near E(Cl), were blocked by the GABA(A) receptor antagonists picrotoxin or bicuculline m

135 gamma-Frequency firing was eliminated by the GABAA receptor antagonist picrotoxin but small (< 5 mV)

136 or mixed effects on GnRH neuron firing, the GABAA receptor antagonist picrotoxin resulted in a consi

137 inephrine or serotonin, was prevented by the GABAA receptor antagonist picrotoxin.

138 Both IPSCs were sensitive to the GABAA receptor antagonists picrotoxin or bicuculline.

139 greatly enhanced by bath application of the GABAA receptor antagonists picrotoxin or bicuculline.

140 In the presence of the GABAA receptor antagonist, picrotoxin, the application o

141 vo are blocked by subconvulsive doses of the GABAA receptor antagonist, picrotoxin.

142 or GABAergic neurotransmission with NMDA or GABA(A) receptor antagonists potently reduced the LC-ind

143 GABA(A) receptor antagonists reduced the holding current

144 Bicuculline, a GABAA receptor antagonist, reduced calcium levels in neu

145 ent data suggesting that picrotoxin (PTX), a GABAA receptor antagonist, rescues certain behavioral an

146 Local application of a GABA(A) receptor antagonist revealed that intracortical

147 GABA(A) receptor antagonists selectively augmented SGC i

148 used to block retinal waves, induced a tonic GABA(A) receptor antagonist-sensitive current in outside

149 ures similar to the convulsant picrotoxin, a GABA(A) receptor antagonist, so their lack of toxicity i

150 y released substances, were depressed by the GABAA receptor antagonist SR95531 and alpha,beta-meATP.

151 Central administration of bicuculline (a GABA(A) receptor antagonist) stimulated feeding of the a

152 e responsible for the REM sleep induction by GABA(A) receptor antagonists through blocking GABA inhib

153 These changes were reversed by delivery of a GABA(A) receptor antagonist to the VMH.

154 Bath application of bicuculline (a GABA(A) receptor antagonist) to brainstems increased hyp

155 In the presence of ionotropic glutamate and GABA(A) receptor antagonists, tolbutamide depolarized an

156 enhanced blocking effect of the low-affinity GABA(A) receptor antagonist, TPMPA [1,2,5,6-tetrahydropy

157 PSC amplitude by a low affinity, competitive GABA(A) receptor antagonist was higher in GAD67-lacking

158 In awake, freely moving, rats a GABA(A) receptor antagonist was infused locally into the

159 GABAA receptor antagonists were also ineffective in alte