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 nd picrotoxin, three structurally dissimilar GABA(A) receptor antagonists.

10 mine receptor antagonists but was blocked by GABA(A) receptor antagonists.

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

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

13 , the VMR was only consistently increased by GABA(A) receptor antagonists.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 the NMDA receptor antagonist MK-801 and the GABA(A) receptor antagonist bicuculline methiodide while

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

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

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

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

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

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

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

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

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

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

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

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

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

52 be blocked by intra-LPBN application of the GABA(A) receptor antagonist bicuculline.

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

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

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

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

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

58 , 0.25, 0.1 and 0.0625 microM doses) and the GABAA receptor antagonist bicuculline (3.0 and 1.0 micro

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

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

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

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

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

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

65 The GABAA receptor antagonist bicuculline methiodide had lit

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

67 The GABAA receptor antagonist bicuculline released glutamate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 tructurally dense (1.64 mcbits/ angstrom(3)) GABA(A) receptor antagonist bilobalide, intermediates en

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

103 intra-BLA administration of a low dose of a GABA(A) receptor antagonist, but not an NMDA/AMPA/kainat

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

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

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

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

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

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

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

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

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

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

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

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

116 Gabazine, a gamma-aminobutyric acid type A (GABA(A)) receptor antagonist, has previously been report

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

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

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

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

121 GABA(A) receptor antagonists inhibited half the recorded

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 on, using intracerebral microinfusion of the GABA(A) receptor antagonist picrotoxin or agonist muscim

142 The mutation imparts resistance to the GABA(A) receptor antagonist picrotoxin, allowing verific

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

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

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

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

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

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

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

150 ffects of post-conditioning infusions of the GABA(A) receptor antagonist, picrotoxin, into the IL on

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

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

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

154 GABA(A) receptor antagonists reduced the holding current

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

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

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

158 GABA(A) receptor antagonists selectively augmented SGC i

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

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

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

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

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

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

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

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

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

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

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

170 GABAA receptor antagonists were also ineffective in alte