ライフサイエンスコーパス: bicuculline

1 absence of the GABA(A) receptor antagonist, bicuculline).

2 sponse of NS to the GABA receptor antagonist bicuculline.

3 rastriatal injection of the GABA antagonist, bicuculline.

4 amic acid, quinine, or strychnine but not by bicuculline.

5 y comicroinjection of the GABA(A) antagonist bicuculline.

6 tion or disinhibiting synaptic activity with bicuculline.

7 by spinal blockade of GABA(A) receptors with bicuculline.

8 etic application of GABA and its antagonist, bicuculline.

9 were resistant to gabazine and inhibited by bicuculline.

10 ted responses were blocked by picrotoxin and bicuculline.

11 the GABAA receptor antagonists picrotoxin or bicuculline.

12 reversed by the GABA(A) receptor antagonist bicuculline.

13 oride reversal potential and were blocked by bicuculline.

14 by strychnine and by picrotoxin, but not by bicuculline.

15 m slow oscillation induced by application of bicuculline.

16 in 5-HT elicited by DAMGO in the presence of bicuculline.

17 at was abolished by perfusion with 30-50 muM bicuculline.

18 duced in the presence of the GABA antagonist bicuculline.

19 activity that was blocked by CNQX but not by bicuculline.

20 t did not affect the EEG amplitude evoked by bicuculline.

21 e speed of cell migration in the presence of bicuculline.

22 cimol and blocked by the specific antagonist bicuculline.

23 so increased dose-dependently in response to bicuculline.

24 LC neurons was diminished in the presence of bicuculline.

25 smaller, and was enhanced in the presence of bicuculline.

26 led to excite PVN neurons in the presence of bicuculline.

27 and AMPA-mESPCs) in the presence of TTX and bicuculline.

28 e GABA(A) receptor blocker and proconvulsant bicuculline.

29 IV-VI neurones at 0.1 Hz in the presence of bicuculline.

30 plication of the GABA(A) receptor antagonist bicuculline.

31 tyric acid (GABA)A receptors were blocked by bicuculline.

32 h were mimicked by muscimol and inhibited by bicuculline.

33 blockade of GABAA R-mediated inhibition with bicuculline.

34 receptor (GABAA R)-mediated inhibition with bicuculline.

35 bition of gating by inverse agonists such as bicuculline.

36 blocked by the application of CNQX, AP-5 and bicuculline.

37 effects were reversed by coadministration of bicuculline.

38 eceded 20 min earlier with administration of bicuculline (0, 7.5, 75, 150, 300 ng) or saclofen (0, 0.

39 th the selective GABA(A) receptor antagonist bicuculline (0.1 microM, 140 min) reversed the SKF38393

40 Muscimol-induced responses were sensitive to bicuculline (1-10 microM) and SR95531 (10 microM) and ba

41 l) were blocked by pre-application of spinal bicuculline (10 microg/50 microl).

42 a GABA-A receptor antagonist; 10 microM) and bicuculline (10 microM) +10 nM of leptin during the seco

43 al GABAergic and glycinergic inhibition with bicuculline (10 microm) and strychnine (300 nm), respect

44 microM) and the GABA(A) receptor antagonist bicuculline (10 microM) diminished and abolished, respec

45 IPSPs were sensitive to bicuculline (10 microM) in all neurones tested and rever

46 Perfusion of the GABAA receptor antagonist bicuculline (10 microM) into the SN prolonged the carbac

47 perfusion of the GABA-A receptor antagonist, bicuculline (10 microm), blocked the METH-induced decrea

48 ts of CTOP but the GABAA receptor antagonist bicuculline (10 mum) did not.

49 Bicuculline (100 microM), a competitive antagonist at GA

50 ing infusion of the GABA(A) receptor blocker bicuculline (100 microM), extracellular 5-HT increased b

51 The evoked currents were inhibited by bicuculline (100 muM) and TPMPA (IC50, 5.9 +/- 0.6 muM),

52 s of single DRN microinjections of muscimol, bicuculline (136 pmol), NMDA, MK-801 (10 pmol) or vehicl

53 njection of the GABA(A) receptor antagonist, bicuculline (2 mM, 30 nl), into RPa increased CSNA (+234

54 gonist picrotoxin (0.25, 0.5 or 1 microg) or bicuculline (20 ng), the GABA(A) agonist muscimol (15 ng

55 jections of the GABA(A) receptor antagonist, bicuculline (20 nl, 1 mm), into the PF region elicited c

56 Bicuculline (3 mg/kg i.v.) immediately (in <1 min) evoke

57 made using the GABA(A) receptor antagonist, bicuculline (3-30 ng), or the GABA(A) receptor agonists,

58 On combination of bicuculline (30 microm) and strychnine (10 microm) the r

59 Bicuculline (30 microm) or strychnine (10 microm) reduce

60 S neurones following local microinjection of bicuculline (30 pmol/60 nl) completely inhibited the ele

61 Bicuculline/4-AP or KCl-induced depolarization reduces,

62 ne sodium (41 %, 1:1), and were depressed by bicuculline (-41 +/- 5.7 %, 5:8) and picrotoxin (-54 %,

63 ain regions, the GABA(A) receptor antagonist bicuculline (50 muM) was infused into a rat ventral tegm

64 n BAT SNA were reversed by microinjection of bicuculline (60 pmol in 60 nl) into the rvmPAG at the le

65 mined the dose-dependent ability of GABA(A) (bicuculline, 75-150 ng) and GABA(B) (saclofen, 1.5-3 mic

66 d not block the induction of active sleep by bicuculline (a GABA(A) antagonist).

67 ve agonist), and the response was reduced by bicuculline (a GABA(A) antagonist).

68 Bath application of bicuculline (a GABA(A) receptor antagonist) to brainstem

69 hallenged with 0, 0.1, 1 or 10 nm of leptin, bicuculline (a GABA-A receptor antagonist; 10 microM) an

70 xytocin receptor [OTR] antagonist) or by (2) bicuculline (a preferent GABA(A) receptor blocker), sugg

71 tion of hypothalami with 10 nM of leptin and bicuculline, a completely blocked the leptin-induced dec

72 conditions, modulation of GABAA receptors by bicuculline, a GABA antagonist, or by diazepam, a GABAer

73 fore and during iontophoretic application of bicuculline, a GABA(A) receptor antagonist.

74 nd spontaneous interictal bursts recorded in bicuculline, a GABA(A) receptor antagonist.

75 Treatment with bicuculline, a GABAA receptor antagonist, decreased DHHC

76 of artificial cerebrospinal fluid (aCSF) or bicuculline, a GABAA receptor antagonist, into the PF-LH

77 Administration of either bicuculline, a GABAA receptor antagonist, or CGP 35348,

78 ked currents were also completely blocked by bicuculline, a selective agent for GABA(A) receptors.

79 significantly attenuated in the presence of bicuculline, a selective antagonist of GABAA receptors.

80 neurones, blockade of GABA(A) receptors with bicuculline abolished inspiratory-phased inhibition and

81 In inspiratory-inhibited motoneurones, bicuculline abolished phasic inhibition, which frequentl

82 nt had no effect, blockade of GABA(A)Rs with bicuculline abolished the BDNF-mediated increase in NMDA

83 The application of 20 microm bicuculline abolished the spontaneous inhibitory post-sy

84 Bicuculline administered alone caused a significant decr

85 GABA(A) receptor antagonist bicuculline, and bicuculline alone were performed in male C57BL/6J mice (

86 Bicuculline also potentiated 8-OH-DPAT-induced phase adv

87 Bicuculline also produced a progressive accumulation of

88 o burst when pharmacologically isolated with bicuculline, although the bursting is not robust in some

89 fore and during iontophoretic application of bicuculline, an antagonist for GABA(A) receptors.

90 ine, an antagonist of glycine receptors, and bicuculline, an antagonist of GABA receptors.

91 gonist, inactivated part of the OMV, whereas bicuculline, an antagonist, disinhibited it.

92 an agonist of GABA, to inactivate the OMV or bicuculline, an antagonist, to block GABA inhibition.

93 ication of the GABA antagonists, picrotoxin, bicuculline and 1,2,5,6-tetrahydropyridine-4-yl methylph

94 Addition of bicuculline and 4-aminopyridine facilitated the occurren

95 ly induced by pharmacological manipulations (bicuculline and 4-aminopyridine) in the entorhinal corte

96 lating the perforant path in the presence of bicuculline and 6 mM K(+).

97 m events were 3.93 +/- 2.76 (+/-STD) min for bicuculline and 6.37 +/- 7.66 min for kainic acid, sugge

98 based on treatment of neuronal cultures with bicuculline and a model of experience-dependent plastici

99 n of GABA-A and GABA-B receptor antagonists, Bicuculline and CGP 35348 (CGP) respectively.

100 antagonist bicuculline, and coapplication of bicuculline and DNQX fully abolished this response.

101 We compared the negative efficacies of bicuculline and gabazine using the general anesthetic pr

102 We also report opposing effects of bicuculline and gabazine, such that bicuculline surprisi

103 1 and CA3 regions of the hippocampus for the bicuculline and kainate models, respectively.

104 iggered [Ca2+]i increments were abolished by bicuculline and partially impaired by (1,2,5,6-tetrahydr

105 nist ICI182,780, but not by GABA antagonist, bicuculline and phaclofen.

106 in current amplitude that were inhibited by bicuculline and picrotoxin and facilitated by diazepam a

107 s, I(phasic)), the GABA(A) receptor blockers bicuculline and picrotoxin caused an outward shift in th

108 However, bicuculline and picrotoxin failed to block it.

109 EC50 concentrations of GABA, were blocked by bicuculline and picrotoxin with IC50 values of 2.7 and 5

110 was also blocked by the GABA(A) antagonists bicuculline and picrotoxin, suggesting that the inhibito

111 for deprivation-induced feeding in that both bicuculline and saclofen administered into the nucleus a

112 cleus accumbens shell and eliminated by both bicuculline and saclofen in the ventral tegmental area.

113 ium was blocked by the GABA(A)-R antagonists bicuculline and SR-95531 (gabazine) and increased in fre

114 Rhythmic activity persisted during combined bicuculline and strychnine application (50 microM each)

115 Disinhibition of the pFL with bicuculline and strychnine led to active expiration.

116 nicotine concentrations, in the presence of bicuculline and tetrodotoxin (TTX), increased the freque

117 inhibition of MCH neurons was eliminated by bicuculline and tetrodotoxin, suggesting that the effect

118 in the size of the receptive field, whereas bicuculline and TPMPA produced comparable 34 and 33 % in

119 tors, the gamma 2L receptors were blocked by bicuculline and were potentiated by pentobarbital and fl

120 uscimol with the GABA(A) receptor antagonist bicuculline, and bicuculline alone were performed in mal

121 y blocked by the GABA(A) receptor antagonist bicuculline, and coapplication of bicuculline and DNQX f

122 ced by 7.5mM [K(+)](o), 4-aminopyridine, and bicuculline, and electrographic seizures induced by high

123 ed with 7.5mM [K(+)](o), 4-aminopyridine, or bicuculline, and in vivo against seizures evoked by 6 Hz

124 synapses, including estrogen and short-term bicuculline, and is essential for upregulating spine den

125 injection of the GABA(A) receptor antagonist bicuculline, and the glutamate agonist kainic acid, into

126 Unexpectedly, we found a markedly enhanced bicuculline- and L-655,708-sensitive background GABA(A)

127 Bicuculline application decreases and GABA application i

128 Bicuculline application produced a greater decrease of t

129 Bicuculline application produces more pronounced broaden

130 Bicuculline application routinely blocked DSC altogether

131 ficking, and synaptic downscaling induced by bicuculline application.

132 Bicuculline applied to the stimulation site changed the

133 MCH neurones exhibited Fos-IR in response to bicuculline as compared to HCRT and other PF-LHA neurone

134 del of seizures (1 h in 0 Mg2+ and 50 microM bicuculline at 35-37 degrees C) reproduced the HCN chann

135 inistration of the GABAA receptor antagonist bicuculline at reactivation, indicating that the disrupt

136 ased 5-HT to approximately 70% above the pre-bicuculline baseline.

137 y the GABA(A) receptor (GABA(A)R) antagonist bicuculline between P0 and P7 but not at P14.

138 amma-aminobutyric acid (GABA) receptors with bicuculline (BIC) phenocopied the dendrite-promoting eff

139 icroinjecting a GABA(A) receptor antagonist, bicuculline (BIC, 0.1 nmol), before and after blocking V

140 Microinjection of the GABA antagonist bicuculline (BIC; 1 nmol) into the same region, to reduc

141 ipsilateral RVLM GABA(A) receptor blockade (bicuculline, BIC, 400 pmol, 100 nl; n=12) in rats with c

142 istration of the GABA(A) receptor antagonist bicuculline blocked induction and expression of the inhi

143 Local application of bicuculline but not the SK-channel blocker apamin attenu

144 DRN single microinjections of bicuculline, but not muscimol, NMDA, or MK-801 induced p

145 n in the presence of 6 mM K(+) and 30 microM bicuculline, CaEDTA slowed the rate at which evoked burs

146 Bicuculline caused the monkey to react in an exaggerated

147 nity for [(3)H]CGP54626 binding sites, while bicuculline compounds had no affinity.

148 treatment with the GABAA receptor antagonist bicuculline confirmed that PSCs were specifically mediat

149 i.c.v.-GnRH and pharmacological stimulation (bicuculline/D,L-homocysteic acid mixture) of the main ol

150 its shows that for the majority of IC units, bicuculline degrades binaural processing involved in dir

151 inal administration of the GABAA antagonist, bicuculline, disrupted A3AR-mediated analgesia.

152 asome, whereas the up-regulation of APs with bicuculline dramatically increased the activity of the p

153 owever, blocking tonic GABA(A) currents with bicuculline enhanced synaptic summation more strongly in

154 Application of the GABA(A)R antagonist bicuculline enhanced the migration rate by 30%, suggesti

155 trast, blocking inhibitory transmission with bicuculline enhanced the reverberation.

156 Bicuculline evoked high-amplitude rhythmic epileptiform

157 Bicuculline exerted a much weaker effect on neuronal res

158 Bicuculline exerted partial protection (by 30%) while GA

159 ished when established pairs were exposed to bicuculline for 3 d, but not by long-term incubation wit

160 roinjection of the GABAA receptor antagonist bicuculline, further demonstrating changes in GABA neuro

161 Prior NTS microinjection of bicuculline (GABA(A) antagonist) prevented the mGluR-med

162 Functionally, the GABA antagonist bicuculline had a greater influence on bursting activity

163 Conversely, in AP rats, microinjection of bicuculline had no effect, whereas kynurenic acid decrea

164 In contrast, injections of bicuculline impaired amplitude decrease adaptation and u

165 along with consistent excitations induced by bicuculline in awake, unrestrained rats, suggest that mo

166 NAC shell pretreatment of either saclofen or bicuculline in rats.

167 ctivity was induced by arterial perfusion of bicuculline in the in vitro isolated guinea pig brain.

168 ted by saclofen and significantly reduced by bicuculline in the nucleus accumbens shell and eliminate

169 of gamma-aminobutyric acid interneurons with bicuculline in the presence of the weak K(+) channel blo

170 muscimol, GABA, bicuculline methiodide, and bicuculline (in order of potency).

171 er, 7 ng of the GABA(A) receptor antagonist, bicuculline, in LS significantly decreased maternal aggr

172 In contrast, the GABAA antagonist bicuculline increased eating behavior at all VP sites, y

173 Inhibiting GABA receptors with bicuculline increased NMDA receptor-induced cAMP synthes

174 infusion of the GABA(A) receptor antagonist bicuculline increased serotonin (5-HT) efflux in the DRN

175 whereas brain-derived nerve growth factor or bicuculline increased the ratio by approximately 1.8-fol

176 The GABA(A) receptor (GABA(A)R) antagonist bicuculline increased the speed of neuroblast migration

177 ipulated sites within that zone by injecting bicuculline (increasing neuronal activity) or muscimol (

178 yer-specific effects of focal application of bicuculline indicate that the GABAergic depolarization i

179 tagonists, evoked IPSCs that were blocked by bicuculline indicating that they are mediated via GABAA

180 al load were reversed by a GABAA antagonist, bicuculline, indicating dependence on GABAA receptor sig

181 me with the addition of the GABAA antagonist bicuculline, indicating that APs are sufficient to activ

182 onal cultures, NOS inhibition attenuated the bicuculline-induced activation of ERK and the expression

183 response was abolished during the period of bicuculline-induced activation.

184 NA expression or genetic deletion blocks the bicuculline-induced decrease in GluR2 expression and mEP

185 Here we report that bicuculline-induced increase in neuronal activity leads

186 igin, spatial extent, and laminar profile of bicuculline-induced interictal-like activity on neocorti

187 In contrast, DG is not required for the bicuculline-induced scaling down of excitatory synaptic

188 cortex of anesthetized rats with and without bicuculline-induced seizures.

189 phosphorylation is specifically required for bicuculline-induced synaptic scaling down in mouse hippo

190 y that suppressive locomotor effects of RMTg bicuculline infusions were due to unintended spread of d

191 orrelation between EEG events at the site of bicuculline injection and discharges in distant areas, m

192 ades to fall short of their targets, whereas bicuculline injections cause most ipsiversive saccades t

193 ns of GABA and a picrotoxin (PTX)-sensitive, bicuculline-insensitive current that probably arises fro

194 astrocytes were identified: classic GABA-A, bicuculline-insensitive GABArho, and GABA-A-GABArho hybr

195 many aspects of the pharmacology of native, bicuculline-insensitive insect GABA receptors.

196 The results revealed that bicuculline insensitivity of the rho1 GABACR was mainly

197 In control rats, microinjection of bicuculline into the DMV increased PES, whereas microinj

198 st muscimol or the GABAA receptor antagonist bicuculline into the IC or NBM during learning or retrie

199 periment showing that bilateral infusions of bicuculline into the VTA produce activation rather than

200 roinjecting the GABA(A) receptor antagonist, bicuculline, into the rostral raphe pallidus (RPa) on ar

201 agonist, saclofen, or the GABA-A antagonist, bicuculline, into the VTA, and then whether VTA baclofen

202 ol/side), or the GABA(A) receptor antagonist bicuculline methiodide (12.5 pmol/side) before being sub

203 The GABA(A) receptor antagonist bicuculline methiodide (8 microM) did not change C4 VR f

204 clamide plus the GABA(A) receptor antagonist bicuculline methiodide (BIC) before performance of a hyp

205 atively, application of the GABAA antagonist bicuculline methiodide (BIC) shortened expirations and c

206 nfusions of the GABA(A) receptor antagonist, bicuculline methiodide (BIC), in nine freely moving maca

207 ) and selective GABA(A) receptor antagonist, bicuculline methiodide (BMI) (100 ng), were administered

208 injection of the GABA(A) receptor antagonist bicuculline methiodide (BMI) 10 pmol (100 nl)(-1) into t

209 inistration of the GABAA receptor antagonist bicuculline methiodide (BMI) also cause rapid enlargemen

210 injection of the GABA(A) receptor antagonist bicuculline methiodide (BMI) into the RP evoked increase

211 n of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in select

212 tical and brief arterial infusions of either bicuculline methiodide (BMI) or 4-aminopyridine (4AP).

213 The GABA(A) receptor antagonist bicuculline methiodide (BMI) was stereotaxically microin

214 e GABA(A) receptor antagonists picrotoxin or bicuculline methiodide (BMI), and had longer decay time

215 diffusion of the GABA(A) receptor antagonist bicuculline methiodide from the tip of a glass recording

216 Bicuculline methiodide has been shown to block mutual in

217 Application of bicuculline methiodide in embryos capable of LB switched

218 es (IISs) were induced with iontophoresis of bicuculline methiodide in rat neocortex.

219 Picrotoxin and bicuculline methiodide inhibited both components, consis

220 and fluoxetine, whereas the GABAA antagonist bicuculline methiodide potentiated the effect of CRH and

221 t MK-801 and the GABA(A) receptor antagonist bicuculline methiodide while recording cellular activity

222 ic acid type A (GABA(A)) receptor antagonist bicuculline methiodide within the dentate gyrus abolishe

223 a dose-dependent fashion by muscimol, GABA, bicuculline methiodide, and bicuculline (in order of pot

224 Following VMH administration of bicuculline methiodide, glucose infusion rates were sign

225 electrical stimulation and chemical (0.3 mM bicuculline methobromide) activation of the dorsal PAG e

226 currents in the presence of tetrodotoxin and bicuculline methobromide.

227 The effect of bicuculline microinjection in the PPN matches that of or

228 maller than the peak increase observed after bicuculline microinjection into the rostral raphe pallid

229 y (EEG) and cranial window techniques in the bicuculline model of sustained generalized seizures in n

230 In non-inhibited motoneurones, neither bicuculline nor strychnine markedly changed inspiratory

231 in the presence of the GABA(A)-R antagonist bicuculline, nor in brain slices from NKCC1-knockout mic

232 unmasking is attributable to the effects of bicuculline on different central auditory processes.

233 roxyisoxazole)hydrobromide (muscimol), 10 ng bicuculline or a combination of the drugs.

234 sessed either by a GABAA receptor antagonist bicuculline or a selective extrasynaptic GABAA receptor

235 compromised central input to HE neurons with bicuculline or by surgical ablation of the central patte

236 Treatment with bicuculline or gabazine to enhance neuronal activity pro

237 In a subset of neurons, GABA(A)R blockers bicuculline or gabazine were applied in addition to iGlu

238 ast, microinjection of a GABA(A) antagonist (bicuculline or gabazine) into the CVLM dramatically atte

239 less GABA-mediated inhibition was reduced by bicuculline or picrotoxin.

240 or microinjection of the GABAA antagonists, bicuculline or SR95531 (60 pmol in 60 nl), into the dors

241 amplitude produced by chronic application of bicuculline or tetrodotoxin is both mimicked and occlude

242 These differences were maintained after bicuculline or tetrodotoxin, indicating they were specif

243 ntagonist kynurenate or the GABAA antagonist bicuculline (P > 0.05).

244 r, in the presence of the GABA(A) antagonist bicuculline, p35 knock-out slices, but not wild-type sli

245 In response to bicuculline perfusion into the PF-LHA, rats exhibited a

246 At the end of aCSF or bicuculline perfusion, rats were killed and c-Fos immuno

247 (ACh) induces increases in the frequency of bicuculline-, picrotoxin-, and 4-aminopyridine-sensitive

248 Finally, systemic injection of bicuculline prevented nicotine-induced firing alteration

249 rneurons, and blockade of GABAA receptors by bicuculline prevented the reduction of CSD amplitudes by

250 In contrast, bicuculline produced an amplitude-dependent dysmetria: i

251 ly, the lipophilic competitive antagonist (+)bicuculline promoted receptor surface expression, includ

252 amate agonist AMPA or the GABA(A) antagonist bicuculline raised RF and the frequency of calls emitted

253 eatment with the GABA(A) receptor antagonist bicuculline, rapidly and robustly induces ubiquitination

254 In addition, bicuculline readily abolished these transients without a

255 ng elicited by NAC shell baclofen, NAC shell bicuculline reduced but did not block feeding elicited b

256 lfotetramine, and the competitive antagonist bicuculline reduced fluorescence near the levels in GABA

257 muscimol, and the GABAa receptor antagonist bicuculline, respectively, on the properties of individu

258 ll mice with the GABA(A) receptor antagonist bicuculline restored corticosterone levels and anxiety-l

259 microdialytic application of L-glutamate or bicuculline resulted in reduced discharge of arousal-rel

260 on, sequential application of strychnine and bicuculline revealed a small (5.2 +/- 1.0 pA) GlyR- but

261 the dorsal hippocampus, with the antagonist bicuculline, reverses the anxiolytic effect of running.

262 Bicuculline, Ro15-4513, finasteride, kainic acid or AMPA

263 hyperpolarized SPNs, an effect that was also bicuculline sensitive.

264 We describe a novel tonically active, bicuculline-sensitive chloride conductance that is insen

265 We conclude that this bicuculline-sensitive conductance needs to be accounted

266 Propofol activated gabazine-resistant, bicuculline-sensitive currents when applied to either pr

267 -21 increased the frequency and amplitude of bicuculline-sensitive currents.

268 a and minaxolone (1 microm) evoked a similar bicuculline-sensitive inhibitory conductance, indicating

269 urring pattern consisting of a monosynaptic, bicuculline-sensitive inhibitory connection from an isle

270 and muscimol attenuated this inhibition in a bicuculline-sensitive manner.

271 With 10 mum GABA, the bicuculline-sensitive tonic currents were approximately

272 xpressing nociceptors, and formed GABAergic, bicuculline-sensitive, synapses onto host neurons.

273 Whereas VTA bicuculline significantly blocked the increased feeding

274 tra-MRN injections of the GABA(A) antagonist bicuculline significantly stimulated SCN 5-HT release, w

275 Moreover, the receptors were resistant to bicuculline, strongly antagonized by (1,2,5,6 tetrahydro

276 Blocking GABAergic inhibition with bicuculline substantially increased neuronal discharge r

277 abolished by the GABA(A) receptor antagonist bicuculline, suggesting that the CB1R-mediated depolariz

278 the presence of tetrodotoxin, AP5, CNQX and bicuculline, supporting an indirect effect.

279 infusions of the GABAA receptor antagonist, bicuculline, suppress robust activations of locomotion e

280 fects of bicuculline and gabazine, such that bicuculline surprisingly activated non-alpha-containing

281 ocker picrotoxin, the competitive antagonist bicuculline, the agonist GABA (gamma-aminobutyric acid),

282 nhibition was blocked by bath application of bicuculline, the incidence of plateau activity increased

283 Application of bicuculline to alpha1beta2gamma2 receptors in the absenc

284 model predictions with published data using bicuculline to block inhibitory GABA inputs supports the

285 Treatment with bicuculline to decrease GABA(A) receptor signaling from

286 Dialysis delivery of bicuculline to the PnO of male mice (n = 18) anesthetize

287 icroinjection of muscimol (to inactivate) or bicuculline (to activate) to these amygdaloid subregions

288 Bicuculline treatment also leads to an increase in the l

289 The 5-HT release induced by intra-DRN bicuculline was also blocked by co-injection of DR4004.

290 ating and REM sleep-suppressing effect of PF bicuculline was not attenuated by systemic administratio

291 e into dendrites and postsynaptic density by bicuculline was prevented in neurons from mice harboring

292 The GABA-A receptor antagonist, bicuculline, was able to reverse the effect of IL-1beta

293 APV, CNQX, and bicuculline were included to block fast synaptic transmi

294 and a specific GABA(A) receptor antagonist, bicuculline, were administered before GHB.

295 ed by the SK(Ca) channel blockers apamin and bicuculline, whereas I(sAHP) is resistant to these agent

296 tivated currents, it prevented inhibition by bicuculline, which acts as an inverse agonist inhibiting

297 In the presence of bicuculline, which blocks inhibitory GABA(A) receptors,

298 ches to inhibit spontaneous GABA(A)R gating, bicuculline, which inhibits spontaneous current in the a

299 l by iontophoresis of the GABA(A) antagonist bicuculline while the rest of the cortex was blocked by

300 ated transmission application of SR-95531 or bicuculline, while abolishing GABAA receptor-mediated ph