ライフサイエンスコーパス: picrotoxin

1 bsence of fast inhibition (blocked by 0.1 mM picrotoxin).

2 s prevented by the GABAA receptor antagonist picrotoxin.

3 nly after slice perfusion with 0 mM Mg2+ and picrotoxin.

4 different chemoconvulsants, pilocarpine and picrotoxin.

5 rents and secretion, which were sensitive to picrotoxin.

6 macological agents, including the convulsant picrotoxin.

7 ted inhibition was reduced by bicuculline or picrotoxin.

8 revent inhibition of the GABA(A) receptor by picrotoxin.

9 e seen with GABA-type-A-receptor blockade by picrotoxin.

10 00 microM), but was unaffected by 100 microM picrotoxin.

11 , but not for the non-competitive antagonist picrotoxin.

12 ric acid alpha subunit) receptor antagonist, picrotoxin.

13 chloride concentration, and is inhibited by picrotoxin.

14 This increase persisted in the presence of picrotoxin.

15 0) = 166 microM), only weakly antagonized by picrotoxin.

16 by GABA and that is blocked substantially by picrotoxin.

17 nal conductance increase that was blocked by picrotoxin.

18 ause the effects of H(2)O(2) were blocked by picrotoxin.

19 nM tetrodotoxin (TTX), but not by 150 microM picrotoxin.

20 using the GABAA antagonists bicuculline and picrotoxin.

21 of BMI or the noncompetitive GABA antagonist picrotoxin.

22 ses converted to paired-pulse depression, by picrotoxin.

23 edium but was ineffective in the presence of picrotoxin.

24 fects can be explained by block of IPSPAs by picrotoxin.

25 he GABA receptor antagonists bicuculline and picrotoxin.

26 low concentrations was sensitive to block by picrotoxin.

27 00 Hz), in either the presence or absence of picrotoxin.

28 Hz, 1 s) in both the absence and presence of picrotoxin.

29 king GABAergic inhibition with intracellular picrotoxin.

30 t can be blocked by an open channel blocker, picrotoxin.

31 -13 but sensitive to the GABA(A)R antagonist picrotoxin.

32 ter L-glutamate and the open-channel blocker picrotoxin.

33 presence of the GABA(A) receptor antagonist picrotoxin.

34 lished by application of the GABA(a) blocker picrotoxin.

35 sive doses of the GABAA receptor antagonist, picrotoxin.

36 entiation of EPSPAs at 50 Hz was enhanced by picrotoxin (0.1 mM) but was not significantly affected b

37 quinpirole (500 ng), the GABA(A) antagonist picrotoxin (0.25, 0.5 or 1 microg) or bicuculline (20 ng

38 ic currents (sIPSCs) by application of 100 M picrotoxin+1 microM strychnine.

39 ceptor antagonists bicuculline (10(-5) M) or picrotoxin (10(-4) M) had no effect on the length of per

40 tor antagonists, bicuculline (10 microM) and picrotoxin (100 microM), inhibited established depolariz

41 mM), pentylenetetrazole (1.5g/L; 11.0mM) and picrotoxin (100mg/L; 0.17mM).

42 es are effectively nullified at low doses of picrotoxin (2.5-5 microM).

43 duce holding currents that were sensitive to picrotoxin (30 microM).

44 ures was then pharmacologically removed with picrotoxin (40 microM) or bicuculline (25 microM) result

45 of nicotine was blocked by a combination of picrotoxin (50 microM) and saclofen (100 microM), and th

46 In the presence of picrotoxin (50 microM), the amplitude of 6-cyano-7-nitro

47 Once again, neither picrotoxin (50 microM, n = 5) nor CNQX (10 microM, n = 5

48 y bath application of the GABA(A) antagonist picrotoxin (50 microM, n = 9) or the glutamate receptor

49 ssed by bicuculline (-41 +/- 5.7 %, 5:8) and picrotoxin (-54 %, 1:1), and the enhancement produced by

50 trongly inhibited and the wave eliminated by picrotoxin, a blocker of GABAA receptor/Cl- channels and

51 After suppressing inhibition with picrotoxin, a GABA(A) receptor antagonist, NMDA receptor

52 e) have structures similar to the convulsant picrotoxin, a GABA(A) receptor antagonist, so their lack

53 This GABA-induced current was blocked by picrotoxin, a GABA(A) receptor blocker.

54 observed in any of our recordings, even when picrotoxin, a GABAA blocker, was included in the interna

55 -cAMPS induced LTD in slices pretreated with picrotoxin, a gamma-aminobutyric acid type A (GABA(A)) r

56 Picrotoxin, a potent antagonist of the inhibitory centra

57 i.p. injection of a subthreshold dose of picrotoxin, a use-dependent gamma-aminobutyric acid rece

58 The GABA(A) receptor antagonist picrotoxin abolished this rescue, while pentobarbital re

59 Following picrotoxin administration in the basolateral amygdala, c

60 minals characteristic of cultures exposed to picrotoxin alone.

61 Picrotoxin also markedly enhanced prefrontal LFP power.

62 hronization is also selectively abolished by picrotoxin, an antagonist of the GABA(A) (gamma-aminobut

63 d widening of EPSPAs at 5 Hz was occluded by picrotoxin and abolished by CGP 35348.

64 However, the GABA antagonists picrotoxin and bicuculline enhanced the on-centre respon

65 Picrotoxin and bicuculline methiodide inhibited both com

66 receptor-mediated responses were blocked by picrotoxin and bicuculline.

67 ased in the presence of the GABA antagonists picrotoxin and CGP55845.

68 The suppression was blocked by picrotoxin and cimetidine, respective antagonists to lob

69 of the IPSC decay indicated a Q10 value of 2.Picrotoxin and cyanotriphenylborate had little or no eff

70 itude that were inhibited by bicuculline and picrotoxin and facilitated by diazepam and zolpidem in a

71 gic and GABAergic inputs with strychnine and picrotoxin and found that TTX in this case had the same

72 its were injected with high and low doses of picrotoxin and gabazine.

73 It is the target of convulsants such as picrotoxin and is mutated in some forms of epilepsy, a d

74 ing equilibrium and can, therefore, displace picrotoxin and prevent inhibition of the GABA(A) recepto

75 s insensitive to the Cl(-) channel blockers, picrotoxin and strychnine, but it was inhibited by a spe

76 Picrotoxin and t-butylbicyclophosphorothionate (TBPS) ar

77 In the absence of episodic GABA application, picrotoxin and TBPS blocked (by 91 +/- 3% and 85 +/- 5%,

78 e noncompetitive GABA(A) receptor antagonist picrotoxin and the competitive GABA(A) receptor antagoni

79 The GABAa/c receptor antagonist picrotoxin and the glycine receptor antagonist strychnin

80 tance that is insensitive to gabazine and to picrotoxin and thus not mediated by conventional GABA re

81 presence of the GABA(A) receptor antagonist picrotoxin and was abolished when both GABA(A) and GABA(

82 GABA were attenuated by (-)-bicuculline and picrotoxin and were potentiated by chlordiazepoxide and

83 This resting conductance was antagonized by picrotoxin and, in the case of the A, G, S, and T substi

84 ed spontaneous openings that were blocked by picrotoxin and, surprisingly, by the competitive antagon

85 ethoxy-4-ethyl-beta-carboline-3-carboxylate, picrotoxin, and amygdala-kindled seizures in mice (ED50

86 were found to suppress zero-Ca2+, low-Ca2+, picrotoxin, and high-K+ epileptiform activity for the du

87 induced by pentylenetetrazole, bicucculine, picrotoxin, and strychnine; also, 2 was not active in di

88 l stimulation could also completely suppress picrotoxin- and high-K+-induced epileptiform activity wi

89 increases in the frequency of bicuculline-, picrotoxin-, and 4-aminopyridine-sensitive miniature IPS

90 ma-aminobutyric acid type A and C receptors, picrotoxin antagonism of the alpha1 homomeric glycine re

91 Picrotoxin antagonism of the embryonic alpha2 homomeric

92 l-blocking mechanism, but the selectivity of picrotoxin antagonism of the embryonic alpha2 homomeric

93 potential oscillations remained after focal picrotoxin applications, and these exhibited the voltage

94 Picrotoxin at 133 pmol elicited eating in the LH, but no

95 Application of the GABA antagonists, picrotoxin, bicuculline and 1,2,5,6-tetrahydropyridine-4

96 diazepines, and neurosteroids) and negative (picrotoxin, bicuculline, and Zn2+) allosteric modulators

97 mpounds that bind with equal affinity to the picrotoxin-binding site on the open-channel form of the

98 (iii) The mechanism indicates that picrotoxin binds to an allosteric site of the receptor w

99 e observations, we proposed a model in which picrotoxin binds to the GABA(C) receptor in both channel

100 In contrast, picrotoxin blockade produces no change in F(TMRM) at the

101 termining use-facilitated characteristics of picrotoxin blockade.

102 wly over the course of 5-20 min, even though picrotoxin blocked both GABA(A) and GABA(C) receptors wi

103 The non-competitive antagonist picrotoxin blocked nearly 50% of GABA-induced fluorescen

104 However, picrotoxin blocked only a part of this GABAC effect, whi

105 Conversely, the GABA(A) receptor antagonist picrotoxin blocked spindle frequency oscillations result

106 Interestingly, the picrotoxin-blocked fraction of the GABA-induced fluoresc

107 Dopamine activity was fully blocked by picrotoxin but not GABAA competitive antagonists, and wa

108 amped neurons and this action was blocked by picrotoxin but not the more selective GABAA antagonist b

109 eliminated by the GABAA receptor antagonist picrotoxin but small (< 5 mV) membrane potential oscilla

110 was converted to paired-pulse enlargement by picrotoxin but was unaffected by CGP 35348.

111 firing was prevented by the GABAA antagonist picrotoxin, but EtOH had no effect on evoked or spontane

112 Ps were blocked by the Cl(-) channel blocker picrotoxin, but not by bicuculline or strychnine, and by

113 t which was antagonized by strychnine and by picrotoxin, but not by bicuculline.

114 d by intracranial pretreatment with 20 ng of picrotoxin, but not by microinjection of 5 micrograms of

115 the presence of the GABA(A) receptor blocker picrotoxin, but not by pretreatment with SR141716A.

116 effect was blocked by the GABA(A) antagonist picrotoxin, but not duplicated by direct application of

117 6N2O2; 62.5, 125, 250 ng/side) or antagonist picrotoxin (C30H34O13; 75, 150, 300 ng/side), respective

118 In dark-adapted retinal slice preparations picrotoxin caused a slow enhancement of glycine-mediated

119 In dark-adapted eyecup preparations picrotoxin caused a slow enhancement of glycinergic IPSP

120 aminobutyric acid type A receptor antagonist picrotoxin caused an activity-dependent and NMDA recepto

121 he GABA(A) receptor blockers bicuculline and picrotoxin caused an outward shift in the holding curren

122 -field locomotor activity, whereas 300 ng of picrotoxin caused locomotor hyperactivity; sensorimotor

123 In the absence of picrotoxin, CGP 35348 also promoted depolarization by en

124 n the presence of various synaptic blockers (picrotoxin, CGP55845, APV, DNQX, E4CPG, and MSPG), we de

125 tion-dependent manner, indicating that these picrotoxin components can bind to the receptor in its op

126 n-use-dependent and nonselective between the picrotoxin components picrotoxinin and picrotin.

127 in slices maintained in standard buffer and picrotoxin-containing buffer.

128 ical agonist site at subunit interfaces, and picrotoxin directly occludes the pore near its cytosolic

129 However, picrotoxin displaceable [(35)S]TBPS binding to alpha1bet

130 lsed depression of EPSPNs in the presence of picrotoxin, effects consistent with its block of GABAB a

131 Muscimol reduced and picrotoxin enhanced bursting and both drugs changed the

132 Applications of bicuculline or picrotoxin enhanced the spontaneous firing rate of corti

133 In addition, low doses of picrotoxin facilitated the expression of unconditioned e

134 However, bicuculline and picrotoxin failed to block it.

135 ce change, but the noncompetitive antagonist picrotoxin failed to elicit optical signals.

136 The channel blockers picrotoxin, fipronil, and tetramethylenedisulfotetramine

137 (i) The apparent dissociation constant of picrotoxin for the open-channel form of the receptor was

138 were used to select those that can displace picrotoxin from the membrane-bound GABA(A) receptor in t

139 that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many action pote

140 dine-4-yl)-methylphosphinic acid (TPMPA) and picrotoxin, GABAC receptor antagonists, reduced the ATPA

141 In the presence of strychnine and picrotoxin, ganglion cells responded to light onset and

142 magnitudes of the shifts in GABA EC(50) and picrotoxin IC(50) as well as the degree of spontaneous o

143 divalent cation Zn(2+) (IC(50)=33.6 microM) picrotoxin (IC(50)=2.4 microM) and blockade of endogenou

144 re blocked by strychnine (IC50 = 630 nm) and picrotoxin (IC50 = 197 mum), where the latter is suggest

145 CSRT) test, we showed that both muscimol and picrotoxin impaired attention (reduced accuracy, increas

146 S firing rate in control, and application of picrotoxin increased both.

147 uscimol inhibited prefrontal firing, whereas picrotoxin increased firing, mainly within bursts.

148 (ii) Picrotoxin increased the channel-closing rate constant (

149 uration, blockade of GABAergic inhibition by picrotoxin increases B8 activity during protraction and

150 increased leak current that was sensitive to picrotoxin, indicating an increased gating efficiency.

151 uctance that was blocked by both 3-APMPA and picrotoxin, indicating spontaneously opening GABA recept

152 re unchanged by the GABA(A) receptor blocker picrotoxin, indicating that alpha7-nAChRs presynapticall

153 These were blocked by tetrodotoxin and picrotoxin, indicating that glucose was acting indirectl

154 application of glycine were not enhanced by picrotoxin, indicating that the enhancement was not caus

155 rrents were sensitive to both strychnine and picrotoxin, indicating that they are mediated by extrasy

156 by application of bicuculline methiodide or picrotoxin, indicating that they are mediated by GABAA r

157 Finally, the allosteric antagonist picrotoxin induced a global conformational change that w

158 simultaneously the coapplication of GABA and picrotoxin induced a large rebound of membrane current.

159 As in other studies, kainate and picrotoxin induced an upsurge in BDNF expression, but BD

160 ed only pre- and/or parasubiculum, evoked or picrotoxin-induced bursts occurred only in deep layer ce

161 behavioural learning paradigm, we show that picrotoxin-induced desynchronization impairs the discrim

162 Compound 3a blocked picrotoxin-induced seizures but was ineffective against

163 ncreased, rats increased response levels for picrotoxin infusion.

164 ; rats discriminated the lever that produced picrotoxin infusions from the lever without consequences

165 Picrotoxin inhibited the channel openings by reducing th

166 In picrotoxin inhibition and in one form of epilepsy, a dec

167 celeration of GABA relaxation were unique to picrotoxin inhibition and were not observed with the com

168 of the experimental findings we observed for picrotoxin inhibition of GABA(C) receptors.

169 e second transmembrane domain that converted picrotoxin inhibition of glycine alpha1 receptors from n

170 e results support an allosteric mechanism of picrotoxin inhibition of ligand-gated chloride channels.

171 noncompetitive mechanisms were observed for picrotoxin inhibition of the GABA(C) receptor.

172 In this study, we investigated the picrotoxin inhibition on perch-rho subunits expressed he

173 inity to the open-channel form and alleviate picrotoxin inhibition.

174 However, the mechanism by which picrotoxin inhibits these receptors is still in debate.

175 More specifically, picrotoxin injected into the tuberal LH (tLH) elicited e

176 properties were modified in vivo by intra-IO picrotoxin injection, which enhances synchronous oscilla

177 movements was greatly reduced, and intra-IO picrotoxin injections did not affect the evoked movement

178 Pressure injection of picrotoxin into the antennal lobe eliminated the oscilla

179 Infusion of picrotoxin into the infralimbic mPFC also reduced fear r

180 oinfusion of the GABA(A) receptor antagonist picrotoxin into the normal adult PFC.

181 Juvenile rats infused with picrotoxin into the prelimbic mPFC and exposed to a thre

182 Infusion of the GABAA antagonist picrotoxin into the VM reduced both high beta power in M

183 ich GABA-mediated currents were blocked with picrotoxin, IPSCs elicited by diffuse illumination were

184 Picrotoxin is a plant alkaloid that is often used to blo

185 our protocol, the GABA-A receptor antagonist picrotoxin is stereotaxically infused in the basolateral

186 ncing synaptic activity in WT, by feeding of picrotoxin is sufficient to increase I(Nap) and promote

187 Given that the OFF response is unmasked with picrotoxin, its direction selectivity cannot be generate

188 to different scope) by low concentrations of picrotoxin (</= 30 muM), which selectively blocked alpha

189 data are consistent with the suggestion that picrotoxin may interact with two domains in ligand-gated

190 ydrogen bonding, directly interacts with the picrotoxin molecule.

191 This was because picrotoxin occluded whereas CGP 35348 blocked the effect

192 e, we present the mechanism of inhibition by picrotoxin of the rat alpha1beta2gamma2L GABA(A) recepto

193 Picrotoxin, on the other hand, was more effective in blo

194 uncoupling is blocked by co-incubation with picrotoxin or alpha-amanitin but is insensitive to nifed

195 blocked by the GABA(A) receptor antagonists picrotoxin or bicuculline methiodide (BMI), and had long

196 pplication of the GABAA receptor antagonists picrotoxin or bicuculline.

197 sensitive to the GABAA receptor antagonists picrotoxin or bicuculline.

198 d in the presence of the GABA(A) antagonists picrotoxin or bicuculline.

199 antennal lobe, and this effect is blocked by picrotoxin or by transgenic RNAi-mediated knockdown of t

200 In the presence of either picrotoxin or CGP 35348 the primed EPSPAs and EPSPNs res

201 and either blocked intra-RE inhibition with picrotoxin or enhanced it with clonazepam.

202 of postsynaptic GABA(A)R with intracellular picrotoxin or gabazine, suggesting that Nxph1 is able to

203 Picrotoxin or muscimol was applied to the cerebellar cor

204 val of extracellular Mg2+ and application of picrotoxin or perfusion with 0.5 mM Mg2+ and 8.5 mM K+-c

205 GABA application during picrotoxin or TBPS administration enhanced alpha1beta2ga

206 Seizure activity was precipitated by picrotoxin or with the BDZ inverse agonist n-methyl-beta

207 Picrotoxin partially blocked glutamate's inhibition of t

208 manipulation with period-altering compounds: picrotoxin, PF-670462 (4-[1-Cyclohexyl-4-(4-fluorophenyl

209 The alkaline shifts persisted in 100 microM picrotoxin (PiTX) but were blocked by 25 microM CNQX/50

210 Finally, chronic picrotoxin pretreatment (100 microM) intended to mimic G

211 The GABAAR and GlyR pore blocker picrotoxin prevented desensitization, consistent with it

212 tterns of neural activity in the presence of picrotoxin prevented the D-V pathfinding errors in the l

213 Picrotoxin (PTX) co-applied with glycine suppressed both

214 The central nervous system convulsant picrotoxin (PTX) inhibits GABA(A) and glutamate-gated Cl

215 Picrotoxin (PTX) is a noncompetitive antagonist of many

216 spiking; TTX+N-methyl-D-aspartic acid (NMDA)+picrotoxin (PTX) or gamma-aminobutyric acid (GABA) to bl

217 ts of GABA-A receptor blockade, finding that picrotoxin (PTX) recapitulated the decrease in sound-evo

218 l disorders with recent data suggesting that picrotoxin (PTX), a GABAA receptor antagonist, rescues c

219 mma-aminobutyric acid (GABA(A&C)) antagonist picrotoxin (PTX), or the inhibitory amino acid GABA and

220 e to millimolar concentrations of GABA and a picrotoxin (PTX)-sensitive, bicuculline-insensitive curr

221 AZINE (GBZ) and the chloride channel blocker picrotoxin (PTX).

222 Antagonists of GABAB (saclofen) and GABAC (picrotoxin) receptors partially inhibited responses to b

223 (including tonic and synaptic currents) with picrotoxin reduced interspike interval (ISI) variability

224 e binding effect is further supported by the picrotoxin resistance of a competitive antagonist-induce

225 the alpha, beta or gamma subunit, can impart picrotoxin resistance to the GABA receptor.

226 gle subunit carrying the 6' mutation imparts picrotoxin resistance.

227 mpal neurons transfected with alpha4 and the picrotoxin-resistant delta(T269Y) subunit showed large r

228 agating into the dorsal neocortex, as do the picrotoxin-resistant fraction of waves in controls.

229 esence of 300 muM picrotoxin, suggesting the picrotoxin-resistant subtype the alphabeta heteromeric G

230 neuron firing, the GABAA receptor antagonist picrotoxin resulted in a consistent suppression of firin

231 application of the GABA(A) receptor blocker, picrotoxin, resulted in motoneurons making dorsal-ventra

232 current and associated noise were reduced by picrotoxin, revealing that epsilon-containing channels a

233 Muscimol, a GABA(A) agonist, disrupted picrotoxin self-infusion, but bicuculline, a GABA(A) ant

234 idal neurons, which in sham treated rats was picrotoxin sensitive.

235 Fast IPSCs are mediated by picrotoxin-sensitive chloride conducting GABA receptors.

236 amp electrophysiology reveals GABA-activated picrotoxin-sensitive chloride currents on PDF+ neurons.

237 for GABA, GAD67, selectively eliminates the picrotoxin-sensitive fraction of these waves.

238 ted byalpha-bungarotoxin-sensitive nAChRs or picrotoxin-sensitive GABA receptors.

239 ry neuronal progenitor responded to GABA via picrotoxin-sensitive GABAA receptor (GABAAR) activation.

240 These inputs were linked to a picrotoxin-sensitive increase of Ca(2+) in the terminals

241 ents were blocked by kynurenic acid, leaving picrotoxin-sensitive IPSCs.

242 In eight neurons, spontaneous picrotoxin-sensitive IPSPs were recorded and found to di

243 Furthermore, picrotoxin-sensitive spontaneous single-channel events r

244 on recordings) by decreased magnitude of the picrotoxin-sensitive tonic current (I(tonic)), but not m

245 on, when mutated to phenylalanine, abolishes picrotoxin sensitivity.

246 Rats treated systemically with picrotoxin showed a dramatic increase in levels of NE wi

247 In addition, picrotoxin significantly accelerated the kinetics of GAB

248 inhibit ligand binding at the GABAA receptor picrotoxin site in the Fischer (F344) rat IC.

249 Rats quickly learned to self-infuse a picrotoxin solution into the anterior VTA; rats discrimi

250 ents reversed around ECl and were blocked by picrotoxin, strychnine, or both, suggesting they were me

251 ponses) which were blocked by bicuculline or picrotoxin, suggesting GABA(A) mediation.

252 e responses to alfaxalone in the presence of picrotoxin, suggesting that alpha4betadelta receptors ma

253 d by the GABA(A) antagonists bicuculline and picrotoxin, suggesting that the inhibitory action of D2

254 Mg2+ deprivation, but not that generated by picrotoxin, suggesting that TRH-mediated increase in GAB

255 ocked by addition of a subconvulsive dose of picrotoxin, suggesting the involvement of GABAA receptor

256 f I(Gly) remained in the presence of 300 muM picrotoxin, suggesting the picrotoxin-resistant subtype

257 rrents reversed near ECl and were blocked by picrotoxin, suggesting they arose from GABAa/c receptors

258 readily antagonized by both bicuculline and picrotoxin than the GABAh response.

259 In the presence of picrotoxin, the action potential amplitude is increased

260 e presence of the GABAA receptor antagonist, picrotoxin, the application of BDNF (100 ng/ml) for 1-5

261 ned the effects of the GABAergic antagonist, picrotoxin, the GABAergic agonist, muscimol, and saline

262 In the presence of strychnine and picrotoxin, the NBQX-induced enhancement of NMDA current

263 embryos were chronically treated in ovo with picrotoxin to block GABA(A) receptors, while light activ

264 F and NT-4 to cerebellar explants exposed to picrotoxin to increase neuronal activity prevented the h

265 Using infusions of picrotoxin to the interpositus nucleus of the rabbit cer

266 Epidural application of picrotoxin to the rat's M1 motor cortex induced Fos in i

267 The most striking effect was that picrotoxin-treated rabbits initially trained with a 250-

268 rd buffer, whereas normal LTP was induced in picrotoxin-treated, disinhibited slices.

269 the application of the GABA receptor blocker picrotoxin unmasks a robust excitatory OFF response in O

270 In 0 Mg(2+) saline with picrotoxin (using a 20 Hz train), the HW measures were s

271 mean open time in the presence of 100 microM picrotoxin was 0.07 +/- 0.01 s (77 openings from 3 patch

272 The change in kinetics induced by picrotoxin was also observed on receptors formed by othe

273 Furthermore, when picrotoxin was applied only at the lateral edge of the a

274 nobutyric acid (GABA)(A) receptor antagonist picrotoxin was applied.

275 At equal concentrations, picrotoxin was approximately twice as effective as bicuc

276 effect is specific to the LH, the antagonist picrotoxin was injected into one of six nearby sites and

277 ation of the mPFC alone with GABA antagonist picrotoxin was insufficient to elicit the stress effect

278 Picrotoxin was more effective than ATPA.

279 Again, picrotoxin was most effective, producing, on average, a

280 The slow enhancement of glycinergic IPSCs by picrotoxin was much weaker in light-adapted preparations

281 gnificantly decreased and the sensitivity to picrotoxin was significantly increased.

282 The reinforcing effect of picrotoxin was site-specific: Anterior VTA regions suppo

283 the GABAA receptor chloride channel blocker picrotoxin, whereas the slow sustained IPSPs were blocke

284 In contrast, picrotoxin, which blocks the GABA-gated Cl- channel, did

285 blocks sodium spiking in amacrine cells, and picrotoxin, which blocks the inhibitory action of GABA,

286 Chronic (7-day) treatment with picrotoxin, which induced a persistent four-fold increas

287 atiotemporal distribution in the presence of picrotoxin, which induced the merging of neuronal cluste

288 idural application of the GABA(A) antagonist picrotoxin, which produces a topographically restricted

289 current, whereas the application of zinc and picrotoxin, which reduce GABAR currents, reduced the hol

290 ons of GABA, were blocked by bicuculline and picrotoxin with IC50 values of 2.7 and 5.1 mum, respecti

291 esting membrane conductances were reduced by picrotoxin, zinc, or penicillin-G.