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 king GABAergic inhibition with intracellular 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 different chemoconvulsants, pilocarpine and picrotoxin.

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

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

21 using the GABAA antagonists bicuculline and picrotoxin.

22 of BMI or the noncompetitive GABA antagonist picrotoxin.

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

24 edium but was ineffective in the presence of picrotoxin.

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

26 he GABA receptor antagonists bicuculline and picrotoxin.

27 low concentrations was sensitive to block by picrotoxin.

28 00 Hz), in either the presence or absence of picrotoxin.

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

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

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

32 at in flies treated with the GABA antagonist picrotoxin.

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

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

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

36 sive doses of the GABAA receptor antagonist, picrotoxin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 We report picrotoxin, a GABA(A)R antagonist, blocks neurotransmiss

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

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

58 Picrotoxin, a potent antagonist of the inhibitory centra

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

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

61 Following picrotoxin administration in the basolateral amygdala, c

62 esistance to the GABA(A) receptor antagonist picrotoxin, allowing verification of mutant subunit inco

63 minals characteristic of cultures exposed to picrotoxin alone.

64 Picrotoxin also markedly enhanced prefrontal LFP power.

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

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

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

68 Picrotoxin and bicuculline methiodide inhibited both com

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

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

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

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

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

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

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

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

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

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

79 Picrotoxin and t-butylbicyclophosphorothionate (TBPS) ar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Picrotoxin antagonism of the embryonic alpha2 homomeric

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

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

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

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

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

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

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

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

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

104 termining use-facilitated characteristics of picrotoxin blockade.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 6N2O2; 62.5, 125, 250 ng/side) or antagonist picrotoxin (C30H34O13; 75, 150, 300 ng/side), respective

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 However, bicuculline and picrotoxin failed to block it.

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

139 The channel blockers picrotoxin, fipronil, and tetramethylenedisulfotetramine

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

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

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

143 xolone (gap junctions blocker), control, and picrotoxin (GABA-A receptor antagonist).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 ncreased, rats increased response levels for picrotoxin infusion.

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

168 Picrotoxin inhibited the channel openings by reducing th

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

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

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

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

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

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

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

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

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

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

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

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

181 In hippocampal slices, picrotoxin-insensitive inhibitory synaptic currents exhi

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

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

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

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

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

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

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

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

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

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

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

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

194 ydrogen bonding, directly interacts with the picrotoxin molecule.

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

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

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

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

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

200 pplication of the GABAA receptor antagonists picrotoxin or bicuculline.

201 sensitive to the GABAA receptor antagonists picrotoxin or bicuculline.

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

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

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

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

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

207 Picrotoxin or muscimol was applied to the cerebellar cor

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

209 GABA application during picrotoxin or TBPS administration enhanced alpha1beta2ga

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

211 Picrotoxin partially blocked glutamate's inhibition of t

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

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

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

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

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

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

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

219 Picrotoxin (PTX) is a noncompetitive antagonist of many

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

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

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

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

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

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

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

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

228 We confirmed picrotoxin resistance and biophysical properties in reco

229 the two receptor populations using mice with picrotoxin resistance engineered into receptors containi

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

231 We used gene editing to confer picrotoxin resistance on delta receptors in mice, then p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 In addition, picrotoxin significantly accelerated the kinetics of GAB

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

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

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

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

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

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

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

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

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

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

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

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

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

268 id nanodiscs is bound to the channel-blocker picrotoxin, the competitive antagonist bicuculline, the

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

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

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

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

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

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

275 and an established animal model of seizure (picrotoxin) to determine the effects of epileptic seizur

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

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

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

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

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

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

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

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

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

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

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

287 Picrotoxin was more effective than ATPA.

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

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

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

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

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

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

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

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

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

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

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

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

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