ライフサイエンスコーパス: TTX

1 TTX (1 mum) significantly increased the occurrence of Ca

2 TTX application abolished the tonic current to a similar

3 TTX at 100 nm, which selectively blocks neuronal isoform

4 TTX blocked this channel with an IC(50) of 1 microM.

5 TTX did not eliminate the effects of PAR1 activation on

6 TTX did not eliminate the synergistic response of the ag

7 TTX increased spontaneous activity through an increase i

8 TTX infusions did not affect the initial acquisition or

9 TTX infusions in the MCP suppressed both CRs and SLRs.

10 TTX injected in the stimulated eye drastically reduced t

11 TTX nearly abolished the expression of maternal retrieva

12 TTX reduced ERG amplitudes measured at fixed times corre

13 TTX reduced PERG amplitude to less than half; simulation

14 TTX-3 and CEH-10 automaintain their expression, thereby

15 TTX-R INa recorded from EGFP-positive hypothalamic neuro

16 TTX-sensitive mitochondrial Ca(2+) influx was largely bl

17 TTX-sensitive sodium current was substantial throughout

18 of the beta subunit with that of Na(v)1.7, a TTX-sensitive Na(+) channel widely expressed in both sma

19 Although none blocked Na(V)1.8, a TTX-resistant isoform, the resulting "activity matrix" r

20 lear nucleus, excitatory synapses activate a TTX-sensitive Na(+) conductance and deactivate a resting

21 nes indicated that channel loss eliminates a TTX-r persistent current.

22 cadherin were decreased, whereas levels of a TTX-soluble 115 kDa VE-cadherin species were increased i

23 We conclude that a TTX-sensitive INa is essential for efficient triggering

24 In addition, TTX still increased frequency and amplitude of mEPSCs in

25 Of importance, after TTX cessation and 7 d of recovery, there was a marked in

26 oma eliminated P50 and reduced P1 amplitude; TTX reduced P50 and hardly altered P1.

27 pt (95%), Nav1.8-immunoreactivity (70%), and TTX-R INa (100%), although not all Nav1.8-expressing neu

28 inhibitors, including local anesthetics and TTX.

29 following infusions (day 3) both the ANI and TTX groups showed significant impairments in allocentric

30 appeared to resolve on day 4 in the ANI and TTX groups, 24 h following infusion.

31 These results show that ANI and TTX inhibit the on-line function of the dorsal hippocamp

32 lthough the combined application of 4-AP and TTX did not rescue responses in pyramidal cells, neither

33 arboxylic acid methyl ester], CNQX, APV, and TTX, and was inhibited in the presence of an extracellul

34 are blocked by nanomolar concentrations and TTX-resistant (TTX-r) channels (NaV1.8 and NaV1.9) inhib

35 ommand voltage, cobalt-sensitive current and TTX-sensitive current were both sizeable at subthreshold

36 nd- and all third-order retinal neurons; and TTX (tetrodotoxin, 6 muM), to block Na+-dependent spikin

37 es of calcium transients with nifedipine and TTX reduced the incidence of differential process outgro

38 als persist after injection of APB, PDA, and TTX, drugs that work to suppress inner and postreceptora

39 PGE2 and TTX (alone or together with PGE2) also increased levels

40 The network and cellular effects of PGE2 and TTX treatments reversed within 1 week.

41 rmine the relative contribution of TTX-s and TTX-r channels to action potential conduction in differe

42 We also show that both TTX-S and TTX-R resurgent currents in DRG neurons are enhanced by

43 vestigated the actions of DHPG on sIPSCs and TTX-insensitive miniature IPSCs (mIPSCs) recorded in mit

44 essed before and following infusions of ANI, TTX, or vehicle (PBS).

45 s blocked by low doses of externally applied TTX or by the internal dialysis of low doses of lidocain

46 t neuronal activity via ion channels such as TTX also influence the function of the dopamine transpor

47 described predator-prey relationship between TTX-bearing Eastern Newts (Notophthalmus viridescens) an

48 We also show that both TTX-S and TTX-R resurgent currents in DRG neurons are en

49 Ps; and vice versa, the inhibition of AP (by TTX or 0 Na, 0 Ca solution) de-synchronized diastolic Ca

50 way, which was reduced by MQC, as well as by TTX, hexamethonium or removal of the submucosal plexus.

51 eurite degeneration, which was attenuated by TTX and KB-R7943, supporting a contribution of sodium ch

52 d neurite degeneration was not attenuated by TTX.

53 erlies both use-dependent and tonic block by TTX.

54 steeply voltage-dependent current blocked by TTX that activates near -60 mV, as well as a sodium "bac

55 In both cases, responses were blocked by TTX, indicating that they were generated by action poten

56 This rhythmic lLN(v) activity is blocked by TTX, voltage-gated sodium blocker, or alpha-bungarotoxin

57 kade of voltage-dependent sodium channels by TTX also reduced CSD.

58 Ch)-induced Cl(-) secretion was decreased by TTX, hexamethonium, and the serosal FFA3 agonists acetat

59 PhNRs that could be eliminated by TTX or severe experimental glaucoma were present in resp

60 hrough extracellular matrix was inhibited by TTX.

61 for the observed resistance to inhibition by TTX.

62 nnels are equally sensitive to inhibition by TTX.

63 mature active responses, mediated in part by TTX- and lidocaine-insensitive channels, were observed i

64 ated eye only and were moderately reduced by TTX.

65 ing potentials were significantly reduced by TTX.

66 ed these transcripts that were suppressed by TTX.

67 In addition, we characterized TTX-sensitive sodium current (I(Na)) and 4AP-sensitive a

68 The latter, as well as the classic TTX, blocked compound action potentials in isolated nerv

69 -R resurgent currents are similar to classic TTX-S resurgent currents in many respects, but not all.

70 After pharmacological blockade with CNQX, TTX still reduced b-wave amplitudes in cone-isolated ERG

71 A substitution conferring TTX resistance to Nav1.7, a channel found in small perip

72 In vivo, injection of liposomes containing TTX and the photosensitizer caused an initial nerve bloc

73 toxin-resistant voltage-gated Na(+) current (TTX-R I(Na)) and a decrease in voltage-gated Ca(2+) curr

74 nce a tetrodotoxin-resistant sodium current (TTX-R I(Na)) and to suppress a delayed rectifier-like po

75 scle mass from a reduction of 51% after 14 d TTX to a reduction of only 24% compared with sham contro

76 urning muscle mass to levels observed at 7 d TTX administration (29% reduction).

77 ifluorination of the aromatic ring decreased TTX affinity by approximately 50-fold, a reduction simil

78 ve at activating this large Na(+)-dependent (TTX sensitive) delayed outward current.

79 n ( approximately 60 s), activity-dependent, TTX- and ouabain-sensitive, hyperpolarization ( approxim

80 The molecular basis of differential TTX sensitivity of mammalian sodium channels has been la

81 Stimulation of mGluR2/3 evoked a direct, TTX-insensitive membrane hyperpolarization in all BLA pr

82 ted spinal cords showed that Hb9 INs display TTX-resistant membrane potential oscillations, suggestin

83 ssion of genes that were most changed during TTX had returned to that of the sham control.

84 attacks and consistently maintained elevated TTX concentrations relative to wild, non-captive individ

85 As with spontaneous EPSCs, TTX-insensitive (action potential-independent) miniature

86 In some experiments, TTX was injected in one eye and saline in the contralate

87 preparation techniques were used to extract TTX from Trumpet shells and pufferfish samples.

88 Extreme TTX resistance has evolved at least five times within th

89 g requires the Otx-type transcription factor TTX-1 and its direct target, the receptor tyrosine kinas

90 ia requires the OTD/OTX transcription factor TTX-1, the fusogen AFF-1 and probably the vascular endot

91 gans, two homeodomain transcription factors, TTX-3 (a LHX2/9 ortholog) and CEH-10 (a CHX10 ortholog),

92 Finally, TTX blocked glucose-dependent mitochondrial Ca(2+) rise,

93 Following TTX (1 muM), or blockade of inhibitory neurotransmission

94 Following TTX application, carbachol (1 muM), substance P (1 muM)

95 first report on the use of ASE as a mean for TTX extraction, the use of UPLC-MS/MS for TTX analysis,

96 lysis, and the validation of this method for TTX in gastropods.

97 or TTX extraction, the use of UPLC-MS/MS for TTX analysis, and the validation of this method for TTX

98 with toxic amphibian prey, which select for TTX-resistant voltage-gated sodium channels (Nav) [12-16

99 nner ear activity is allowed to recover from TTX treatments, retracted NL dendrites regrow to their n

100 cking TNFalpha signaling, early scaling (6 h TTX) was not, unless TNFalpha signaling was first blocke

101 The highest TTX levels in gonads, livers, intestines and skins of fe

102 However, TTX blocked, and in some cases MLA reduced, the potentia

103 However, TTX rats required a greater number of trials than did co

104 We tested if TTX can be induced by exposing populations of adult and

105 Importantly, TTX-induced downregulation of mIPSC was attenuated in Ga

106 Spontaneous activity in TTX had broader, smaller spikes than normal pacemaking a

107 ecies was present on the cell surface and in TTX-insoluble fractions, consistent with junctional loca

108 ast, although the tonic current decreased in TTX, it was still enhanced by GLP-1 or exendin-4.

109 Induction of LTP in TTX-treated neurons leads to insertion of AMPA receptors

110 This depolarization persisted in TTX or when fast synaptic potentials were blocked, indic

111 n paradigms, lid suture (LS) and intraocular TTX, affect the local microcircuit within layer 2/3 of r

112 urrent-voltage curve was dominated by inward TTX-sensitive persistent sodium current (I(NaP)) that ac

113 gly inhibits MCH neurons, an effect which is TTX insensitive, and blocked by the intracellular presen

114 opening of a Na(+) permeant and yet largely TTX insensitive ion channel.

115 tic spikes with intracellular QX314 or local TTX application prevented LTP in the GluR1 knock-out mic

116 In nerves from NaV1.8(-/-) mice, TTX-r C-CAPs could not be detected.

117 uld be a widespread mechanism for modulating TTX sensitivity of sodium channels in diverse invertebra

118 Similarly, visual deprivation with monocular TTX injections results in synaptic accumulation of GluR2

119 Moreover, TTX inactivation of the ventral hippocampus restores DA

120 Moreover, TTX reduced GFP levels in interneurons, suggesting that

121 Above -55 mV, TTX-sensitive voltage-dependent "persistent" Na current

122 based current as a substitute for the native TTX-sensitive Na(+) currents, which were pharmacological

123 Neither TTX nor MLA reduced the potentiation of IPSC frequencies

124 ry to findings in the somatosensory neurons, TTX-R VGSCs are not preferentially expressed in the noci

125 ion in the preBotC of 10 microM RIL or 20 nM TTX does not perturb respiratory frequency, even in the

126 ersistent" sodium current, a noninactivating TTX-sensitive current present at subthreshold voltages.

127 TRPV1-specific antagonist SB366791, but not TTX, strongly attenuated thermal responses.

128 Here we report a novel TTX-resistant (TTX-R) resurgent current recorded from ra

129 In vitro, 5.6% of TTX was released upon NIR irradiation, which could be re

130 IPSC bursts were identical in the absence of TTX, although the burst incidence increased 5-fold, indi

131 In the absence of TTX, these independent pathways appear to act in a coope

132 /MS method was developed for the analysis of TTX and validated following the guidelines contained in

133 ver-1 expression requires direct binding of TTX-1 to ver-1 regulatory sequences, and is induced in d

134 Unlike all other cases of TTX resistance in vertebrates, H. platirhinos lacks the

135 channels (blocked by a low concentration of TTX) are required for long-term potentiation (LTP) in th

136 To determine the relative contribution of TTX-s and TTX-r channels to action potential conduction

137 a of 18, 42, and 69% after 3, 7, and 14 d of TTX, respectively.

138 olarizing shift in the voltage dependence of TTX-S I(Na) inactivation, reduced persistent TTX-R I(Na)

139 een developed for rapid, robust detection of TTX; however, these assays focus on detection of unbound

140 ent indicate that there is a large effect of TTX-induced inactivation on retrieval behavior latencies

141 compartments, we investigated the effects of TTX on C-fiber-mediated compound action potentials (C-CA

142 antly reduced only the additional effects of TTX on the mixed rod-cone ERG observed under mesopic con

143 Effects of TTX were seen under all background conditions, but were

144 xamine the repeatability of the evolution of TTX resistance in an undescribed predator-prey relations

145 al thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle noc

146 Moreover, infusion of TTX into the ventral hippocampus (vHPC) reversed both be

147 e before and after intravitreal injection of TTX (approximately 3 microm) alone, 3-6 weeks after opti

148 t affect b-wave amplitudes, and injection of TTX in eyes with ONTx reduced b-wave amplitudes by the s

149 ar interactions, we used focal injections of TTX to block activity in small local populations, while

150 ound that that local newts contain levels of TTX dangerous enough to dissuade most predators, and tha

151 Changes in the levels of TTX in the gonads, livers, intestines, skins and muscles

152 echanical calculations applied to a model of TTX binding to benzene.

153 estigate the mechanisms of FFA modulation of TTX-sensitive voltage-gated sodium current.

154 duced AAS-IPSCs persisted in the presence of TTX and TEA but not 4-AP.

155 TEA-sensitive K+ channels in the presence of TTX significantly increased EPSP amplification, arguing

156 this view, and found that in the presence of TTX, mGluR5 agonists evoked GABA release that could inst

157 ic magnocellular neurones in the presence of TTX, which implicated a coordinated mechanism of spike-i

158 glutamate photo-uncaging in the presence of TTX.

159 ues VP gene transcription in the presence of TTX.

160 lity of small DRG neurons in the presence of TTX.

161 The apparent expanding prevalence of TTX supports a growing need for screening assays that ca

162 ntial initiation and increased prevalence of TTX-sensitive spontaneous Ca2+ transients.

163 of the density and biophysical properties of TTX-R I(Na), and the high level of intracellular Cl(-) i

164 TTX-R I(Na), a prolonged rate of recovery of TTX-R I(Na) from inactivation, and reduced cell surface

165 bing a qualitative pharmacological survey of TTX-sensitive Na(V)1 isoforms responsible for propagatin

166 lled by the different VGSC isoforms based on TTX sensitivity and effects of siRNA-mediated gene silen

167 ly reported, severe experimental glaucoma or TTX eliminated photopic negative responses, N95, and N2;

168 aces the permeation pathway where it orients TTX optimally and interacts with permeant ions.

169 Nav1.7 (PF-04856264, IC50, 28 nM) vs. other TTX-sensitive or resistant (i.e., Nav1.5) sodium channel

170 ugh several of these currents, in particular TTX-R I(Na), appear to contribute to the sensitization o

171 ts contribute to this property: a persistent TTX-sensitive sodium current and a ruthenium red-sensiti

172 sodium channels and also enhances persistent TTX-resistant current near threshold.

173 TTX-S I(Na) inactivation, reduced persistent TTX-R I(Na), a prolonged rate of recovery of TTX-R I(Na)

174 pheral nerves of mice and nonhuman primates, TTX reduced the C-CAP amplitude to 16% of the baseline.

175 conditions while longitudinally quantifying TTX concentrations.

176 e skeletal muscle sodium channel that reduce TTX binding, suggesting that physiological resistance in

177 nits, encoded by Scn2b, selectively regulate TTX-S alpha subunit mRNA and protein expression, ultimat

178 trodotoxin-sensitive (TTX-S) and -resistant (TTX-R) Na(+) current (I(Na)) mediated by voltage-gated N

179 toxin did not act on tetrodotoxin-resistant (TTX-r) Na(V)1.8 currents; discrimination was based on te

180 m indicated that the tetrodotoxin-resistant (TTX-R) voltage-gated sodium channels (VGSC) are preferen

181 nanomolar concentrations and TTX-resistant (TTX-r) channels (NaV1.8 and NaV1.9) inhibited by millimo

182 Here we report a novel TTX-resistant (TTX-R) resurgent current recorded from rat DRG neurons.

183 show for the first time that TTX-resistant (TTX-R) VGSCs (Nav1.5) potentiate VEGF-induced ERK1/2 act

184 pharmacologic blockade of the inner retina (TTX) and postreceptoral retinal circuitry (APB and PDA),

185 DRG) neurons express tetrodotoxin-sensitive (TTX-S) and -resistant (TTX-R) Na(+) current (I(Na)) medi

186 ination was based on tetrodotoxin-sensitive (TTX-s) Na(+) channel expression.

187 Tetrodotoxin-sensitive (TTX-S) resurgent currents have been described in many di

188 y divided into tetrodotoxin (TTX)-sensitive (TTX-s) channels (NaV1.1-NaV1.4, NaV1.6-NaV1.7) that are

189 These results suggest that slow TTX-R resurgent currents in DRG neurons are mediated by

190 We propose that these slow TTX-R resurgent currents contribute to the membrane exci

191 mmunoassay for a seafood toxin, specifically TTX.

192 gly, this arachnid channel showed surprising TTX resistance.

193 Tetrodotoxin (TTX) is a key chemical defense trait in North American a

194 Tetrodotoxin (TTX) is a potent blocker of voltage-gated sodium channel

195 Tetrodotoxin (TTX) is one of the most potent marine neurotoxins report

196 Tetrodotoxin (TTX) stopped spontaneous activity and usually resulted i

197 Tetrodotoxin (TTX), a small molecular weight neurotoxin, is responsibl

198 Tetrodotoxin (TTX)-sensitive sodium channels carry large transient cur

199 he presence of bicuculline and tetrodotoxin (TTX), increased the frequency but did not change the amp

200 ple Na(+) channel antagonists: tetrodotoxin (TTX; 20 nM), riluzole (RIL; 10 microM), and the intracel

201 tage-gated Na+ channel blocker tetrodotoxin (TTX) abolished the effects of SKF81297 on sEPSP amplific

202 of the sodium channel blocker tetrodotoxin (TTX) into the MCP.

203 use the sodium channel blocker tetrodotoxin (TTX) is typically used in such studies.

204 of the sodium channel blocker tetrodotoxin (TTX) on depolarizations generated by two-photon uncaging

205 -gated sodium channel blocker, tetrodotoxin (TTX), the metabotropic glutamate receptor (mGluR6) agoni

206 chronic blockade of firing by tetrodotoxin (TTX) for two days resulted in increases both in the freq

207 ed by KCl and downregulated by tetrodotoxin (TTX) in cultured primary neurons.

208 n potentials were inhibited by tetrodotoxin (TTX), inhibitory postsynaptic currents decreased and cur

209 ligodendrocytes was blocked by tetrodotoxin (TTX), much of the NAAG-evoked current in oligodendrocyte

210 e functional and suppressed by tetrodotoxin (TTX).

211 The liposomes contained tetrodotoxin (TTX), which has ultrapotent local anesthetic properties.

212 In the first experiment, tetrodotoxin (TTX) was used to chemically inactivate the mPFC during t

213 Voltage-gated tetrodotoxin (TTX)-sensitive Na(+) currents (Na(V)1.6/1.7) contribute

214 longed activity blockade [24 h tetrodotoxin (TTX)] was prevented by blocking TNFalpha signaling, earl

215 f human nociceptors, including tetrodotoxin (TTX)-resistant, SCN10A-dependent sodium currents and res

216 ften functionally divided into tetrodotoxin (TTX)-sensitive (TTX-s) channels (NaV1.1-NaV1.4, NaV1.6-N

217 und squirrel cb5b, has a large tetrodotoxin (TTX)-sensitive Na(+) current.

218 Potent neurotoxins like tetrodotoxin (TTX) and saxitoxin (STX) that are highly toxic to humans

219 Finally, we show that local tetrodotoxin (TTX) application to the soma blocked LTP in adults, but

220 ous firing activity with 10 nM tetrodotoxin (TTX) abolished the protective effect of NTR1 against Abe

221 dy investigated the effects of tetrodotoxin (TTX) blockade of Na(v) channels on the b-wave, an ERG wa

222 The toxicity of tetrodotoxin (TTX) in pufferfish (Lagocephalus sceleratus) from Mersin

223 activity by the application of tetrodotoxin (TTX) reduced mIPSC amplitudes and the levels of GAD67 an

224 Convergent evolution of tetrodotoxin (TTX) resistance, at both the phenotypic and genetic leve

225 In the presence of tetrodotoxin (TTX), 8-Br-cGMP decreased the exogenous postsynaptic inw

226 characterized as inhibitors of tetrodotoxin (TTX)-resistant sodium channels in amphibian dorsal root

227 h persisted in the presence of tetrodotoxin (TTX).

228 ry activity in the presence of tetrodotoxin (TTX).

229 ilateral infusion of saline or tetrodotoxin (TTX) within the VH to transiently inactivate local circu

230 een CMMCs, exhibited prolonged tetrodotoxin (TTX; 1 mum)-sensitive Ca(2+) transients that peaked appr

231 were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav

232 , are exquisitely sensitive to tetrodotoxin (TTX), and a functional differentiation of these presents

233 ptation, extreme resistance to tetrodotoxin (TTX), has arisen in several species of snakes through co

234 All APs were sensitive to tetrodotoxin (TTX), indicating that they were driven by voltage-gated

235 One such toxin, tetrodotoxin (TTX), blocks sodium channels with nanomolar affinity onl

236 cts on EPSCs were blocked with tetrodotoxin (TTX) (1 microM), but not by methyllycaconitine (MLA) (50

237 Pharmacologic antagonism with tetrodotoxin (TTX) in differentiated THP-1 cells or absence of functio

238 ibiting neuronal activity with tetrodotoxin (TTX) increased the percentage of mobile mitochondria in

239 hermore, after incubation with tetrodotoxin (TTX), a sodium channel blocker, there was a significant

240 al or temporary treatment with tetrodotoxin (TTX), leads to rapid and significant retraction of affec

241 s anterior muscle in rats with tetrodotoxin (TTX)-administered to the common peroneal nerve-resulted

242 trophysiological analysis with tetrodotoxin (TTX)-dependent block of the Na(+) channel, and molecular

243 network-activity blockade with tetrodotoxin (TTX).

244 activity by treating them with tetrodotoxin (TTX, 1 mum; 48 h).

245 nanomolar concentrations of (-)-tetrodotoxin(TTX) but not (+)-saxitoxin (STX) and (+)-gonyautoxin-III

246 nsitive current was consistently larger than TTX-sensitive current at interspike voltages from -70 to

247 We found that TTX also eliminated this delayed outward component in ra

248 We show that TTX inhibits glucose-dependent depolarization and blocks

249 Here, we show that TTX-induced synaptic scaling in cultured visual cortical

250 dditionally, we show for the first time that TTX-resistant (TTX-R) VGSCs (Nav1.5) potentiate VEGF-ind

251 The TTX level in the muscle of female fish in winter was 2.8

252 The TTX- and Cs(+)-resistant background Na(+) leak current i

253 The TTX-increased frequency was blunted by 2-AG or JZL184 an

254 The TTX-R resurgent currents are similar to classic TTX-S re

255 osure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not

256 gonist SSR 180711 (3.0 mg/kg) eliminated the TTX-induced performance deficits.

257 mands showed that D623N channels enhance the TTX-sensitive inward current, persistent at subthreshold

258 Moreover, mRNA and immunoreactivity for the TTX-R VGSC molecules Na(V)1.8 and Na(V)1.9 were present

259 However, the TTX-R resurgent currents exhibit much slower kinetics, o

260 reby eliminating a ganglion cell role in the TTX effects.

261 b) increased: (i) 140 kDa VE-cadherin in the TTX-insoluble fraction, (ii) VE-cadherin intensity at AJ

262 Mutations in the TTX-sensitive voltage-gated sodium channel subtype Nav1.

263 ast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel.

264 ilities, but the molecular identities of the TTX- and Cs(+)-resistant Na(+) leak conductance are tota

265 ansporter substrate d-aspartate reversed the TTX-induced increase in the percentage of mobile mitocho

266 drial Na(+) influx and is tuned to sense the TTX-sensitive cytosolic Na(+) responses.

267 rating conditioning flash indicated that the TTX effects were primarily on cone circuits contributing

268 ined data supporting the hypothesis that the TTX-R sodium currents are similarly distributed between

269 nel Nav1.6 is the major contributor to these TTX-S resurgent currents.

270 rons were rescued by the addition of 4-AP to TTX, and decreased when presynaptic firing in Cajal-Retz

271 nsitivity of invertebrate sodium channels to TTX remains poor, in part because of limited success in

272 experiments in which slices were exposed to TTX plus PGE2 suggest that the two substances evoke dist

273 Exposure to TTX hyperpolarized resting potential by 7mV, increased c

274 Tonic vasodilation was insensitive to TTX, as well as a variety of synaptic and extrasynaptic

275 on potential dependent, being insensitive to TTX, but is abolished by the L-type Ca(2+) channel block

276 neurons in vitro fail to respond normally to TTX treatment by scaling up synaptic parameters.

277 contrast, >30% of the C-CAP was resistant to TTX in distal peripheral branches of monkeys and WT and

278 Eastern Hog-nosed Snakes are so resistant to TTX that the potential for current reciprocal selection

279 es within newt range are highly resistant to TTX.

280 resting sodium conductance not sensitive to TTX.

281 We found that ultrasound triggers TTX-sensitive neuronal activity in the absence of a rise

282 hat NaV1.8 is the primary isoform underlying TTX-r conduction in distal axons of somatosensory C-fibe

283 e generated by the same mechanism underlying TTX-S resurgent currents.

284 rs in both the ON and OFF pathways, and used TTX-sensitive sodium channels to boost signal transfer a

285 The hyperpolarisation was TTX-resistant and was accompanied by decreased input res

286 Whereas TTX-R sodium currents have been documented in lung vagal

287 To test whether TTX is attracted to Tyr401 of NaV1.4 through a cation-pi

288 As with TTX-S resurgent currents, they are activated by membrane

289 ockade of voltage-gated sodium channels with TTX and reverse (Ca(2+)-importing) mode of the sodium-ca

290 a growing number of foods contaminated with TTX and a larger number of waters and associated countri

291 ric Wnt/beta-catenin pathway cooperates with TTX-3 to directly restrict ceh-10 expression to only one

292 Inhibition of Na(+) currents with TTX reduced glucose-stimulated (6-20 mmol/l) insulin sec

293 take, or reversed-Na(+)/Ca(2+)-exchange with TTX, TFB-TBOA, or YM-244769, respectively, increases mit

294 ctivation (with NMDA) and inactivation (with TTX) of the ilPFC and plPFC on dopamine neuron activity,

295 age and region-specific as rats infused with TTX into the VH at PD32, or into the dorsal hippocampus

296 synaptic terminals, whereas inhibition with TTX blocked AbetaO synaptic localization and reduced Abe

297 interspike voltages from -70 to -50 mV, with TTX-sensitive current larger at voltages positive to -45

298 e silenced cultured hippocampal neurons with TTX at 7 days in vitro, during rapid synaptogenesis, and

299 replaced by N-methyl-D-glucamine (NMDG) with TTX present, cells hyperpolarized by an average of -11 m

300 revealed by NMDG replacement for sodium with TTX present.