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 at 100 nm, which selectively blocks neuronal isoform

3 TTX concentration within poison glands is related to the

4 TTX did not eliminate the effects of PAR1 activation on

5 TTX did not eliminate the synergistic response of the ag

6 TTX infusions did not affect the initial acquisition or

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

8 TTX injected in the stimulated eye drastically reduced t

9 TTX nearly abolished the expression of maternal retrieva

10 TTX reduced PERG amplitude to less than half; simulation

11 TTX release can be adjusted by tuning the hydrophilicity

12 TTX was detected in mucous glands in both populations, c

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

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

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

16 TTX-sensitive sodium current was substantial throughout

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

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

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

20 e species of newts appear to be engaged in a TTX-mediated arms race with Th. couchii.

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

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

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

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

25 Nav1.6 channels, vincristine failed to alter TTX-S Na+ current density in medium dorsal root ganglion

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

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

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

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

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

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

41 0-15%) from tetrodotoxin (TTX)-sensitive and TTX-resistant sodium channels and hyperpolarization-acti

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

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

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

45 Marine organisms seem to bioaccumulate TTX from their food or acquire it from symbiotic bacteri

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

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

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

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

50 d neurite degeneration was not attenuated by TTX.

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

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

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

54 on on outflow facility and IOP is blocked by TTX.

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

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

57 hrough extracellular matrix was inhibited by TTX.

58 for the observed resistance to inhibition by TTX.

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

60 ated eye only and were moderately reduced by TTX.

61 ed these transcripts that were suppressed by TTX.

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

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

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

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

66 Some of the tissues contained TTX contents close to or above 2 mg/kg.

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

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

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

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

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

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

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

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

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

76 however, Na(V)1.8 transcripts, which encode TTX-resistant channels, were more prevalent in TRPM8-neg

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

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

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

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

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

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

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

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

85 using two-photon Ca(2+) photometry and focal TTX application.

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

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

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

89 We then screened bacterial culture media for TTX using LC-MS/MS and identified TTX-producing bacteria

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

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

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

93 lity of low-cost and user-friendly tools for TTXs detection will contribute to guarantee seafood safe

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

95 arms race induces variation in T. granulosa TTX levels, from very high to undetectable.

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

97 Taricha granulosa can exhibit high TTX levels, presumably concentrated in skin poison gland

98 knowledge, this is the first report of high TTX levels in small L. sceleratus individuals.

99 stance at the northern latitudes, and higher TTX levels and snake resistance at southern latitudes.

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

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

102 media for TTX using LC-MS/MS and identified TTX-producing bacterial strains from four genera, includ

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

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

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

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

107 The increase in TTX-S Na+ current density is likely mediated by Nav1.6,

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

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

110 emonstrate that interpopulation variation in TTX levels is related to poison gland morphology.

111 impair inactivation, significantly increase TTX-resistant resurgent sodium currents mediated by Nav1

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

116 newts expressed Na(v) channels with modified TTX binding sites, conferring extreme physiological resi

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 reduced GFP levels in interneurons, suggesting that

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

121 wide range of voltage-gated ion channels: Na(TTXs), Na(TTXr), Na(p), K(dr), K(M), K(A), and HCN chann

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

123 nificantly among localities, with lower newt TTX levels and snake TTX resistance at the northern lati

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

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

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

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

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

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

130 rats were killed and corneal application of TTX though ICP remained elevated.

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

132 data demonstrate that open-channel block of TTX-resistant currents, enhanced by gain-of-function mut

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

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

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

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

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

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

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

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

141 zbromarone and Ani9 inhibited the effects of TTX, L-NNA and ODQ.

142 blocker (GSK 7975 A) reversed the effects of TTX, L-NNA and ODQ.

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

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

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

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

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

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

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

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

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

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

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

154 -HRMS, the latter confirming the presence of TTX.

155 glutamate photo-uncaging in the presence of TTX.

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

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

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

159 ere we report a system where slow release of TTX conjugated to a biocompatible and biodegradable poly

160 esistant predatory snakes, but the source of TTX in newts is unknown.

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

162 In vivo, 1.0-80.0 ug of TTX released from these polymers produced a range of dur

163 imals revealed a significant upregulation of TTX-S Na+ current in medium but not small neurons.

164 This tool revealed the presence of TTXs in both individuals.

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

166 er Vglut3(lineage) neurons rely primarily on TTX-resistant Na(V) channels.

167 ncy was prevented by bath-applied EGTA-AM or TTX.

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

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

172 thermore, after recovery of muscle mass post TTX-induced atrophy in rats, UBR5 was hypomethylated and

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

174 eria isolated from toxic newts could produce TTX.

175 conditions while longitudinally quantifying TTX concentrations.

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

177 ntly alter T790A current density but reduces TTX-resistant resurgent currents by 56%.

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

179 Nerve block by the released TTX is enhanced by administration in a carrier with chem

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

181 etrodotoxin-sensitive (TTX-S) and resistant (TTX-R) sodium currents in dorsal root ganglion neurons f

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

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

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

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

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

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

188 characterization of tetrodotoxin-sensitive (TTX-S) and resistant (TTX-R) sodium currents in dorsal r

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

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

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

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

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

194 lities, with lower newt TTX levels and snake TTX resistance at the northern latitudes, and higher TTX

195 tetrodotoxin (TTX) levels and matching snake TTX resistance.

196 mmunoassay for a seafood toxin, specifically TTX.

197 gly, this arachnid channel showed surprising TTX resistance.

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

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

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

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

202 Tetrodotoxin (TTX), one of the most toxic substances in nature, is pre

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

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

205 odium channel blockers such as tetrodotoxin (TTX) are extremely potent, and can provide very long ner

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

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

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

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

210 Newts are defended by tetrodotoxin (TTX), a neurotoxin that binds to voltage-gated sodium ch

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

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

213 e functional and suppressed by tetrodotoxin (TTX).

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

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

216 st contribution (~10-15%) from tetrodotoxin (TTX)-sensitive and TTX-resistant sodium channels and hyp

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

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

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

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

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

222 ey exhibiting hotspots of newt tetrodotoxin (TTX) levels and matching snake TTX resistance.

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

224 lter the inhibitory effects of tetrodotoxin (TTX) in pharmacological studies.

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

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

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

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

229 howed similar distributions of tetrodotoxin (TTX)-sensitive Na(V) transcripts between TRPM8-positive

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

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

232 ntiated cells exhibited robust tetrodotoxin (TTX)-sensitive sodium currents, and acute infection sign

233 We found that tetrodotoxin (TTX), an inhibitor of nitric oxide (NO) synthesis, L-NNA

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

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

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

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

238 newts (Taricha granulosa) use tetrodotoxin (TTX) to block voltage-gated sodium (Na(v)) channels as a

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

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

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

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

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

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

245 network-activity blockade with tetrodotoxin (TTX).

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

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

248 ied to the rapid screening of tetrodotoxins (TTXs), potent neurotoxins that constitute a food safety

249 Thus, these data demonstrate that TTX-sensitive Na(V)s drive action potential firing in me

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

251 Ca(2+) imaging revealed that TTX, L-NNA and ODQ increased Ca(2+) transient firing in

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

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

254 Our data show that TTX-S sodium channel Nav1.6 is involved in the functiona

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 nferring extreme physiological resistance to TTX.

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

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

277 ted traits, with some snakes so resistant to TTX they would be unaffected by any sympatric newt.

278 es within newt range are highly resistant to TTX.

279 resting sodium conductance not sensitive to TTX.

280 ncoded protein (Na(v)1.4) less vulnerable 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 Upon TTX (tetrodotoxin) exposure, mitochondria near Na(V)1.5

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

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

287 to the volume of a single cell type in which TTX occurs exclusively in distinctive secretory granules

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

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

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

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

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

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

298 ttributed to a coevolutionary arms race with TTX-resistant predatory snakes, but the source of TTX in

299 revealed by NMDG replacement for sodium with TTX present.

300 independent, persisting after treatment with TTX.