ライフサイエンスコーパス: tetrodotoxin

1 terminals after blocking Na(+) channels with tetrodotoxin.

2 on and hyperpolarization that was blocked by tetrodotoxin.

3 the pore and therefore did not interact with tetrodotoxin.

4 d these transcripts from being suppressed by tetrodotoxin.

5 re up-regulated by KCl and down-regulated by tetrodotoxin.

6 ons known to increase Na(v)1.4 resistance to tetrodotoxin.

7 or monocular retinal inactivation (MI) with tetrodotoxin.

8 ich was blocked by the addition of 1 mumol/L tetrodotoxin.

9 triggered by nsPEF, even in the presence of tetrodotoxin.

10 miniature IPSCs recorded in the presence of tetrodotoxin.

11 d by preventing action potential firing with tetrodotoxin.

12 (+) current, as they were rapidly blocked by tetrodotoxin.

13 features in common with the complex alkaloid tetrodotoxin.

14 ial INaP after blocking endogenous INaP with tetrodotoxin.

15 8 h silencing with the Na(+) channel blocker tetrodotoxin.

16 in cortical slices electrically silenced by tetrodotoxin.

17 This latter effect was prevented by tetrodotoxin.

18 s characterized by their high sensitivity to tetrodotoxin.

19 Ca(2+) homeostasis were prevented by 100 nM tetrodotoxin.

20 voltage-gated sodium (Na(V)) channel blocker tetrodotoxin.

21 of STX and an allied guanidinium derivative, tetrodotoxin.

22 in Ca2+ homeostasis were prevented by 100 nm tetrodotoxin.

23 als and IPSPs that remain in the presence of tetrodotoxin.

24 ity to the highly selective 4D-Na(v) blocker tetrodotoxin.

25 pathway to the dioxaadamantane core of (+/-)-tetrodotoxin.

26 oride (100 microM, an antagonist for ASICs), tetrodotoxin (0.5 microM, a sodium channel blocker), cad

27 ellular responses to DHPG were unaffected by tetrodotoxin (0.5-1 mum) or perfusion with low Ca(2+)(0.

28 The remaining responses were abolished by tetrodotoxin (1 microM).

29 Tetrodotoxin (1 micromol/L) also reduced cardiac contrac

30 (+) current inhibitors Ran (5 micromol/L) or tetrodotoxin (1 micromol/L).

31 Tetrodotoxin (1 muM) caused a significant depolarization

32 This effect can be reversed by tetrodotoxin (1 muM) or PD184352 (2 muM) treatment, furt

33 g vs. Old mice (P 0.05) and was inhibited by tetrodotoxin (1 mum).

34 l pharmacological inhibition of the NAc with tetrodotoxin (1 mum; 0.5 mul/side) abolished the prefere

35 Tetrodotoxin (1 mumol/L) and ranolazine significantly at

36 n was eliminated by blocking Na(V) channels (tetrodotoxin, 1 mum), persistent Na(+) current (I (NaP);

37 t did not stop the spontaneous activity, and tetrodotoxin (10 microM), to block Na+ channels, had lit

38 Ds that were suppressed by the I(Na) blocker tetrodotoxin (10 micromol/L), as well as the I(Ca,L) blo

39 Low concentrations of tetrodotoxin (200 nmol/L) abolished the effect of BjIP o

40 In additon, in the presence of tetrodotoxin, (2R,6R)-HNK increased the frequency, but n

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

42 ockade of excitatory neurotransmission using tetrodotoxin, 6-cyano-7-nitroquinoxaline-2,3-dione, or 2

43 muOR because endocytosis was not affected by tetrodotoxin, a blocker of endogenous neurotransmitter r

44 t evoked rapid increases in acetycholine and tetrodotoxin, a blocker of Na(+) channels, that lowered

45 Tetrodotoxin, a potent neurotoxin that blocks action pot

46 Local perfusion of tetrodotoxin, a sodium channel blocker, into the striatu

47 vernight silencing of synaptic activity with tetrodotoxin, a treatment that allows progression of arr

48 nal weeks) were not completely eliminated by tetrodotoxin--a drug that blocks action potential firing

49 In the presence of tetrodotoxin, Abeta(1-42) at 100 nM evoked the release o

50 Tetrodotoxin abolished the inward current, suggesting th

51 mechanisms: (1) pore obstruction mediated by tetrodotoxin and (2) altered inactivation dynamics media

52 The vasodilatation was inhibited by 1 mum tetrodotoxin and 5 mum guanethidine, although not by the

53 ions were blocked by the Na+ channel blocker tetrodotoxin and a Ca2+ channel mutation but could be mi

54 fested as inward currents in the presence of tetrodotoxin and bicuculline methobromide.

55 manipulated by blocking native channels with tetrodotoxin and by creating virtual channels and anti-c

56 OS S1412 phosphorylation that was blocked by tetrodotoxin and by inhibitors of the protein kinase Akt

57 that in vivo, and the effect was blocked by tetrodotoxin and CNQX.

58 uide, Lorentz et al. discuss the function of tetrodotoxin and its distribution in the animal kingdom.

59 Tetrodotoxin and KB-R7943 increased the repetition thres

60 n-induced miniature EPSCs in the presence of tetrodotoxin and omega-conotoxin-MVIIC, consistent with

61 orted effects of experimental application of tetrodotoxin and riluzole in respiratory circuits are di

62 imal nerves or dorsal roots, is resistant to tetrodotoxin and that, in mice, this effect is mediated

63 Oxidation currents were reduced by tetrodotoxin and were blocked in calcium-free solutions.

64 eous action potentials that are abolished by tetrodotoxin, and all display spontaneous excitatory pos

65 letely blocked by NMDA receptor antagonists, tetrodotoxin, and calcium chelator BAPTA-AM.

66 uency and was diminished by the neurotoxins, tetrodotoxin, and omega-conotoxin GVIA.

67 g-accepted view that the 1.7 isoform is both tetrodotoxin- and saxitoxin-sensitive and identify the o

68 However, the Na(v) channel-inhibitor tetrodotoxin antagonized hBD-2 mechanisms, but not those

69 ne potential was detected in the presence of tetrodotoxin, AP5, CNQX and bicuculline, supporting an i

70 he H(2)O(2)-induced current was inhibited by tetrodotoxin as well as the cation channel blockers, 9-p

71 e-gated Na(+) current (I(Na)) amplitude, and tetrodotoxin, at doses that reduced I(Na) as moderately

72 We found that inactivation of mPFC by tetrodotoxin attenuates the ability of the vSub to drive

73 The arms race between tetrodotoxin-bearing Pacific newts (Taricha) and their g

74 as its capacity to interfere with subsequent tetrodotoxin binding, greatly expands its scope as a rea

75 Key tetrodotoxin-binding residues are outer carboxylates in

76 We analyzed it by using experimental data on tetrodotoxin block of sodium channels.

77 ): (1) ipRGC signaling to DACs is blocked by tetrodotoxin both in vitro and in vivo, indicating that

78 mediated depolarization was not blocked with tetrodotoxin but was significantly reduced by replacemen

79 These EADs were abolished by caffeine and tetrodotoxin (but not ranolazine), suggesting that sarco

80 blockade of spontaneous retinal activity by tetrodotoxin, but not visual deprivation, retarded synap

81 esponse that is blocked by actinomycin D and tetrodotoxin, by inhibitors of ionotropic glutamate rece

82 allowed building of a NavAb-based model with tetrodotoxin-channel contacts similar to those proposed

83 neous IPSCs and miniature IPSCs (recorded in tetrodotoxin) confirmed that layer II stellate cell hype

84 ACSF or the selective Na(v) channel blocker tetrodotoxin consistently depolarized action potential t

85 at the mouse neuromuscular junction, using a tetrodotoxin cuff in vivo, increased synaptic strength b

86 versely, suppression of neuronal activity by tetrodotoxin decreased APP endocytosis and insertion.

87 are mediated in part by neuronal activity as tetrodotoxin decreases the oscillations and cortical neu

88 Blocking spike-mediated communication with tetrodotoxin did not disrupt overall Per1::GFP induction

89 t2 abolished this effect, but application of tetrodotoxin did not, indicating that the SST effect is

90 ivity in PdN6 with sodium-free saline and/or tetrodotoxin disrupted the motor pattern in a reversible

91 Blockade of neuronal depolarisation by tetrodotoxin during preconditioning attenuated but did n

92 Tetrodotoxin eliminated the majority of events, indicati

93 Upon TTX (tetrodotoxin) exposure, mitochondria near Na(V)1.5 chann

94 lcium-free extracellular medium and in 1 muM tetrodotoxin, findings suggesting that the oscillations

95 physiological resistance of garter snakes to tetrodotoxin found in their newt (Taricha) prey.

96 1 mmol/l glucose was inhibited by 40-70% by tetrodotoxin, heteropodatoxin-2, stromatoxin, omega-agat

97 d dimethyl sulfide in marine communities and tetrodotoxin in riparian communities.

98 ombination was maintained in the presence of tetrodotoxin in spinal cord slices suggests that synergy

99 volution of resistance to the lethal poison, tetrodotoxin, in six snake species representing three di

100 tion of glomerular mAChRs in the presence of tetrodotoxin increased IPSCs in all glomerular neurons,

101 tion persists in the presence of gabazine or tetrodotoxin, indicating a direct action.

102 tic currents, and are blocked by gabazine or tetrodotoxin, indicating an indirect action.

103 mitter release induced by NGF was blocked by tetrodotoxin, indicating neuronal origin of this respons

104 or 3 d, but not by long-term incubation with tetrodotoxin, indicating that spontaneous GABA release d

105 s calcium oscillations were blocked by 1 muM tetrodotoxin, indicating that they are action potential-

106 nexpectedly, ATP secretion is not blocked by tetrodotoxin, indicating that transmitter release from t

107 , prolonged blockade of sodium channels with tetrodotoxin induced homeostatic synaptic scaling in wil

108 ynapse density, accompanied by a decrease in tetrodotoxin induced spine plasticity.

109 utamatergic signals were highly sensitive to tetrodotoxin-induced blockade of voltage-regulated sodiu

110 importantly, KN-62 significantly suppressed tetrodotoxin-induced contractile response in mouse colon

111 nt for specific AMPAR subunit during chronic tetrodotoxin-induced HSP using hippocampal cultures deri

112 tify Arc as a SUMO substrate involved in the tetrodotoxin-induced increase in AMPAR surface expressio

113 down of excitatory synaptic strength or the tetrodotoxin-induced scaling down of inhibitory synaptic

114 the blockade of action potentials (APs) with tetrodotoxin inhibited the activity of the proteasome, w

115 also converted our previous racemic route to tetrodotoxin into an enantioselective one.

116 ced by chronic application of bicuculline or tetrodotoxin is both mimicked and occluded by altered Rp

117 emic diene intermediate for the synthesis of tetrodotoxin is described.

118 hanged by inhibition of synaptic activity by tetrodotoxin, it increased in dendritic synapses and dec

119 Focal application of tetrodotoxin localized the spike initiation zone to the

120 Based on muscimol and tetrodotoxin microinfusions, these glutamate transients

121 In the tetrodotoxin model, we used 16-channel microarrays and m

122 as neither blocking the sodium channels with tetrodotoxin nor NMDA receptors with dl-APV altered the

123 5, and led to neuronal death under long-term tetrodotoxin or AP5 treatment in rat hippocampal organot

124 ing synaptic transmission in the NAcore with tetrodotoxin or by inhibiting glutamatergic afferents to

125 scimol was eliminated in a medium containing tetrodotoxin or cadmium.

126 otential were inhibited pharmacologically by tetrodotoxin or genetically by small interfering RNAs (s

127 Trpa1(-/-) mice; this effect was reduced by tetrodotoxin or N(G)-nitro-l-arginine methyl ester.

128 enteric neurons, and release was blocked by tetrodotoxin or omega-conotoxin GVIA.

129 f intracellular calcium, but were blocked by tetrodotoxin, ouabain, or the removal of extracellular p

130 high-affinity block by the guanidinium toxin tetrodotoxin, primarily due to an electrostatic attracti

131 Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed

132 ated sodium currents, inhibition of which by tetrodotoxin reduced both basal and glutamine-stimulated

133 EPSCs were eliminated by tetrodotoxin, reinstated by 4-aminopyridine, and blocked

134 nitude of tetrodotoxin-sensitive relative to tetrodotoxin -resistant whole cell current.

135 beta2 on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) Na(v)1 in vivo.

136 The toxin did not act on tetrodotoxin-resistant (TTX-r) Na(V)1.8 currents; discri

137 the new mu-conotoxins were likely to target tetrodotoxin-resistant (TTX-r) sodium channels.

138 Persistent tetrodotoxin-resistant (TTX-r) sodium currents up-regula

139 the somatosensory system indicated that the tetrodotoxin-resistant (TTX-R) voltage-gated sodium chan

140 Nav1.8 (also known as PN3) is a tetrodotoxin-resistant (TTx-r) voltage-gated sodium chan

141 peripheral nerves and its use dependence in tetrodotoxin-resistant (TTXr) sodium channel (Nav 1.8, N

142 ripheral nerves, and the contribution of the tetrodotoxin-resistant (TTXr) sodium channels Nav 1.8 an

143 In these cells, a tetrodotoxin-resistant background N(+) conductance is cr

144 h in expression of tetrodotoxin-sensitive to tetrodotoxin-resistant channels in reactive astrocytes.

145 sodium channel blocker that potently blocks tetrodotoxin-resistant currents (IC(50) = 140 nM) and th

146 t combinations of tetrodotoxin sensitive and tetrodotoxin-resistant Na(+) channels that underlie the

147 mouse myenteric neurons exhibit two types of tetrodotoxin-resistant Na(+) currents: an early inactiva

148 Nav1.8 is a tetrodotoxin-resistant sodium channel present in large s

149 Activation of tetrodotoxin-resistant sodium channels contributes to ac

150 part, from the capacity of BDNF to enhance a tetrodotoxin-resistant sodium current (TTX-R I(Na)) and

151 H attenuated PGE(2)-induced sensitization of tetrodotoxin-resistant sodium current, in small-diameter

152 1.9-/- mice, the non-inactivating persistent tetrodotoxin-resistant sodium TTXr-Per current is absent

153 r previously described [i.e., an increase in tetrodotoxin-resistant voltage-gated Na(+) current (TTX-

154 Increased peripheral expression of tetrodotoxin-resistant voltage-gated sodium channel 1.8

155 rs by relieving resting slow inactivation of tetrodotoxin-resistant voltage-gated sodium channels and

156 in three minutes) increased the frequency of tetrodotoxin-resistant, miniature IPSCs (mIPSCs) in 67%

157 imately 80% reduction in peak density of the tetrodotoxin-resistant, voltage-gated sodium current I(N

158 prevented by tetraethylammonium chloride and tetrodotoxin, respectively.

159 ing neurogenic activity with veratridine and tetrodotoxin, respectively.

160 D/+) CA1 hippocampal neurons were blocked by tetrodotoxin, riluzole, and SN-6, implicating elevated p

161 cn8a(medtg) mice that lack Na(v)1.6, reduces tetrodotoxin-S sodium currents, suggesting isoform-speci

162 glion (DRG) express distinct combinations of tetrodotoxin sensitive and tetrodotoxin-resistant Na(+)

163 These currents were tetrodotoxin sensitive but resistant to MTSEA, a specifi

164 e dorsal root ganglion (DRG) neurons express tetrodotoxin-sensitive (TTX-S) and -resistant (TTX-R) Na

165 vided the first detailed characterization of tetrodotoxin-sensitive (TTX-S) and resistant (TTX-R) sod

166 physiological examination of fluphenazine at tetrodotoxin-sensitive (TTX-S) and resistant (TTX-R) vol

167 /- mice to determine the effects of beta2 on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistan

168 (V)1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na(+) channel expression.

169 Tetrodotoxin-sensitive (TTX-S) resurgent currents have b

170 sion of Na(V)1.2 in HEK-293 cells revealed a tetrodotoxin-sensitive [Ca(2+)](i) rise.

171 These inputs depended on tetrodotoxin-sensitive action potentials, had kinetics t

172 and glial driven responses consisted of both tetrodotoxin-sensitive and -insensitive components.

173 ignificant increase in the peak amplitude of tetrodotoxin-sensitive and resistant sodium currents.

174 The AfD is well explained by a tetrodotoxin-sensitive and voltage-dependent Na(+) persi

175 Electrical stimulation of the colon evoked a tetrodotoxin-sensitive chloride secretion.

176 sic outward current, with an early transient tetrodotoxin-sensitive component followed by a slowly ac

177 y increases density and shifts activation of tetrodotoxin-sensitive currents in a hyperpolarized dire

178 juvenile null animals resulted in increased tetrodotoxin-sensitive INa but only in the cell midsecti

179 juvenile null animals resulted in increased tetrodotoxin-sensitive INa but only in the cell midsecti

180 among other effects, increased amplitude of tetrodotoxin-sensitive INa, delayed after-depolarization

181 The amplitude of the tetrodotoxin-sensitive INaL was 0.1709 +/- 0.0299 pA pF(

182 The amplitude of the tetrodotoxin-sensitive INaL was 0.1709 +/- 0.0299 pA pF-

183 ded lidocaine inhibition of voltage-clamped, tetrodotoxin-sensitive Na currents in mouse Purkinje neu

184 -channel block, we recorded voltage-clamped, tetrodotoxin-sensitive Na currents in Purkinje and nucle

185 epends on K(ATP) channel activity but not on tetrodotoxin-sensitive Na(+) channels.

186 Interestingly, tetrodotoxin-sensitive Na(+) currents and 1,3-benzenedic

187 Tetrodotoxin-sensitive Na(+) currents have been extensiv

188 -sensitive delayed rectifying K(+)-channels, tetrodotoxin-sensitive Na(+)-currents, and low-threshold

189 cn3a mRNA, suggesting increased abundance of tetrodotoxin-sensitive NaV 1.3 protein and yet its exclu

190 cn3a mRNA, suggesting increased abundance of tetrodotoxin-sensitive NaV1.3 protein and yet its exclus

191 riments suggest that selective activation of tetrodotoxin-sensitive neuronal sodium channels can safe

192 tial and produced a hyperpolarizing shift of tetrodotoxin-sensitive persistent voltage-gated sodium c

193 mata showing a reduction in the magnitude of tetrodotoxin-sensitive relative to tetrodotoxin -resista

194 oot ganglion (DRG) neurons revealed enhanced tetrodotoxin-sensitive resurgent and persistent current

195 ntifies a previously unknown requirement for tetrodotoxin-sensitive sodium channels in action potenti

196 lack Judean scorpion that activates neuronal tetrodotoxin-sensitive sodium channels.

197 direct application of estradiol modulated a tetrodotoxin-sensitive sodium current in isolated GnRH n

198 ene expression coincided with a reduction in tetrodotoxin-sensitive sodium current, a requirement for

199 namic manner, with a switch in expression of tetrodotoxin-sensitive to tetrodotoxin-resistant channel

200 In these neurons, the tetrodotoxin-sensitive voltage-gated Na(+) channels resp

201 The Na(V)1.7 tetrodotoxin-sensitive voltage-gated sodium channel isof

202 pecific antigens revealed voltage-dependent, tetrodotoxin-sensitive, inward Na+ currents and voltage-

203 calcium release in the mutant myocytes were tetrodotoxin-sensitive.

204 and this action persisted in the presence of tetrodotoxin, suggesting a postsynaptic site of action.

205 t CGP 52432 but persisted in the presence of tetrodotoxin, suggesting direct postsynaptic effects.

206 e- 3-carboxamide], a CB1R antagonist, and by tetrodotoxin, suggesting no postsynaptic effect on eithe

207 Release of Up4A was reduced by tetrodotoxin, suggesting that at least a portion of Up4A

208 CH neurons was eliminated by bicuculline and tetrodotoxin, suggesting that the effect was mediated in

209 Although tetrodotoxin, TFB-TBOA, or YM-244769 increased Ca(2+) si

210 tor, (2) an alpha7 nAChR antagonist, and (3) tetrodotoxin to block action potential firing.

211 Furthermore, experiments using tetrodotoxin to block action potentials revealed that GA

212 treating myotube cultures with potassium or tetrodotoxin to block contraction and disrupt myofibril

213 Second, exposure to 10 mum tetrodotoxin to block I(Na) also reduced the Ca(2+) tran

214 In SCN explants treated with tetrodotoxin to block spike-dependent signaling, neurons

215 tact Casq2-/- cardiomyocytes pretreated with tetrodotoxin to inhibit sodium channels and isolate the

216 dark exposure and retinal inactivation with tetrodotoxin to promote anatomical recovery in the dorsa

217 s that were treated with either glutamate or tetrodotoxin to stimulate an increase or decrease in neu

218 ions at three sets of excitatory synapses in tetrodotoxin-treated organotypic hippocampal cultures.

219 Chronic tetrodotoxin treatment greatly reduced the percentage of

220 In the presence of tetrodotoxin, TRH induced inward currents that were asso

221 Effects on EPSCs were blocked with tetrodotoxin (TTX) (1 microM), but not by methyllycaconi

222 The voltage-gated Na+ channel blocker tetrodotoxin (TTX) abolished the effects of SKF81297 on

223 ucing spontaneous firing activity with 10 nM tetrodotoxin (TTX) abolished the protective effect of NT

224 Potent neurotoxins like tetrodotoxin (TTX) and saxitoxin (STX) that are highly t

225 Finally, we show that local tetrodotoxin (TTX) application to the soma blocked LTP i

226 Site 1 sodium channel blockers such as tetrodotoxin (TTX) are extremely potent, and can provide

227 This study investigated the effects of tetrodotoxin (TTX) blockade of Na(v) channels on the b-w

228 we report that chronic blockade of firing by tetrodotoxin (TTX) for two days resulted in increases bo

229 m conjunctivum (BC) with small injections of tetrodotoxin (TTX) has been reported to have no effect o

230 were upregulated by KCl and downregulated by tetrodotoxin (TTX) in cultured primary neurons.

231 Pharmacologic antagonism with tetrodotoxin (TTX) in differentiated THP-1 cells or abse

232 n reversibly alter the inhibitory effects of tetrodotoxin (TTX) in pharmacological studies.

233 The toxicity of tetrodotoxin (TTX) in pufferfish (Lagocephalus sceleratu

234 o is completely blocked by a 2 h exposure to tetrodotoxin (TTX) in the culture medium, and this TTX i

235 Inhibiting neuronal activity with tetrodotoxin (TTX) increased the percentage of mobile mi

236 y an injection of the sodium channel blocker tetrodotoxin (TTX) into the MCP.

237 Tetrodotoxin (TTX) is a key chemical defense trait in No

238 Tetrodotoxin (TTX) is a potent blocker of voltage-gated

239 Tetrodotoxin (TTX) is one of the most potent marine neur

240 component because the sodium channel blocker tetrodotoxin (TTX) is typically used in such studies.

241 toxic newt prey exhibiting hotspots of newt tetrodotoxin (TTX) levels and matching snake TTX resista

242 ing the effect of the sodium channel blocker tetrodotoxin (TTX) on depolarizations generated by two-p

243 Na currents were decreased by tetrodotoxin (TTX) or increased by beta-pompilidotoxin (

244 uppression of activity by the application of tetrodotoxin (TTX) reduced mIPSC amplitudes and the leve

245 Convergent evolution of tetrodotoxin (TTX) resistance, at both the phenotypic an

246 Tetrodotoxin (TTX) stopped spontaneous activity and usua

247 xposed cultured slices of mouse neocortex to tetrodotoxin (TTX) to block SSA, which normally occurs b

248 Rough-skinned newts (Taricha granulosa) use tetrodotoxin (TTX) to block voltage-gated sodium (Na(v))

249 Comparison of PSCs before and during tetrodotoxin (TTX) treatment showed TTX decreased PSC fr

250 In the first experiment, tetrodotoxin (TTX) was used to chemically inactivate the

251 -treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast N

252 ved a single bilateral infusion of saline or tetrodotoxin (TTX) within the VH to transiently inactiva

253 In the presence of tetrodotoxin (TTX), 8-Br-cGMP decreased the exogenous po

254 Newts are defended by tetrodotoxin (TTX), a neurotoxin that binds to voltage-g

255 Tetrodotoxin (TTX), a small molecular weight neurotoxin,

256 Previously, we demonstrated that tetrodotoxin (TTX), a sodium channel blocker that tempor

257 Furthermore, after incubation with tetrodotoxin (TTX), a sodium channel blocker, there was

258 We found that tetrodotoxin (TTX), an inhibitor of nitric oxide (NO) sy

259 , 1.6, and 1.7, are exquisitely sensitive to tetrodotoxin (TTX), and a functional differentiation of

260 One such toxin, tetrodotoxin (TTX), blocks sodium channels with nanomola

261 Tetrodotoxin (TTX), but not postsynaptic receptor blocka

262 One such adaptation, extreme resistance to tetrodotoxin (TTX), has arisen in several species of sna

263 trations, in the presence of bicuculline and tetrodotoxin (TTX), increased the frequency but did not

264 All APs were sensitive to tetrodotoxin (TTX), indicating that they were driven by

265 When action potentials were inhibited by tetrodotoxin (TTX), inhibitory postsynaptic currents dec

266 cochlea removal or temporary treatment with tetrodotoxin (TTX), leads to rapid and significant retra

267 response in oligodendrocytes was blocked by tetrodotoxin (TTX), much of the NAAG-evoked current in o

268 Tetrodotoxin (TTX), one of the most toxic substances in

269 of the voltage-gated sodium channel blocker, tetrodotoxin (TTX), the metabotropic glutamate receptor

270 The liposomes contained tetrodotoxin (TTX), which has ultrapotent local anesthet

271 ng the tibialis anterior muscle in rats with tetrodotoxin (TTX)-administered to the common peroneal n

272 imaging, electrophysiological analysis with tetrodotoxin (TTX)-dependent block of the Na(+) channel,

273 Na channels in the heart are composed of the tetrodotoxin (TTX)-resistant (KD, 2 to 6 micromol/L) "ca

274 Because tetrodotoxin (TTX)-resistant Na+ channels are a critical

275 es previously characterized as inhibitors of tetrodotoxin (TTX)-resistant sodium channels in amphibia

276 l properties of human nociceptors, including tetrodotoxin (TTX)-resistant, SCN10A-dependent sodium cu

277 mammals are often functionally divided into tetrodotoxin (TTX)-sensitive (TTX-s) channels (NaV1.1-Na

278 s, with a modest contribution (~10-15%) from tetrodotoxin (TTX)-sensitive and TTX-resistant sodium ch

279 cell, the ground squirrel cb5b, has a large tetrodotoxin (TTX)-sensitive Na(+) current.

280 Voltage-gated tetrodotoxin (TTX)-sensitive Na(+) currents (Na(V)1.6/1.

281 ybridization showed similar distributions of tetrodotoxin (TTX)-sensitive Na(V) transcripts between T

282 Tetrodotoxin (TTX)-sensitive sodium channels carry large

283 Differentiated cells exhibited robust tetrodotoxin (TTX)-sensitive sodium currents, and acute

284 hronic (60 h) network-activity blockade with tetrodotoxin (TTX).

285 e channels were functional and suppressed by tetrodotoxin (TTX).

286 /90 MSNs, which persisted in the presence of tetrodotoxin (TTX).

287 hmic oscillatory activity in the presence of tetrodotoxin (TTX).

288 ing during prolonged activity blockade [24 h tetrodotoxin (TTX)] was prevented by blocking TNFalpha s

289 Tetrodotoxin (TTX, 0.3 microM), a voltage-dependent sodi

290 pic slices of activity by treating them with tetrodotoxin (TTX, 1 mum; 48 h).

291 ade of Na(+)-dependent spiking activity with tetrodotoxin (TTX, 1 to 2 muM, n = 3), blockade of ionot

292 quiescent between CMMCs, exhibited prolonged tetrodotoxin (TTX; 1 mum)-sensitive Ca(2+) transients th

293 aP) with multiple Na(+) channel antagonists: tetrodotoxin (TTX; 20 nM), riluzole (RIL; 10 microM), an

294 ocked by low nanomolar concentrations of (-)-tetrodotoxin(TTX) but not (+)-saxitoxin (STX) and (+)-go

295 eloped and applied to the rapid screening of tetrodotoxins (TTXs), potent neurotoxins that constitute

296 n all experiments the sodium channel blocker tetrodotoxin was used to prevent indirect neuronal activ

297 erpolarisations persisted in the presence of tetrodotoxin, were mimicked by 5-HT(2C) receptor agonist

298 ow that suppression of network activity with tetrodotoxin, which increases surface expression of AMPA

299 effective block of INaP by low concentration tetrodotoxin will stop respiratory rhythm generation in

300 opic glutamate receptor (iGluR) antagonists, tetrodotoxin, ziconotide (Ca(2+) channel blocker), two i