ライフサイエンスコーパス: tetrodotoxin

1 d these transcripts from being suppressed by tetrodotoxin.

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

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

4 or monocular retinal inactivation (MI) with tetrodotoxin.

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

6 miniature IPSCs recorded in the presence of tetrodotoxin.

7 in cortical slices electrically silenced by tetrodotoxin.

8 d by preventing action potential firing with tetrodotoxin.

9 ium channel blocker cadmium and abolished by tetrodotoxin.

10 This latter effect was prevented by tetrodotoxin.

11 and after blockade of neuronal activity with tetrodotoxin.

12 e dependent, being blocked by treatment with tetrodotoxin.

13 tures in which depolarization was blocked by tetrodotoxin.

14 s characterized by their high sensitivity to tetrodotoxin.

15 features in common with the complex alkaloid tetrodotoxin.

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

17 of STX and an allied guanidinium derivative, tetrodotoxin.

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

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

20 ial INaP after blocking endogenous INaP with tetrodotoxin.

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

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

23 8 h silencing with the Na(+) channel blocker tetrodotoxin.

24 on and hyperpolarization that was blocked by tetrodotoxin.

25 the pore and therefore did not interact with 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 tions were blocked by atropine (1 microm) or tetrodotoxin (1 microm).

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

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

32 Tetrodotoxin (1 muM) caused a significant depolarization

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

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

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

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

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

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

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

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

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

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

43 Tetrodotoxin, a potent neurotoxin that blocks action pot

44 of dendritic spines even in the presence of Tetrodotoxin, a sodium channel blocker, indicating that

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

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

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

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

49 Tetrodotoxin abolished the coordination between the CM c

50 Tetrodotoxin abolished the inward current, suggesting th

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

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

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

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

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

56 Tetrodotoxin and KB-R7943 increased the repetition thres

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

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

59 ro studies using neurohumoral inhibitors and tetrodotoxin and the use of SMCs demonstrate direct rela

60 ocess because it was seen in the presence of tetrodotoxin and was blunted by decreasing the temperatu

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

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

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

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

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

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

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

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

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

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

71 Key tetrodotoxin-binding residues are outer carboxylates in

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

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

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

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

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

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

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

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

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

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

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

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

84 al drugs acting on sodium channels displaced tetrodotoxin-dependent [(3)H]BW202W92 binding, and most

85 Tetrodotoxin-dependent binding was stereoselective (the

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

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

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

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

90 m was relatively poor, low concentrations of tetrodotoxin (EC(50) = 2-3 nM) greatly enhanced the bind

91 Tetrodotoxin eliminated the majority of events, indicati

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

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

94 1 mmol/l glucose was inhibited by 40-70% by tetrodotoxin, heteropodatoxin-2, stromatoxin, omega-agat

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

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

97 erve conduction was at least as sensitive to tetrodotoxin in Trembler-J nerves as in wild-type nerves

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

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

100 Experiments performed in tetrodotoxin indicate that the maintenance of a stable d

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 Tetrodotoxin inhibited evoked purinergic Ca2+ transients

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

116 res spontaneous Na+-based action potentials (tetrodotoxin inhibits, (+/-)-2-amino-4-phosphonobutyric

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

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

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

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

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

122 Based on muscimol and tetrodotoxin microinfusions, these glutamate transients

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

124 naptic Ca2+ chelation, low concentrations of tetrodotoxin, omega-conotoxin MVIIC, calcium/calmodulin-

125 5, and led to neuronal death under long-term tetrodotoxin or AP5 treatment in rat hippocampal organot

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

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

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

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

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

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

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

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

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

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

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

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

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

139 The tetrodotoxin-resistant (TTX-r) persistent Na(+) current,

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

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

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

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

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

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

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

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

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

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

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

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

152 Despite the presence of Nav1.8, a tetrodotoxin-resistant sodium channel, sciatic nerve con

153 Activation of tetrodotoxin-resistant sodium channels contributes to ac

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

155 1.9-/- mice, the non-inactivating persistent tetrodotoxin-resistant sodium TTXr-Per current is absent

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

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

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

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

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

161 ing neurogenic activity with veratridine and tetrodotoxin, respectively.

162 prevented by tetraethylammonium chloride and tetrodotoxin, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Burst firing persisted in concentrations of tetrodotoxin that produced half-block of sodium current.

211 In the presence of apamin and tetrodotoxin, the slow AHP was strongly reduced by 5-HT,

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

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

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

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

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

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

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

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

220 Chronic tetrodotoxin treatment greatly reduced the percentage of

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

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

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

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

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

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

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

228 Pretreatment with tetrodotoxin (TTX) for 24-72 h subsequently suppressed p

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

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

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

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

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 a sodium channel blocker that temp

240 The deadly neurotoxin tetrodotoxin (TTX) is found in a variety of animal phyla

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

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

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

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

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

246 Likewise, bath application of tetrodotoxin (TTX) reduced the SNR and contrast sensitiv

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

248 Tetrodotoxin (TTX) stopped spontaneous activity and usua

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

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

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

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

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

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

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

259 ng application of the sodium channel blocker tetrodotoxin (TTX), and in the presence of glutamatergic

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

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

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

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

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

273 sociated bladder afferent neurons exhibiting tetrodotoxin (TTX)-resistant action potentials from NGF-

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 p, dissociated HH cells exhibited functional tetrodotoxin (TTX)-sensitive Na(+) and tetraethylammoniu

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 old, slowly inactivating, voltage-dependent, tetrodotoxin (TTX)-sensitive Na+ current and a TTX-insen

282 Tetrodotoxin (TTX)-sensitive sodium channels carry large

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

284 /90 MSNs, which persisted in the presence of tetrodotoxin (TTX).

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

286 rizing sodium currents that are sensitive to tetrodotoxin (TTX).

287 hronic (60 h) network-activity blockade with 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 as abolished by external Na+ replacement and tetrodotoxin (TTX, 1 microM).

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

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

293 e Na+ current (I(Na)) is highly sensitive to tetrodotoxin (TTX, Kd = 2.2 nM).

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

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

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

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

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

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

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