ライフサイエンスコーパス: tetraethylammonium

1 8)Te(0.22)Hf(0.2)Sn(0.3)Pt(0.1))Cl(6) (TEA = tetraethylammonium).

2 el function with permeability to K+ > Na+ >> tetraethylammonium.

3 expressing cells is insensitive to 25 mmol/L tetraethylammonium.

4 illations, as they are completely blocked by tetraethylammonium.

5 enaline, 50 microM 2-chloroadenosine or 5 mM tetraethylammonium.

6 s partially sensitive to 4-aminopyridine and tetraethylammonium.

7 in, 3,4-diaminopyridine, 4-aminopyridine and tetraethylammonium.

8 ter tension when K+ channels were blocked by tetraethylammonium.

9 sulfonate and alter reversible inhibition by tetraethylammonium.

10 sensitive to the potassium channel inhibitor tetraethylammonium.

11 ficantly lower than a LOD of less lipophilic tetraethylammonium.

12 ions but did not affect plateaus unmasked by tetraethylammonium.

13 otic frequency evoked by bath application of tetraethylammonium (1-10 mM) was significantly enhanced

14 y of SjAQP was inhibited by 1 mM HgCl2, 3 mM tetraethylammonium, 1 mM ZnCl2, and 1 mM CuSO4.

15 Tetraethylammonium 10(-3) mol/L but not glibenclamide 10

16 ntrast, the non-specific K+ channel blockers tetraethylammonium (10 mM) and 4-aminopyridine (10 mM) m

17 The SOR and RD were blocked by external tetraethylammonium (10 mM) and Ba2+ (0.1-0.5 mM).

18 The K+ channel blocker tetraethylammonium (10 mM) generated inward currents sim

19 (5 mM), tetrapentylammonium (10 microM) and tetraethylammonium (10 mM).

20 TRESK-2 was insensitive to 1 mm tetraethylammonium, 100 nm apamin, 1 mm 4-aminopyridine,

21 To assess Oct1 function, the model substrate tetraethylammonium ([(14)C]TEA) was administered intrave

22 ptake of the quaternary organic cation [14C]-tetraethylammonium ([14C]-TEA), with a Km of 38 micromol

23 ne (15% inhibition) and insensitive to 10 mM tetraethylammonium, 2 mM Ca2+, 1 mM Cd2+ and 50 microM L

24 was inhibited by 4-aminopyridine (10 mM) and tetraethylammonium (4-25 mM), but insensitive to charybd

25 f the potassium delayed rectifier current by tetraethylammonium (5 mM) or the hyperpolarization-activ

26 t density and currents that are inhibited by tetraethylammonium (5 mmol/L) or charybdotoxin (100 nmol

27 Tetraethylammonium, a pore blocker, did not affect the r

28 h variants abolished OCT1-mediated uptake of tetraethylammonium, a typical OCT1 substrate, and were n

29 imulated by flufenamic acid and inhibited by tetraethylammonium; a voltage-gated inward Na+ current;

30 ive to 4-aminopyridine but is insensitive to tetraethylammonium, alpha-dendrotoxin, and E-4031.

31 e widely used Kv channel blockers, including tetraethylammonium, alpha-dendrotoxin, phrixotoxin-2, an

32 Treatment with 500 microM tetraethylammonium also decreased the latency to AP gene

33 The K+ channel blocker tetraethylammonium also inhibited oligodendrocyte progen

34 cate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduction.

35 In contrast, 1.5 mM tetraethylammonium, an organic cation, blocked uptake of

36 the rate of transport of the fixed cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e.

37 d-spectrum of K+ channel blockers, including tetraethylammonium and 4-aminopyridine, and insensitive

38 Unexpectedly, also the organic cations Tetraethylammonium and Acetylcholine were transported in

39 the nonselective potassium channel blockers tetraethylammonium and barium.

40 nels were Ca2+-dependent and were blocked by tetraethylammonium and charybdotoxin in normal and infla

41 eLa cells, the cDNA induces the transport of tetraethylammonium and guanidine.

42 f this particular mutation on the binding of tetraethylammonium and hydroxylamine, support the hypoth

43 Inhibition by tetraethylammonium and iberiotoxin suggested that these

44 Tetraethylammonium and iberiotoxin, preferential KCa-cha

45 ubthreshold voltages was unaffected by 10 mM tetraethylammonium and likely represents I(A), because i

46 retic uptake of K+ and other cations such as tetraethylammonium and lysine by rat liver mitochondria

47 and Cs+, but the organic monovalent cations tetraethylammonium and N-methyl-D-glucamine are much les

48 oth small monovalent organic cations such as tetraethylammonium and N1-methylnicotinamide and bulkier

49 a calcium spike elicited in the presence of tetraethylammonium and tetrodotoxin.

50 tocatalyst [NEt(4)](2)[CeCl(6)] (NEt(4) (+), tetraethylammonium), and RO* are not intermediates.

51 omponent of K+ current sensitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 value

52 lso increased fluorescence, whereas choline, tetraethylammonium, and N-methyl-D-glucamine did not.

53 Quaternary amines (tetramethylammonium, tetraethylammonium, and tetrapropylammonium, TMA, TEA, a

54 large pore as inferred from permeability to tetraethylammonium (approximately 8.5 angstroms diameter

55 ntally with a calcium selective membrane and tetraethylammonium as a model interfering agent, and the

56 halide ions in an aqueous sample containing tetraethylammonium benzoate, (b) capture of the released

57 anion-exchange cartridges with solutions of tetraethylammonium bicarbonate, perchlorate or tosylate

58 Internal application of tetraethylammonium blocked BK channel activity in a mann

59 oncentration of permeant ions, we argue that tetraethylammonium blocks by occluding the external end

60 In contrast, simulations indicate that tetraethylammonium blocks movement of metal cations.

61 ative measurements of atenolol, tioconazole, tetraethylammonium bromide, and tetrabutylammonium iodid

62 For the tetraethylammonium bromide/carbon tetrabromide dyad, the

63 to alpha-dendrotoxin, paxilline, apamin, and tetraethylammonium but sensitive to 4-aminopyridine and

64 e insensitive to 20 microM verapamil or 1 mM tetraethylammonium, but inhibited by 0.5 mM Ba(2+) or 0.

65 rganic anions, but not by the organic cation tetraethylammonium, by the multidrug resistance ATPase i

66 d in a near-homogeneous system that utilizes tetraethylammonium carbonate as base, 8-hydroxyquinoline

67 The tetraethylammonium carceplex, 1b, has been characterized

68 these states may be controlled by using the tetraethylammonium cation (TEA(+)) and/or iodide anion (

69 storage times in UW solution as assessed by tetraethylammonium cation transport (TEA).

70 In contrast, the addition of a tetraethylammonium cation, which binds more effectively

71 ions and simulations reveal that introducing tetraethylammonium cations as ion sieves can dynamically

72 ut affecting the affinity of the channel for tetraethylammonium, charybdotoxin, and nifedipine.

73 ofilium and 4-aminopyridine and partially by tetraethylammonium, charybdotoxin, dendrotoxin, and kali

74 e inhibition was not blocked by low doses of tetraethylammonium chloride (1 mM), barium, or glibencla

75 acellular electrodes in solutions containing tetraethylammonium chloride (10 mM) and BaCl2, (1 mM).

76 mide (10 microM), 4-aminopyridine (3 mM) and tetraethylammonium chloride (10 mM) did not affect L-lac

77 ith 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na(+)

78 ly blocked by 4-aminopyridine (4 mM) but not tetraethylammonium chloride (30 mM) and did not show ina

79 ing various concentrations of the ionic salt tetraethylammonium chloride (TEA(+)Cl(-)) or the zwitter

80 ns could be induced easily by Bay K8644 plus tetraethylammonium chloride (TEA) or [TEA]o after Cs+ re

81 Tetraethylammonium chloride (TEA) was used to inhibit K(

82 nnel blockers, including chlorotoxin (Ctx),, tetraethylammonium chloride (TEA), and tamoxifen.

83 lamp in the presence of 15 mM CsCl and 15 mM tetraethylammonium chloride (TEA-Cl) to eliminate K+ cha

84 waves and phasic contractions stimulated by tetraethylammonium chloride (TEA; 10 mM), but did not si

85 were separated in 100% methanol with 12.5 mM tetraethylammonium chloride added as a charge carrier.

86 outward and inward components, prevented by tetraethylammonium chloride and tetrodotoxin, respective

87 not affected at 10(-2) M; on the other hand, tetraethylammonium chloride failed to inhibit either che

88 f MIN6 cells with glucose in the presence of tetraethylammonium chloride generated concomitant Ca2+ a

89 ibition of K+ channels with charybdotoxin or tetraethylammonium chloride produced a modest transient

90 The effects of lidocaine were not blocked by tetraethylammonium chloride, 4-aminopyridine, glibenclam

91 ed potassium channels (blocked by 250 microM tetraethylammonium chloride, 70 nM charybdotoxin, or 100

92 and econazole, and the K+ channel blockers, tetraethylammonium chloride, apamin, and charybdotoxin,

93 amine-containing compounds tetramethyl- and tetraethylammonium chloride, glutamine, and urea.

94 application of potassium channel antagonist tetraethylammonium chloride, iberiotoxin, or 4-aminopyri

95 annels were already blocked by submillimolar tetraethylammonium chloride, indicating that Cav2.1 (Q-t

96 arbor depended upon voltage-gated sodium and tetraethylammonium chloride-sensitive potassium channels

97 tidine or with the potassium channel blocker tetraethylammonium chloride.

98 e channel blockers glyburide, gadolinium, or tetraethylammonium-Cl did not alter hypotonic-induced sw

99 (+), and Rb(+) and was not inhibited by high tetraethylammonium concentrations.

100 inhibited by K+ channel blockers, including tetraethylammonium, Cs+, and Ba2+.

101 of CMECs was blocked to a similar extent by tetraethylammonium, currents in the stretched endothelia

102 by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22, carnitine, PHA (p-amin

103 ium to the inactivated channel, although the tetraethylammonium does not interact directly with the K

104 Under voltage clamp conditions, tetraethylammonium evokes inward currents that are conce

105 Demetalation with tetraethylammonium fluoride quantitatively generates the

106 hat which determines sensitivity to external tetraethylammonium for voltage-gated potassium channels

107 Tetraethylammonium, glibenclamide, and a high concentrat

108 T transports classic OCT substrates, such as tetraethylammonium, guanidine, and histamine.

109 epolarized conditioning blocked the TOC, but tetraethylammonium had no effect.

110 nents were both blocked potently by external tetraethylammonium (half-block by 150 microm) and 4-amin

111 IK2 were sensitive to high concentrations of tetraethylammonium (half-maximal block at approximately

112 spinal fluid (ACSF), 5 mM Cs+ in ACSF, 20 mM tetraethylammonium in ACSF, or 1 mM 4-aminopyridine in A

113 l and attenuated by glibenclamide as well as tetraethylammonium, in agreement with established respon

114 heir ability to transport the organic cation tetraethylammonium indicating that their effect on carni

115 minopyridine, Ca2+ (10(-8) to 10(-6) M), and tetraethylammonium (internal or external) were without e

116 s are more sensitive to blockade by internal tetraethylammonium ion (TEA) than KvLQT1 channels.

117 Unlike the tetraethylammonium ion (TEA), neither JC638.2alpha nor C

118 We propose that 4AP, like tetraethylammonium ion and other quaternary ammonium ion

119 The tetraethylammonium ion fits snugly in the interior of th

120 ly with KCNQ5 by patch clamp analysis of the tetraethylammonium ion sensitivity of the resulting curr

121 ansport down its diffusion gradient, whereas tetraethylammonium ion substitution for K+ did not affec

122 with a molecule (diethyl ether) or a cation (tetraethylammonium ion) trapped inside.

123 potentiation occurred in the presence of the tetraethylammonium ion, a K+-channel blocker.

124 In the first, we constructed a mutant tetraethylammonium ion-sensitive KCNQ4 subunit and teste

125 y, at very low and at high concentrations of tetraethylammonium ion.

126 +10 mV, indicating increased permeability of tetraethylammonium ion.

127 was confirmed by studying simple transfer of tetraethylammonium ion.

128 er currents by using the BK channel blockers tetraethylammonium ions (TEA(+); 1 mM) or iberiotoxin (2

129 e silent arteries by charybdotoxin (CTX) and tetraethylammonium ions (TEA) induced dose-dependent dep

130 ns, the K+ channel blockers 4-aminopyridine, tetraethylammonium ions and XE991.

131 ation was perturbed by application of either tetraethylammonium ions or the Shaker (Sh)B peptide to t

132 efflux is approximately 0.1 mM), but not by tetraethylammonium ions or verapamil.

133 The IK(V) was blocked by tetraethylammonium ions with an IC50 of 5.2 mM and was u

134 in the axons, using the K(+) channel blocker tetraethylammonium ions, we suggest this may explain the

135 inopyridine and quinine and insensitivity to tetraethylammonium ions.

136 nt cations including tetramethylammonium and tetraethylammonium ions.

137 Since inhibition by external tetraethylammonium is sensitive to voltage and to the in

138 nd stichodactylatoxin, and is insensitive to tetraethylammonium, kaliotoxin, and charybdotoxin.

139 urrent that is blocked by externally applied tetraethylammonium (Kd = 30 +/- 7 mM), charybdotoxin (Kd

140 thiosulfonate ethylammonium (MTSEA) and MTS tetraethylammonium (MTSET) was tested.

141 ost of the Cl- with largely impermeant ions (tetraethylammonium, N-methyl-D-glucamine and methanesulp

142 s (Ik) were small and were inhibited by 1 mM tetraethylammonium or 100 nM charybdotoxin (CTX; a speci

143 Exchanging the sodium cation with tetraethylammonium or didodecyldimethylammonium expands

144 Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not

145 K(+) currents were suppressed by tetraethylammonium or N-methylglucamine in the solutions

146 iation (LTP) induced either chemically (with tetraethylammonium), or by high-frequency (200-Hz) elect

147 y extracellular tetrodotoxin, nimodipine, or tetraethylammonium, or by intracellular dialysis with 4-

148 on exchange with either tetramethylammonium, tetraethylammonium, or tetrabutylammonium cations to yie

149 Among the cations tested, tetraethylammonium provides the most favorable balance,

150 nsensitivity to all other inhibitors tested (tetraethylammonium, quinine, Cs(+), tetrodotoxin, verapa

151 In addition, 0.5 mM tetraethylammonium reduced I(M), suggesting that I(M) wa

152 The IK blocker tetraethylammonium reversed the ischemia-induced suppres

153 xceeding 10(14) M(-1) have been measured for tetraethylammonium salts in chloroform by employing a va

154 sted for binding to seven monovalent anions (tetraethylammonium salts, wet chloroform as solvent).

155 components of the whole-cell current were a tetraethylammonium-sensitive (IC50 = 9 mM), iberiotoxin-

156 hat CrMP decreases the open probability of a tetraethylammonium-sensitive (TEA-sensitive) 105 pS K ch

157 eous vasodilatation is mediated, in part, by tetraethylammonium-sensitive calcium-dependent potassium

158 units underlie the more slowly inactivating, tetraethylammonium-sensitive component of I(K, slow).

159 s absent (n=6), the density of the 20-mmol/L tetraethylammonium-sensitive component of I(K,slow) was

160 VLM- and PVN-projecting neurons had similar, tetraethylammonium-sensitive IK.

161 The ensuing decrease in tetraethylammonium-sensitive K(+) current activation slo

162 Onset cells have a unique high-threshold tetraethylammonium-sensitive K(+) current.

163 ional tetrodotoxin (TTX)-sensitive Na(+) and tetraethylammonium-sensitive K(+) currents.

164 In somatic membrane patches, we observed tetraethylammonium-sensitive K(DR) currents that activat

165 of different ratios of 4-aminopyridine- and tetraethylammonium-sensitive K+ currents.

166 In many nigral neurons, I(CAN) is masked by tetraethylammonium-sensitive potassium conductances, but

167 Tetraethylammonium-sensitive voltage-gated fibroblast cu

168 ) differed from ventricular muscle in having tetraethylammonium sensitivity and slower recovery.

169 as DPP6 knockdown reduced, I(to) density and tetraethylammonium sensitivity in canine PF but not in v

170 on and inactivation parameters, and external tetraethylammonium sensitivity were all similar to those

171 annels endows SK channels with an equivalent tetraethylammonium sensitivity, indicating that the oute

172 d tetraethylammonium, with Tyr185 conferring tetraethylammonium sensitivity.

173 hift in the concentration-response curve for tetraethylammonium; similar results were evident with ib

174 vated potassium channels by charybdotoxin or tetraethylammonium slowed the repolarizing phase of the

175 rmation of the occluded, economical template tetraethylammonium (TEA(+) ) has been systematically exa

176 ted WiS (IC-WiS) electrolytes containing the tetraethylammonium (TEA(+) ) inert cation is reported.

177 lipid bilayers reduced the effectiveness of tetraethylammonium (TEA(+)) as a blocker of K(+) translo

178 tigate the kinetics of the rapid transfer of tetraethylammonium (TEA(+)) at the 1,2-dichloroethane/wa

179 K(+) currents, which were inhibited by 5 mM tetraethylammonium (TEA(+)) chloride.

180 of S. mitis and C. matruchotii membranes to tetraethylammonium (TEA(+)) probe ions but also to real-

181 en Li(+) was the countercation compared with tetraethylammonium (TEA(+)), due to the coordination of

182 TP), LTP induced by the K(+) channel blocker tetraethylammonium (TEA) (TEA-LTP), and mossy fiber (MF)

183 Replacing external Na+ with tetraethylammonium (TEA) abolished the decrease in Gm.

184 epolarizations, and could be blocked by both tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

185 sion with the potassium channel antagonists, tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

186 f delayed rectifier K+ currents inhibited by tetraethylammonium (TEA) and 4-aminopyridine, with simil

187 sitive to block by external charybdotoxin or tetraethylammonium (TEA) and by internal Ba2+.

188 in the presence of the external pore blocker tetraethylammonium (TEA) and depended on a residue requi

189 lity and spike broadening in the presence of tetraethylammonium (TEA) and nifedipine.

190 ult-type nicotinic acetylcholine receptor by tetraethylammonium (TEA) and related quaternary ammonium

191 sistent with this possibility, extracellular tetraethylammonium (TEA) and tetramethylammonium applica

192 ely 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-amino

193 The location of the tetraethylammonium (TEA) binding site in the outer vesti

194 a mixed alkali metal reaction gel containing tetraethylammonium (TEA) cations.

195 ice, the addition of apamin with glucose and tetraethylammonium (TEA) caused a similar elevation in [

196 ained outward current that can be blocked by tetraethylammonium (TEA) characteristic of a delayed rec

197 Here we show that the nonmercurial compound, tetraethylammonium (TEA) chloride, reduces the water per

198 The K+ channel inhibitors Ba2+, Cs+, and tetraethylammonium (TEA) had distinct effects on differe

199 The uptake of [14C]tetraethylammonium (TEA) in oocytes injected with the cR

200 ions of 4-AP (1 mM) in combination with 5 mM tetraethylammonium (TEA) induce spontaneous synchronized

201 veratridine or blockage of K+ channels with tetraethylammonium (TEA) inhibit oligodendrocyte progeni

202 Intracellular tetraethylammonium (TEA) inhibition was studied at the s

203 Changes in the chemical structure of the tetraethylammonium (TEA) ion reduce binding affinity at

204 Tetraethylammonium (TEA) is frequently used to inhibit d

205 ected by 0.5 mM 4-aminopyridine (4-AP), 1 mM tetraethylammonium (TEA) or 1-10 nM margatoxin.

206 Exposure to the inhibitors of IK, tetraethylammonium (TEA) or 4-aminopyridine (4-AP), redu

207 annel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA) or dendrotoxin (DTX).

208 We show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) whi

209 -40 mV was slowly activating, long-lasting, tetraethylammonium (TEA) sensitive and showed little ste

210 GluR agonists and the K+ channel blocker tetraethylammonium (TEA) strongly inhibited delayed rect

211 Tetraethylammonium (TEA) transport also was investigated

212 The prototype for organic cations tetraethylammonium (TEA) was also transported by SlCAT2.

213 tive muscarinic potassium channels (KACh) by tetraethylammonium (TEA) was studied at 35 degrees C in

214 Internal Cs+ and external tetraethylammonium (TEA) were used to suppress outward c

215 imilar selectivity for some substrates (e.g. tetraethylammonium (TEA)), they have distinct selectivit

216 MLA, applied topically to skin surface), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4

217 ), a non-specific NOS inhibitor; (iii) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blo

218 Using tetraethylammonium (TEA), a presynaptic potassium channe

219 e of the membrane (trans-ions), and external tetraethylammonium (TEA), an I(Ks) pore-blocker.

220 ester (l-NAME), (3) a KCa channel inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

221 A nonselective K(+) channel blocker, tetraethylammonium (TEA), and a large-conductance Ca(2+)

222 , the nonselective potassium channel blocker tetraethylammonium (TEA), and the selective adenosine tr

223 We previously observed that tetraethylammonium (TEA), high extracellular potassium,

224 K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellular Cs+ decreased

225 t using various chloride salts, specifically tetraethylammonium (TEA), tetrapropylammonium (TPA), tet

226 ified in blLPM vesicles, including thiamine, tetraethylammonium (TEA), tri-n-butyl-methylammonium (TB

227 Because all K+ channels are blocked by tetraethylammonium (TEA), we asked if TEA would inhibit

228 ective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), which block the potassium chan

229 ult rat hippocampal slices with BDNF or with tetraethylammonium (TEA), which induces a chemical form

230 They were also inhibited by tetraethylammonium (TEA),an inhibitor of Ca2+-activated

231 ter exocytosis, because it was observed that tetraethylammonium (TEA)-induced inhibition of the delay

232 PMA had no significant effect on the 1 mM tetraethylammonium (TEA)-insensitive outward current or

233 Z: type 1 cells, with 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive and CdCl(2)-sensitive

234 ow that repolarization is composed of a fast tetraethylammonium (TEA)-sensitive component, determinin

235 extracellular Cs+ (0 K+), there were large, tetraethylammonium (TEA)-sensitive currents.

236 al excitability through inhibition of highly tetraethylammonium (TEA)-sensitive ion channels that con

237 -sensitive K(+) channels at the same site as tetraethylammonium (TEA).

238 the inward current by approximately 50%, and tetraethylammonium (TEA+) and choline were relatively im

239 Iberiotoxin or 1 mM tetraethylammonium (TEA+) constricted intact arteries.

240 Tetraethylammonium (TEA+) is widely used for reversible

241 channel, unlike native Shaker, to close with tetraethylammonium (TEA+) or the long-chain TEA-derivati

242 Movement of Ca2+, K+, and tetraethylammonium (TEA+) through the model RyR2 pore we

243 a2+ or K+ channel antagonists, verapamil and tetraethylammonium (TEA+).

244 Tetraethylammonium (TEA, 1-10 mM) had little effect on t

245 ng the application of the K+ channel blocker tetraethylammonium (TEA, 10 mM), implicating the involve

246 Tetraethylammonium (TEA; 1 mM) similarly enhanced KCa ex

247 electively blocked by a low concentration of tetraethylammonium (TEA; 1 mM).

248 Tetraethylammonium (TEA; 10 mM), 1 and 5 mM 4-aminopyrid

249 d by Ba2+ (1 mM), 4-aminopyridine (1 mM) and tetraethylammonium (TEA; 20 mM), with an IC50 for TEA of

250 Tetraethylammonium (TEA; 30 mM) reduced the voltage-depe

251 Caesium (100 microM), barium (1 mM), tetraethylammonium (TEA; 5 mM), apamin (10 nM) and 4-ami

252 om) and high concentrations of extracellular tetraethylammonium (TEA; IC(50) = 11.8 mM), but no speci

253 ted K(+) current that is blocked potently by tetraethylammonium (TEA; IC(50), 0.14 mm).

254 We investigated the effect of 1.0 mM tetraethylammonium (TEA; which blocks Kv3 channels) on i

255 riant with changes in [Cl(-)], [Na(+)], and [tetraethylammonium] ([TEA(+)]), but dependent on [H(+)].

256 We found that dimethylamine, triethylamine, tetraethylammonium, tetrabutylammonium, tetrapropylammon

257 lam-functionalized quartz nanopipettes, with tetraethylammonium tetrafluoroborate (TEATFB) in MeCN as

258 bstrate (l-carnitine) and the organic cation tetraethylammonium, three variants showed functional dif

259 potentiated by the binding of extracellular tetraethylammonium to the inactivated channel, although

260 n, even though it allows large ions, such as tetraethylammonium, to permeate readily.

261 In the presence of glucose and tetraethylammonium, transgenically derived beta-cells (b

262 on followed by Western blotting) and reduced tetraethylammonium transport by OCT2 expressed in Chines

263 [(3)H]tetraethylammonium uptake in HeLa cells stably expressin

264 Na(+) (approximately 1.25), insensitivity to tetraethylammonium, voltage independence, and partial se

265 rved in the presence of Bay K 8644, NMDA, or tetraethylammonium were abolished in low-sodium buffer a

266 Low concentrations of tetraethylammonium were used to broaden the presynaptic

267 eation of AgAQP1 is inhibited by HgCl(2) and tetraethylammonium, with Tyr185 conferring tetraethylamm

268 thiolate complexes (Et4N)Ni(X-pyS)3 (Et4N = tetraethylammonium; X = 5-H (1a), 5-Cl (1b), 5-CF3 (1c),