ライフサイエンスコーパス: 4-AP

1 4-AP (5 mM) reduced the early current but increased outw

2 4-AP also increased the second messenger inositol trisph

3 4-AP also unmasked tonic firing in phasic PGN (average m

4 4-AP and 3,4-diaminopyridine (3,4-DiAP), which have rela

5 4-AP blocked voltage-sensitive K(+) currents in astrocyt

6 4-AP decreased the chemosensory activities in normoxia b

7 4-AP had no consistent effect in restoring conduction to

8 4-AP has differential actions on distinct ASICs, strongl

9 4-AP inhibited outward current at potentials negative to

10 4-AP preferentially blocked IA and prevented the spike n

11 4-AP was further found to increase the maximum following

12 4-AP, 4-(aminomethyl)pyridine, 4-(methylamino)pyridine,

13 4-AP-induced spontaneous discharges are blocked by 20 mi

14 itivity of this assay enables detection of 2.4 AP sites per 10(7) bases.

15 ound density of AP sites in DNA fibers was 5.4 AP sites/10(6) nt, while newly replicated DNA containe

16 5-HT activated a 4-AP-sensitive current with a reversal potential of -95

17 y by 50 microM 4-aminopyridine (4-AP), and a 4-AP-insensitive component that is blocked by 25 mM TEA;

18 K(V)1.6 in Xenopus oocytes also generated a 4-AP-sensitive K(+) current with a threshold for activat

19 We conclude that adenosine acts to inhibit a 4-AP-sensitive current in isolated type I cells of the r

20 labelled, PVN-RVLM neurones indicate that a 4-AP sensitive, TEA insensitive current, with biophysica

21 In the context of rhythmic network activity, 4-AP caused irregular respiratory-related motor output o

22 Two additional 4-AP- and charybdotoxin-insensitive K+ channels (approxi

23 ed dendritic excitability when applied after 4-AP.

24 Also, 4-AP did not evoke any rise in [Ca2+]i in glomus cells e

25 Although 4-AP and 3,4-DiAP were effective in preventing attacks i

26 Although 4-AP, a blocker of the transient outward current (I(to))

27 e active form responsible for 4-aminophenol (4-AP) oxidase activity in both G4DFsc and 3His-G4DFsc(Mu

28 on of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP) within 45 seconds though the hydrogenation process

29 on of p-nitrophenol (4-NP) to p-aminophenol (4-AP) as a model system.

30 nal cortex slices bathed in 4-aminopirydine (4-AP) as an experimental paradigm model to evaluate the

31 specific K+ channel blocker 4-aminopurydine (4-AP) prevented UV-irradiation-induced apoptosis in the

32 ifedipine (to block ICa) or 4-aminopyridine (4-AP) (to block the transient outward current, ITO) furt

33 t K(+) (K(V)) currents with 4-aminopyridine (4-AP) an outward current containing inactivating (I(tran

34 nels [blocked by 100 microM 4-aminopyridine (4-AP) and 0.5-1 microM alpha-dendrotoxin (alpha-DTX)] pl

35 um (TEA; 10 mM), 1 and 5 mM 4-aminopyridine (4-AP) and 20 nM charybdotoxin all failed to evoke a sign

36 with the K+ channel blocker 4-aminopyridine (4-AP) and by varying the extracellular Ca2+ concentratio

37 and high concentrations of 4-aminopyridine (4-AP) and TEA.

38 ts for selective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), which block the pota

39 type current was blocked by 4-aminopyridine (4-AP) and was inhibited by flecainide, with an IC(50) of

40 similar to those seen with 4-aminopyridine (4-AP) application.

41 Aminopyridines such as 4-aminopyridine (4-AP) are widely used as voltage-activated K(+) (Kv) cha

42 not considered part of the 4-aminopyridine (4-AP) binding site, unlike the L4 heptad leucine, Phe su

43 Toxin I and 4-aminopyridine (4-AP) both increased the frequency of spontaneous dorsal

44 ethyl ammonium chloride and 4-aminopyridine (4-AP) both inhibited short-term copper-induced K(+) effl

45 to the K(+) channel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA) or dendrotoxin (D

46 sium (K(+)) channel blocker 4-aminopyridine (4-AP) constitutes the most promising treatment, although

47 4-Aminopyridine (4-AP) has been used extensively to study transient outwa

48 However, although 4-aminopyridine (4-AP) inhibited peak I(A) activated by step depolarizati

49 4-Aminopyridine (4-AP) is a well known convulsant that enhances the relea

50 d K(+) (Kv) channel blocker 4-aminopyridine (4-AP) is used to target symptoms of the neuroinflammator

51 Perfusion of 4-aminopyridine (4-AP) mimicked a known effect of behavioral conditioning

52 udies indicate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduct

53 y we analyzed the effect of 4-aminopyridine (4-AP) on free cytosolic calcium concentration ([Ca(2+)](

54 th application of 50 microM 4-aminopyridine (4-AP) or 250 nM veratridine both clearly reduced DSI, ev

55 potassium channel blockers 4-aminopyridine (4-AP) or alpha-dendrotoxin (DTX).

56 bition of KV1 channels with 4-aminopyridine (4-AP) or treatment with the epidermal growth factor rece

57 in sensitivity to block by 4-aminopyridine (4-AP) over a 1000-fold range.

58 The A-channel antagonist 4-aminopyridine (4-AP) produced a voltage-dependent block (IC50, approxim

59 shold K+ current, which was 4-aminopyridine (4-AP) sensitive and showed significant steady-state inac

60 alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block these conductances.

61 e potassium channel blocker 4-aminopyridine (4-AP) to induce large amplitude population spikes and 4-

62 demonstrated the ability of 4-aminopyridine (4-AP) to restore electrophysiological and/or behavioral

63 n Ito and IK(ur) of TEA and 4-aminopyridine (4-AP) was not different in cells isolated from WT and NG

64 raethyl ammonium (TEA), and 4-aminopyridine (4-AP) were applied in the superfusate.

65 traethylammonium (TEA) plus 4-aminopyridine (4-AP) which suppressed the Ca2+ sensitive and other K+ c

66 EA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV, and a slowly i

67 2+ but unaffected by 0.5 mM 4-aminopyridine (4-AP), 1 mM tetraethylammonium (TEA) or 1-10 nM margatox

68 of a K(+) channel blocker, 4-aminopyridine (4-AP), 5-HT left unaltered the presynaptic Ca(2+) transi

69 s cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ current, on intracellul

70 4-Aminopyridine (4-AP), a nonselective blocker of K(v) voltage-gated pota

71 ebrospinal fluid containing 4-aminopyridine (4-AP), a potassium channel blocker.

72 tage-gated K+ channels with 4-aminopyridine (4-AP), a treatment known to increase neurotransmitter re

73 g(+)) uptake is enhanced by 4-aminopyridine (4-AP), a well known voltage-sensitive potassium ion chan

74 ed selectively by 50 microM 4-aminopyridine (4-AP), and a 4-AP-insensitive component that is blocked

75 e potassium channel blocker 4-aminopyridine (4-AP), at a low (50 microM) and at a higher (2500 microM

76 cid (BAPTA), application of 4-Aminopyridine (4-AP), expression of a Kv4.2 dominant negative subunit,

77 iaminopyridine (3,4-DAP) or 4-aminopyridine (4-AP), inhibitors of K(V) channels.

78 tetraethylammonium (TEA) or 4-aminopyridine (4-AP), reduced the control current elicited by a voltage

79 ical synapses in sustaining 4-aminopyridine (4-AP)-evoked network activity recorded extracellularly f

80 filin in hippocampus due to 4-aminopyridine (4-AP)-induced seizures/epileptiform activity in vivo and

81 crease in susceptibility to 4-aminopyridine (4-AP)-induced spontaneous ectopic firing.

82 v1.5 is thought to encode a 4-aminopyridine (4-AP)-sensitive component of the current I(K,slow) in th

83 mping showed a reduction of 4-aminopyridine (4-AP)-sensitive current (Kv current) from smooth muscle

84 kinje cell dendrites, and a 4-aminopyridine (4-AP)-sensitive potassium channel underlies these membra

85 D) is a slowly inactivating 4-aminopyridine (4-AP)-sensitive potassium current of hippocampal pyramid

86 e weak K(+) channel blocker 4-aminopyridine (4-AP).

87 t is largely insensitive to 4-aminopyridine (4-AP).

88 etraethylammonium (TEA) and 4-aminopyridine (4-AP).

89 ium conductances blocked by 4-aminopyridine (4-AP).

90 of epileptiform activity by 4-aminopyridine (4-AP).

91 f the K+ channel antagonist 4-aminopyridine (4-AP).

92 etraethylammonium (TEA) and 4-aminopyridine (4-AP).

93 e potassium channel blocker 4-aminopyridine (4-AP).

94 use SVZ: type 1 cells, with 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive and CdCl(2)-sen

95 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spiking.

96 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for spike activation

97 tassium conductance blocker 4-aminopyridine (4-AP, 100 microM) abolished the inhibitory effects of ME

98 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both whole-cell and somat

99 d by a low concentration of 4-aminopyridine (4-AP, 40 microM), a significant facilitation of the [Ca2

100 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of the control outwa

101 A-type K+ current blocker, 4-aminopyridine (4-AP, 5 mM) in the pipette also antagonised the effects

102 d by applications of either 4-aminopyridine (4-AP, at micromolar levels), alpha-dendrotoxin at nanomo

103 d K+ (KCa) channel blocker; 4-aminopyridine (4-AP; 1 mM), a voltage-gated K+ (KV) channel blocker; ma

104 a maximal concentration of 4-aminopyridine (4-AP; 10 mM) blocked only 40% of the current.

105 e potassium channel blocker 4-aminopyridine (4-AP; 100 microM) and a 12-lipoxygenase inhibitor, baica

106 ication of TEA (0.5 mm) and 4-aminopyridine (4-AP; 30 mum).

107 ich was potently blocked by 4-aminopyridine (4-AP; IC50, 232 microM), but was almost insensitive to T

108 other potassium channels by aminopyridines (4-AP and 3,4-DAP) may also explain the paraesthesiae ind

109 ive to both tetraethyl ammonium chloride and 4-AP.

110 DTX- and 4-AP-sensitive channels were activated during sodium-dep

111 as less sensitive to TEA (K(D) = 0.8 mM) and 4-AP (K(D) approximately 6 mM).

112 ioxidant; and a combination of ryanodine and 4-AP reduced diazoxide (100 microM)-induced dilation in

113 mimicked and occluded the effects of TEA and 4-AP in NTS and dorsal column nuclei neurones, but not i

114 f the TS evoked EPSPs and IPSPs, and TEA and 4-AP increased the average amplitude and decreased the p

115 TEA alone had as much effect as TEA and 4-AP together, suggesting that there are at least two co

116 Dose-response relations for TEA and 4-AP were obtained by exposing single cells to ten conce

117 um currents, which were sensitive to TEA and 4-AP, respectively.

118 ough the inhibition of voltage-gated TEA and 4-AP-sensitive K+ channels (e.g. maxi-K or KO2 channels)

119 r -85 mV, and a slowly inactivating TEA- and 4-AP-sensitive current (IKIS, tau approximately 145 msec

120 the K(+) channel blockers Ba(2+), XE991, and 4-AP.

121 In astrocytes, 4-AP treatment potentiated the sustained phase of the [C

122 P was accelerated by 1S,3R-ACPD, and because 4-AP occluded any further actions of 1S,3R-ACPD.

123 interneuronal network activity occurs before 4-AP-induced seizures and therefore supports a role of i

124 Bicuculline/4-AP or KCl-induced depolarization reduces, whereas high

125 ices in vitro, the potassium channel blocker 4-AP and GABAA receptor antagonist bicuculline together

126 ted by the broad-spectrum K+ channel blocker 4-AP.

127 2 cells, with Ca(2+)-sensitive K(+) and both 4-AP/TEA-sensitive and -insensitive currents; type 3 cel

128 blockade of micro-opioid inhibition by both 4-AP and baicalein was reduced.

129 Conductances blocked by 4-AP also contributed to the repolarization of the actio

130 Since citrate efflux was blocked by 4-AP, K(+) appears to serve as a counterion during coppe

131 rast, the depression phase was eliminated by 4-AP.

132 of dopamine release and unaltered [Ca2+]i by 4-AP are not consistent with the implied meaning of the

133 The [Ca(2+)](i) elevation induced by 4-AP was concentration-dependent and consisted of two ph

134 The potassium current was inhibited by 4-AP and by Heteropodatoxin, a specific blocker of Kv4.2

135 Whole-cell currents were inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating fun

136 We report here inhibition by 4-AP of HERG (the human ether-a-go-go-related gene) K+ c

137 cillations were abolished by TEA, but not by 4-AP.

138 urrent density, with no further reduction by 4-AP.

139 calcium entry was potentiated severalfold by 4-AP, in astrocytes and muscle cells but not in neurons.

140 blocked by 1 mM Ba2+ but were unaffected by 4-AP or TEA.

141 By blocking Kv channels, 4-AP facilitates action potential conduction and neurotr

142 Because at higher concentrations 4-AP blocks a large array of K(+) channels and is a proc

143 In contrast, 4-AP had no effect on Cav3.2 channels expressed in HEK29

144 In contrast, 4-AP only partially blocked the actions of baclofen.

145 constricted further in response to 3,4-DAP, 4-AP or correolide, but not to rAgTX2.

146 Also consistent with such enhancement, 4-AP also greatly increased the latency to first spike a

147 current pulses, with two components: a fast 4-AP-sensitive component (A-type conductance), contribut

148 for TEA (K1 = 0.215 mM) and low affinity for 4-AP (K1 = 12.3 mM).

149 This effect is specific for 4-AP compared with its heterocyclic base, pyridine, and

150 In G4DFsc, 4-AP increases the coordination of the biferrous site, w

151 armacological profiles of the voltage-gated, 4-AP-sensitive K(+) channel in rat and RCE cells resembl

152 Surprisingly, as first demonstrated here, 4-AP inhibits neuronal degenerin/epithelial Na(+) (Deg/E

153 However, 4-AP had prominent effects that did not involve demyelin

154 However, 4-AP seizures had no overt short-term structural effects

155 nt current is a steady-state K(+) current (I(4-AP)).

156 If 4-AP blocks the open channel by promoting closure of the

157 In 4-AP bursts of large amplitude action potentials were fo

158 In 4-AP the excitatory phase of the reflex was followed by

159 These deletions produced no change in 4-AP sensitivity in the mutant channel and approximately

160 annel, we demonstrate a 400-fold increase in 4-AP sensitivity following substitution of L4 with pheny

161 tion confirmed the presence of inhibition in 4-AP, and its reduction in Toxin I.

162 ort the expression of a slowly inactivating, 4-AP-sensitive potassium current (K4-AP) at significantl

163 L1F (L457) and L3F (L471) increase 4-AP sensitivity by 8- and 150-fold, respectively, and p

164 titutions at L2 (L464) or L5 (L485) increase 4-AP sensitivity by 400-fold, as seen previously in the

165 t the view that changes at L4 which increase 4-AP sensitivity are largely due to 4-AP binding and may

166 lations between altered gating and increased 4-AP sensitivity.

167 ier type K(+) channels demonstrate increased 4-AP sensitivity upon mutation of the L4 heptad leucine

168 nel closed state may contribute to increased 4-AP sensitivity by amplifying the mechanism of 4-AP blo

169 Instead, 4-AP restores the severely diminished precision of pacem

170 homozygous SWAP myocytes, the 50-micromol/L 4-AP-sensitive component of IK,slowwas absent (n=6), the

171 did not prolong in response to 30 micromol/L 4-AP.

172 Constriction to 3 mmol/L 4-AP was reduced in vessels exposed to HG (13+/-5%, P<0.

173 e a compromised responsiveness to either low 4-AP concentrations or elevated extracellular Ca(2+).

174 gion, spanning the S4-S5 linker, exhibit low 4-AP sensitivity, while channels with phenylalanine exhi

175 outward current sensitive to 100-200 microM 4-AP was accelerated by 1S,3R-ACPD, and because 4-AP occ

176 was mimicked in WT cells by exposure to 1 mM 4-AP, which partially blocked Ito, completely blocked IK

177 n additional 25-30 % in the presence of 1 mM 4-AP.

178 5.9 x 10(4) ions per cell per sec with 1 mM 4-AP.

179 recordings of spontaneous pacemaking, 10 mM 4-AP slowed rather than speeded firing, consistent with

180 d by 50 mV/s ramp enhanced >15-fold by 10 mM 4-AP).

181 .0 x 10(8) ions per cell per sec with 0.2 mM 4-AP.

182 .5 x 10(4) ions per cell per sec with 0.5 mM 4-AP and 5.9 x 10(4) ions per cell per sec with 1 mM 4-A

183 ordings, a combination of 10 mM TEA and 5 mM 4-AP failed to depolarize type I cells.

184 In contrast, 10 mM TEA + 5 mM 4-AP had little effect on the current-voltage relationsh

185 Treatment with 5 mM 4-AP inhibited peak IHERG during an applied action poten

186 tive role of fast inactivation in modulating 4-AP block, N-terminal deletions of the fast inactivatio

187 isted in the presence of TTX and TEA but not 4-AP.

188 ely responsible for the beneficial action of 4-AP in multiple sclerosis patients.

189 phenomenon was not due to a direct action of 4-AP on presynaptic Ca2+ channels, but to cumulative sup

190 It was concluded that the actions of 4-AP and Toxin I on the isolated preparation of rat spin

191 4-methylpyridine; and akin to the actions of 4-AP on the structurally unrelated Kv channels, dose- an

192 be considered when evaluating the actions of 4-AP.

193 waves may be due, in part, to activation of 4-AP-sensitive, 'delayed rectifier' K+ channels.

194 xplain some of the therapeutic activities of 4-AP as a neurotransmission enhancer.

195 interneurons were rescued by the addition of 4-AP to TTX, and decreased when presynaptic firing in Ca

196 remaining K(+) current with the addition of 4-AP, TEA-Cl, and glibenclamide; and 4) blocking I(Ca) w

197 Although the combined application of 4-AP and TTX did not rescue responses in pyramidal cells

198 tivity that can be induced by application of 4-AP.

199 Furthermore, blockade of 4-AP- and TEA-sensitive K+ channels in the presence of T

200 not blocked by a saturating concentration of 4-AP (8 mM) but was reduced during the application of th

201 The threshold concentration of 4-AP was 1 microM, with EC50 at 20 microM.

202 we have found that higher concentrations of 4-AP (1 mM) in combination with 5 mM tetraethylammonium

203 Low concentrations of 4-AP (approximately 100 microM) readily induce synchroni

204 was blocked by micromolar concentrations of 4-AP and TEA (K(D) approximately 140 microM).

205 he IKr channel, millimolar concentrations of 4-AP can modulate ventricular repolarisation independent

206 only believed, therapeutic concentrations of 4-AP do not increase the inhibitory drive of cerebellar

207 t in wild-type neurons low concentrations of 4-AP facilitate glutamatergic and GABAergic transmission

208 current-clamp recordings, concentrations of 4-AP that blocked the current through Kv3.1b channels al

209 Half-blocking concentrations of 4-AP were correlated with the time constant of deactivat

210 Thus, the state dependence of 4-AP binding to the channels underlying I(A) can result

211 vation gate is not a critical determinant of 4-AP sensitivity in Kv1.4 channels.

212 The apparent free energy differences of 4-AP binding in each mutant suggest enhanced drug-channe

213 y enhanced by a single, 2 mg/kg i.v. dose of 4-AP.

214 Finally, the effect of 4-AP on B-cell action potentials and on the postsynaptic

215 BDS-I, did not mimic or alter the effect of 4-AP on HVACCs.

216 The occlusion of the effects of 4-AP by paired training was not attributable to a satura

217 If so, the dominant effects of 4-AP in multiple sclerosis patients are independent of d

218 Analysis of the effects of 4-AP on firing properties suggests that the K4-AP curren

219 mimic or change the potentiating effects of 4-AP on neurotransmitter release from sensory and motor

220 These effects of 4-AP were completely and promptly reversible.

221 mode of action, the therapeutic efficacy of 4-AP was comparable, and not additive, to chlorzoxazone,

222 These data demonstrate the existence of 4-AP-sensitive neuronal networks within SG that can gene

223 in part on differences in the expression of 4-AP-sensitive K(+) channels.

224 P sensitivity by amplifying the mechanism of 4-AP block.

225 Within 30 minutes of 4-AP injection, animals developed recurrent seizures (du

226 eous dorsal root activity in the presence of 4-AP and Toxin I differed.

227 s also showed differences in the presence of 4-AP and Toxin I.

228 A introduced into the VSI in the presence of 4-AP by means of the dynamic-clamp technique restored sp

229 the astrocytic responses in the presence of 4-AP required the presence of both MCPG and the ionotrop

230 was virtually eliminated in the presence of 4-AP, but it could be restored by lowering [Ca2+]o.

231 rong oscillatory activity in the presence of 4-AP, but little such activity in the presence of Toxin

232 In the presence of 4-AP, synchronized calcium oscillations become independe

233 rying [CA2+]o in the absence and presence of 4-AP.

234 To examine the action(s) of 4-AP in demyelinating disorders, the drug was administer

235 Superfusion of 4-AP (0.8 mM) reversibly depolarized a low frequency cel

236 Superfusion of 4-AP (50 microM) induced two types of activity, the firs

237 The likely target of 4-AP at the concentrations used are the K(v)1 family of

238 the curve appeared to be parallel to that of 4-AP.

239 and octanol (1 mM) attenuated both types of 4-AP-induced activity.

240 lupirtine (30muM) had a depressant effect on 4-AP-induced excitation in SG such that the frequency of

241 either increased extracellular potassium or 4-AP.

242 conductance channels were blocked by TEA or 4-AP or 140 mM RbCl.

243 als have demonstrated that 4-amino-pyridine (4-AP), a potassium channel-blocking agent, improves symp

244 educe events stimulated by 4-amino-pyridine (4-AP; 10 mM).

245 However, during remyelination, 4-AP profoundly increased both compound action potential

246 ct was attenuated by MnTMPyP and ryanodine + 4-AP.

247 Since 4-AP preconditioning affords extensive protection agains

248 e, variable-field (VTVH) MCD spectroscopies, 4-AP is found to bind directly to the biferrous sites of

249 nations of N-type (Cav2.2) channel subunits, 4-AP potentiated Ca(2+) currents primarily through the i

250 iring threshold while profoundly suppressing 4-AP-induced spontaneous firing, demonstrating a functio

251 o when a 'blocking solution' containing TEA, 4-AP, Ni(2+) and zero extracellular Ca(2+) was used.

252 o conventional K(+) channel inhibitors (TEA, 4-AP and Ba(2+)) but completely inhibited by tetracaine

253 IBTX and TEA/4-AP did not affect the basal [Ca(2+) ]i in isolated glo

254 not affect the rise in [Ca(2+) ]i , but TEA/4-AP strongly ( approximately 3-fold) enhanced [Ca(2+) ]

255 ts of inhibitors of BK (IBTX) and BK/Kv (TEA/4-AP) on [Ca(2+) ]i responses to a wide range of hypoxia

256 We conclude that 4-AP is able to affect calcium homeostasis at multiple l

257 Here, we present novel evidence that 4-AP and several of its analogs directly stimulate high

258 endent of demyelination, and it follows that 4-AP may be beneficial in other neurological disorders i

259 2 ratiometric calcium imaging, we found that 4-AP increased [Ca(2+)](i) in type I astrocytes, neurons

260 capacitative calcium entry, indicating that 4-AP effects on [Ca(2+)](i) were not caused by the block

261 le-cell current-clamp recordings showed that 4-AP changed the envelope of depolarization underlying i

262 These data suggest that 4-AP might act by enhancing synaptic efficacy, as well a

263 ant activation of caspase-3, suggesting that 4-AP preconditioning is effective primarily against necr

264 indings challenge the conventional view that 4-AP facilitates synaptic and neuromuscular transmission

265 The 4-AP-sensitive current continues to increase after the o

266 orylation was significantly increased by the 4-AP preconditioning, although bcl-2 expression was not

267 Thus, Kv1.5 encodes the 4-AP-sensitive component of I(K,slow) in the mouse ventr

268 We conclude that in the 4-AP seizure model, interneuronal network activity occur

269 Neither the 4-AP-sensitive, slowly inactivating K+ current, IK,slow,

270 The voltage dependence of the 4-AP block and the single binding site for this inhibito

271 second postnatal week, the activation of the 4-AP-sensitive current, by now contributing about half o

272 ed gene targeting to replace mKv1.5 with the 4-AP-insensitive channel rKv1.1 (SWAP mice) and directly

273 rebellar Purkinje cell somas confirmed these 4-AP-sensitive currents with half maximal activation at

274 Thus, 4-AP might be useful where silver is used as antimicrobi

275 mutase and catalase increased contraction to 4-AP in HG CAs.

276 increase 4-AP sensitivity are largely due to 4-AP binding and may, in part, arise from alterations in

277 V (n = 2) in high frequency cells exposed to 4-AP (0.8 mM).

278 In some slices exposed to 4-AP and TEA, smaller-amplitude asynchronous responses a

279 Under current-clamp conditions, exposure to 4-AP or flecainide depolarized the membrane potential by

280 (IC50, 2.6 mM) but relatively insensitive to 4-AP (37% block at 20 mM).

281 fering significantly from it with respect to 4-AP sensitivity (IC50, 352 microM), activation rate, an

282 Delayed rectifier currents sensitive to 4-AP are important determinants of rhythmicity but not a

283 rger fraction of the current is sensitive to 4-AP.

284 e mouse ventricle and confers sensitivity to 4-AP-induced prolongation of APD and QTC: Compensatory u

285 ously linked to I(D) by their sensitivity to 4-AP: reduction in input conductance and enhanced excita

286 and sensitive to TEA and DTX but less so to 4-AP.

287 In many recordings, a transient 4-AP-insensitive outward current was evoked from a holdi

288 ke by the cells increased significantly when 4-AP was added to the solution.

289 binding enables a two-electron process where 4-AP is oxidized to benzoquinone imine and O2 is reduced

290 g ramps can be explained by a model in which 4-AP binds tightly to closed channels but must unbind be

291 ine release by microsensors without and with 4-AP (0.2, 1.0 and 2.0 mM in CO2-HCO3- buffer) and recor

292 nd -insensitive currents; type 3 cells, with 4-AP/TEA-sensitive and -insensitive K(+) and small Na(+)

293 ation gating, which is known to compete with 4-AP in rapidly inactivating A-type K(+) channels.

294 site for this inhibitor are consistent with 4-AP binding in the pore of Deg/ENaC channels as it does

295 tly, the current results are consistent with 4-AP influencing the symptoms of MS as well as the cours

296 ; 62+/-2, controls, n=9), and injection with 4-AP prolonged QTc only in controls (63+/-1, homozygotes

297 hange in sensitivity to the neurotoxins with 4-AP could be explained in terms of a nonlinear relation

298 pig brain preparation during perfusion with 4-AP.

299 as 4.8 x 10(7) ions per cell per sec without 4-AP compared with 1.0 x 10(8) ions per cell per sec wit

300 as 1.5 x 10(4) ions per cell per sec without 4-AP vs. 3.5 x 10(4) ions per cell per sec with 0.5 mM 4