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 restores neurotransmission and number of propriocep

12 4-AP was further found to increase the maximum following

13 4-AP, 4-(aminomethyl)pyridine, 4-(methylamino)pyridine,

14 4-AP-induced spontaneous discharges are blocked by 20 mi

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

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

17 5-HT activated a 4-AP-sensitive current with a reversal potential of -95

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

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

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

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

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

23 In addition, 4-AP treatment with pharmacological inhibition of p53-de

24 ed dendritic excitability when applied after 4-AP.

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

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

27 chlorophenol (2,4-DP) and 4-aminoantipyrine (4-AP) to produce an obvious red product.

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

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

30 product of paracetamol, i.e., 4-aminophenol (4-AP), and two antibacterials, namely, cefadroxil (CFD,

31 such as hydroquinone (HQ) and 4-aminophenol (4-AP), were detected amperometrically in flow-injection

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 4-Aminopyridine (4-AP) has been used extensively to study transient outwa

49 d potassium channel blocker 4-aminopyridine (4-AP) improves motor behavior in both sexes of a severe

50 ure focus with injection of 4-aminopyridine (4-AP) in somatosensory cortex.

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

52 4-Aminopyridine (4-AP) is a well known convulsant that enhances the relea

53 4-aminopyridine (4-AP) is used and licensed as a symptomatic treatment to

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

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

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

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

58 ( p-H(2)) and a substrate (4-aminopyridine (4-AP) or 4-methylpyridine (4-MP)) into [Ir(H)(2)(IMes)(s

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

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

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

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

63 ty by the FDA-approved drug 4-aminopyridine (4-AP) rescues the number and function of central and per

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

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

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

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

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

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

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

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

72 2+ but unaffected by 0.5 mM 4-aminopyridine (4-AP), 1 mM tetraethylammonium (TEA) or 1-10 nM margatox

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

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

75 4-Aminopyridine (4-AP), a nonselective blocker of K(v) voltage-gated pota

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spiking.

99 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for spike activation

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

101 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both whole-cell and somat

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

103 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of the control outwa

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

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

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

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

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

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

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

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

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

113 ch is responsible for motor neuron death and 4-AP, results in additive beneficial effects on the sens

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 2 cells, with Ca(2+)-sensitive K(+) and both 4-AP/TEA-sensitive and -insensitive currents; type 3 cel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 ith the experimental data, during concurrent 4-AP therapy, degeneration of the macular retinal nerve

146 generation between 52 patients on continuous 4-AP therapy and 51 matched controls.

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

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

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

150 at in addition to those symptomatic effects, 4-AP can prevent neuroaxonal loss in the CNS.

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

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

153 her sensitivity, 7 nmol L(-1), was noted for 4-AP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 histology and in vitro experiments indicated 4-AP stabilization of myelin and oligodendrocyte precurs

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

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

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

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

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

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

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

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

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

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

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

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

185 .0 x 10(8) ions per cell per sec with 0.2 mM 4-AP.

186 .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

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

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

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

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

191 In experimental optic neuritis, 4-AP potentiated the effects of immunomodulatory treatme

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

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

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

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

196 4-methylpyridine; and akin to the actions of 4-AP on the structurally unrelated Kv channels, dose- an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 esults indicate disease-modifying effects of 4-AP beyond symptomatic therapy and provide support for

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

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

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

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

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

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

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

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

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

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

229 ion of deuterium into the ortho positions of 4-AP, where the source of deuterium is the solvent, meth

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

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

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

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

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

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

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

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

240 either increased extracellular potassium or 4-AP.

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

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

243 As extended release 4-AP is already licensed for symptomatic multiple sclero

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

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

246 Since 4-AP preconditioning affords extensive protection agains

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

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

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

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

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

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

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

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

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

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

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

258 2 ratiometric calcium imaging, we found that 4-AP increased [Ca(2+)](i) in type I astrocytes, neurons

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

260 Our in vivo study reveals that 4-AP-induced increase of neuronal activity restores syna

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

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

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

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

281 The amperometric response to 4-AP was linear in the concentration range between 0.05

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 less potent than 4AP; and 2-trifluoromethyl-4-AP (2CF(3)4AP) was found to be about 60-fold less acti

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 reduction in retinal neurodegeneration with 4-AP in models of experimental optic neuritis and optic

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