ライフサイエンスコーパス: 4-aminopyridine

1 D-C) amplitude and/or K(+) channel-blockade (4-aminopyridine).

2 e less sensitive to the K(+) channel blocker 4-aminopyridine.

3 ed by local injection of the chemoconvulsant 4-aminopyridine.

4 ot by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine.

5 an IC50 of 5.2 mM and was unaffected by 1 mM 4-aminopyridine.

6 pig brain with the potassium channel blocker 4-aminopyridine.

7 ng the potassium channel blockers barium and 4-aminopyridine.

8 e firing induced by the K(+)-channel blocker 4-aminopyridine.

9 ation was reduced by 46.2 +/- 10.3 % in 5 mM 4-aminopyridine.

10 vation on epileptiform discharges induced by 4-aminopyridine.

11 cking K+ currents with extracellular TEA and 4-aminopyridine.

12 reshold current steps was greatly reduced by 4-aminopyridine.

13 lective cyclization promoted by N,N-dimethyl-4-aminopyridine.

14 tetraethylammonium chloride, iberiotoxin, or 4-aminopyridine.

15 nd aspartate from CA1 synaptosomes evoked by 4-aminopyridine.

16 ences in APD25 are still present in 3 mmol/L 4-aminopyridine.

17 yanodine on residual release was reversed by 4-aminopyridine.

18 ive to charybdotoxin (200 nM) but blocked by 4-aminopyridine.

19 re increased after blocking Kv channels with 4-aminopyridine.

20 nd block of the transient outward current by 4-aminopyridine.

21 o seizures induced by topical application of 4-aminopyridine.

22 ctal events elicited with focal injection of 4-aminopyridine.

23 outward current that was also suppressed by 4-aminopyridine (0.5 mM).

24 rophenylsulfonyloxy)phenoxy]ethyl]-N- methyl-4 -aminopyridine (1), has been determined to 2.20 A reso

25 IPO was blocked by Ba2+ (1 mM), 4-aminopyridine (1 mM) and tetraethylammonium (TEA; 20 m

26 Application of 4-aminopyridine (1 mM) to normal TTX-resistant bladder a

27 Transient outward current (I(to)) block with 4-aminopyridine (1 to 2 mmol/L) or quinidine (5 micromol

28 allergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and allergic rats tr

29 ockers of other types of K(+) channels (1 mM 4-aminopyridine, 1 mM TEA+, and 10 mu M glibenclamide),

30 The current was inhibited by 4-aminopyridine (10 mM) and tetraethylammonium (4-25 mM)

31 nnel blockers tetraethylammonium (10 mM) and 4-aminopyridine (10 mM) markedly increased the amplitude

32 ic cells were disclosed after application of 4-aminopyridine (100 microM), indicating that these syna

33 d with oral, extended-release dalfampridine (4-aminopyridine) 10mg twice daily.

34 al Ba2+ and Cs+, slightly attenuated by 5 mM 4-aminopyridine (15% inhibition) and insensitive to 10 m

35 BaCl2 (1 mM) and 4-aminopyridine (2 mM) did not alter the effect of CCK.

36 normal window width I(CaL,D-C) or subsequent 4-aminopyridine (2 mm), window I(CaL,D-C) narrowing (10

37 separate sites, the K(V) channel antagonist, 4-aminopyridine (26.6 mm), was co-perfused with each vas

38 channel blockers glibenclamide (10 microM), 4-aminopyridine (3 mM) and tetraethylammonium chloride (

39 t was antagonized by a high concentration of 4-aminopyridine (3 mM).

40 a compound able to increase axon conduction, 4-aminopyridine-3-methanol, promotes further improvement

41 caused by U69593 was blocked by low doses of 4-aminopyridine (30 microM) and the selective peptide to

42 e potency to 4AP and the PET tracer 3-fluoro-4-aminopyridine (3F4AP).

43 Specifically, 3-methyl-4-aminopyridine (3Me4AP) was found to be approximately 7

44 and 3F4AP; 3-methoxy- and 3-trifluoromethyl-4-aminopyridine (3MeO4AP and 3CF(3)4AP) were found to be

45 larized potentials was reversibly blocked by 4-aminopyridine (4 mM) but not tetraethylammonium chlori

46 ontrols) (n = 6); allergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and

47 ent addition of nifedipine (to block ICa) or 4-aminopyridine (4-AP) (to block the transient outward c

48 voltage-dependent K(+) (K(V)) currents with 4-aminopyridine (4-AP) an outward current containing ina

49 pe potassium channels [blocked by 100 microM 4-aminopyridine (4-AP) and 0.5-1 microM alpha-dendrotoxi

50 Tetraethylammonium (TEA; 10 mM), 1 and 5 mM 4-aminopyridine (4-AP) and 20 nM charybdotoxin all faile

51 action potential with the K+ channel blocker 4-aminopyridine (4-AP) and by varying the extracellular

52 cked by Cs+, Ba2+ and high concentrations of 4-aminopyridine (4-AP) and TEA.

53 model also accounts for selective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), whi

54 The A-type current was blocked by 4-aminopyridine (4-AP) and was inhibited by flecainide,

55 of the dendrites similar to those seen with 4-aminopyridine (4-AP) application.

56 Aminopyridines such as 4-aminopyridine (4-AP) are widely used as voltage-activa

57 ugh L2 and L5 are not considered part of the 4-aminopyridine (4-AP) binding site, unlike the L4 hepta

58 Toxin I and 4-aminopyridine (4-AP) both increased the frequency of s

59 el blockers tetraethyl ammonium chloride and 4-aminopyridine (4-AP) both inhibited short-term copper-

60 nd was sensitive to the K(+) channel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA)

61 sently, the potassium (K(+)) channel blocker 4-aminopyridine (4-AP) constitutes the most promising tr

62 4-Aminopyridine (4-AP) has been used extensively to stud

63 h the FDA-approved potassium channel blocker 4-aminopyridine (4-AP) improves motor behavior in both s

64 rtical acute seizure focus with injection of 4-aminopyridine (4-AP) in somatosensory cortex.

65 However, although 4-aminopyridine (4-AP) inhibited peak I(A) activated by

66 4-Aminopyridine (4-AP) is a well known convulsant that e

67 4-aminopyridine (4-AP) is used and licensed as a symptom

68 The voltage-gated K(+) (Kv) channel blocker 4-aminopyridine (4-AP) is used to target symptoms of the

69 Perfusion of 4-aminopyridine (4-AP) mimicked a known effect of behavi

70 Conduction studies indicate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters nor

71 In this study we analyzed the effect of 4-aminopyridine (4-AP) on free cytosolic calcium concent

72 Nevertheless, bath application of 50 microM 4-aminopyridine (4-AP) or 250 nM veratridine both clearl

73 of para-hydrogen ( p-H(2)) and a substrate (4-aminopyridine (4-AP) or 4-methylpyridine (4-MP)) into

74 serotonin or the potassium channel blockers 4-aminopyridine (4-AP) or alpha-dendrotoxin (DTX).

75 Inhibition of KV1 channels with 4-aminopyridine (4-AP) or treatment with the epidermal g

76 (+) channels vary in sensitivity to block by 4-aminopyridine (4-AP) over a 1000-fold range.

77 The A-channel antagonist 4-aminopyridine (4-AP) produced a voltage-dependent bloc

78 f neuronal activity by the FDA-approved drug 4-aminopyridine (4-AP) rescues the number and function o

79 ansient, low-threshold K+ current, which was 4-aminopyridine (4-AP) sensitive and showed significant

80 The current blocked by low concentrations of 4-aminopyridine (4-AP) showed marked inactivation, sugge

81 er 2-3 PNs, using alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block these conductances.

82 lity that uses the potassium channel blocker 4-aminopyridine (4-AP) to induce large amplitude populat

83 cal studies have demonstrated the ability of 4-aminopyridine (4-AP) to restore electrophysiological a

84 The effect on Ito and IK(ur) of TEA and 4-aminopyridine (4-AP) was not different in cells isolat

85 amine (RAMH), tetraethyl ammonium (TEA), and 4-aminopyridine (4-AP) were applied in the superfusate.

86 show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) which suppressed the Ca2+ sensiti

87 aethylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 m

88 ibited by 1 mM Ba2+ but unaffected by 0.5 mM 4-aminopyridine (4-AP), 1 mM tetraethylammonium (TEA) or

89 , in the presence of a K(+) channel blocker, 4-aminopyridine (4-AP), 5-HT left unaltered the presynap

90 arotid body glomus cells was tested by using 4-aminopyridine (4-AP), a known suppressant of K+ curren

91 4-Aminopyridine (4-AP), a nonselective blocker of K(v) v

92 ng artificial cerebrospinal fluid containing 4-aminopyridine (4-AP), a potassium channel blocker.

93 inhibition of voltage-gated K+ channels with 4-aminopyridine (4-AP), a treatment known to increase ne

94 hat silver ion (Ag(+)) uptake is enhanced by 4-aminopyridine (4-AP), a well known voltage-sensitive p

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

96 ing step using the potassium channel blocker 4-aminopyridine (4-AP), at a low (50 microM) and at a hi

97 'N'-tetraacetic acid (BAPTA), application of 4-Aminopyridine (4-AP), expression of a Kv4.2 dominant n

98 blocked by 3,4-diaminopyridine (3,4-DAP) or 4-aminopyridine (4-AP), inhibitors of K(V) channels.

99 nhibitors of IK, tetraethylammonium (TEA) or 4-aminopyridine (4-AP), reduced the control current elic

100 ectrical and chemical synapses in sustaining 4-aminopyridine (4-AP)-evoked network activity recorded

101 in F-actin and cofilin in hippocampus due to 4-aminopyridine (4-AP)-induced seizures/epileptiform act

102 wed a fivefold increase in susceptibility to 4-aminopyridine (4-AP)-induced spontaneous ectopic firin

103 e K(+) channel mKv1.5 is thought to encode a 4-aminopyridine (4-AP)-sensitive component of the curren

104 le-cell patch clamping showed a reduction of 4-aminopyridine (4-AP)-sensitive current (Kv current) fr

105 of cerebellar Purkinje cell dendrites, and a 4-aminopyridine (4-AP)-sensitive potassium channel under

106 I(D) is a slowly inactivating 4-aminopyridine (4-AP)-sensitive potassium current of hi

107 ng produced by the potassium channel blocker 4-aminopyridine (4-AP).

108 he presence of the weak K(+) channel blocker 4-aminopyridine (4-AP).

109 rd K+ current that is largely insensitive to 4-aminopyridine (4-AP).

110 blocked by both tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

111 cesium and potassium conductances blocked by 4-aminopyridine (4-AP).

112 in the presence of the K+ channel antagonist 4-aminopyridine (4-AP).

113 el antagonists, tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

114 IK was specifically blocked by 100 microM 4-aminopyridine (4-AP).

115 or the induction of epileptiform activity by 4-aminopyridine (4-AP).

116 s in the adult mouse SVZ: type 1 cells, with 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitiv

117 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spikin

118 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for

119 tage-dependent potassium conductance blocker 4-aminopyridine (4-AP, 100 microM) abolished the inhibit

120 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both who

121 annels was blocked by a low concentration of 4-aminopyridine (4-AP, 40 microM), a significant facilit

122 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of

123 Inclusion of the A-type K+ current blocker, 4-aminopyridine (4-AP, 5 mM) in the pipette also antagon

124 lls were inhibited by applications of either 4-aminopyridine (4-AP, at micromolar levels), alpha-dend

125 nce Ca2+-activated K+ (KCa) channel blocker; 4-aminopyridine (4-AP; 1 mM), a voltage-gated K+ (KV) ch

126 M, 5 cells) while a maximal concentration of 4-aminopyridine (4-AP; 10 mM) blocked only 40% of the cu

127 ed by 65% with the potassium channel blocker 4-aminopyridine (4-AP; 100 microM) and a 12-lipoxygenase

128 sensitive to application of TEA (0.5 mm) and 4-aminopyridine (4-AP; 30 mum).

129 thylammonium (TEA; 5 mM), apamin (10 nM) and 4-aminopyridine (4-AP; 4 mM) each completely prevented t

130 tivating I(Kv) which was potently blocked by 4-aminopyridine (4-AP; IC50, 232 microM), but was almost

131 The drug 4-aminopyridine (4AP) blocks voltage-dependent potassium

132 ically, the potassium channel blocking agent 4-aminopyridine (4AP) can sometimes cause ectopic activi

133 The convulsant 4-aminopyridine (4AP) facilitates the synchronous firing

134 4-aminopyridine (4AP) is a potassium (K(+)) channel bloc

135 4-Aminopyridine (4AP) is a specific blocker of voltage-g

136 We present a model for the action of 4-aminopyridine (4AP) on K channels.

137 en the two channel types were also found for 4-aminopyridine (4AP).

138 nels and using the potassium channel blocker 4-aminopyridine (4AP).

139 ns of either bicuculline methiodide (BMI) or 4-aminopyridine (4AP).

140 uscript reports on the sustained delivery of 4-Aminopyridine (4AP, molecular weight 94.1146 g/mol), a

141 rizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammon

142 Blockade of Kv channels by 4-aminopyridine (5 mM) depolarized pulmonary artery myoc

143 othreitol or TEA (10 mM) or by extracellular 4-aminopyridine (5 mM), glibenclamide (20 microM) or TEA

144 e identity of I(A) was confirmed by applying 4-aminopyridine (5 mM), which significantly inhibited I(

145 t density and currents that are inhibited by 4-aminopyridine (5 mmol/L).

146 Conversely, 4-aminopyridine (50 microM), a potassium channel antagon

147 eous epileptiform activity induced in CA3 by 4-aminopyridine (50-100 microM) was investigated.

148 The SOR was not affected by 4-aminopyridine (6 mM).

149 Application of 2 mM 4-aminopyridine (a dose sufficient to cause channel bloc

150 ore opening and is absent in the presence of 4-aminopyridine, a compound that prevents the last gatin

151 4-Aminopyridine, a K+ channel blocker, broadened the com

152 4-Aminopyridine, a powerful modulator of sperm motility,

153 a(2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel block

154 a(2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel block

155 ng 1-s pacing cycle length in the absence of 4-aminopyridine, adding a virtual Ito-like current (n=11

156 The K(v) channel blocker 4-aminopyridine also inhibited oxyhb-induced cerebral ar

157 ts were induced by neocortical injections of 4-aminopyridine, an inhibitor of voltage-gated K+ channe

158 l vein myocytes, in the presence of 5 mmol/L 4-aminopyridine, an outwardly rectifying K+ current was

159 min, and tetraethylammonium but sensitive to 4-aminopyridine and 0.5 mM Ba2+, consistent with A-type

160 e complexes cis-[Ru(phen)2(Apy)2](2+), Apy = 4-aminopyridine and 3,4-aminopyridine, are stable in aqu

161 urrent using the specific channel antagonist 4-aminopyridine and a long-lasting delayed rectified K c

162 y rectifying current that was insensitive to 4-aminopyridine and barium.

163 ate, and increased survival were observed in 4-aminopyridine and EPI groups.

164 in F2 increased in controls but decreased in 4-aminopyridine and EPI groups.

165 Leukotriene B4 decreased in 4-aminopyridine and EPI groups.

166 plication of neuromodulators such as DCG IV, 4-aminopyridine and forskolin as well as a paired train

167 ocampal epileptiform activity is promoted by 4-aminopyridine and inhibited by GABA(B) receptor agonis

168 riefer and less frequent upon coinjection of 4-aminopyridine and leptin.

169 ur)) antagonized completely by clofilium and 4-aminopyridine and partially by tetraethylammonium, cha

170 as inhibition by hypoxia, low sensitivity to 4-aminopyridine and quinine and insensitivity to tetraet

171 nt in lactotrophs was partially sensitive to 4-aminopyridine and tetraethylammonium.

172 cked with tetrodotoxin, 3,4-diaminopyridine, 4-aminopyridine and tetraethylammonium.

173 urther and renders this channel sensitive to 4-aminopyridine and Zn(2+).

174 y by potassium ions that was reduced by 1 mM 4-aminopyridine and/or 100 nM iberiotoxin but unaffected

175 1 mm tetraethylammonium, 100 nm apamin, 1 mm 4-aminopyridine, and 10 microm glybenclamide.

176 leptiform bursts induced by 7.5mM [K(+)](o), 4-aminopyridine, and bicuculline, and electrographic sei

177 re eliminated by tetrodotoxin, reinstated by 4-aminopyridine, and blocked by ionotropic glutamate rec

178 l blockers, including tetraethylammonium and 4-aminopyridine, and insensitive to intracellular Ca2+.

179 scribe the preparation of a series of 2-acyl-4-aminopyridines, and their use as catalysts for the hyd

180 lated with expression of different ratios of 4-aminopyridine- and tetraethylammonium-sensitive K+ cur

181 ed vasoconstriction stimulated by Psora-4 or 4-aminopyridine, another KV channel inhibitor.

182 We found that during 4-aminopyridine application, both spontaneous seizure-li

183 4-Aminopyridines are valuable scaffolds for the chemical

184 en)2(Apy)2](2+), Apy = 4-aminopyridine and 3,4-aminopyridine, are stable in aqueous solution with str

185 IK(N) showed a similar sensitivity to 4-aminopyridine as IK(A) and IK(V), with 49% inhibition

186 ivating, fast inactivating, and sensitive to 4-aminopyridine at 3 mm), and I(K) (slowly activating, n

187 ating, slowly inactivating, and sensitive to 4-aminopyridine at 30 microm), I(A) (fast activating, fa

188 lammonium, or by intracellular dialysis with 4-aminopyridine, ATP, ryanodine, or heparin.

189 of K(+) antagonists used in animal research, 4-aminopyridine blocked E. coli chemotaxis between 10(-3

190 Islow is highly sensitive to 4-aminopyridine but is insensitive to tetraethylammonium

191 length, EADs were blocked by the Ito blocker 4-aminopyridine, but reappeared when a virtual current w

192 2O2-elicited dilation to a similar extent as 4-aminopyridine, but the selective KV1.3 blocker phenoxy

193 Internal 4-aminopyridine, Ca2+ (10(-8) to 10(-6) M), and tetraeth

194 4-Aminopyridines can also be prepared directly from 4-me

195 Enhancement of transmitter release with 4-aminopyridine caused a significant increase in quantal

196 In the presence of 4-aminopyridine, depolarizing pulses evoked transient ou

197 sion in muscle cells, we identified a unique 4-aminopyridine derivative exhibiting an embedded partia

198 4-Aminopyridine derivatives yielded oligoadenylates as l

199 However, 4-aminopyridine did not affect the adaptation of rapidly

200 4-Aminopyridine did not change DeltaV(-)(m)/DeltaV(+)(m)

201 lation was inhibited by paxilline but not by 4-aminopyridine, diphenylphosphine oxide-1, or 5-(4-phen

202 Addition of bicuculline and 4-aminopyridine facilitated the occurrence of large even

203 ngle-cell resolution, the dynamics of acute (4-aminopyridine) focal cortical seizures as they origina

204 4-aminopyridine, gaboxadol hydrochloride and N-acetylneu

205 4-Aminopyridine gave extensive protection against a numb

206 not blocked by tetraethylammonium chloride, 4-aminopyridine, glibenclamide, apamin or MK-499.

207 stamine level was higher in controls and the 4-aminopyridine group but reduced in the EPI group.

208 Metabolic acidosis was prevented in the 4-aminopyridine group.

209 d in controls and EPI group and decreased in 4-aminopyridine group; prostaglandin F2 increased in con

210 ethylammonium (half-block by 150 microm) and 4-aminopyridine (half-block by 110 microm).

211 combination with low, subepileptic levels of 4-aminopyridine, Halorhodopsin activation rapidly induce

212 eatment of central vestibular disorders with 4-aminopyridine has been extended to patients with ataxi

213 es in nystagmus treatment, like the usage of 4-aminopyridine, have added potent medications to the ph

214 by its sensitivity to low concentrations of 4-aminopyridine (IC50 <100 mum) and block by the peptide

215 Clinical studies suggested that fampridine (4-aminopyridine) improves motor function in people with

216 F, 20 mM tetraethylammonium in ACSF, or 1 mM 4-aminopyridine in ACSF.

217 Pharmacological reduction of Ito by 4-aminopyridine in control myocytes decreased the notch

218 state outward current was eliminated by 1 mM 4-aminopyridine in Kv1.4+/+, Kv1.4+/- and Kv1.4-/- myocy

219 perfusion with the potassium channel blocker 4-aminopyridine in Mg(2+)-free medium.

220 rizations were observed after application of 4-aminopyridine in Tg mice.

221 We induced focal neocortical seizures with 4-aminopyridine in transgenic mice expressing green fluo

222 armacological manipulations (bicuculline and 4-aminopyridine) in the entorhinal cortex and in the hip

223 Conversely, 4-aminopyridine increased resting tension with an EC50 (

224 ke with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequency of dopamine tran

225 ding a dominant-negative Kv4.2 construct and 4-aminopyridine, increased the amplitude of plateau pote

226 of the K+ channel blockers glibenclimide and 4-aminopyridine indicating that their protective mechani

227 55 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, indicating that LC causes vasodilation

228 Potassium channel blockers, such as 4-aminopyridine, induce vasoconstriction.

229 However, the 4-aminopyridine-induced GABA-dependent negative potentia

230 4-Aminopyridine-induced hyperactivation even in cells su

231 locker) decreased the cumulative duration of 4-aminopyridine-induced ictal-like activities, with a sl

232 lular electrophysiological recordings during 4-aminopyridine-induced neocortical spikes and seizures.

233 T because directly broadening the spike with 4-aminopyridine induces adult-like SDD synaptic facilita

234 urons from lean mice, the Kv channel blocker 4-aminopyridine inhibited leptin-induced changes in inpu

235 currents contribute to the Ca(2+)-dependent 4-aminopyridine-insensitive component of the transient o

236 IK1 was a 4-aminopyridine-insensitive current with a negative half

237 nels underlie the transient Ca(2+)-activated 4-aminopyridine-insensitive current, which contributes t

238 sting membrane potential, in the presence of 4-aminopyridine, ionotropic glutamate receptor antagonis

239 ked transmitter release could be reversed by 4-aminopyridine, it is suggested that the effect on rele

240 Low doses of 4-aminopyridine (<100 microm) reduced the oscillations a

241 tion of cholinergic interneuron spiking with 4-aminopyridine mimicked the effects of exogenous agonis

242 We have addressed this issue in the 4-aminopyridine model of epilepsy in vitro by comparing

243 We conclude that, in the 4-aminopyridine model of epilepsy in vitro, connexin36 i

244 the mouse entorhinal cortex in the in vitro 4-aminopyridine model of epileptiform synchronization.

245 ns in the entorhinal cortex, in the in vitro 4-aminopyridine model.

246 t Kv3.1b does not account for the effects of 4-aminopyridine on central myelinated tracts.

247 Application of 4-aminopyridine on slices resulted in spontaneous networ

248 te intraocular pressure increases induced by 4-aminopyridine or a selective agonist of the A3 adenosi

249 Blockade of the current by low doses of 4-aminopyridine or alpha-dendrotoxin dramatically slows

250 y of neither sEPSCs nor mEPSCs stimulated by 4-aminopyridine or capsaicin differed significantly betw

251 4-Aminopyridine or depolarized conditioning blocked the

252 uced epileptiform activity induced by either 4-aminopyridine or Mg(2+)-free medium alone.

253 4-aminopyridine or related voltage-dependent K channel b

254 campal slices perfused with 7.5mM [K(+)](o), 4-aminopyridine, or bicuculline, and in vivo against sei

255 alen, or broad-spectrum K(+) channel blocker 4-Aminopyridine, or by knockdown of Kv1.3 expression via

256 s targeting different convulsant mechanisms (4-Aminopyridine, Pentylenetetrazole, Pilocarpine and Str

257 rast, blockade of motor neuron K channels by 4-aminopyridine prolonged the action potential and intro

258 Our data point to I(to) block (4-aminopyridine, quinidine) as an effective pharmacologi

259 s, the relatively broad K(+) channel blocker 4-aminopyridine reduced the fast repolarization, resulti

260 The potassium channel blocker 4-aminopyridine reliably induces seizure-like events in

261 only likely permeant ion is Cl- to identify 4-aminopyridine-resistant unitary Ca(2+)-activated Cl- c

262 f a rapidly activating, slowly inactivating, 4-aminopyridine sensitive outward K+ current.

263 el evidence that oxyhb selectively decreases 4-aminopyridine sensitive, voltage-dependent K(+) channe

264 IK2 was a 4-aminopyridine-sensitive current (half-maximal block at

265 IK,A was a 4-aminopyridine-sensitive current with a negative inacti

266 Block of 4-aminopyridine-sensitive K(+) currents increased the am

267 frequency of bicuculline-, picrotoxin-, and 4-aminopyridine-sensitive miniature IPSCs (mIPSCs) media

268 g was the presence of very high conductance, 4-aminopyridine-sensitive multistate channels resembling

269 inwardly rectifying K(+) (Kir) channels and 4-aminopyridine-sensitive outwardly rectifying voltage-g

270 O2 reversibly inhibits a 58-pS voltage- and 4-aminopyridine-sensitive potassium channel, causing mem

271 icant increase (approximately 1.5-fold) in a 4-aminopyridine-sensitive transient outward K+ current (

272 cting NTS neurons displayed large transient, 4-aminopyridine-sensitive, A-type currents (IKA).

273 y receive, and the density of low-threshold, 4-aminopyridine-sensitive, transient K+ current.

274 In isolated pulmonary arteries, 4-aminopyridine significantly inhibited NO-induced relax

275 current was insensitive to nifedipine, TEA, 4-aminopyridine, SK&F 96365 and S-nitroso-N-acetyl-penic

276 formation and parasite growth depends on its 4-aminopyridine substructure.

277 el and with the potassium channel inhibitor, 4-aminopyridine, suggested that D1-type receptors enhanc

278 ulse duration and remains in the presence of 4-aminopyridine, suggesting the existence of an intrinsi

279 c administration of the K(+) channel blocker 4-aminopyridine, suggesting the presence of latent conne

280 g them, [(18)F]3F4AP-a fluorinated analog of 4-aminopyridine-targets voltage-gated potassium channels

281 d K+ concentrations, the K+ channel blockers 4-aminopyridine, tetraethylammonium ions and XE991.

282 ucturally diverse polycyclic fused and spiro-4-aminopyridines that are prepared in only three steps f

283 erimental condition (ie, bath application of 4-aminopyridine), the initiation of low-voltage, fast an

284 are decreased markedly by acetazolamide and 4-aminopyridine, the primary treatments for EA2, suggest

285 ive of this study was to test the ability of 4-aminopyridine to restore blood pressure and increase s

286 All allergic 4-aminopyridine-treated rats survived after the inductio

287 voltage-dependent K+ channel inhibition with 4-aminopyridine treatment restores blood pressure and in

288 The IA channel blocker 4-aminopyridine triggered AP generation in TNs and preve

289 convenient substrates for the preparation of 4-aminopyridines under thermal metal-free conditions.

290 However, only 4-aminopyridine was able to reduce the transient hyperpo

291 ponse of [Ca2+]cyt to the KV channel blocker 4-aminopyridine was significantly attenuated in PPH-PASM

292 The convulsant 4-aminopyridine was used to induce interictal activity a

293 4-Aminopyridine was well tolerated up to 2.6 mg/kg per d

294 Nifedipine and 4-aminopyridine were applied to inhibit the L-type calci

295 Likewise, 4-aminopyridine, which augments transmitter release at p

296 tions also abolished Shaker's sensitivity to 4-aminopyridine, which is a pharmacological tool to isol

297 nor the kinetics of AMPA EPSC was altered by 4-aminopyridine, while the maximal number of quanta incr

298 The reaction of 3-halo-4-aminopyridines with acyl chlorides and triethylamine i

299 ensitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 values of 21.7 micromol/L, 1.

300 ts inhibited by tetraethylammonium (TEA) and 4-aminopyridine, with similar Kd values to that of Kv2.1