ライフサイエンスコーパス: 4-aminopyridine

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

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

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

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

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

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

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

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

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

10 tetraethylammonium chloride, iberiotoxin, or 4-aminopyridine.

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

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

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

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

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

16 vation on epileptiform discharges induced by 4-aminopyridine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 4-Aminopyridine (4-AP) has been used extensively to stud

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

57 4-Aminopyridine (4-AP) is a well known convulsant that e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 4-Aminopyridine (4-AP), a nonselective blocker of K(v) v

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spikin

106 4-aminopyridine (4-AP, 0.5 mM) reduced the threshold for

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

108 4-Aminopyridine (4-AP, 2 mm) attenuated I(A) in both who

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

110 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 4-Aminopyridine, a K+ channel blocker, broadened the com

137 4-Aminopyridine, a powerful modulator of sperm motility,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 1 mm tetraethylammonium, 100 nm apamin, 1 mm 4-aminopyridine, and 10 microm glybenclamide.

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

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

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

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

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

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

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

166 4-Aminopyridines are valuable scaffolds for the chemical

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

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

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

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

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

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

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

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

175 2O2-elicited dilation to a similar extent as 4-aminopyridine, but the selective KV1.3 blocker phenoxy

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

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

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

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

180 4-Aminopyridine derivatives yielded oligoadenylates as l

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

182 4-Aminopyridine did not change DeltaV(-)(m)/DeltaV(+)(m)

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

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

185 4-aminopyridine, gaboxadol hydrochloride and N-acetylneu

186 4-Aminopyridine gave extensive protection against a numb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 55 nM iberiotoxin, and unmodified by 0.8 mM 4-aminopyridine, indicating that LC causes vasodilation

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

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

211 4-Aminopyridine-induced hyperactivation even in cells su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 4-Aminopyridine or depolarized conditioning blocked the

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

233 4-aminopyridine or related voltage-dependent K channel b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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