| Name | sodium channel (protein family or complex) |
|---|---|
| Synonyms | Sodium channel |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11586111 | Dumont RJ, Verma S, Okonkwo DO, Hurlbert RJ, Boulos PT, Ellegala DB, Dumont AS: Acute spinal cord injury, part II: contemporary pharmacotherapy. Clin Neuropharmacol. 2001 Sep-Oct;24(5):265-79. Myriad treatment modalities, including corticosteroids, 21-aminosteroids, opioid receptor antagonists, gangliosides, (TRH) and TRH analogs, antioxidants and free radical scavengers, calcium channel blockers, replacement therapy, sodium channel blockers, N -methyl-D- receptor antagonists, alpha-amino-3--5-methylisoxazole-4--kainate receptor antagonists, modulators of arachadonic acid metabolism, neurotrophic growth factors, antagonists, antibodies against inhibitors of axonal regeneration, potassium channel blockers (4-aminopyridine), paclitaxel, clenbuterol, gabexate mesylate, activated protein C, caspase inhibitors, tacrolimus, antibodies against adhesion molecules, and other immunomodulatory therapy have been studied to date. |
31(0,1,1,1) | Details |
| 12645037 | Caputi L, Hainsworth A, Guatteo E, Tozzi A, Stefani A, Spadoni F, Leach M, Bernardi G, Mercuri NB: Actions of the sodium channel inhibitor 202W92 on rat midbrain dopaminergic neurons. Synapse. 2003 Jun 1;48(3):123-30. It also inhibited the frequency of 4-aminopyridine (4-AP)- and electrically evoked excitatory postsynaptic currents (EPSCs) and GABAergic inhibitory postsynaptic currents (IPSCs), with > 80% inhibition at 10 microM (IC (50) 1.5 microM). |
3(0,0,0,3) | Details |
| 15851155 | Fish JM, Antzelevitch C: Role of and calcium channel block in unmasking the Brugada syndrome. Heart Rhythm. 2004 Jul;1(2):210-7. Terfenadine-induced ST segment elevation was normalized and arrhythmias suppressed following I (to) block with 4-aminopyridine (0.5-2 mM). The ECG sign of BS is often concealed, but can be unmasked with potent sodium channel blockers. |
2(0,0,0,2) | Details |
| 12580050 | Fu LY, Li Y, Xia GJ, Yao WX, Jiang MX: [Effects of 4-aminopyridine on currents and currents in guinea pig ventricular myocytes]. Yao Xue Xue Bao. 2001 Apr;36(4):250-3. METHODS: L-type calcium channel and sodium channel currents were recorded in guinea pig single ventricular myocyte using whole-cell patch-clamp techniques. |
2(0,0,0,2) | Details |
| 11325354 | Liu X, Zhou JL, Chung K, Chung JM: Ion channels associated with the ectopic discharges generated after segmental spinal nerve injury in the rat. Brain Res. 2001 May 4;900(1):119-27. The main focus of the study was to examine the effect of the sodium channel blocker, tetrodotoxin (TTX), in order to identify important subtype (s) (i.e. |
2(0,0,0,2) | Details |
| 10852214 | Lefebvre C, Fisher K, Cahill CM, Coderre TJ: Evidence that -induced nociception depends on release from primary afferent C-fibres. Neuroreport. 2000 Jun 5;11(8):1631-5. Pretreatment with drugs that have been shown to inhibit release, including a group II metabotropic glutamate receptor (mGluR) agonist (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate ((2R,4R)-APDC), a group III mGluR agonist L-2-amino-4-phosphonobutyrate (L-AP4), or the use-dependent sodium channel blockers 3,5-diamino-6-(2,3-diclorophenyl)-1,2,4-triazine and 2-amino-6-trifluoromethoxybenzothiazole (riluzole), produced dose-dependent reductions in (RS)--induced SNBs. We have also shown that incubation of rat lumbar spinal cord slices with (RS)- potentiates 4-aminopyridine-evoked (4-AP) release of |
1(0,0,0,1) | Details |
| 11431490 | Nunemaker CS, DeFazio RA, Geusz ME, Herzog ED, Pitts GR, Moenter SM: Long-term recordings of networks of immortalized GnRH neurons reveal episodic patterns of electrical activity. J Neurophysiol. 2001 Jul;86(1):86-93. Long-term, multi-site recordings of GT1-7 cells revealed repeated episodes of increased firing rate with an interval of 24.8 +/- 1.3 (SE) min that were completely eliminated by tetrodotoxin, a sodium channel blocker. The A-type potassium-channel antagonist 4-aminopyridine (1 mM) increased both firing rate and GnRH secretion, demonstrating the presence of A-type currents in these cells and supporting the hypothesis that electrical activity is associated with GnRH release. |
1(0,0,0,1) | Details |
| 11374879 | Denda M, Ashida Y, Inoue K, Kumazawa N: Skin surface electric potential induced by ion-flux through epidermal cell layers. Biochem Biophys Res Commun. 2001 Jun 1;284(1):112-7. and sodium channel blockers also reduced the potential. |
1(0,0,0,1) | Details |
| 11701138 | Caputi L, Hainsworth AH, Lavaroni F, Leach MJ, McNaughton NC, Mercuri NB, Randall AD, Spadoni F, Swan JH, Stefani A: Neuroprotective actions in vivo and electrophysiological actions in vitro of 202W92. Brain Res. 2001 Nov 23;919(2):259-68. The drug inhibited the amplitude and frequency of 4-aminopyridine-evoked glutamatergic excitatory post-synaptic currents (EPSCs). In conclusion, 202W92 is an effective neuroprotective agent when administered post-ischaemia and a potent sodium channel inhibitor in vitro. |
1(0,0,0,1) | Details |
| 19111909 | Chindo BA, Anuka JA, McNeil L, Yaro AH, Adamu SS, Amos S, Connelly WK, Lees G, Gamaniel KS: Anticonvulsant properties of saponins from Ficus platyphylla stem bark. Brain Res Bull. 2009 Mar 30;78(6):276-82. Epub 2008 Dec 26. SFG impaired membrane excitability; a property shared by most anticonvulsants particularly the voltage-gated sodium channel (VGSC) blocking drugs, thus supporting the isolation and development of the saponin components of this plant as anticonvulsant agents. SFG neither abolished the spontaneous discharges induced by 4-aminopyridine in a neonatal rat brain slice model of tonic-clonic epilepsy nor could it modulate currents through (A) receptor channel complex in cultured cortical cells. |
1(0,0,0,1) | Details |
| 15472024 | Pennec JP, Talarmin H, Droguet M, Giroux-Metges MA, Gioux M, Dorange G: Characterization of the voltage-activated currents in cultured atrial myocytes isolated from the heart of the common oyster Crassostrea gigas. J Exp Biol. 2004 Oct;207(Pt 22):3935-44. When they exist, the fast sodium channel is blocked by tetrodotoxin. |
1(0,0,0,1) | Details |
| 11322931 | Ambrosio AF, Silva AP, Malva JO, Soares-da-Silva P, Carvalho AP, Carvalho CM: Inhibition of release by BIA 2-093 and BIA 2-024, two novel derivatives of carbamazepine, due to blockade of but not channels. Biochem Pharmacol. 2001 May 15;61(10):1271-5. The AEDs inhibited the release of evoked by 4-aminopyridine (4-AP) or veratridine in a concentration-dependent manner, being CBZ more potent than the other AEDs. The results indicate that BIA 2-093 and BIA 2-024 have sodium channel-blocking properties, but CBZ and OXC are more potent than the new AEDs. |
1(0,0,0,1) | Details |
| 19558973 | Baylor K, Stecker MM: Peripheral nerve at extreme low temperatures 2: pharmacologic modulation of temperature effects. Cryobiology. 2009 Aug;59(1):12-8. Epub 2009 Feb 5. The reduction in conduction velocity with temperature was shown to be independent of the ionic composition of the perfusate and was unaffected by or sodium channel blockade. Blockade of channels and chronic membrane depolarization produced by high perfusate concentrations or high dose 4-aminopyridine impair the resistance of the nerve to hypothermia and enhance the injury to the nerve produced by cycles of cooling and rewarming. |
1(0,0,0,1) | Details |
| 15546779 | Sitges M, Nekrassov V: Vinpocetine prevents 4-aminopyridine-induced changes in the EEG, the auditory brainstem responses and hearing. Clin Neurophysiol. 2004 Dec;115(12):2711-7. OBJECTIVE: The purpose of the present study was to investigate if the sodium channel blocker and memory enhancer, vinpocetine, was capable to overcome the epileptic cortical activity, the abnormalities in the later waves of the auditory brainstem responses (ABRs) and the hearing loss induced by 4-AP at a convulsing dose in the guinea pig in vivo. |
1(0,0,0,1) | Details |
| 19118105 | Acker CD, Antic SD: Quantitative assessment of the distributions of membrane conductances involved in action potential backpropagation along basal dendrites. J Neurophysiol. 2009 Mar;101(3):1524-41. Epub 2008 Dec 31. The best-fit model included a nonuniform sodium channel distribution with decreasing conductance with distance from the soma, together with a nonuniform (increasing) A-type conductance. |
1(0,0,0,1) | Details |
| 12763062 | Lee JH, Marcus DC: Endolymphatic homeostasis by Reissner's membrane. Neuroscience. 2003;119(1):3-8. I (sc) was inhibited by amiloride analogs in the potency sequence benzamil> amiloride>> ethylisopropylamiloride, consistent with Na (+) absorption through an epithelial sodium channel in the apical cell membrane. I (sc) was also inhibited by an inhibitor of Na (+),K (+)-ATPase, ouabain, and by the K (+) channel blockers Ba (2+), 4-aminopyridine and quinine but not tetraethylammonium nor glibenclamide, consistent with the presence of a voltage-activated K (+) channel. |
1(0,0,0,1) | Details |
| 19955484 | Jiang P, Rushing SN, Kong CW, Fu J, Lieu DK, Chan CW, Deng W, Li RA: Electrophysiological properties of human induced pluripotent stem cells. . Am J Physiol Cell Physiol. 2010 Mar;298(3):C486-95. Epub 2009 Dec 2. By contrast, 4-aminopyridine (4-AP) inhibited viability (EC (50) = 4.5 +/- 0.5 mM) but had less effect on proliferation (EC (50) = 0.9 +/- 0.5 mM). |
0(0,0,0,0) | Details |
| 16187302 | Smith GT: Pharmacological characterization of ionic currents that regulate high-frequency spontaneous activity of electromotor neurons in the weakly electric fish, Apteronotus leptorhynchus. J Neurobiol. 2006 Jan;66(1):1-18. As in pacemaker neurons, high-frequency firing of EMNs was regulated primarily by tetrodotoxin-sensitive currents and by currents that were sensitive to 4-aminopyridine and kappaA-conotoxin SIVA, but resistant to tetraethylammonium. |
0(0,0,0,0) | Details |
| 15122647 | Pizzo AB, Beleboni RO, Fontana AC, Ribeiro AM, Miranda A, Coutinho-Netto J, dos Santos WF: Characterization of the actions of AvTx 7 isolated from Agelaia vicina (Hymenoptera: Vespidae) wasp venom on synaptosomal uptake and release. J Biochem Mol Toxicol. 2004;18(2):61-8. AvTx 7 potentiates release in the presence of K (+) channel blockers tetraethylammonium and 4-aminopyridine, indicating that the toxin may act through these drugs-sensible K (+) channels. |
0(0,0,0,0) | Details |
| 10640333 | Smith GT, Zakon HH: Pharmacological characterization of ionic currents that regulate the pacemaker rhythm in a weakly electric fish. J Neurobiol. 2000 Feb 5;42(2):270-86. Two potassium channel blockers, 4-aminopyridine (4AP) and kappaA-conotoxin SIVA, increased pacemaker firing rates by approximately 20% and then stopped pacemaker firing. |
0(0,0,0,0) | Details |