| Name | calcium channel (protein family or complex) |
|---|---|
| Synonyms | calcium channel |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17724889 | Fiszer M, Kolacinski Z, Rechcinski T: [The application of 4-aminopyridine in calcium channel inhibitors acute poisoning]. Przegl Lek. 2007;64(4-5):293-7. |
33(0,1,1,3) | Details |
| 19046383 | Padmanabhan S, Lambert NA, Prasad BM: Activity-dependent regulation of the dopamine transporter is mediated by Ca (2+)/calmodulin-dependent protein kinase signaling. Eur J Neurosci. 2008 Nov;28(10):2017-27. Chronic treatment with an L-type calcium channel blocker (nifedipine) or CaM kinase inhibitor (KN93) decreased dopamine transporter-mediated uptake and occluded the effects of tetrodotoxin and 4-aminopyridine. |
31(0,1,1,1) | Details |
| 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 |
| 14506322 | Magdalan J: New treatment methods in poisoning: experimental studies. Pol J Pharmacol. 2003 May-Jun;55(3):425-32. The aim of this study was to evaluate the effectiveness of the treatment with 4-aminopyridine (4-AP, potassium channel inhibitor) and Bay K 8644 (calcium channel activator) in experimentally evoked poisoning in rats and to compare the results of this treatment with the effectiveness of widely accepted methods compounds). |
31(0,1,1,1) | Details |
| 10780986 | Bonanno G, Sala R, Cancedda L, Cavazzani P, Cossu M, Raiteri M: Release of from human neocortex nerve terminals evoked by different stimuli involving extra- and intraterminal Br J Pharmacol. 2000 Apr;129(8):1780-6. Exposure of synaptosomes to 25 microM of the broad spectrum calcium channel blocker CdCl (2) strongly inhibited the 4-aminopyridine-induced tritium overflow while that evoked by ionomycin remained unaffected. |
31(0,1,1,1) | Details |
| 12163346 | Giovannini F, Sher E, Webster R, Boot J, Lang B: Calcium channel subtypes contributing to release from normal, 4-aminopyridine-treated and myasthenic syndrome auto-antibodies-affected neuromuscular junctions. Br J Pharmacol. 2002 Aug;136(8):1135-45. |
6(0,0,1,1) | Details |
| 11865685 | Amorim S, Dias P, Rocha G, Gama G, de Campos M, Pires S: Poisoning with calcium channel blockers--a case report and review of the literature. Rev Port Cardiol. 2001 Dec;20(12):1249-57. There are alternative and adjuvant drugs such as amrinone, insulin- 4-aminopyridine and entry promoters. |
4(0,0,0,4) | Details |
| 16820010 | Cho S, Meriney SD: The effects of presynaptic calcium channel modulation by roscovitine on transmitter release at the adult frog neuromuscular junction. Eur J Neurosci. 2006 Jun;23(12):3200-8. |
3(0,0,0,3) | Details |
| 10670441 | Vilchis C, Bargas J, Ayala GX, Galvan E, Galarraga E: Ca2+ channels that activate Ca2+-dependent K+ currents in neostriatal neurons. Neuroscience. 2000;95(3):745-52. Previous work made clear that different calcium channel types contribute with a similar amount of current to whole-cell current in neostriatal neurons. Transient currents were reduced by 4-aminopyridine and currents were blocked by tetrodotoxin. |
3(0,0,0,3) | 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. |
3(0,0,0,3) | Details |
| 15051158 | Wang SJ, Wang KY, Wang WC: Mechanisms underlying the riluzole inhibition of release from rat cerebral cortex nerve terminals (synaptosomes). Neuroscience. 2004;125(1):191-201. Riluzole inhibited the -dependent release of that was evoked by exposing cerebrocortical synaptosomes to the potassium channel blocker 4-aminopyridine, and this presynaptic inhibition was concentration-dependent. A possible effect of riluzole on synaptosomal channels was confirmed in experiments where synaptosomes pretreated with P/Q-type calcium channel blocker omega-agatoxin IVA, which abolished the riluzole-mediated inhibition of release. |
2(0,0,0,2) | Details |
| 16424798 | Lam FF, Yeung JH, Cheung JH, Or PM: Pharmacological evidence for calcium channel inhibition by danshen (Salvia miltiorrhiza) on rat isolated femoral artery. J Cardiovasc Pharmacol. 2006 Jan;47(1):139-45. A 3.3-fold shift was produced on the concentration-response curve of danshen when the artery rings were pretreated with a mixture of 10 mM TEA, 1 mM 4-aminopyridine (K (V) blocker), 1 microM glibenclamide (K (ATP) blocker), 100 nM iberiotoxin (BK (Ca) blocker), and 100 microM barium (K (IR) blocker). |
1(0,0,0,1) | 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. In addition, the effects of and calcium channel blockers were also tested for comparison with the results of previous studies. |
1(0,0,0,1) | 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. The nonspecific calcium channel blockers and cadmium reduced pacemaker firing rates by approximately 15-20%. |
1(0,0,0,1) | Details |
| 18365869 | Rampino T, Gregorini M, Guidetti C, Broggini M, Marchini S, Bonomi R, Maggio M, Roscini E, Soccio G, Tiboldo R, Dal Canton A: KCNA1 and TRPC6 ion channels and NHE1 exchanger operate the biological outcome of HGF/scatter factor in renal tubular cells. Growth Factors. 2007 Dec;25(6):382-91. In previous study, we found that HGF upregulated in epithelial tubular cell line (HK2) 3 genes: potassium channel KCNA1, calcium channel (transient receptor potential channel, subfamily C, member 6, TRPC6) and Na (+)/H (+) exchanger-1 (NHE1). To investigate whether KCNA1, TRPC6, NHE1 mediate the changes induced by HGF in HK2, we studied the effects of their inhibitors: 4-aminopyridine, charybdotoxin, dendrotoxin K inhibitors of KCNA1, lanthanum, N-(p-amylcinnamoyl) inhibitors of TRPC6, 5-(N-ethyl-N-isopropyl) amiloride, cariporide inhibitors of NHE1. |
1(0,0,0,1) | Details |
| 19627466 | Lee SY, Myung SC, Lee MY, Kim TH, Kim SC, Kim KD, Park SH, Kim WY: The effects of /- (DHEAS) on the contraction responses of the clitoral cavernous smooth muscle from female rabbits. J Sex Med. 2009 Oct;6(10):2653-60. Epub 2009 Jul 21. Various K channel blockers, tetraethylammonium (TEA; 1 mM, 10 mM), 4-aminopyridine (10 microM) and glibenclamide (10 microM) did not affect the /DHEAS-induced relaxation on muscle strips contracted by PE. CONCLUSIONS: /DHEAS was found to induce a relaxation response in rabbit clitoral cavernosal smooth muscle, and this is thought to be mediated by direct inhibition of a voltage-dependent calcium channel. |
1(0,0,0,1) | Details |
| 17395137 | Strupp M, Zwergal A, Brandt T: Episodic ataxia type 2. . Neurotherapeutics. 2007 Apr;4(2):267-73. Episodic ataxia type 2 (EA 2) is a rare neurological disorder of autosomal dominant inheritance resulting from dysfunction of a voltage-gated calcium channel. Two effective treatment options have been established for EA 2: acetazolamide (ACTZ), which probably changes the intracellular pH and thereby the transmembraneous potential, and 4-aminopyridine (4-AP), a potassium channel blocker. |
2(0,0,0,2) | 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). |
2(0,0,0,2) | Details |
| 15900025 | Strupp M, Kalla R, Freilinger T, Dichgans M, Brandt T: Dysfunction of the brain calcium channel CaV2.1 in absence epilepsy and episodic ataxia--a comment. Brain. 2005 Jun;128(Pt 6):E32; author reply E33. |
1(0,0,0,1) | Details |
| 11447345 | Wang SJ, Sihra TS, Gean PW: inhibition of release from isolated cerebrocortical nerve terminals (synaptosomes) by suppression of voltage-activated calcium channel activity. Neuroreport. 2001 Jul 20;12(10):2255-8. The present study was aimed at investigating the effect of LAG on the 4-aminopyridine (4AP)-evoked release in cerebrocortical nerve terminals (synaptosomes). |
1(0,0,0,1) | Details |
| 14767864 | Peuler JD, Warfield RK, Phelps LE: Attenuation by 4-aminopyridine of delayed vasorelaxation by troglitazone. Metabolism. 2004 Feb;53(2):147-52. Recently, a novel experiment was reported in which troglitazone caused a 2-phase relaxation of perfused resistance arteries, namely, an acute relaxation (within the first 20 minutes of treatment), which was blocked by a nonselective calcium channel blocker and a delayed relaxation (after 2 hours), which was not. |
1(0,0,0,1) | Details |
| 17295025 | Gupta S, Lozano-Cuenca J, Villalon CM, de Vries R, Garrelds IM, Avezaat CJ, van Kats JP, Saxena PR, MaassenVanDenBrink A: Pharmacological characterisation of -induced relaxations in human and porcine isolated arteries. Naunyn Schmiedebergs Arch Pharmacol. 2007 Mar;375(1):29-38. Epub 2007 Feb 13. Concentration response curves to were constructed in the absence or presence of the CGRP receptor antagonist olcegepant (BIBN4096BS, 1 microM), the neurokinin NK1 receptor antagonist L-733060 (0.5 microM), the voltage-sensitive calcium channel blocker ruthenium red (100 microM), the TRPV1 receptor antagonist capsazepine (5 microM), the synthetase inhibitor Nomega-nitro- methyl ester HCl (L-NAME; 100 microM), the gap junction blocker 18alpha-glycyrrhetinic acid (10 microM), as well as the RhoA kinase inhibitor Y-27632 (1 microM). Further, we also used the K+ channel inhibitors 4-aminopyridine (1 mM), charybdotoxin (0.5 microM) + apamin (0.1 microM) and iberiotoxin (0.5 microM) + apamin (0.1 microM). |
1(0,0,0,1) | Details |
| 11698549 | Xiong ZQ, Stringer JL: Prolonged bursts occur in normal in hippocampal slices after raising excitability and blocking synaptic transmission. J Neurophysiol. 2001 Nov;86(5):2625-8. Spontaneous interictal activity was induced in CA1 and CA3 by perfusing hippocampal slices with high potassium, cesium, 4-aminopyridine, or tetraethylammonium in normal levels of Synaptic transmission was then blocked by the addition of neurotransmitter receptor blockers (6-cyano-7-nitroquinoxaline-2,3-dione, D,L-2-amino-5-phosphonopentanoic acid, and bicuculline) or the calcium channel blocker cadmium, resulting in complete blockade of the interictal discharges and the appearance of spontaneous seizure-like events (ictal-like discharges) primarily in CA1 and the dentate gyrus. |
1(0,0,0,1) | Details |
| 12753410 | Uhrenholt TR, Nedergaard OA: channels involved in release from sympathetic neurones in rabbit carotid artery. Pharmacol Toxicol. 2003 May;92(5):226-33. The potassium channel blocking agent 4-aminopyridine (10-5-10-3 M) enhanced the stimulation-evoked 3H overflow up to 5 times. 4-Aminopyridine (10 (-4) M) did not alter the inhibitory effect of omega-conotoxin GVIA (3 x 10 (-8) M). The selective N-type calcium channel blocking agent omega-conotoxin GVIA (single concentrations: 3 x 10 (-10)-10 (-8) M) caused a slowly developing reduction of the stimulation-evoked 3H overflow. |
1(0,0,0,1) | Details |
| 18718350 | Strupp M, Kalla R, Glasauer S, Wagner J, Hufner K, Jahn K, Brandt T: Aminopyridines for the treatment of cerebellar and ocular motor disorders. Prog Brain Res. 2008;171:535-41. Animal experiments have shown that aminopyridines [3,4-diaminopyridine (3,4-DAP) and 4-aminopyridine (4-AP)], nonselective blockers of the Kv family of voltage-gated potassium channels, increase Purkinje-cell (PC) excitability. On the basis of these assumptions, we evaluated the efficacy and underlying mechanisms of aminopyridines in DBN and UBN as well as in another cerebellar disorder with an impaired PC function: episodic ataxia type 2 (EA2), which is caused by mutations of the PQ-calcium channel. |
1(0,0,0,1) | Details |
| 11551668 | Lopez E, Oset-Gasque MJ, Figueroa S, Albarran JJ, Gonzalez MP: Calcium channel types involved in intrinsic amino acid neurotransmitters release evoked by depolarizing agents in cortical neurons. Neurochem Int. 2001 Oct;39(4):283-90. Based on our results, we have reached the following conclusions: (1) Ca2+ channel types P/Q, N and L mediate Ca2+ entry evoked by high KCl and veratridine, and P/Q and N but not L-type Ca2+ channels are involved when the effector is 4-aminopyridine (4-AP); (2) When we compare the relationship between the amino acid release and the Ca2+ channels which are opened by different depolarizing agents, we find that the release of a particular amino acid neurotransmitter not only depends on the opening of the voltage-dependent Ca2+ channel but also on the effector which produces the opening; and (3) the amount of amino acid release evoked by the different depolarizing agents is not correlated with the elevation of intracellular Ca2+ produced by them. |
1(0,0,0,1) | Details |
| 16151435 | Wu BN, Tu HF, Welsh DG, Chen IJ: KMUP-1 activates BKCa channels in basilar artery myocytes via cyclic nucleotide-dependent protein kinases. Br J Pharmacol. 2005 Nov;146(6):862-71. Voltage-dependent L-type Ca2+ current was significantly suppressed by KMUP-1 (1 microM), and nearly abolished by a calcium channel blocker (nifedipine, 1 microM). |
1(0,0,0,1) | Details |
| 20050319 | : Changing the "channel": aminopyridines potentiate synaptic and neuromuscular transmission by targeting the voltage-activated calcium channel beta subunit. J Biol Chem. 2009 Dec 25;284(52):e99971. |
1(0,0,0,1) | Details |
| 12580063 | Zheng LX: [Effect of 4-aminopyridine on -regulated release of amino acid from rat cortical synaptosomes]. Yao Xue Xue Bao. 2001 Apr;36(4):307-9. CONCLUSION: may regulate release through presynaptic L-type calcium channel and also act on Asp- and -nereve terminal to regulate Asp and release in rat cortex. |
1(0,0,0,1) | Details |
| 11842444 | Wang SJ: Inhibition of release by fluspirilene in cerebrocortical nerve terminals (synaptosomes). Synapse. 2002 Apr;44(1):36-41. Besides its well-known actions on the receptors, fluspirilene also displays calcium channel-blocking activity. The aim of this study was to investigate the effect of fluspirilene on the 4-aminopyridine (4AP)-evoked release in the cerebrocortical nerve terminals (synaptosomes). |
1(0,0,0,1) | Details |
| 16579053 | Raginov IS, Cherepnev GV, Garaev RS: [Effect of xymedone on high-voltage-activated Ca2+ currents in pyramidal neurons of the entorhinal cortex]. Eksp Klin Farmakol. 2006 Jan-Feb;69(1):18-20. The sample slices were superfused with artificial cerebrospinal fluid containing tetrodotoxin, 4-aminopyridine, and tetraethylammonium for the blocking of Na+ and K+ channels, respectively. The obtained data showed for the first time that xymedone exhibits a calcium channel blocker activity in neurons. |
1(0,0,0,1) | Details |
| 18342060 | Shipley E, Krim E, Deminiere C, Lagueny A: [Lambert-Eaton Myasthenic Syndrome associated with vocal cord carcinoma] . Rev Neurol. 2008 Jan;164(1):72-6. Epub 2008 Jan 30. Diagnosis of LEMS was confirmed by electrophysiologic study and anti-voltage gated calcium channel antibodies (90pM, positive value greater or equal to 70pM). |
1(0,0,0,1) | Details |
| 15353504 | Thebaud B, Michelakis ED, Wu XC, Moudgil R, Kuzyk M, Dyck JR, Harry G, Hashimoto K, Haromy A, Rebeyka I, Archer SL: -sensitive Kv channel gene transfer confers responsiveness to preterm rabbit and remodeled human ductus arteriosus: implications for infants with patent ductus arteriosus. Circulation. 2004 Sep 14;110(11):1372-9. Epub 2004 Sep 7. This is associated with decreased mRNA and protein expression of certain O2-sensitive Kv channels (Kv1.5 and Kv2.1) but equivalent expression of the L-type calcium channel. |
1(0,0,0,1) | Details |
| 16686648 | Weiergraber M, Henry M, Krieger A, Kamp M, Radhakrishnan K, Hescheler J, Schneider T: Altered seizure susceptibility in mice lacking the Ca (v) 2.3 E-type Ca2+ channel. Epilepsia. 2006 May;47(5):839-50. In addition, convulsive seizure activity was induced by systemic administration of either 4-aminopyridine (4-AP; 10 mg/kg, i.p.) or pentylenetetrazol (PTZ; 80 mg/kg, s.c.) to reveal possible alterations in seizure susceptibility. |
0(0,0,0,0) | Details |
| 10583911 | Hendriks R, Morest DK, Kaczmarek LK: Role in neuronal cell migration for high-threshold currents in the chicken hindbrain. J Neurosci Res. 1999 Dec 15;58(6):805-14. These currents were completely suppressed by the potassium channel blockers, 1.0 mM tetraethylammonium (TEA) or 1.0 mM 4-aminopyridine (4-AP). |
0(0,0,0,0) | Details |
| 15843617 | Weisz CJ, Raike RS, Soria-Jasso LE, Hess EJ: Potassium channel blockers inhibit the triggers of attacks in the calcium channel mouse mutant tottering. J Neurosci. 2005 Apr 20;25(16):4141-5. These mutations predict reduced currents, particularly in cerebellar Purkinje cells, where these channels are most abundant. 4-Aminopyridine (4-AP), a nonselective blocker of K (v) voltage-gated potassium channels, alleviates attacks of ataxia in EA2 patients. |
1(0,0,0,1) | Details |
| 20157397 | Kim JK, Han WH, Lee MY, Myung SC, Kim SC, Kim MK: relaxes rabbit seminal vesicle by calcium channel inhibition. . Korean J Physiol Pharmacol. 2008 Apr;12(2):73-7. Epub 2008 Apr 30. Various K (+) channel blockers, such as tetraethylammonium (TEA; 10 mM), iberiotoxin (0.1 microM), 4-aminopyridine (4-AP, 10 microM), or glibenclamide (10 microM) rarely affected these relaxations. |
1(0,0,0,1) | Details |
| 11041555 | Kurtz A, Hamann M, Gotz K: Role of channels in the control of renin secretion from isolated perfused rat kidneys. Pflugers Arch. 2000 Oct;440(6):889-95. For this purpose we examined the effects of the K+ channel blockers 4-aminopyridine (1 mmol/l), barium (100 micromol/l), tetraethylammonium (2 mmol/l) and apamin (200 nmol/l) on basal renin secretion, on renin secretion stimulated by isoproterenol (10 nmol/l) and on the inhibition of renin secretion by angiotensin II (100-300 pmol/l) in the isolated rat kidney perfused at constant pressure. |
0(0,0,0,0) | 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 |
| 12798424 | Workman AJ, Kane KA, Russell JA, Norrie J, Rankin AC: Chronic beta-adrenoceptor blockade and human atrial cell electrophysiology: evidence of pharmacological remodelling. Cardiovasc Res. 2003 Jun 1;58(3):518-25. The I (TO) blocker 4-aminopyridine largely mimicked the changes in phase 1 and ERP associated with chronic beta-blockade, in cells from non-beta-blocked patients. |
0(0,0,0,0) | Details |
| 14716629 | Fish JM, Antzelevitch C: Cellular and ionic basis for the sex-related difference in the manifestation of the Brugada syndrome and progressive conduction disease phenotypes. J Electrocardiol. 2003;36 Suppl:173-9. Male preparations pretreated with 4-aminopyridine to inhibit Ito displayed progressive conduction impairment but not Brugada syndrome. We hypothesized that these differences may be related to a larger transient outward current (Ito)-mediated right ventricular (RV) epicardial (Epi) action potential (AP) notch in males versus females, resulting in a higher incidence of all-or-none repolarization at the end of phase 1 and phase 2 re-entry (P2R) when challenged with and calcium channel block. |
1(0,0,0,1) | Details |
| 19850918 | Wu ZZ, Li DP, Chen SR, Pan HL: Aminopyridines potentiate synaptic and neuromuscular transmission by targeting the voltage-activated calcium channel beta subunit. J Biol Chem. 2009 Dec 25;284(52):36453-61. Epub 2009 Oct 22. Aminopyridines such as 4-aminopyridine (4-AP) are widely used as voltage-activated K (+) (Kv) channel blockers and can improve neuromuscular function in patients with spinal cord injury, myasthenia gravis, or multiple sclerosis. |
1(0,0,0,1) | Details |