| Name | SNAP |
|---|---|
| Synonyms | RIC 4; RIC4; SEC 9; SEC9; SNAP; SNAP 25; SNAP25; SUP… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 10618154 | Ghisdal P, Gomez JP, Morel N: Action of a NO donor on the excitation-contraction pathway activated by in rat superior mesenteric artery. J Physiol. 2000 Jan 1;522 Pt 1:83-96. Responses to SNAP were unaffected by the following K+ channel blockers: glibenclamide, 4-aminopyridine, apamin and charybdotoxin, and by increasing the KCl concentration to 25 mM. |
11(0,0,1,6) | Details |
| 10832600 | Terluk MR, da Silva-Santos JE, Assreuy J: Involvement of soluble guanylate cyclase and -activated channels in the long-lasting hyporesponsiveness to induced by in rat aorta. Naunyn Schmiedebergs Arch Pharmacol. 2000 May;361(5):477-83. Contraction of rings without endothelium by (0.1 nM to 100 microM) was decreased by 50-60% after incubation (30 min) with sodium nitroprusside (3-300 microM) or S-nitroso-acetyl-D,L-penicillamine (SNAP; 70-200 microM). In contrast, 4-aminopyridine (1 mM) and glibenclamide (10 microM) had no effect. |
1(0,0,0,1) | Details |
| 16474412 | Romano MR, Lograno MD: Cannabinoid agonists induce relaxation in the bovine ophthalmic artery: evidences for CB1 receptors, and channels. Br J Pharmacol. 2006 Apr;147(8):917-25. In endothelium-intact arteries, the synthase inhibitor, N (G)-monomethyl- (L-NMMA, 300 microM), completely blocked the - and WIN55212-2-relaxant responses; by contrast, the donor S-nitroso-N-acetylpenicillamine (SNAP, 100 microM) induced an increase in vasorelaxant responses to cannabinoid agonists. Relaxations to and WIN55212-2 were inhibited by iberiotoxin (IbTX, 200 nM), a blocker of large conductance, Ca2+-activated K+ channel (BK (Ca)), and by 4-aminopyridine (4-AP; 1 mM), a blocker of delayed rectifier K+ channel, whereas the blockade of K (ATP) channels by glibenclamide (5 microM) and of small conductance Ca2+-activated K+ channels (SK (Ca)) by apamin (100 nM) did not produce any effects. |
1(0,0,0,1) | Details |
| 10978741 | Adler M, Keller JE, Sheridan RE, Deshpande SS: Persistence of botulinum neurotoxin A demonstrated by sequential administration of serotypes A and E in rat EDL muscle. Toxicon. 2001 Feb-Mar;39(2-3):233-43. Botulinum neurotoxin serotypes A (BoNT/A) and E (BoNT/E) inhibit neurotransmitter release from peripheral cholinergic nerve terminals by cleaving different sites on SNAP-25, a protein involved in synaptic vesicle docking and exocytosis. |
2(0,0,0,2) | Details |
| 10781419 | Janssen LJ, Premji M, Lu-Chao H, Cox G, Keshavjee S: NO (+) but not NO radical relaxes airway smooth muscle via -independent release of internal Ca (2+). Am J Physiol Lung Cell Mol Physiol. 2000 May;278(5):L899-905. SNAP evoked a rise in [Ca (2+)](i) that was unaffected by removing external Ca (2+) but was markedly reduced by depleting the internal Ca (2+) pool using cyclopiazonic acid (10 (-5) M). SNAP relaxations were sensitive to charybdotoxin (10 (-7) M) or tetraethylammonium (30 mM) but not to 4-aminopyridine (1 mM). |
1(0,0,0,1) | Details |
| 16716281 | Zhang Y, Tazzeo T, Chu V, Janssen LJ: Membrane currents in human radial artery and their regulation by donor. Cardiovasc Res. 2006 Jul 15;71(2):383-92. Epub 2006 Apr 21. The donor SNAP augmented membrane K (+) currents in a concentration-dependent fashion; the augmentation was completely suppressed by TEA, but was relatively insensitive to the guanylate cyclase inhibitor ODQ. The K (+) currents were predominantly sensitive to the K (Ca) blocker tetraethylammonium (TEA; 63.9+/-12.1% inhibition, p <0.05), less sensitive to the Kv blocker 4-aminopyridine (4-AP; 32.8+/-4.4% inhibition, p <0.05), and the K (ATP) blocker glibenclamide (28.7+/-8.5% inhibition), at -20 mV testing potential. |
1(0,0,0,1) | Details |
| 10763852 | Mazzuco TL, Andre E, Calixto JB: Contribution of prostanoids and Ca (2+)-activated K+ channels to the relaxant response of bradykinin in the guinea pig bronchus in vitro. Naunyn Schmiedebergs Arch Pharmacol. 2000 Apr;361(4):383-90. However, ODQ almost abolished SNAP-induced relaxation. In contrast, 4-aminopyridine, apamin or glibenclamide did not affect BK-induced relaxation. |
1(0,0,0,1) | Details |
| 20054493 | Lee JJ: modulation of GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons. Korean J Physiol Pharmacol. 2009 Dec;13(6):461-7. Epub 2009 Dec 31. Blockade of presynaptic K (+) channels by 4-aminopyridine, a K (+) channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic Ca (2+) channels by Cd (2+), a general voltage-dependent Ca (2+) channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. |
1(0,0,0,1) | Details |
| 11485374 | Hermann A, Erxleben C: activates voltage-dependent currents of crustacean skeletal muscle. Nitric Oxide. 2001 Aug;5(4):361-9. Both currents were blocked by extracellular 4-aminopyridine and tetraethylammonium; the currents were not blocked by charybdotoxin or apamin. |
0(0,0,0,0) | Details |
| 14746926 | Schrofner S, Zsombok A, Hermann A, Kerschbaum HH: decreases a -activated current via activation of phosphodiesterase 2 in Helix U-cells. Brain Res. 2004 Feb 27;999(1):98-105. KCa-current amplitude in U-cells was sensitive to Ba2+, TEA, iberiotoxin, kaliotoxin and charybdotoxin (ChTX), but not to 4-aminopyridine (4-AP) (up to 30 mM) and apamin (up to 300 nM). |
0(0,0,0,0) | Details |
| 17869444 | Yang Q, Chen SR, Li DP, Pan HL: Kv1.1/1.2 channels are downstream effectors of on synaptic release to preautonomic neurons in the paraventricular nucleus. Neuroscience. 2007 Oct 26;149(2):315-27. Epub 2007 Aug 8. Surprisingly, blocking of voltage-gated potassium channels (Kv) with 4-aminopyridine or alpha-dendrotoxin eliminated the effect of on mIPSCs in all labeled PVN neurons tested. |
0(0,0,0,0) | Details |
| 10844005 | Bergsman JB, Tsien RW: Syntaxin modulation of channels in cortical synaptosomes as revealed by botulinum toxin C1. J Neurosci. 2000 Jun 15;20(12):4368-78. Similar results were obtained when Ca (2+) influx arose from repetitive firing induced by the K (+)-channel blocker 4-aminopyridine. |
0(0,0,0,0) | Details |
| 11883949 | Magga JM, Kay JG, Davy A, Poulton NP, Robbins SM, Braun JE: ATP dependence of the SNARE/caveolin 1 interaction in the hippocampus. . Biochem Biophys Res Commun. 2002 Mar 15;291(5):1232-8. Previously, we reported that application of 4-aminopyridine to hippocampal slices resulted in a persistent potentiation of synaptic transmission and the induction of a short-lasting and specific 40-kDa complex composed of synaptosomal associated protein of 25 kDa (SNAP25) and caveolin1. |
82(1,1,1,2) | Details |
| 15993634 | Costa RS, Assreuy J: Multiple channels mediate -induced inhibition of rat vascular smooth muscle cell proliferation. Nitric Oxide. 2005 Sep;13(2):145-51. In this report, we show that tetraethylammonium (TEA, a non-selective blocker of KC, 300 microM), and 4-aminopyridine (a selective blocker of voltage-dependent KC, 100 microM) prevented SNAP inhibitory effects on cell proliferation, whereas glibenclamide (a selective blocker of ATP-dependent KC, 1 microM) was ineffective. |
33(0,1,1,3) | Details |