| Name | GABA receptor (protein family or complex) |
|---|---|
| Synonyms | GABA receptor; GABA receptors; GABA(A) receptor; GABA(A) receptors; Gamma aminobutyric acid receptor; Gamma aminobutyric acid receptors |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12213259 | Wong JY, Ross SA, McColl C, Massalas JS, Powney E, Finkelstein DI, Clark M, Horne MK, Berkovic SF, Drago J: Proconvulsant-induced seizures in alpha (4) nicotinic acetylcholine receptor subunit knockout mice. Neuropharmacology. 2002 Jul;43(1):55-64. We investigated the response of alpha (4) nAChR subunit knockout mice to the (GABA) receptor antagonists; pentylenetetrazole (PTZ) and bicuculline (BIC), the glutamate receptor agonist kainic acid (KA), the glycine receptor antagonist strychnine and the K (+) channel blocker 4-aminopyridine (4-AP). |
33(0,1,1,3) | Details |
| 16806308 | Inaba Y, Biagini G, Avoli M: The H current blocker ZD7288 decreases epileptiform hyperexcitability in the rat neocortex by depressing synaptic transmission. Neuropharmacology. 2006 Sep;51(3):681-91. Epub 2006 Jun 27. Here, we addressed this issue by using field and intracellular recordings to study the effects of ZD7288 (10-100 microM), a bradycardic agent known to abolish Ih, on the epileptiform discharges (duration = 2.5 +/- 0.3 s, mean +/- SEM; interval of occurrence = 34.2 +/- 3.3 s, n = 30 slices) induced in rat neocortical slices by 4-aminopyridine and GABA receptor antagonists. |
31(0,1,1,1) | Details |
| 12438533 | Motalli R, D'Antuono M, Louvel J, Kurcewicz I, D'Arcangelo G, Tancredi V, Manfredi M, Pumain R, Avoli M: Epileptiform synchronization and GABA (B) receptor antagonism in the juvenile rat hippocampus. J Pharmacol Exp Ther. 2002 Dec;303(3):1102-13. The GABA (B) receptor agonist baclofen enhances the epileptiform activity induced by 4-aminopyridine (4AP) in juvenile rat hippocampal slices. Bath application of 4AP (50 microM) induced spontaneous interictal and ictal discharges along with synchronous GABA receptor-mediated potentials. |
3(0,0,0,3) | Details |
| 19291222 | Uva L, Avoli M, de Curtis M: Synchronous GABA-receptor-dependent potentials in limbic areas of the in-vitro isolated adult guinea pig brain. Eur J Neurosci. 2009 Mar;29(5):911-20. We found that arterial perfusion of this preparation with 4-aminopyridine caused the appearance of glutamatergic-independent interictal potentials that were reversibly abolished by (A) receptor antagonism. |
1(0,0,0,1) | Details |
| 17910585 | Cepeda C, Andre VM, Wu N, Yamazaki I, Uzgil B, Vinters HV, Levine MS, Mathern GW: Immature neurons and networks may contribute to epileptogenesis in pediatric cortical dysplasia. Epilepsia. 2007;48 Suppl 5:79-85. Because is the main neurotransmitter in early cortical development, we hypothesized increased GABA receptor-mediated synaptic function in CD tissue. Evoked synaptic responses mediated by were also prominent, and bath application of 4-aminopyridine induced rhythmic depolarizations that were blocked by bicuculline. |
1(0,0,0,1) | Details |
| 15919713 | Qian J, Noebels JL: Visualization of transmitter release with zinc fluorescence detection at the mouse hippocampal mossy fibre synapse. J Physiol. 2005 Aug 1;566(Pt 3):747-58. Epub 2005 May 26. Manipulating release probability with the application of neuromodulators such as DCG IV, 4-aminopyridine and forskolin as well as a paired train stimulation protocol altered both the [Zn2+] t and the field excitatory postsynaptic potential (fEPSP) coordinately, strongly indicating that zinc is co-released with during exocytosis. Since zinc ions colocalize with in small clear vesicles and modulate postsynaptic excitability at and GABA receptors, the findings establish zinc as a cotransmitter during physiological signalling at the mossy fibre synapse. |
1(0,0,0,1) | Details |
| 11412897 | Wong M, Yamada KA: Developmental characteristics of epileptiform activity in immature rat neocortex: a comparison of four in vitro seizure models. Brain Res Dev Brain Res. 2001 Jun 29;128(2):113-20. A leading hypothesis to explain an increased seizure susceptibility of the immature nervous system involves ontogenetic changes in different neurotransmitter systems, such as specific and GABA receptors. The present study investigated developmental changes in epileptiform activity in rat neocortical slices from four age groups (postnatal days P4--7, P13--16, P23--26, P41--47) due to four pharmacological conditions (4-aminopyridine, low picrotoxin, CGP-35348) that differentially modulate and systems. |
1(0,0,0,1) | Details |
| 15051526 | Gu Y, Ge SY, Ruan DY: Effect of 4-aminopyridine on synaptic transmission in rat hippocampal slices. Brain Res. 2004 May 1;1006(2):225-32. The and GABA receptor-associated ligand-gated currents were obtained from dissociated single hippocampal pyramidal cells. |
1(0,0,0,1) | Details |
| 12213266 | Cozzi A, Meli E, Carla V, Pellicciari R, Moroni F, Pellegrini-Giampietro DE: Metabotropic glutamate 1 (mGlu1) receptor antagonists enhance GABAergic neurotransmission: a mechanism for the attenuation of post-ischemic injury and epileptiform activity?. Neuropharmacology. 2002 Aug;43(2):119-30. In a mouse cortical wedge model, both muscimol and 3-MATIDA reduced the frequency of spontaneous bursts induced by 4-aminopyridine and this reduction was prevented by co-perfusion with bicuculline. Taken together, our results suggest that the release of and the subsequent activation of GABA receptors, may contribute to the attenuation of post-ischemic neuronal damage and epileptiform activity induced by mGlu1 receptor antagonists. |
1(0,0,0,1) | Details |
| 15537816 | Skov J, Nedergaard S, Andreasen M: New type of synaptically mediated epileptiform activity independent of known and GABA receptors. J Neurophysiol. 2005 Apr;93(4):1845-56. Epub 2004 Nov 10. The effect of Cs+ was partly mimicked by 4-aminopyridine (4-AP; 2 mM), suggesting that an increase in transmitter release is involved. |
1(0,0,0,1) | Details |
| 16725129 | Skov J, Andreasen M, Nedergaard S: Postnatal development of a new type of epileptiform activity in the rat hippocampus. Brain Res. 2006 Jun 22;1096(1):61-9. Epub 2006 May 24. Long-term application of Cs (+) (5 mM) induces an epileptiform field potential (Cs-FP) in area CA1 of the rat hippocampus, which is independent of and non- glutamate receptors and (GABA)(A) receptors. In the presence of 4-aminopyridine, potentials resembling the Cs-FP were evoked. |
1(0,0,0,1) | Details |
| 10973624 | Haberek G, Tomczyk T, Zuchora B, Wielosz M, Turski WA, Urbanska EM: Proconvulsive effects of the mitochondrial respiratory chain inhibitor--3-nitropropionic acid. Eur J Pharmacol. 2000 Sep 8;403(3):229-33. An inhibitor of mitochondrial complex III, 3-nitropropionic acid, which is known to evoke convulsions per se, and was used here in subthreshold dose, enhanced seizures generated by electric current and application of 4-aminopyridine. |
0(0,0,0,0) | Details |
| 20083165 | Henderson Z, Lu CB, Janzso G, Matto N, McKinley CE, Yanagawa Y, Halasy K: Distribution and role of Kv3.1b in neurons in the medial septum diagonal band complex. Neuroscience. 2010 Mar 31;166(3):952-69. Epub 2010 Jan 18. The results for the MS/DB were as follows: (1) cholinergic cells did not express GFP in either GAD67-GFP or VGluT2-GFP mice, and there was GAD67 immunoreactivity in GFP-positive neurons in GAD67-GFP mice and in a small proportion (6%) of GFP-positive neurons in VGluT2-GFP mice. (2) Kv3.1b immunofluorescence was associated with the somata of GABAergic neurons, especially those that contained parvalbumin, and with a minority of glutamatergic neurons, but not with cholinergic neurons, and with GABAergic axonal terminal-like processes around certain GABAergic neurons. (3) Both Kv3.1b-positive and -negative GABAergic neurons were septo-hippocampal, and there was a minor projection to hippocampus from VGluT2-GFP neurons. (4) Kainate-induced theta oscillations in the MS/DB slice were potentiated rather than inhibited by the Kv3.1 blocker 4-aminopyridine, and this agent on its own produced theta frequency oscillations in MS/DB slices that were reduced by ionotropic and GABA receptor antagonists and abolished by low extracellular |
0(0,0,0,0) | Details |