| Name | glutamate receptors (protein family or complex) |
|---|---|
| Synonyms | Glutamate receptor; Glutamate receptors |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11113304 | Pena F, Tapia R: Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of - and -mediated neurotransmission and of ion channels. Neuroscience. 2000;101(3):547-61. We conclude that 4-aminopyridine stimulates the release of from nerve endings and that the resultant augmented extracellular is directly related to the neurodegeneration and is involved in the generation of epileptiform discharges through the concomitant overactivation of glutamate receptors. |
6(0,0,1,1) | Details |
| 19445932 | Vilagi I, Dobo E, Borbely S, Czege D, Molnar E, Mihaly A: Repeated 4-aminopyridine induced seizures diminish the efficacy of glutamatergic transmission in the neocortex. Exp Neurol. 2009 Sep;219(1):136-45. Epub 2009 May 13. Changes in general neuronal excitability and pharmacological sensitivity of glutamate receptors were tested in ex vivo electrophysiological experiments on brain slices. |
3(0,0,0,3) | Details |
| 16181416 | Kopniczky Z, Dobo E, Borbely S, Vilagi I, Detari L, Krisztin-Peva B, Bagosi A, Molnar E, Mihaly A: Lateral entorhinal cortex lesions rearrange afferents, glutamate receptors, increase seizure latency and suppress seizure-induced c-fos expression in the hippocampus of adult rat. J Neurochem. 2005 Oct;95(1):111-24. Here we analysed the effects of one-sided lateral EC (LEC) and temporoammonic (alvear) path lesion on the development and properties of 4-aminopyridine-induced seizures. |
2(0,0,0,2) | Details |
| 14623765 | White AM, Kylanpaa RA, Christie LA, McIntosh SJ, Irving AJ, Platt B: Presynaptic group I metabotropic glutamate receptors modulate synaptic transmission in the rat superior colliculus via 4-AP sensitive K (+) channels. Br J Pharmacol. 2003 Dec;140(8):1421-33. Epub 2003 Nov 17. The K+ channel antagonist 4-aminopyridine (4-AP, 50-100 microm) converted the inhibitory effect of into facilitation. |
2(0,0,0,2) | Details |
| 11744755 | Daniel H, Crepel F: Control of Ca (2+) influx by cannabinoid and metabotropic glutamate receptors in rat cerebellar cortex requires K (+) channels. J Physiol. 2001 Dec 15;537(Pt 3):793-800. |
2(0,0,0,2) | Details |
| 12126879 | Gulyas-Kovacs A, Doczi J, Tarnawa I, Detari L, Banczerowski-Pelyhe I, Vilagi I: Comparison of spontaneous and evoked epileptiform activity in three in vitro epilepsy models. Brain Res. 2002 Aug 2;945(2):174-80. We conclude that the contribution of and AMPA types of glutamate receptors to the development and maintenance of epileptiform activity in cortical cell assemblies is different in the three models. Rat neocortical slices express spontaneous epileptiform activity after incubation with (A) receptor blocker bicuculline (BIC, 20 microM), with potassium channel blocker 4-aminopyridine (4-AP, 50 microM) or in Mg (2+)-free medium (LMG). |
2(0,0,0,2) | Details |
| 17822807 | Oleskovicz SP, Martins WC, Leal RB, Tasca CI: Mechanism of -induced neuroprotection in rat hippocampal slices submitted to - deprivation. Neurochem Int. 2008 Feb;52(3):411-8. Epub 2007 Aug 1. derivatives are spontaneously released to the extracellular space from cultured astrocytes during - deprivation (OGD) and may act as trophic factors, glutamate receptors blockers or transport modulators, thus promoting neuroprotection. Nifedipine (a Ca (2+) channel blocker) increased the neuroprotective effect of and 4-aminopyridine, a K (+) channel blocker, reversed the neuroprotective effect of |
1(0,0,0,1) | Details |
| 16183639 | Lenz G, Avruch J: Glutamatergic regulation of the p70S6 kinase in primary mouse neurons. . J Biol Chem. 2005 Nov 18;280(46):38121-4. Epub 2005 Sep 22. Thus the mTOR-S6K pathway in neurons, a critical component of the late phase of LTP, is activated by glutamatergic stimulation in a /calmodulin-dependent fashion through a pool controlled by postsynaptic voltage-dependent channels, whereas sustained stimulation of extrasynaptic glutamate receptors is inhibitory. After 12 days in culture, the response to direct glutamatergic activation is attenuated but can be uncovered by suppression of interneurons with bicuculline in the presence of the weak K (+) channel blocker 4-aminopyridine (4-AP). |
1(0,0,0,1) | Details |
| 14770276 | Wejksza K, Rzeski W, Parada-Turska J, Zdzisinska B, Rejdak R, Kocki T, Okuno E, Kandefer-Szerszen M, Zrenner E, Turski WA: production in cultured bovine aortic endothelial cells. Naunyn Schmiedebergs Arch Pharmacol. 2004 Mar;369(3):300-4. Epub 2004 Feb 10. (KYNA) is a broad-spectrum antagonist at all subtypes of ionotropic glutamate receptors, but is preferentially active at the strychnine-insensitive allosteric site of the (NMDA) receptor and is also a non-competitive antagonist at the alpha7 nicotinic receptor. KYNA production was inhibited by the aminotransferase inhibitor aminooxyacetic acid but was not affected by a depolarising concentration of K (+) or by 4-aminopyridine. |
1(0,0,0,1) | Details |
| 12617942 | Zheng F, Johnson SW: Metabotropic glutamate and muscarinic cholinergic receptor-mediated preferential inhibition of component of transmissions in rat ventral tegmental area. Neuroscience. 2003;116(4):1013-20. Intracellular voltage clamp recordings were made from neurons in rat ventral tegmental area in slice preparations. (+/-)-1-Aminocyclopentane-trans-1,3-dicarboxylic acid (agonist for groups I and II metabotropic glutamate receptors) and L (+)-2-amino-4-phosphonobutyric acid (L-AP4; agonist for group III metabotropic glutamate receptors) were significantly more potent for inhibiting N-methyl-D-aspartate receptor-mediated excitatory postsynaptic currents, as compared with inhibition of excitatory postsynaptic currents mediated by alpha-amino-3--5-methyl-4-isoxazolepropionic acid receptors. Interestingly, the release stimulator 4-aminopyridine (30 microM) and the uptake inhibitor L-anti-endo-3,4-methanopyrrolidine dicarboxylate (300 microM) preferentially increased the amplitude of excitatory postsynaptic currents.Thus, agonists for metabotropic and muscarinic cholinergic receptors act presynaptically to cause a preferential reduction in the component of excitatory synaptic transmissions. |
1(0,0,0,1) | Details |
| 11311981 | Sequeira SM, Malva JO, Carvalho AP, Carvalho CM: Presynaptic N-methyl-D-aspartate receptor activation inhibits neurotransmitter release through formation in rat hippocampal nerve terminals. Brain Res Mol Brain Res. 2001 Apr 18;89(1-2):111-8. Novel evidence indicates that glutamate receptors may play a presynaptic role in synaptic plasticity. dose-dependently inhibited the release of evoked by 4-aminopyridine (IC (50)=155 microM), and this effect was reversed by the N-methyl-D-aspartate receptor antagonist D-(-)-2-amino-5-phosphopentanoic acid and by the synthase inhibitor, L-nitroarginine, in synaptosomes isolated from whole hippocampus, CA3 and CA1 areas, but not from the dentate gyrus. |
1(0,0,0,1) | Details |
| 10987837 | Sistiaga A, Sanchez-Prieto J: Protein phosphatase 1 and 2A inhibitors prolong the switch in the control of release by group I metabotropic glutamate receptors: characterization of the inhibitory pathway. J Neurochem. 2000 Oct;75(4):1566-74. |
2(0,0,0,2) | Details |
| 12364493 | Lee AC, Wong RK, Chuang SC, Shin HS, Bianchi R: Role of synaptic metabotropic glutamate receptors in epileptiform discharges in hippocampal slices. J Neurophysiol. 2002 Oct;88(4):1625-33. Addition of 4-aminopyridine (4-AP; 100 microM) prolonged these bursts to 0.7-2 s. |
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 |
| 10658620 | Kearney JA, Albin RL: Intrasubthalamic nucleus metabotropic glutamate receptor activation: a behavioral, Fos immunohistochemical and [14C] 2-deoxyglucose autoradiographic study. Neuroscience. 2000;95(2):409-16. Previous results have shown that unilateral stimulation of metabotropic glutamate receptors in the subthalamic nucleus with the non-subtype-selective metabotropic glutamate receptor agonist 1S,3R-1-amino-1,3-cyclopentane dicarboxylate results in contralateral rotation in rats and Fos expression in the subthalamic nucleus. |
2(0,0,0,2) | Details |
| 14499451 | Ruscheweyh R, Sandkuhler J: Epileptiform activity in rat spinal dorsal horn in vitro has common features with neuropathic pain. Pain. 2003 Sep;105(1-2):327-38. Application of the convulsant 4-aminopyridine (100 microM) evoked epileptiform activity that was most pronounced in superficial dorsal horn and involved nociceptive lamina I neurons with a projection to the brain. The epileptiform activity was dependent on fast excitatory and inhibitory synaptic transmission through ionotropic glutamate receptors and (A) receptors. |
1(0,0,0,1) | Details |
| 11801366 | Doi A, Ishibashi H, Jinno S, Kosaka T, Akaike N: Presynaptic inhibition of GABAergic miniature currents by metabotropic glutamate receptor in the rat CNS. Neuroscience. 2002;109(2):299-311. The modulation of spontaneous miniature GABAergic inhibitory postsynaptic currents (mIPSC) by the metabotropic glutamate receptors was investigated in the mechanically dissociated rat nucleus basalis of Meynert neurons using the conventional whole-cell patch recording configuration. The application of K+ channel blockers such as 4-aminopyridine, Cs+, Ba2+ or tetraethylammonium increased the mIPSC frequency, but failed to inhibit the tACPD action on mIPSC. |
1(0,0,0,1) | Details |
| 16258845 | Wejksza K, Rzeski W, Okuno E, Kandefer-Szerszen M, Albrecht J, Turski WA: Demonstration of aminotransferases I and II and characterization of synthesis in oligodendrocyte cell line (OLN-93). Neurochem Res. 2005 Aug;30(8):963-8. KYNA production in OLN-93 cells was depressed in the presence of aminotransferase inhibitor, aminooxyacetic acid and was not affected by depolarizing agents such as 50 mM K+ and 4-aminopyridine. |
0(0,0,0,0) | 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. We conclude that long-term exposure to Cs+ induces a state where excitatory synaptic transmission can exist between area CA3 and CA1 in the hippocampus, independent of ionotropic and metabotropic glutamate receptors and (A) receptors. 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 |
| 16289841 | Taccola G, Nistri A: Fictive locomotor patterns generated by tetraethylammonium application to the neonatal rat spinal cord in vitro. Neuroscience. 2006;137(2):659-70. Epub 2005 Nov 14. Rhythmic alternating patterns elicited by tetraethylammonium on ventral roots were relatively stereotypic, had limited synergy with fictive locomotion induced by dorsal root stimuli, and were not accelerated by 4-aminopyridine. Rhythmic alternating patterns were suppressed by blockers of (A) and glycine receptors, disclosing a background of depolarizing bursts inhibited by antagonism of group I metabotropic glutamate receptors. |
1(0,0,0,1) | Details |
| 18789952 | Ayala GX, Tapia R: HSP70 expression protects against hippocampal neurodegeneration induced by endogenous in vivo. Neuropharmacology. 2008 Dec;55(8):1383-90. Epub 2008 Sep 9. The K+ channel blocker 4-aminopyridine (4-AP) stimulates the release of from nerve endings and induces seizures and neurodegeneration when perfused by microdialysis in rat hippocampus. These results suggest that HSP70 induction is an important cellular mechanism to protect vulnerable neurons from excitotoxic overactivation of glutamate receptors by endogenous and may be relevant to pathological conditions in which extracellular endogenous is augmented, such as ischemia. |
1(0,0,0,1) | Details |
| 15473972 | Cai X, Liang CW, Muralidharan S, Kao JP, Tang CM, Thompson SM: Unique roles of SK and Kv4.2 channels in dendritic integration. Neuron. 2004 Oct 14;44(2):351-64. Focal activation of glutamate receptors in distal dendrites of hippocampal pyramidal cells triggers voltage-dependent Ca (2+) channel-mediated plateau potentials that are confined to the stimulated dendrite. Manipulations that blocked Kv4.2 A-type K (+) channels, including a dominant-negative Kv4.2 construct and 4-aminopyridine, increased the amplitude of plateau potentials by allowing them to recruit neighboring dendrites. |
1(0,0,0,1) | Details |
| 11773238 | Hirasawa H, Shiells R, Yamada M: A metabotropic glutamate receptor regulates transmitter release from cone presynaptic terminals in carp retinal slices. J Gen Physiol. 2002 Jan;119(1):55-68. The role of group III metabotropic glutamate receptors (mGluRs) in photoreceptor-H1 horizontal cell (HC) synaptic transmission was investigated by analyzing the rate of occurrence and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in H1 HCs uncoupled by in carp retinal slices. During L-APB application, recovery of sEPSC rate occurred with 500 microM (s)-2-methyl-2-amino-4-phosphonobutyrate (MAP4), a selective antagonist of group III mGluR, and with 200 microM 4-aminopyridine (4-AP), a blocker of voltage-dependent channels. |
1(0,0,0,1) | Details |
| 11877514 | Watabe AM, Carlisle HJ, O'Dell TJ: Postsynaptic induction and presynaptic expression of group 1 mGluR-dependent LTD in the hippocampal CA1 region. J Neurophysiol. 2002 Mar;87(3):1395-403. Activation of metabotropic glutamate receptors (mGluRs) with the group I mGluR selective agonist (R,S)-3,5-dihydroxyphenylglycine induces a long-term depression (LTD) of excitatory synaptic transmission in the CA1 region of the hippocampus. Enhancing Ca (2+) influx by prolonging action potential duration with bath applications of the K (+) channel blocker 4-aminopyridine (4-AP) also strongly reduced the effects of in the presence of normal [Ca (2+)](o) (2 mM). |
1(0,0,0,1) | Details |
| 16162834 | Kang N, Xu J, Xu Q, Nedergaard M, Kang J: Astrocytic release-induced transient depolarization and epileptiform discharges in hippocampal CA1 pyramidal neurons. J Neurophysiol. 2005 Dec;94(6):4121-30. Epub 2005 Sep 14. The neuronal STC is mediated by ionotropic glutamate receptors leading to the TD and epileptiform discharges; while the astrocytic TC is reuptake current resulting from transporting released into the patched astrocyte. |
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. Selective antagonists of mGlu1 metabotropic glutamate receptors attenuate neuronal death in models of cerebral ischemia. 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. |
1(0,0,0,1) | Details |
| 19657079 | Deng P, Pang ZP, Lei Z, Xu ZC: Excitatory roles of protein kinase C in striatal cholinergic interneurons. J Neurophysiol. 2009 Oct;102(4):2453-61. Epub 2009 Aug 5. These excitatory effects of PKC could be partially mimicked and occluded by blockade of I (A) with potassium channel blocker 4-aminopyridine. Furthermore, activation of group I metabotropic glutamate receptors (mGluRs) led to an inhibition of I (A) through a PKC-dependent pathway. |
1(0,0,0,1) | Details |
| 12015207 | Pena F, Bargas J, Tapia R: Paired pulse facilitation is turned into paired pulse depression in hippocampal slices after epilepsy induced by 4-aminopyridine in vivo. Neuropharmacology. 2002 May;42(6):807-12. Modifications in synaptic plasticity seem to play a key role in the origin and persistence of epilepsy. 4-Aminopyridine (4-AP) induces intense and long lasting epileptic seizures and neurodegeneration when applied into the hippocampus in vivo, effects that seem to be mediated by overactivation of glutamate receptors due to the enhancement of release from nerve endings. |
81(1,1,1,1) | Details |
| 17725506 | Taccola G, Nistri A: Oscillatory circuits underlying locomotor networks in the rat spinal cord. . Crit Rev Neurobiol. 2006;18(1-2):25-36. In fact, activation of metabotropic group I glutamate receptors or block of certain K+ currents by 4-aminopyridine generates non-locomotor discharges, and, at the same time, facilitates evoked locomotor activity, which then suppresses any other interfering rhythmicity. |
81(1,1,1,1) | Details |