Excitoprotective effect of felbamate in cultured cortical neurons
References (48)
Glutamate neurotoxicity and diseases of the nervous system
Neuron
(1988)- et al.
Selective antagonism of the anticonvulsant effects of felbamate by glycine
Eur. J. Pharmacol.
(1994) - et al.
The influence of strychnine-insensitive glycine receptor agonists and antagonists on generalized seizure thresholds
Brain Res.
(1991) - et al.
Excitatory amino acid neurotransmission through both NMDA and non-NMDA receptors is involved in the anticonvulsant activity of felbamate in DBA/2 mice
Eur. J. Pharmacol.
(1994) - et al.
A new generation of Ca2+ indicators with greatly improved fluorescence properties
J. Biol. Chem.
(1985) - et al.
Quantitative determination of glutamate mediated cortical neuronal injury in cell cultures by lactate dehydrogenase efflux
J. Neurosci. Methods
(1987) - et al.
N-Methyl-d-aspartic acid-induced lethality in mice: selective antagonism by pencyclidine-like drugs
Brain Res.
(1988) - et al.
Strychnine-insensitive glycine site antagonists attenuate a cardiac arrest-induced movement disorder
Eur. J. Pharmacol.
(1995) Mechanism of action of new antiepileptic drugs: rational design and serendipitous findings
Trends Pharmacol. Sci.
(1994)- et al.
Interaction of felbamate with [3H]DCKA-labeled strychnine-insensitive glycine receptors in human postmortem brain
Exp. Neurol.
(1994)
Felbamate reduces hypoxic-ischemic brain damage in vivo
Eur. J. Pharmacol.
Mechanisms of excitotoxicity in neurologic diseases
FASEB J.
Many agents that antagonize the NMDA receptor-channel complex in vivo also causes disturbances of motor coordination
J. Pharmacol. Exp. Ther.
Effects of NMDA and strychnine-insensitive glycine site antagonists on NMDA-mediated convulsions and learning
Psychopharmacology
Ionic dependence of glutamate neurotoxicity in cortical cell culture
J. Neurosci.
Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists
J. Neurosci.
The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death
Annu. Rev. Neurosci.
The role of excitatory amino acids and NMDA receptors in traumatic brain injury
Science
7-Chlorokynurenate blocks NMDA receptor-mediated neurotoxicity in murine cortical culture
Eur. J. Neurosci.
Glutamate receptor-induced 45Ca2+ accumulation in cortical cell culture correlates with subsequent neuronal degeneration
J. Neurosci.
Glycine potentiates the NMDA responses in cultured mouse brain neurons
Nature
7-Chlorokynureic acid is a selective antagonist at the glycine site of N-methyl-d-asparate receptor complex
Requirement for glycine in activation of NMDA receptor expressed in Xenopus oocytes
Science
Selective blockade of N-methyl-d-aspartate (NMDA)-induced convulsions by NMDA antagonists and putative glycine antagonists: relationship with phencyclidine-like behavioral effects
J. Pharmacol. Exp. Ther.
Cited by (18)
Characterization of the gating conformational changes in the felbamate binding site in NMDA channels
2007, Biophysical JournalCitation Excerpt :However, Subramanian et al. (6) showed that FBM competitively inhibited [3H]MK-801 binding but not [3H]5,7-DCKA binding. Also, exogenous addition of glycine failed to modulate the excitoprotective effect of FBM on cultured cortical neurons exposed to glutamate or NMDA (14), and there were no competitive interactions between FBM and glycine in studies of NMDA currents (5). Furthermore, it has been reported that FBM produced an increase rather than a decrease in [3H]glycine binding to the NMDA channel (15).
Suppression of caspase-3-dependent proteolytic activation of protein kinase Cδ by small interfering RNA prevents MPP<sup>+</sup>-induced dopaminergic degeneration
2004, Molecular and Cellular NeurosciencePositive and negative modulation of the GABA(A) receptor and outcome after traumatic brain injury in rats
2000, Brain ResearchCitation Excerpt :Although the precise mechanisms of diazepam's beneficial effects is speculative, it is well documented that TBI produces neuronal depolarization that triggers a cascade of events that can lead to cell death by enabling intracellular levels of Ca2+ to rise [5, 53]. Increasing neuronal hyperpolarization with diazepam may be effective in preventing the increase in intracellular Ca2+, as anticonvulsants have been shown to reduce Ca2+ influx [21, 23, 29, 30]. In addition to reducing Ca2+ influx, the anticonvulsant felbanate also protects CA1 neurons from TBI [49].
New antiepileptic drugs
2000, Journal of Clinical NeuroscienceElectrophysiological effects of felbamate
1998, Life Sciences