NMDA receptor-mediated long-term alterations in epileptiform activity in experimental chronic epilepsy

[1]  D. Manahan‐Vaughan,et al.  Metabotropic glutamate receptor 1 (mGluR1) and 5 (mGluR5) regulate late phases of LTP and LTD in the hippocampal CA1 region in vitro , 2008, The European journal of neuroscience.

[2]  S. Dudek,et al.  Synapse elimination accompanies functional plasticity in hippocampal neurons , 2008, Proceedings of the National Academy of Sciences.

[3]  Alison L. Barth,et al.  Ongoing in Vivo Experience Triggers Synaptic Metaplasticity in the Neocortex , 2008, Science.

[4]  David R Grosshans,et al.  NMDA receptor trafficking at recurrent synapses stabilizes the state of the CA3 network. , 2007, Journal of neurophysiology.

[5]  Kazunari Hattori,et al.  Discovery of novel and orally active NR2B-selective N-methyl-D-aspartate (NMDA) antagonists, pyridinol derivatives with reduced HERG binding affinity. , 2007, Bioorganic & medicinal chemistry letters.

[6]  D. Manahan‐Vaughan,et al.  Antagonism of group III metabotropic glutamate receptors results in impairment of LTD but not LTP in the hippocampal CA1 region, and prevents long‐term spatial memory , 2007, The European journal of neuroscience.

[7]  H. Beck,et al.  Loss of Metabotropic Glutamate Receptor-Dependent Long-Term Depression via Downregulation of mGluR5 after Status Epilepticus , 2007, The Journal of Neuroscience.

[8]  F. Dudek,et al.  How Does the Balance of Excitation and Inhibition Shift during Epileptogenesis? , 2007, Epilepsy currents.

[9]  J. Macdonald,et al.  G protein-coupled receptors control NMDARs and metaplasticity in the hippocampus. , 2007, Biochimica et biophysica acta.

[10]  M. Bear,et al.  Activation of NR2B-containing NMDA receptors is not required for NMDA receptor-dependent long-term depression , 2007, Neuropharmacology.

[11]  Antonio Malgaroli,et al.  LTP and adaptation to inactivity: Overlapping mechanisms and implications for metaplasticity , 2007, Neuropharmacology.

[12]  Z. Xiong,et al.  Differential Roles of NR2A- and NR2B-Containing NMDA Receptors in Activity-Dependent Brain-Derived Neurotrophic Factor Gene Regulation and Limbic Epileptogenesis , 2007, The Journal of Neuroscience.

[13]  J. Hablitz,et al.  NR2B antagonists restrict spatiotemporal spread of activity in a rat model of cortical dysplasia , 2006, Epilepsy Research.

[14]  F. Dudek,et al.  Interictal Spikes and Epileptogenesis , 2006, Epilepsy currents.

[15]  Damien J. Ferraro,et al.  The use of radiotelemetry to evaluate electrographic seizures in rats with kainate-induced epilepsy , 2006, Journal of Neuroscience Methods.

[16]  Andrew M. White,et al.  Efficient unsupervised algorithms for the detection of seizures in continuous EEG recordings from rats after brain injury , 2006, Journal of Neuroscience Methods.

[17]  D. Debanne,et al.  A Brief Period of Epileptiform Activity Strengthens Excitatory Synapses in the Rat Hippocampus in Vitro , 2006, Epilepsia.

[18]  G. Woodhall,et al.  Tonic Facilitation of Glutamate Release by Presynaptic NR2B-Containing NMDA Receptors Is Increased in the Entorhinal Cortex of Chronically Epileptic Rats , 2006, The Journal of Neuroscience.

[19]  D. Lowenstein,et al.  Posttraumatic Epilepsy: A Major Problem in Desperate Need of Major Advances , 2006, Epilepsy currents.

[20]  E.L.J.M. van Luijtelaar,et al.  The preferential mGlu2/3 receptor antagonist, LY341495, reduces the frequency of spike–wave discharges in the WAG/Rij rat model of absence epilepsy , 2005, Neuropharmacology.

[21]  U. Heinemann,et al.  Induction of sharp wave–ripple complexes in vitro and reorganization of hippocampal networks , 2005, Nature Neuroscience.

[22]  J. González-Martínez,et al.  The NMDA receptor NR2B subunit contributes to epileptogenesis in human cortical dysplasia , 2005, Brain Research.

[23]  F Edward Dudek,et al.  Chemoconvulsant Model of Chronic Spontaneous Seizures , 2005, Current protocols in neuroscience.

[24]  Mu-ming Poo,et al.  Shrinkage of Dendritic Spines Associated with Long-Term Depression of Hippocampal Synapses , 2004, Neuron.

[25]  J. Montgomery,et al.  Discrete synaptic states define a major mechanism of synapse plasticity , 2004, Trends in Neurosciences.

[26]  M. Bear,et al.  LTP and LTD An Embarrassment of Riches , 2004, Neuron.

[27]  G. Collingridge,et al.  Differential Roles of NR2A and NR2B-Containing NMDA Receptors in Cortical Long-Term Potentiation and Long-Term Depression , 2004, The Journal of Neuroscience.

[28]  B. Gähwiler,et al.  Epileptiform activity in rat hippocampus strengthens excitatory synapses , 2004, The Journal of physiology.

[29]  J. Swann,et al.  Postsynaptic contributions to hippocampal network hyperexcitability induced by chronic activity blockade in vivo , 2003, The European journal of neuroscience.

[30]  P. Rutecki,et al.  Group I metabotropic glutamate receptor activation produces prolonged epileptiform neuronal synchronization and alters evoked population responses in the hippocampus , 2003, Epilepsy Research.

[31]  R. Wong,et al.  Role of synaptic metabotropic glutamate receptors in epileptiform discharges in hippocampal slices. , 2002, Journal of neurophysiology.

[32]  P. J. Sjöström,et al.  Spike timing, calcium signals and synaptic plasticity , 2002, Current Opinion in Neurobiology.

[33]  J. Bains,et al.  Statistical model relating CA3 burst probability to recovery from burst-induced depression at recurrent collateral synapses. , 2001, Journal of neurophysiology.

[34]  G. Dannhardt,et al.  The NMDA receptor complex: a promising target for novel antiepileptic strategies. , 2001, Current medicinal chemistry.

[35]  M. Bear,et al.  Chemical induction of mGluR5- and protein synthesis--dependent long-term depression in hippocampal area CA1. , 2001, Journal of neurophysiology.

[36]  J E Lisman,et al.  Three Ca2+ levels affect plasticity differently: the LTP zone, the LTD zone and no man's land , 2001, The Journal of physiology.

[37]  R. Wong,et al.  Group I mGluR activation turns on a voltage-gated inward current in hippocampal pyramidal cells. , 2000, Journal of neurophysiology.

[38]  I. Fried,et al.  Hippocampal N‐methyl‐D‐aspartate receptor subunit mRNA levels in temporal lobe epilepsy patients , 1999, Annals of neurology.

[39]  Kevin J. Staley,et al.  Reciprocal interactions between CA3 network activity and strength of recurrent collateral synapses , 1999, Nature Neuroscience.

[40]  F. Edward Dudek,et al.  Spontaneous motor seizures of rats with kainate-induced epilepsy: effect of time of day and activity state , 1999, Epilepsy Research.

[41]  Kevin J. Staley,et al.  Presynaptic modulation of CA3 network activity , 1998, Nature Neuroscience.

[42]  C Kentros,et al.  Abolition of long-term stability of new hippocampal place cell maps by NMDA receptor blockade. , 1998, Science.

[43]  F. Edward Dudek,et al.  Recurrent spontaneous motor seizures after repeated low-dose systemic treatment with kainate: assessment of a rat model of temporal lobe epilepsy , 1998, Epilepsy Research.

[44]  S Shinnar,et al.  Do seizures beget seizures? An assessment of the clinical evidence in humans. , 1997, Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society.

[45]  S. Urwyler,et al.  Biphenyl-derivatives of 2-amino-7-phosphono-heptanoic acid, a novel class of potent competitive N-Methyl-D-aspartate receptor antagonists—II. Pharmacological characterization in vivo , 1996, Neuropharmacology.

[46]  R. Nicoll,et al.  Ca2+ Signaling Requirements for Long-Term Depression in the Hippocampus , 1996, Neuron.

[47]  P. Somogyi,et al.  High-resolution immunogold localization of AMPA type glutamate receptor subunits at synaptic and non-synaptic sites in rat hippocampus , 1995, Neuroscience.

[48]  E. Bertram,et al.  The evolution of a rat model of chronic spontaneous limbic seizures , 1994, Brain Research.

[49]  J. Schneiderman,et al.  Hippocampal plasticity following epileptiform bursting produced by GABAA antagonists , 1994, Neuroscience.

[50]  R. Traub,et al.  Neuronal Networks of the Hippocampus , 1991 .

[51]  R. Traub,et al.  Role of EPSPs in initiation of spontaneous synchronized burst firing in rat hippocampal neurons bathed in high potassium. , 1990, Journal of neurophysiology.

[52]  W. W. Anderson,et al.  NMDA antagonists differentiate epileptogenesis from seizure expression in an in vitro model. , 1989, Science.

[53]  Y. Ben-Ari,et al.  Long‐lasting modification of the synaptic properties of rat CA3 hippocampal neurones induced by kainic acid. , 1988, The Journal of physiology.

[54]  Y. Ben-Ari,et al.  Limbic seizure and brain damage produced by kainic acid: Mechanisms and relevance to human temporal lobe epilepsy , 1985, Neuroscience.

[55]  G. Celesia,et al.  Effects of ketamine in epilepsy , 1975, Neurology.

[56]  R. Racine,et al.  Modification of seizure activity by electrical stimulation. II. Motor seizure. , 1972, Electroencephalography and clinical neurophysiology.

[57]  Y. Dan,et al.  Spike timing-dependent plasticity: a Hebbian learning rule. , 2008, Annual review of neuroscience.

[58]  M. Rudin,et al.  Biphenyl-derivatives of 2-amino-7-phosphono-heptanoic acid, a novel class of potent competitive N-methyl-D-aspartate receptor antagonists--II. Pharmacological characterization in vivo. , 1996, Neuropharmacology.

[59]  R. Racine.  Modification of seizure activity by electrical stimulation: cortical areas. , 1975, Electroencephalography and clinical neurophysiology.