Excitation in Neocortical Layer V Pyramidal Cells Decrease in Synaptic Inhibition and Increase in Acute Injury to Superficial Cortex Leads to a

[1]  L. Benardo,et al.  Nootropic agents enhance the recruitment of fast GABAA inhibition in rat neocortex. , 2005, Cerebral cortex.

[2]  D. Katz,et al.  Update of Neuropathology and Neurological Recovery After Traumatic Brain Injury , 2005, The Journal of head trauma rehabilitation.

[3]  R. D’Ambrosio,et al.  Epilepsy after head injury , 2004, Current opinion in neurology.

[4]  Margaret Fahnestock,et al.  Kindling and status epilepticus models of epilepsy: rewiring the brain , 2004, Progress in Neurobiology.

[5]  Igor Timofeev,et al.  Hyperexcitability of intact neurons underlies acute development of trauma‐related electrographic seizures in cats in vivo , 2003, The European journal of neuroscience.

[6]  Igor Timofeev,et al.  Partial cortical deafferentation promotes development of paroxysmal activity. , 2003, Cerebral cortex.

[7]  S. Hestrin,et al.  Synaptic Interactions of Late-Spiking Neocortical Neurons in Layer 1 , 2003, The Journal of Neuroscience.

[8]  D. Prince,et al.  Synaptic activity in chronically injured, epileptogenic sensory-motor neocortex. , 2002, Journal of neurophysiology.

[9]  Wolfgang Löscher,et al.  Animal models of epilepsy for the development of antiepileptogenic and disease-modifying drugs. A comparison of the pharmacology of kindling and post-status epilepticus models of temporal lobe epilepsy , 2002, Epilepsy Research.

[10]  L. Benardo,et al.  Laminar properties of 4-aminopyridine-induced synchronous network activities in rat neocortex , 2002, Neuroscience.

[11]  John F. Crary,et al.  Protein kinase Mζ is necessary and sufficient for LTP maintenance , 2002, Nature Neuroscience.

[12]  Lie Yang,et al.  Valproate Prevents Epileptiform Activity After Trauma in an In Vitro Model in Neocortical Slices , 2000, Epilepsia.

[13]  J. Eberwine,et al.  Traumatic injury induces differential expression of cell death genes in organotypic brain slice cultures determined by complementary DNA array hybridization , 2000, Neuroscience.

[14]  G Lynch,et al.  Positive Modulation of AMPA Receptors Increases Neurotrophin Expression by Hippocampal and Cortical Neurons , 2000, The Journal of Neuroscience.

[15]  L. Benardo,et al.  Restrictions on inhibitory circuits contribute to limited recruitment of fast inhibition in rat neocortical pyramidal cells. , 1999, Journal of neurophysiology.

[16]  N R Temkin,et al.  Valproate therapy for prevention of posttraumatic seizures: a randomized trial. , 1999, Journal of neurosurgery.

[17]  L. Satin,et al.  Enhancement of AMPA-Mediated Current after Traumatic Injury in Cortical Neurons , 1999, The Journal of Neuroscience.

[18]  F Angeleri,et al.  Posttraumatic Epilepsy Risk Factors: One‐Year Prospective Study After Head Injury , 1999, Epilepsia.

[19]  M. Nuwer,et al.  Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring. , 1999, Journal of neurosurgery.

[20]  M. Kaste,et al.  Early and Late Posttraumatic Seizures in Traumatic Brain Injury Rehabilitation Patients: Brain Injury Factors Causing Late Seizures and Influence of Seizures on Long‐Term Outcome , 1999, Epilepsia.

[21]  T. H. Brown,et al.  Methods for whole-cell recording from visually preselected neurons of perirhinal cortex in brain slices from young and aging rats , 1998, Journal of Neuroscience Methods.

[22]  Lie Yang,et al.  Removal of superficial inhibition releases hyperexcitability in middle and deep horizontal slices from rat somatosensory neocortex , 1998, Neuroscience Letters.

[23]  Andreas Lüthi,et al.  Modulation of AMPA receptor unitary conductance by synaptic activity , 1998, Nature.

[24]  Lie Yang,et al.  Epileptogenesis following neocortical trauma from two sources of disinhibition. , 1997, Journal of neurophysiology.

[25]  D. Debanne,et al.  Lesion-induced axonal sprouting and hyperexcitability in the hippocampus in vitro: Implications for the genesis of posttraumatic epilepsy , 1997, Nature Medicine.

[26]  L. Benardo,et al.  Recruitment of GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex. , 1997, Journal of neurophysiology.

[27]  P A Salin,et al.  Electrophysiological mapping of GABAA receptor-mediated inhibition in adult rat somatosensory cortex. , 1996, Journal of neurophysiology.

[28]  Paul Antoine Salin,et al.  Axonal sprouting in layer V pyramidal neurons of chronically injured cerebral cortex , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[29]  I. Módy,et al.  Tonic inhibition originates from synapses close to the soma , 1995, Neuron.

[30]  D. Choi Calcium: still center-stage in hypoxic-ischemic neuronal death , 1995, Trends in Neurosciences.

[31]  L. Benardo,et al.  Properties of isolated GABAB-mediated inhibitory postsynaptic currents in hippocampal pyramidal cells , 1994, Neuroscience.

[32]  P A Salin,et al.  Chronic neocortical epileptogenesis in vitro. , 1994, Journal of neurophysiology.

[33]  I. Módy,et al.  Noise analysis of miniature IPSCs in adult rat brain slices: properties and modulation of synaptic GABAA receptor channels. , 1994, Journal of neurophysiology.

[34]  S. Lipton,et al.  Excitatory amino acids as a final common pathway for neurologic disorders. , 1994, The New England journal of medicine.

[35]  U. Ungerstedt,et al.  Epileptic seizure activity in the acute phase following cortical impact trauma in rat , 1994, Brain Research.

[36]  C. Gall Seizure-Induced Changes in Neurotrophin Expression: Implications for Epilepsy , 1993, Experimental Neurology.

[37]  E. G. Jones,et al.  GABAergic neurons and their role in cortical plasticity in primates. , 1993, Cerebral cortex.

[38]  R. Silver,et al.  Estimated conductance of glutamate receptor channels activated during EPSCs at the cerebellar mossy fiber-granule cell synapse , 1993, Neuron.

[39]  D. Prince,et al.  Epileptogenesis in chronically injured cortex: in vitro studies. , 1993, Journal of neurophysiology.

[40]  D. Choi Excitotoxic cell death. , 1992, Journal of neurobiology.

[41]  P. Greengard,et al.  Enhancement of the glutamate response by cAMP-dependent protein kinase in hippocampal neurons , 1991, Science.

[42]  M. Salter,et al.  Regulation of kainate receptors by cAMP-dependent protein kinase and phosphatases , 1991, Science.

[43]  I. Módy,et al.  Perpetual inhibitory activity in mammalian brain slices generated by spontaneous GABA release , 1991, Brain Research.

[44]  L. W. Jenkins,et al.  Excitatory amino acid receptor subtype binding following traumatic brain injury , 1990, Brain Research.

[45]  N R Temkin,et al.  A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. , 1990, The New England journal of medicine.

[46]  B W Connors,et al.  Synchronized excitation and inhibition driven by intrinsically bursting neurons in neocortex. , 1989, Journal of neurophysiology.

[47]  F. A. Edwards,et al.  A thin slice preparation for patch clamp recordings from neurones of the mammalian central nervous system , 1989, Pflügers Archiv.

[48]  R. Vink,et al.  The role of excitatory amino acids and NMDA receptors in traumatic brain injury. , 1989, Science.

[49]  Jordan Grafman,et al.  Epilepsy after penetrating head injury. I. Clinical correlates , 1985, Neurology.

[50]  B. Ramamurthi,et al.  Convulsions with meningiomas: incidence and significance. , 1980, Surgical neurology.

[51]  L. Elveback,et al.  Seizures after head trauma , 1980, Neurology.

[52]  T. Sacktor,et al.  Protein kinase Mζ enhances excitatory synaptic transmission by increasing the number of active postsynaptic AMPA receptors , 2006, Hippocampus.

[53]  Anita E Bandrowski,et al.  Cortical injury affects short-term plasticity of evoked excitatory synaptic currents. , 2005, Journal of neurophysiology.

[54]  A. Thomson,et al.  Interlaminar connections in the neocortex. , 2003, Cerebral cortex.

[55]  W. Hauser,et al.  A population-based study of seizures after traumatic brain injuries. , 1998, The New England journal of medicine.

[56]  Lowenstein Dh Recent advances related to basic mechanisms of epileptogenesis. , 1996 .

[57]  D Colquhoun,et al.  Mechanisms of activation of glutamate receptors and the time course of excitatory synaptic currents. , 1995, Annual review of physiology.

[58]  Barry W. Connors,et al.  Epilepsy: Generation of epileptiform discharge by local circuits of neocortex , 1993 .

[59]  C. Gall,et al.  Regulation of brain neurotrophin expression by physiological activity. , 1992, Trends in pharmacological sciences.

[60]  C. Gall,et al.  Kainic acid-induced seizures stimulate increased expression of nerve growth factor mRNA in rat hippocampus. , 1991, Brain research. Molecular brain research.

[61]  R. Wong,et al.  GABAA receptor function is regulated by phosphorylation in acutely dissociated guinea‐pig hippocampal neurones. , 1990, The Journal of physiology.

[62]  G. Collingridge,et al.  Excitatory amino acids in synaptic transmission in the Schaffer collateral‐commissural pathway of the rat hippocampus. , 1983, The Journal of physiology.