Altered calcium homeostasis in motor neurons following AMPA receptor but not voltage-dependent calcium channels’ activation in a genetic model of amyotrophic lateral sclerosis

[1]  M. Ciotti,et al.  Modulation of AMPA Receptors in Cultured Cortical Neurons Induced by the Antiepileptic Drug Levetiracetam , 2007, Epilepsia.

[2]  C. Zona,et al.  Voltage-dependent sodium channels in spinal cord motor neurons display rapid recovery from fast inactivation in a mouse model of amyotrophic lateral sclerosis. , 2006, Journal of neurophysiology.

[3]  J. Zhu,et al.  Amyotrophic Lateral Sclerosis 2-Deficiency Leads to Neuronal Degeneration in Amyotrophic Lateral Sclerosis through Altered AMPA Receptor Trafficking , 2006, The Journal of Neuroscience.

[4]  W. Robberecht,et al.  The role of excitotoxicity in the pathogenesis of amyotrophic lateral sclerosis. , 2006, Biochimica et biophysica acta.

[5]  K. Abe,et al.  Parvalbumin and calbindin D-28k immunoreactivity in transgenic mice with a G93A mutant SOD1 gene , 2006, Brain Research.

[6]  Nicola B Mercuri,et al.  Temperature sensitivity of dopaminergic neurons of the substantia nigra pars compacta: involvement of transient receptor potential channels. , 2005, Journal of neurophysiology.

[7]  B. Keller,et al.  Ca2+, mitochondria and selective motoneuron vulnerability: implications for ALS , 2005, Trends in Neurosciences.

[8]  M. Sheng,et al.  PDZ domain proteins of synapses , 2004, Nature Reviews Neuroscience.

[9]  G. Bernardi,et al.  Cu/Zn-superoxide dismutase (GLY93→ALA) mutation alters AMPA receptor subunit expression and function and potentiates kainate-mediated toxicity in motor neurons in culture , 2004, Neurobiology of Disease.

[10]  B. Keller,et al.  Impact of mitochondrial inhibition on excitability and cytosolic Ca2+ levels in brainstem motoneurones from mouse , 2004, The Journal of physiology.

[11]  G. Rotilio,et al.  Overexpression of superoxide dismutase 1 protects against β-amyloid peptide toxicity: effect of estrogen and copper chelators , 2004, Neurochemistry International.

[12]  M. Wong-Riley,et al.  Postnatal changes in cytochrome oxidase expressions in brain stem nuclei of rats: implications for sensitive periods. , 2003, Journal of applied physiology.

[13]  G. Bernardi,et al.  α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate receptors in spinal cord motor neurons are altered in transgenic mice overexpressing human Cu,Zn superoxide dismutase (Gly93→Ala) mutation , 2003, Neuroscience.

[14]  C. Zona,et al.  Altered excitability of motor neurons in a transgenic mouse model of familial amyotrophic lateral sclerosis , 2003, Neuroscience Letters.

[15]  M. Brini,et al.  Ca2+ signalling in mitochondria: mechanism and role in physiology and pathology , 2003 .

[16]  A. Tozzi,et al.  Involvement of transient receptor potential‐like channels in responses to mGluR‐I activation in midbrain dopamine neurons , 2003, The European journal of neuroscience.

[17]  I. Kanazawa,et al.  Human spinal motoneurons express low relative abundance of GluR2 mRNA: an implication for excitotoxicity in ALS , 2003, Journal of neurochemistry.

[18]  W. Webb,et al.  Spatial profiles of store‐dependent calcium release in motoneurones of the nucleus hypoglossus from newborn mouse , 2003, The Journal of physiology.

[19]  I. Forsythe,et al.  Presynaptic Mitochondrial Calcium Sequestration Influences Transmission at Mammalian Central Synapses , 2002, The Journal of Neuroscience.

[20]  M. Pericak-Vance,et al.  The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis , 2001, Nature Genetics.

[21]  S. Scherer,et al.  A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2 , 2001, Nature Genetics.

[22]  J. Roder,et al.  The Influence of Glutamate Receptor 2 Expression on Excitotoxicity in GluR2 Null Mutant Mice , 2001, The Journal of Neuroscience.

[23]  A. Ludolph,et al.  Calcineurin A and calbindin immunoreactivity in the spinal cord of G93A superoxide dismutase transgenic mice , 2001, Brain Research.

[24]  Richard L. Huganir,et al.  Postsynaptic organisation and regulation of excitatory synapses , 2000, Nature Reviews Neuroscience.

[25]  W. Robberecht,et al.  AMPA Receptor Current Density, Not Desensitization, Predicts Selective Motoneuron Vulnerability , 2000, The Journal of Neuroscience.

[26]  R. Huganir,et al.  PDZ domains in synapse assembly and signalling. , 2000, Trends in cell biology.

[27]  M. Tymianski,et al.  Molecular mechanisms of calcium-dependent excitotoxicity , 2000, Journal of Molecular Medicine.

[28]  G. Bernardi,et al.  Pharmacologic reversal of cortical hyperexcitability in patients with ALS , 2000, Neurology.

[29]  S. Sensi,et al.  AMPA Exposures Induce Mitochondrial Ca2+ Overload and ROS Generation in Spinal Motor Neurons In Vitro , 2000, The Journal of Neuroscience.

[30]  E. Avignone,et al.  Upregulation of GABA Neurotransmission Suppresses Hippocampal Excitability and Prevents Long-Term Potentiation in Transgenic Superoxide Dismutase-Overexpressing Mice , 1999, The Journal of Neuroscience.

[31]  D. Cleveland.  From Charcot to SOD1 Mechanisms of Selective Motor Neuron Death in ALS , 1999, Neuron.

[32]  R. Huganir,et al.  Organization and regulation of proteins at synapses. , 1999, Current opinion in cell biology.

[33]  M. Charlton,et al.  Distinct Influx Pathways, Not Calcium Load, Determine Neuronal Vulnerability to Calcium Neurotoxicity , 1998, Journal of neurochemistry.

[34]  G. Bernardi,et al.  Intracellular sodium and calcium homeostasis during hypoxia in dopamine neurons of rat substantia nigra pars compacta. , 1998, Journal of Neurophysiology.

[35]  S. Sensi,et al.  Rapid Ca2+ Entry through Ca2+-Permeable AMPA/Kainate Channels Triggers Marked Intracellular Ca2+Rises and Consequent Oxygen Radical Production , 1998, The Journal of Neuroscience.

[36]  B. Keller,et al.  Endogenous calcium buffering in motoneurones of the nucleus hypoglossus from mouse , 1998, The Journal of physiology.

[37]  J. Powell,et al.  Mutations in all five exons of SOD‐1 may cause ALS , 1998, Annals of neurology.

[38]  P. Ince,et al.  Glutamate, excitotoxicity and amyotrophic lateral sclerosis , 1997, Journal of Neurology.

[39]  B. Hille,et al.  Mitochondrial Participation in the Intracellular Ca2+ Network , 1997, The Journal of cell biology.

[40]  P N Leigh,et al.  Excitotoxicity in ALS , 1996, Neurology.

[41]  J. Weiss,et al.  Motor Neurons Are Selectively Vulnerable to AMPA/Kainate Receptor-Mediated Injury In Vitro , 1996, The Journal of Neuroscience.

[42]  J. Belleroche,et al.  Amyotrophic Lateral Sclerosis: Recent Advances in Understanding Disease Mechanisms , 1996, Journal of neuropathology and experimental neurology.

[43]  Charles Tator,et al.  Normal and abnormal calcium homeostasis in neurons: a basis for the pathophysiology of traumatic and ischemic central nervous system injury. , 1996, Neurosurgery.

[44]  S. Budd,et al.  A Reevaluation of the Role of Mitochondria in Neuronal Ca2+ Homeostasis , 1996, Journal of neurochemistry.

[45]  J. Rothstein,et al.  Neuroprotective Strategies in a Model of Chronic Glutamate‐Mediated Motor Neuron Toxicity , 1995, Journal of neurochemistry.

[46]  J. Weiss,et al.  In vitro kainate injury to large, SMI-32(+) spinal neurons is Ca2+ dependent , 1995, Neuroreport.

[47]  M E Greenberg,et al.  Calcium signaling in neurons: molecular mechanisms and cellular consequences. , 1995, Science.

[48]  V. Meininger,et al.  Identification of new mutations in the Cu/Zn superoxide dismutase gene of patients with familial amyotrophic lateral sclerosis. , 1995, American journal of human genetics.

[49]  V. La Bella,et al.  The role of calcium‐binding proteins in selective motoneuron vulnerability in amyotrophic lateral sclerosis , 1994, Annals of neurology.

[50]  I. Kanazawa,et al.  A two basepair deletion in the SOD 1 gene causes familial amyotrophic lateral sclerosis. , 1994, Human molecular genetics.

[51]  M. Gurney,et al.  Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. , 1994, Science.

[52]  J. Rothstein,et al.  Chronic inhibition of glutamate uptake produces a model of slow neurotoxicity. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[53]  Charles Tator,et al.  Source specificity of early calcium neurotoxicity in cultured embryonic spinal neurons , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[54]  M E Greenberg,et al.  Regulation of gene expression in hippocampal neurons by distinct calcium signaling pathways. , 1993, Science.

[55]  J. Haines,et al.  Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis , 1993, Nature.

[56]  J. Rothstein,et al.  Decreased glutamate transport by the brain and spinal cord in amyotrophic lateral sclerosis. , 1992, The New England journal of medicine.

[57]  J. Coyle,et al.  Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis , 1990, Annals of neurology.

[58]  T. Takahashi.  Membrane currents in visually identified motoneurones of neonatal rat spinal cord. , 1990, The Journal of physiology.

[59]  Norbert,et al.  Cyclopiazonic acid is a specific inhibitor of the Ca2+-ATPase of sarcoplasmic reticulum. , 1989, The Journal of biological chemistry.

[60]  J. Vallat,et al.  Kainic acid induces early and delayed degenerative neuronal changes in rat spinal cord , 1989, Neuroscience Letters.

[61]  J. Vallat,et al.  Glutamate dehydrogenase and aspartate aminotransferase in leukocytes of patients with motor neuron disease , 1989, Neurology.

[62]  D. Choi,et al.  Glutamate neurotoxicity and diseases of the nervous system , 1988, Neuron.

[63]  J. Caroscio,et al.  Abnormal glutamate metabolism in amyotrophic lateral sclerosis , 1987, Annals of neurology.

[64]  R. Tsien,et al.  A new generation of Ca2+ indicators with greatly improved fluorescence properties. , 1985, The Journal of biological chemistry.

[65]  B. Sakmann,et al.  Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches , 1981, Pflügers Archiv.

[66]  C. Heckman,et al.  Hyperexcitability of cultured spinal motoneurons from presymptomatic ALS mice. , 2004, Journal of neurophysiology.

[67]  S. Heinemann,et al.  Cloned glutamate receptors. , 1994, Annual review of neuroscience.