Altered Voltage Dependent Calcium Currents in a Neuronal Cell Line Derived From the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Down Syndrome

[1]  J. Segura-Aguilar,et al.  Effect of the knockdown of amyloid precursor protein on intracellular calcium increases in a neuronal cell line derived from the cerebral cortex of a trisomy 16 mouse , 2008, Experimental Neurology.

[2]  E. Rojas,et al.  Endosomal abnormalities related to amyloid precursor protein in cholesterol treated cerebral cortex neuronal cells derived from trisomy 16 mice, an animal model of Down syndrome , 2007, Neuroscience Letters.

[3]  W. Sather,et al.  AKAP79/150 Anchoring of Calcineurin Controls Neuronal L-Type Ca2+ Channel Activity and Nuclear Signaling , 2007, Neuron.

[4]  D. D. Allen,et al.  Neuronal dysfunction in Down syndrome: Contribution of neuronal models in cell culture , 2006, Journal of Physiology-Paris.

[5]  S. Rapoport,et al.  Altered calcium currents in cultured sensory neurons of normal and trisomy 16 mouse fetuses, an animal model for human trisomy 21 (Down syndrome). , 2006, Biological research.

[6]  J. Buxbaum,et al.  Aβ localization in abnormal endosomes: association with earliest Aβ elevations in AD and Down syndrome , 2004, Neurobiology of Aging.

[7]  S. Sampaio,et al.  Expression of ion channels during differentiation of a human skeletal muscle cell line , 1997, Journal of Muscle Research & Cell Motility.

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

[9]  C. Epstein,et al.  App Gene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome , 2003, The Journal of Neuroscience.

[10]  S. Rapoport,et al.  Cell Lines Derived from Hippocampal Neurons of the Normal and Trisomy 16 Mouse Fetus (a Model for Down Syndrome) Exhibit Neuronal Markers, Cholinergic Function, and Functional Neurotransmitter Receptors , 2002, Experimental Neurology.

[11]  S. Rapoport,et al.  Establishment and characterization of immortalized neuronal cell lines derived from the spinal cord of normal and trisomy 16 fetal mice, an animal model of Down syndrome , 2002, Journal of neuroscience research.

[12]  S. Rapoport,et al.  Impaired cholinergic function in cell lines derived from the cerebral cortex of normal and trisomy 16 mice , 2000, The European journal of neuroscience.

[13]  M. Hattori,et al.  The DNA sequence of human chromosome 21 , 2000, Nature.

[14]  S. Rapoport,et al.  Calcium signals in cell lines derived from the cerebral cortex of normal and trisomy 16 mice. , 1999, Neuroreport.

[15]  W. Müller,et al.  Altered Ca2+ Signaling and Mitochondrial Deficiencies in Hippocampal Neurons of Trisomy 16 Mice: A Model of Down’s Syndrome , 1998, The Journal of Neuroscience.

[16]  S. Rapoport,et al.  Increased expression of voltage-activated calcium channels in cultured hippocampal neurons from mouse trisomy 16, a model for Down syndrome. , 1998, Brain research. Molecular brain research.

[17]  U. Heinemann,et al.  Altered Ca 2 1 Signaling and Mitochondrial Deficiencies in Hippocampal Neurons of Trisomy 16 Mice : A Model of Down ’ s Syndrome , 1998 .

[18]  R. Penner,et al.  Silent calcium channels generate excessive tail currents and facilitation of calcium currents in rat skeletal myoballs. , 1996, The Journal of physiology.

[19]  S. Rapoport,et al.  Increased inward current in septal neurons from the trisomy 16 mouse, a model for Down's syndrome , 1995, Brain Research.

[20]  C. Epstein,et al.  Regional alteration of cholinergic function in central neurons of trisomy 16 mouse fetuses, an animal model of human trisomy 21 (Down syndrome) , 1994, Brain Research.

[21]  Maria V. Sanchez-Vives,et al.  Calcium‐dependent chloride current induced by axotomy in rat sympathetic neurons. , 1994, The Journal of physiology.

[22]  E. Jaimovich,et al.  Calcium fluxes, ion currents and dihydropyridine receptors in a new immortal cell line from rat heart muscle. , 1993, Journal of molecular and cellular cardiology.

[23]  S. Rapoport,et al.  Cultured hippocampal neurons from trisomy 16 mouse, a model for Down's syndrome, have an abnormal action potential due to a reduced inward sodium current , 1993, Brain Research.

[24]  H. Sullivan.  Ionic Channels of Excitable Membranes, 2nd Ed. , 1992, Neurology.

[25]  K. Currie,et al.  Calcium‐activated currents in cultured neurones from rat dorsal root ganglia , 1992, British journal of pharmacology.

[26]  S. Barnes,et al.  Modulation of calcium-activated chloride current via pH-induced changes of calcium channel properties in cone photoreceptors , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[27]  S. Rapoport,et al.  The role of altered sodium currents in action potential abnormalities of cultured dorsal root ganglion neurons from trisomy 21 (down syndrome) human fetuses , 1990, Brain Research.

[28]  A. Hodgkin,et al.  A quantitative description of membrane current and its application to conduction and excitation in nerve , 1990, Bulletin of mathematical biology.

[29]  S. Rapoport,et al.  Neurophysiological abnormalities in cultured dorsal root ganglion neurons from the trisomy-16 mouse fetus, a model for Down syndrome , 1989, Brain Research.

[30]  D. Armstrong.  Calcium channel regulation by calcineurin, a Ca2+-activated phosphatase in mammalian brain , 1989, Trends in Neurosciences.

[31]  Stanley I. Rapoport,et al.  Electrical properties of cultured dorsal root ganglion neurons from normal and trisomy 21 human fetal tissue , 1988, Brain Research.

[32]  J. Haxby,et al.  Dementia in Down's syndrome , 1988, Neurology.

[33]  D. Chelmow.  The Neurobiology of Down Syndrome , 1987, The Yale Journal of Biology and Medicine.

[34]  M. Oster-Granite.  The neurobiologic consequences of autosomal trisomy in mice and men , 1986, Brain Research Bulletin.

[35]  C. Epstein.  The Consequences of Chromosome Imbalance: The Consequences of Chromosome Imbalance , 1986 .

[36]  D. Cox,et al.  Mouse Trisomy 16: An Animal Model of Human Trisomy 21 (Down Syndrome) a , 1985, Annals of the New York Academy of Sciences.

[37]  B. Hille,et al.  Ionic channels of excitable membranes , 2001 .

[38]  R. Tsien,et al.  High selectivity of calcium channels in single dialysed heart cells of the guinea‐pig. , 1984, The Journal of physiology.

[39]  S. Hagiwara,et al.  The calcium channel , 1983, Trends in Neurosciences.

[40]  T. Petit,et al.  Neurobiology of Down's syndrome , 1983, Progress in Neurobiology.

[41]  E Neher,et al.  Sodium and calcium channels in bovine chromaffin cells , 1982, The Journal of physiology.

[42]  W. Gibbons,et al.  Effects of low-chloride solutions on action potentials of sheep cadiac purkinje fibers , 1977, The Journal of general physiology.

[43]  Johnson Rc,et al.  The behavioral competence of mongoloid and non-mongoloid retardates. , 1969 .

[44]  R. C. Johnson,et al.  The behavioral competence of mongoloid and non-mongoloid retardates. , 1969, American journal of mental deficiency.

[45]  D. Loesch-Mdzewska.  Some aspects of the neurology of Down's syndrome. , 2008, Journal of mental deficiency research.

[46]  P. Véghelyi.  EMERGENCY HYPOTHERMIC IN MENINGOCOCCAL MENINGITIS. , 1965, Lancet.

[47]  R TURPIN,et al.  Somatic chromosomes in mongolism. , 1962, Research publications - Association for Research in Nervous and Mental Disease.

[48]  J. Lejeune,et al.  [Mongolism; a chromosomal disease (trisomy)]. , 1959, Bulletin de l'Academie nationale de medecine.