Functional Characterization and Neuronal Modeling of the Effects of Childhood Absence Epilepsy Variants of CACNA1H, a T-Type Calcium Channel
暂无分享,去创建一个
E. Perez-Reyes | Iuliia Vitko | Yucai Chen | J. Arias | Yen-Ting Shen | Xi-ru Wu | Edward Perez-Reyes | Iuliia Vitko | Xi-Ru Wu | Yucai Chen | Juan M Arias | Yen Shen
[1] P. Barrett,et al. Stimulation of recombinant Cav3.2, T‐type, Ca2+ channel currents by CaMKIIγC , 2002 .
[2] E. Perez-Reyes,et al. Gating Kinetics of the α1i T-Type Calcium Channel , 2001, The Journal of general physiology.
[3] R. Llinás,et al. Electrophysiology of mammalian thalamic neurones in vitro , 1982, Nature.
[4] P. Lory,et al. Plasma Membrane Expression of T-type Calcium Channel α1 Subunits Is Modulated by High Voltage-activated Auxiliary Subunits* , 2004, Journal of Biological Chemistry.
[5] D. McCormick,et al. On the cellular and network bases of epileptic seizures. , 2001, Annual review of physiology.
[6] D. Baillie,et al. Molecular and Functional Characterization of a Family of Rat Brain T-type Calcium Channels* , 2001, The Journal of Biological Chemistry.
[7] T. Sander. The genetics of idiopathic generalized epilepsy: implications for the understanding of its aetiology. , 1996, Molecular medicine today.
[8] M. de Curtis,et al. Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[9] M. Ferrari,et al. 2 A Cacna 1 a Knockin Migraine Mouse Model with Increased Susceptibility to Cortical Spreading Depression , 2006 .
[10] P. Lory,et al. Overexpression of T‐type calcium channels in HEK‐293 cells increases intracellular calcium without affecting cellular proliferation , 2000, FEBS letters.
[11] P. Gloor,et al. Generalized epilepsy: some of its cellular mechanisms differ from those of focal epilepsy , 1988, Trends in Neurosciences.
[12] Y. Zhang,et al. Cloning and characterization of alpha1H from human heart, a member of the T-type Ca2+ channel gene family. , 1998, Circulation research.
[13] Alain Destexhe,et al. LTS cells in cerebral cortex and their role in generating spike-and-wave oscillations , 2001, Neurocomputing.
[14] D. Prince,et al. Characterization of ethosuximide reduction of low‐threshold calcium current in thalamic neurons , 1989, Annals of neurology.
[15] Vincenzo Crunelli,et al. The ‘window’ T‐type calcium current in brain dynamics of different behavioural states , 2005, The Journal of physiology.
[16] Jung-Ha Lee,et al. Cloning and Expression of a Novel Member of the Low Voltage-Activated T-Type Calcium Channel Family , 1999, The Journal of Neuroscience.
[17] R Ottman,et al. Identification of epilepsy genes in human and mouse. , 2001, Annual review of genetics.
[18] R. Llinás,et al. Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[19] Jung-Ha Lee,et al. Comparison of the Ca2 + currents induced by expression of three cloned α1 subunits, α1G, α1H and α1I, of low‐voltage‐activated T‐type Ca2 + channels , 1999 .
[20] Yusuke Nakamura,et al. JSNP: a database of common gene variations in the Japanese population , 2002, Nucleic Acids Res..
[21] M. Gardiner,et al. Genetics of childhood epilepsy , 2000, Archives of disease in childhood.
[22] H R Parri,et al. On the Action of the Anti-Absence Drug Ethosuximide in the Rat and Cat Thalamus , 1998, The Journal of Neuroscience.
[23] C. Lingle,et al. Kinetic and pharmacological properties of low voltage-activated Ca2+ current in rat clonal (GH3) pituitary cells. , 1992, Journal of neurophysiology.
[24] Jung-Ha Lee,et al. Cloning and expression of the human T-type channel Ca(v)3.3: insights into prepulse facilitation. , 2002, Biophysical journal.
[25] E. Perez-Reyes,et al. State-Dependent Inactivation of the α1g T-Type Calcium Channel , 1999, The Journal of general physiology.
[26] A. Depaulis,et al. Low-voltage-activated calcium channel subunit expression in a genetic model of absence epilepsy in the rat. , 2000, Brain research. Molecular brain research.
[27] D. Bayliss,et al. A role for T-type Ca2+channels in the synergistic control of aldosterone production by ANG II and K. , 1999, American journal of physiology. Renal physiology.
[28] B. Delisle,et al. Mechanism of inactivation gating of human T-type (low-voltage activated) calcium channels. , 2002, Biophysical journal.
[29] F. Döring,et al. Endogenous calcium channels in human embryonic kidney (HEK293) cells , 1996, British journal of pharmacology.
[30] J. Huguenard. Neuronal circuitry of thalamocortical epilepsy and mechanisms of antiabsence drug action. , 1999, Advances in neurology.
[31] V. Crunelli,et al. Cortical-area specific block of genetically determined absence seizures by ethosuximide , 2004, Neuroscience.
[32] Zhijian Yao,et al. Association between genetic variation of CACNA1H and childhood absence epilepsy , 2003, Annals of neurology.
[33] Yi Zhang,et al. Mutations in High-Voltage-Activated Calcium Channel Genes Stimulate Low-Voltage-Activated Currents in Mouse Thalamic Relay Neurons , 2002, The Journal of Neuroscience.
[34] Daesoo Kim,et al. Lack of the Burst Firing of Thalamocortical Relay Neurons and Resistance to Absence Seizures in Mice Lacking α1G T-Type Ca2+ Channels , 2001, Neuron.
[35] T. Sejnowski,et al. Ionic mechanisms underlying synchronized oscillations and propagating waves in a model of ferret thalamic slices. , 1996, Journal of neurophysiology.
[36] T J Sejnowski,et al. In vivo, in vitro, and computational analysis of dendritic calcium currents in thalamic reticular neurons , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[37] M L Hines,et al. Neuron: A Tool for Neuroscientists , 2001, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry.
[38] T-type calcium channel gene alpha (1G) is not associated with childhood absence epilepsy in the Chinese Han population , 2003, Neuroscience Letters.
[39] P. Lory,et al. Electrophysiological properties of the hypokalaemic periodic paralysis mutation (R528H) of the skeletal muscle α 1S subunit as expressed in mouse L cells , 1996, FEBS letters.
[40] C. Bader,et al. T-type alpha 1H Ca2+ channels are involved in Ca2+ signaling during terminal differentiation (fusion) of human myoblasts. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[41] C. Kuo,et al. Recovery from Inactivation of T-Type Ca2+ Channels in Rat Thalamic Neurons , 2001, The Journal of Neuroscience.
[42] R. Lambert,et al. T-Type Ca 2 1 Current Properties Are Not Modified by Ca 2 1 Channel b Subunit Depletion in Nodosus Ganglion Neurons , 1997 .
[43] Edmund M. Talley,et al. Differential Distribution of Three Members of a Gene Family Encoding Low Voltage-Activated (T-Type) Calcium Channels , 1999, The Journal of Neuroscience.
[44] P. Lory,et al. Specific contribution of human T‐type calcium channel isotypes (α1G, α1H and α1I) to neuronal excitability , 2002 .
[45] T. Sejnowski,et al. Interactions between membrane conductances underlying thalamocortical slow-wave oscillations. , 2003, Physiological reviews.
[46] D. Prince,et al. A novel T-type current underlies prolonged Ca(2+)-dependent burst firing in GABAergic neurons of rat thalamic reticular nucleus , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[47] H. Fukuda,et al. Pharmacological profiles of generalized absence seizures in lethargic, stargazer and γ-hydroxybutyrate-treated model mice , 1997, Neuroscience Research.
[48] Aaron M. Beedle,et al. The CACNA1F Gene Encodes an L-Type Calcium Channel with Unique Biophysical Properties and Tissue Distribution , 2004, The Journal of Neuroscience.
[49] C. Arnoult,et al. Identification and Localization of T-type Voltage-operated Calcium Channel Subunits in Human Male Germ Cells , 2002, The Journal of Biological Chemistry.
[50] J. Gargus,et al. Unraveling monogenic channelopathies and their implications for complex polygenic disease. , 2003, American journal of human genetics.
[51] C. Altier,et al. Gating Effects of Mutations in the Cav3.2 T-type Calcium Channel Associated with Childhood Absence Epilepsy* , 2004, Journal of Biological Chemistry.
[52] M. Weiergräber,et al. Block of cloned human T-type calcium channels by succinimide antiepileptic drugs. , 2001, Molecular pharmacology.
[53] F. H. Lopes da Silva,et al. Cortical Focus Drives Widespread Corticothalamic Networks during Spontaneous Absence Seizures in Rats , 2002, The Journal of Neuroscience.
[54] A. Destexhe,et al. Dendritic Low-Threshold Calcium Currents in Thalamic Relay Cells , 1998, The Journal of Neuroscience.
[55] A. George,et al. Molecular Basis of an Inherited Epilepsy , 2002, Neuron.
[56] J. Bossu,et al. Inactivation of the low‐threshold transient calcium current in rat sensory neurones: evidence for a dual process. , 1986, The Journal of physiology.
[57] E. Perez-Reyes. Molecular physiology of low-voltage-activated t-type calcium channels. , 2003, Physiological reviews.
[58] M. Steriade. Impact of network activities on neuronal properties in corticothalamic systems. , 2001, Journal of neurophysiology.
[59] O. Devinsky,et al. Epilepsy-Associated Dysfunction in the Voltage-Gated Neuronal Sodium Channel SCN1A , 2003, The Journal of Neuroscience.
[60] I. Scheffer,et al. Genetic variation of CACNA1H in idiopathic generalized epilepsy , 2004, Annals of neurology.
[61] V. Crunelli,et al. Childhood absence epilepsy: Genes, channels, neurons and networks , 2002, Nature Reviews Neuroscience.
[62] L. Cribbs,et al. Arachidonic acid modulation of α1H, a cloned human T-type calcium channel , 2000 .
[63] Simon Kaja,et al. A Cacna1a Knockin Migraine Mouse Model with Increased Susceptibility to Cortical Spreading Depression , 2004, Neuron.