Effects of the T-type calcium channel CaV3.2 R1584P mutation on absence seizure susceptibility in GAERS and NEC congenic rats models

[1]  G. van Luijtelaar,et al.  The impact of early-life environment on absence epilepsy and neuropsychiatric comorbidities , 2022, IBRO neuroscience reports.

[2]  D. D. Markov,et al.  Sucrose Preference Test as a Measure of Anhedonic Behavior in a Chronic Unpredictable Mild Stress Model of Depression: Outstanding Issues , 2022, Brain sciences.

[3]  Pablo M. Casillas-Espinosa,et al.  An Integrated Multi-Omic Network Analysis Identifies Seizure-Associated Dysregulated Pathways in the GAERS Model of Absence Epilepsy , 2022, International journal of molecular sciences.

[4]  Pablo M. Casillas-Espinosa,et al.  Disease-modifying effects of sodium selenate in a model of drug-resistant, temporal lobe epilepsy , 2022, bioRxiv.

[5]  J. Tu,et al.  Neural Burst Firing and Its Roles in Mental and Neurological Disorders , 2021, Frontiers in Cellular Neuroscience.

[6]  I. Scheffer,et al.  Contribution of rare genetic variants to drug response in absence epilepsy , 2021, Epilepsy Research.

[7]  Casey R. Vickstrom,et al.  T-Type Calcium Channels Contribute to Burst Firing in a Subpopulation of Medial Habenula Neurons , 2020, eNeuro.

[8]  G. Carvill,et al.  CACNA1H variants are not a cause of monogenic epilepsy , 2020, Human mutation.

[9]  Pablo M. Casillas-Espinosa,et al.  Harmonization of pipeline for detection of HFOs in a rat model of post-traumatic epilepsy in preclinical multicenter study on post-traumatic epileptogenesis , 2019, Epilepsy Research.

[10]  Pablo M. Casillas-Espinosa,et al.  Harmonization of the pipeline for seizure detection to phenotype post-traumatic epilepsy in a preclinical multicenter study on post-traumatic epileptogenesis , 2019, Epilepsy Research.

[11]  Pablo M. Casillas-Espinosa,et al.  Disease-modifying effects of a novel T-type calcium channel antagonist, Z944, in a model of temporal lobe epilepsy , 2019, Progress in Neurobiology.

[12]  Pablo M. Casillas-Espinosa,et al.  Multiunit cluster firing patterns of piriform cortex and mediodorsal thalamus in absence epilepsy , 2019, Epilepsy & Behavior.

[13]  Zheng Wang,et al.  A statistical analysis plan for a randomized clinical trial to evaluate the efficacy and safety of ethosuximide in patients with treatment-resistant depression , 2019, Medicine.

[14]  Armen R. Sargsyan,et al.  A universal automated tool for reliable detection of seizures in rodent models of acquired and genetic epilepsy , 2019, Epilepsia.

[15]  M. Koenig,et al.  Expanding the Phenotypic Spectrum of CACNA1H Mutations. , 2019, Pediatric neurology.

[16]  Michael R. Johnson,et al.  Ultra-rare genetic variation in the epilepsies: a whole-exome sequencing study of 17,606 individuals , 2019, bioRxiv.

[17]  S. Scheggi,et al.  Making Sense of Rodent Models of Anhedonia , 2018, The international journal of neuropsychopharmacology.

[18]  P. Lory,et al.  Modulation of T-type Ca2+ channels by Lavender and Rosemary extracts , 2017, PloS one.

[19]  S. Charpier,et al.  Building Up Absence Seizures in the Somatosensory Cortex: From Network to Cellular Epileptogenic Processes , 2017, Cerebral cortex.

[20]  Pablo M. Casillas-Espinosa,et al.  Evaluating whole genome sequence data from the Genetic Absence Epilepsy Rat from Strasbourg and its related non-epileptic strain , 2017, PLoS ONE.

[21]  Michael R. Johnson,et al.  Ultra-rare genetic variation in common epilepsies: a case-control sequencing study , 2017, The Lancet Neurology.

[22]  M. Salzberg,et al.  Environmental enrichment imparts disease-modifying and transgenerational effects on genetically-determined epilepsy and anxiety , 2016, Neurobiology of Disease.

[23]  Olivier David,et al.  The genetic absence epilepsy rat from Strasbourg as a model to decipher the neuronal and network mechanisms of generalized idiopathic epilepsies , 2016, Journal of Neuroscience Methods.

[24]  Pablo M. Casillas-Espinosa,et al.  Z944, a Novel Selective T-Type Calcium Channel Antagonist Delays the Progression of Seizures in the Amygdala Kindling Model , 2015, PloS one.

[25]  A. Depaulis,et al.  Seizure expression, behavior, and brain morphology differences in colonies of Genetic Absence Epilepsy Rats from Strasbourg , 2014, Epilepsia.

[26]  F. Jensen,et al.  The challenge and promise of anti-epileptic therapy development in animal models , 2014, The Lancet Neurology.

[27]  A. Nehlig,et al.  Anxiety and locomotion in Genetic Absence Epilepsy Rats from Strasbourg (GAERS): Inclusion of Wistar rats as a second control , 2014, Epilepsia.

[28]  Hatim A. Zariwala,et al.  Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement , 2014, The Journal of Neuroscience.

[29]  T. Snutch,et al.  T-type calcium channels in burst-firing, network synchrony, and epilepsy. , 2013, Biochimica et biophysica acta.

[30]  Pablo M. Casillas-Espinosa,et al.  Regulators of synaptic transmission: Roles in the pathogenesis and treatment of epilepsy , 2012, Epilepsia.

[31]  J. Hallak,et al.  Psychiatric comorbidities in temporal lobe epilepsy: possible relationships between psychotic disorders and involvement of limbic circuits. , 2012, Revista brasileira de psiquiatria.

[32]  T. Snutch,et al.  T-Type Calcium Channel Blockers That Attenuate Thalamic Burst Firing and Suppress Absence Seizures , 2012, Science Translational Medicine.

[33]  P. Schauwecker The relevance of individual genetic background and its role in animal models of epilepsy , 2011, Epilepsy Research.

[34]  P. Lory,et al.  Role of voltage-gated calcium channels in epilepsy , 2010, Pflügers Archiv - European Journal of Physiology.

[35]  Gary F. Egan,et al.  Morphometric abnormalities and hyperanxiety in genetically epileptic rats: A model of psychiatric comorbidity? , 2009, NeuroImage.

[36]  C. Reid,et al.  A Cav3.2 T-Type Calcium Channel Point Mutation Has Splice-Variant-Specific Effects on Function and Segregates with Seizure Expression in a Polygenic Rat Model of Absence Epilepsy , 2009, The Journal of Neuroscience.

[37]  E. Donner,et al.  Stepwise developmental regression associated with novel CACNA1A mutation. , 2008, Pediatric neurology.

[38]  Bruce Hermann,et al.  The neurobehavioural comorbidities of epilepsy: can a natural history be developed? , 2008, The Lancet Neurology.

[39]  Michael R. Salzberg,et al.  Elevated anxiety and depressive-like behavior in a rat model of genetic generalized epilepsy suggesting common causation , 2008, Experimental Neurology.

[40]  I. Scheffer,et al.  Extended spectrum of idiopathic generalized epilepsies associated with CACNA1H functional variants , 2007, Annals of neurology.

[41]  Scott B Patten,et al.  Psychiatric Comorbidity in Epilepsy: A Population‐Based Analysis , 2007, Epilepsia.

[42]  S. Charpier,et al.  Deep Layer Somatosensory Cortical Neurons Initiate Spike-and-Wave Discharges in a Genetic Model of Absence Seizures , 2007, The Journal of Neuroscience.

[43]  Y. Jiang,et al.  Common Polymorphisms in the CACNA1H Gene Associated with Childhood Absence Epilepsy in Chinese Han Population , 2007, Annals of human genetics.

[44]  P. Lory,et al.  The I–II Loop Controls Plasma Membrane Expression and Gating of Cav3.2 T-Type Ca2+ Channels: A Paradigm for Childhood Absence Epilepsy Mutations , 2007, The Journal of Neuroscience.

[45]  G. Stuart,et al.  Inherited cortical HCN1 channel loss amplifies dendritic calcium electrogenesis and burst firing in a rat absence epilepsy model , 2007, The Journal of physiology.

[46]  Diego Contreras,et al.  The role of T-channels in the generation of thalamocortical rhythms. , 2006, CNS & neurological disorders drug targets.

[47]  Yan Shen,et al.  New variants in the CACNA1H gene identified in childhood absence epilepsy , 2006, Neuroscience Letters.

[48]  K. Campbell,et al.  CaV3.2 is the major molecular substrate for redox regulation of T‐type Ca2+ channels in the rat and mouse thalamus , 2006, The Journal of physiology.

[49]  A. Heils,et al.  Evaluation of CACNA1H in European patients with childhood absence epilepsy , 2006, Epilepsy Research.

[50]  D. Hanck,et al.  A profile of alternative RNA splicing and transcript variation of CACNA1H, a human T-channel gene candidate for idiopathic generalized epilepsies. , 2006, Human molecular genetics.

[51]  C. Bladen,et al.  Functional Analysis of Cav3.2 T‐type Calcium Channel Mutations Linked to Childhood Absence Epilepsy , 2006 .

[52]  Pierre Jallon,et al.  Epidemiology of Idiopathic Generalized Epilepsies , 2005, Epilepsia.

[53]  R. Dahl,et al.  A genetic epidemiologic perspective on comorbidity of depression and anxiety. , 2005, Child and adolescent psychiatric clinics of North America.

[54]  Terence J O'Brien,et al.  Cellular and network mechanisms of genetically-determined absence seizures. , 2005, Thalamus & related systems.

[55]  E. Perez-Reyes,et al.  Functional Characterization and Neuronal Modeling of the Effects of Childhood Absence Epilepsy Variants of CACNA1H, a T-Type Calcium Channel , 2005, The Journal of Neuroscience.

[56]  C. Bladen,et al.  Effects of Cav3.2 channel mutations linked to idiopathic generalized epilepsy , 2005, Annals of neurology.

[57]  J. Noebels,et al.  Elevated Thalamic Low-Voltage-Activated Currents Precede the Onset of Absence Epilepsy in the SNAP25-Deficient Mouse Mutant Coloboma , 2004, The Journal of Neuroscience.

[58]  Robert Nitsch,et al.  An impaired neocortical Ih is associated with enhanced excitability and absence epilepsy , 2004, The European journal of neuroscience.

[59]  Francisco E. Baralle,et al.  Genomic variants in exons and introns: identifying the splicing spoilers , 2004, Nature Reviews Genetics.

[60]  D. Gauguier,et al.  Polygenic Control of Idiopathic Generalized Epilepsy Phenotypes in the Genetic Absence Rats from Strasbourg (GAERS) , 2004, Epilepsia.

[61]  I. Scheffer,et al.  Genetic variation of CACNA1H in idiopathic generalized epilepsy , 2004, Annals of neurology.

[62]  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.

[63]  A. Kanner Depression in epilepsy: a frequently neglected multifaceted disorder , 2003, Epilepsy & Behavior.

[64]  M. Kulikov,et al.  Depressive-like behavioral alterations and c-fos expression in the dopaminergic brain regions in WAG/Rij rats with genetic absence epilepsy , 2003, Behavioural Brain Research.

[65]  Zhijian Yao,et al.  Association between genetic variation of CACNA1H and childhood absence epilepsy , 2003, Annals of neurology.

[66]  Suresh Gurbani,et al.  Behavioral Disorders in Pediatric Epilepsy: Unmet Psychiatric Need , 2003, Epilepsia.

[67]  Alain Destexhe,et al.  The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity. , 2002, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.

[68]  V. Crunelli,et al.  Childhood absence epilepsy: Genes, channels, neurons and networks , 2002, Nature Reviews Neuroscience.

[69]  D. Pietrobon,et al.  Calcium channels and channelopathies of the central nervous system , 2002, Molecular Neurobiology.

[70]  Thomas D. Schmittgen,et al.  Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.

[71]  E. Vicaut,et al.  The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel. , 2001, The New England journal of medicine.

[72]  I. Kalcheva,et al.  Genome-tagged mice (GTM): two sets of genome-wide congenic strains. , 2001, Genomics.

[73]  Mark S. Seidenberg,et al.  Psychiatric Comorbidity in Chronic Epilepsy: Identification, Consequences, and Treatment of Major Depression , 2000, Epilepsia.

[74]  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.

[75]  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.

[76]  L. Danober,et al.  Pathophysiological mechanisms of genetic absence epilepsy in the rat , 1998, Progress in Neurobiology.

[77]  S. Berkovic,et al.  Epilepsies in twins: Genetics of the major epilepsy syndromes , 1998, Annals of neurology.

[78]  C. Ebeling,et al.  Theoretical and empirical issues for marker-assisted breeding of congenic mouse strains , 1997, Nature Genetics.

[79]  M. Weil,et al.  Genotype selection to rapidly breed congenic strains. , 1997, Genetics.

[80]  M. Meisler,et al.  Mutation of the Ca2+ Channel β Subunit Gene Cchb4 Is Associated with Ataxia and Seizures in the Lethargic (lh) Mouse , 1997, Cell.

[81]  P. Loiseau,et al.  Absence Epilepsies , 1995, Epilepsia.

[82]  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.

[83]  M. de Curtis,et al.  Thalamic regulation of epileptic spike and wave discharges. , 1994, Functional neurology.

[84]  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.

[85]  A. Coenen,et al.  Genetic models of absence epilepsy, with emphasis on the WAG/Rij strain of rats , 1992, Epilepsy Research.

[86]  A. Depaulis,et al.  Ontogeny of spontaneous petit mal-like seizures in Wistar rats , 1986 .

[87]  H. Lux,et al.  A low voltage-activated, fully inactivating Ca channel in vertebrate sensory neurones , 1984, Nature.

[88]  R L Sidman,et al.  Inherited epilepsy: spike-wave and focal motor seizures in the mutant mouse tottering. , 1979, Science.

[89]  G. Snell Methods for the study of histocompatibility genes , 1948, Journal of Genetics.

[90]  Jason H. Moore,et al.  Evidence for epistatic interactions in antiepileptic drug resistance , 2011, Journal of Human Genetics.

[91]  Andrew Charles,et al.  The neurobiology of migraine. , 2010, Handbook of clinical neurology.

[92]  A. Heils,et al.  EVALUATION OF CACNA 1 H IN EUROPEAN PATIENTS WITH CHILDHOOD ABSENCE EPILEPSY , 2008 .

[93]  T. Snutch,et al.  Calcium channelopathies: voltage-gated calcium channels. , 2007, Sub-cellular biochemistry.

[94]  C. Bladen,et al.  Functional analysis of Ca3.2 T-type calcium channel mutations linked to childhood absence epilepsy. , 2006, Epilepsia.

[95]  I. Davis,et al.  Transgenic mice. , 2006, Paediatric respiratory reviews.

[96]  C. Bladen,et al.  Effects of Cav 3 . 2 Channel Mutations Linked to Idiopathic Generalized Epilepsy , 2005 .

[97]  E. Perez-Reyes Molecular physiology of low-voltage-activated t-type calcium channels. , 2003, Physiological reviews.

[98]  A. Depaulis,et al.  Genetic absence epilepsy in rats from Strasbourg--a review. , 1992, Journal of neural transmission. Supplementum.

[99]  M. Gutnick,et al.  Electrophysiological properties of neurons in the lateral habenula nucleus: an in vitro study. , 1988, Journal of neurophysiology.

[100]  A. Depaulis,et al.  Ontogeny of spontaneous petit mal-like seizures in Wistar rats. , 1986, Brain research.

[101]  A. Depaulis,et al.  [A genetic form of petit mal absence in Wistar rats]. , 1984, Revue neurologique.