Corrigendum to “Long-term valproic acid exposure increases the number of neocortical neurons in the developing rat brain” [Neurosci. Lett. 580 (2014) 12–16] A possible new animal model of autism

[1]  H. Markram,et al.  General developmental health in the VPA-rat model of autism , 2013, Front. Behav. Neurosci..

[2]  I. Chiu,et al.  The mood stabilizer valproate activates human FGF1 gene promoter through inhibiting HDAC and GSK‐3 activities , 2013, Journal of neurochemistry.

[3]  Mogens Vestergaard,et al.  Prenatal valproate exposure and risk of autism spectrum disorders and childhood autism. , 2013, JAMA.

[4]  J. Foster,et al.  In utero exposure to valproic acid and autism--a current review of clinical and animal studies. , 2013, Neurotoxicology and teratology.

[5]  K. Meador,et al.  Fetal antiepileptic drug exposure and cognitive outcomes at age 6 years (NEAD study): a prospective observational study , 2013, The Lancet Neurology.

[6]  T. Chomiak,et al.  Alterations of neocortical development and maturation in autism: insight from valproic acid exposure and animal models of autism. , 2013, Neurotoxicology and teratology.

[7]  Marta García-Fiñana,et al.  The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs , 2013, Journal of Neurology, Neurosurgery & Psychiatry.

[8]  Se Jin Jeon,et al.  Prenatal exposure to valproic acid increases the neural progenitor cell pool and induces macrocephaly in rat brain via a mechanism involving the GSK-3β/β-catenin pathway , 2012, Neuropharmacology.

[9]  W. Hauser,et al.  Comparative safety of antiepileptic drugs during pregnancy , 2012, Neurology.

[10]  Kristopher T Kahle,et al.  The GABA Excitatory/Inhibitory Shift in Brain Maturation and Neurological Disorders , 2012, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry.

[11]  T. Tomson,et al.  Dose-dependent risk of malformations with antiepileptic drugs: an analysis of data from the EURAP epilepsy and pregnancy registry , 2011, The Lancet Neurology.

[12]  J. Piven,et al.  Early brain overgrowth in autism associated with an increase in cortical surface area before age 2 years. , 2011, Archives of general psychiatry.

[13]  D. Guilloteau,et al.  Fetal exposure to teratogens: Evidence of genes involved in autism , 2011, Neuroscience & Biobehavioral Reviews.

[14]  Kwang Ho Ko,et al.  The critical period of valproate exposure to induce autistic symptoms in Sprague-Dawley rats. , 2011, Toxicology letters.

[15]  S. Essock,et al.  Valproate prescription prevalence among women of childbearing age. , 2011, Psychiatric services.

[16]  B. Hu,et al.  Altering the trajectory of early postnatal cortical development can lead to structural and behavioural features of autism , 2010, BMC Neuroscience.

[17]  Yoshio Imura,et al.  Nonexploratory movement and behavioral alterations in a thalidomide or valproic acid-induced autism model rat , 2010, Neuroscience Research.

[18]  A. Ornoy Valproic acid in pregnancy: how much are we endangering the embryo and fetus? , 2009, Reproductive toxicology.

[19]  H. Markram,et al.  Hyper-Connectivity and Hyper-Plasticity in the Medial Prefrontal Cortex in the Valproic Acid Animal Model of Autism , 2008, Frontiers in neural circuits.

[20]  Henry Markram,et al.  The Intense World Syndrome – an Alternative Hypothesis for Autism , 2007, Front. Neurosci..

[21]  Yehezkel Ben-Ari,et al.  Fetal Exposure to GABA‐Acting Antiepileptic Drugs Generates Hippocampal and Cortical Dysplasias , 2007, Epilepsia.

[22]  Ben S. Wittner,et al.  Association of valproate‐induced teratogenesis with histone deacetylase inhibition in vivo , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[23]  M. Narita,et al.  Maternal administration of thalidomide or valproic acid causes abnormal serotonergic neurons in the offspring: implication for pathogenesis of autism , 2005, International Journal of Developmental Neuroscience.

[24]  Eric Courchesne,et al.  Brain overgrowth in autism during a critical time in development: implications for frontal pyramidal neuron and interneuron development and connectivity , 2005, International Journal of Developmental Neuroscience.

[25]  P. Rodier,et al.  The teratology of autism , 2005, International Journal of Developmental Neuroscience.

[26]  D. O’Carroll,et al.  Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression , 2002, The EMBO journal.

[27]  Ping Zhu,et al.  Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells , 2001, The EMBO journal.

[28]  J R Nyengaard,et al.  Tissue shrinkage and unbiased stereological estimation of particle number and size * , 2001, Journal of microscopy.

[29]  M. Guenther,et al.  Histone Deacetylase Is a Direct Target of Valproic Acid, a Potent Anticonvulsant, Mood Stabilizer, and Teratogen* , 2001, The Journal of Biological Chemistry.

[30]  R. Przewłocki,et al.  Nociceptive changes in rats after prenatal exposure to valproic acid. , 2001, Polish journal of pharmacology.

[31]  Ruth A. Carper,et al.  Unusual brain growth patterns in early life in patients with autistic disorder , 2001, Neurology.

[32]  B. Kerr,et al.  Fetal valproate syndrome and autism: additional evidence of an association , 2001, Developmental medicine and child neurology.

[33]  P. Rodier,et al.  Prenatal exposure of rats to valproic acid reproduces the cerebellar anomalies associated with autism. , 2000, Neurotoxicology and teratology.

[34]  P. Rodier,et al.  Linking etiologies in humans and animal models: studies of autism. , 1997, Reproductive toxicology.

[35]  P. Rodier,et al.  Embryological origin for autism: Developmental anomalies of the cranial nerve motor nuclei , 1996, The Journal of comparative neurology.

[36]  J. Kromberg,et al.  Fetal Valproate Syndrome: Clinical and Neuro‐developmental Features in Two Sibling Pairs , 1994 .

[37]  C. Gillberg,et al.  AUTISM IN THALIDOMIDE EMBRYOPATHY: A POPULATION STUDY , 1994, Developmental medicine and child neurology.

[38]  C. Vorhees,et al.  Teratogenicity and developmental toxicity of valproic acid in rats. , 1987, Teratology.

[39]  C. Curry,et al.  The fetal valproate syndrome. , 1984, American journal of medical genetics.

[40]  J. Petrere,et al.  Teratogenesis of calcium valproate in rats. , 1983, Fundamental and applied toxicology : official journal of the Society of Toxicology.

[41]  A. Czeizel,et al.  VALPROIC ACID AND SPINA BIFIDA , 1982, The Lancet.

[42]  H. Nau,et al.  A new model for embryotoxicity testing: teratogenicity and pharmacokinetics of valproic acid following constant-rate administration in the mouse using human therapeutic drug and metabolite concentrations. , 1981, Life sciences.

[43]  Evans Da Letter: Coeliac disease and HL-A8. , 1973 .

[44]  Ryszard Przewłocki,et al.  Behavioral Alterations in Rats Prenatally Exposed to Valproic Acid: Animal Model of Autism , 2005, Neuropsychopharmacology.

[45]  C. Vorhees,et al.  Behavioral teratogenicity of valproic acid: selective effects on behavior after prenatal exposure to rats , 2004, Psychopharmacology.

[46]  B. Kerr,et al.  Fetal valproate syndrome and autism , 2001 .

[47]  O. Ladefoged,et al.  Total number and mean cell volume of neocortical neurons in rats exposed to 2,5-hexanedione with and without acetone. , 1991, Neurotoxicology and teratology.

[48]  J. Piven,et al.  Magnetic resonance imaging and head circumference study of brain size in autism: birth through age 2 years. , 2005, Archives of general psychiatry.