Research Topics
| Veronique M AndreSummaryAffiliation: University of California Country: USA Publications
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Detail Information
Publications
Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasiaVeronique M Andre
Mental Retardation Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA
J Neurosci Res 86:3151-62. 2008....
Differential electrophysiological changes in striatal output neurons in Huntington's diseaseVeronique M Andre
Department of Psychiatry and Biobehavioral Sciences, University of California, LA, CA 90095, USA
J Neurosci 31:1170-82. 2011..Stereotypic behavior at an early stage could be explained by increased glutamate activity and DA tone in direct pathway neurons, whereas hypokinesia at later stages could result from reduced input onto these neurons...- Dopamine and glutamate in Huntington's disease: A balancing actVeronique M Andre
Intellectual and Developmental Disabilities Research Center, Semel Institute, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, USA
CNS Neurosci Ther 16:163-78. 2010..Restoring the balance between glutamate and dopamine could be helpful to treat HD symptoms... - Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoidsVeronique M Andre
Mental Retardation Research Center, David Geffen School of Medicine at UCLA, Semel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, NPI 58 258, Los Angeles, CA 90095, USA
Eur J Neurosci 31:14-28. 2010..We suggest that activation of postsynaptic dopamine receptors controls endocannabinoid mobilization, acting on presynaptic CB1Rs, thus modulating glutamate release differently in glutamate terminals projecting to D1 and D2 cells... 
Altered cortical glutamate receptor function in the R6/2 model of Huntington's diseaseVeronique M Andre
Mental Retardation Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
J Neurophysiol 95:2108-19. 2006..Altered glutamate receptor function could contribute to changes in cortical output and may underlie some of the cognitive and motor impairments in this animal model of HD...- Differential electrophysiological properties of dopamine D1 and D2 receptor-containing striatal medium-sized spiny neuronsCarlos Cepeda
Mental Retardation Research Center, David Geffen School of Medicine, NPI Room 58 258, 760 Westwood Plaza, University of California, Los Angeles, CA 90095, USA
Eur J Neurosci 27:671-82. 2008..This could help to explain the increased vulnerability of D2 MSSNs in neurodegenerative disorders... - Immature neurons and GABA networks may contribute to epileptogenesis in pediatric cortical dysplasiaCarlos Cepeda
Mental Retardation Research Center, David Geffen School of Medicine, University of California, Los Angeles, California 90024, USA
Epilepsia 48:79-85. 2007..These results could partially explain the increased excitability of the cortical network in pediatric CD... - A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's diseaseDamian M Cummings
Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, California 90095, USA
J Neurophysiol 107:677-91. 2012.... - A hypothesis regarding the pathogenesis and epileptogenesis of pediatric cortical dysplasia and hemimegalencephaly based on MRI cerebral volumes and NeuN cortical cell densitiesGary W Mathern
Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA 90095 1769
Epilepsia 48:74-8. 2007.... - Cytomegalic interneurons: a new abnormal cell type in severe pediatric cortical dysplasiaVeronique M Andre
Mental Retardation Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA
J Neuropathol Exp Neurol 66:491-504. 2007.... - Age-dependent alterations of corticostriatal activity in the YAC128 mouse model of Huntington diseasePrasad R Joshi
Mental Retardation Research Center, The David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
J Neurosci 29:2414-27. 2009.... - Enhanced GABAergic network and receptor function in pediatric cortical dysplasia Type IIB compared with Tuberous Sclerosis ComplexCarlos Cepeda
Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90024, USA
Neurobiol Dis 45:310-21. 2012..These differences support the notion that the mechanisms of epileptogenesis could differ in patients with TSC and CDIIB. Consequently, pharmacologic therapies should take these findings into consideration... - NMDA receptor alterations in neurons from pediatric cortical dysplasia tissueVeronique M Andre
Mental Retardation Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Cereb Cortex 14:634-46. 2004..Taken together, these results demonstrate the presence of NMDA receptors with altered subunit composition and Mg(2+) sensitivity that could contribute to functional abnormalities in CD... - Interneurons, GABAA currents, and subunit composition of the GABAA receptor in type I and type II cortical dysplasiaVeronique M Andre
Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
Epilepsia 51:166-70. 2010..These findings support the hypothesis that patients with type I and type II CD will respond differently to GABA receptor-mediated antiepileptic drugs and that cytomegalic neurons have features similar to immature neurons... - Contralateral hemimicrencephaly and clinical-pathological correlations in children with hemimegalencephalyNoriko Salamon
Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
Brain 129:352-65. 2006..In addition, our findings support the hypothesis that HME pathogenesis probably involves somatic mutations that affect each developing cerebral hemisphere differently with more neurons than expected on the HME side... - Alterations in N-methyl-D-aspartate receptor sensitivity and magnesium blockade occur early in development in the R6/2 mouse model of Huntington's diseaseAmaal J Starling
Mental Retardation Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
J Neurosci Res 82:377-86. 2005..These alterations may contribute to an enhancement of NMDA responses at hyperpolarized membrane potentials that may be a key factor in striatal neuronal dysfunction... - Alterations in cortical excitation and inhibition in genetic mouse models of Huntington's diseaseDamian M Cummings
Mental Retardation Research Center, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, Los Angeles, CA 90095, USA
J Neurosci 29:10371-86. 2009..Furthermore, the differences between synaptic phenotypes in cortex and striatum are important for the development of future therapeutic approaches, which may need to be targeted early in the development of the phenotype... - Are cytomegalic neurons and balloon cells generators of epileptic activity in pediatric cortical dysplasia?Carlos Cepeda
Mental Retardation Research Center, David Geffen School of Medicine, University of California Los Angeles, California 90024, USA
Epilepsia 46:82-8. 2005..These aberrant cells could participate in the generation of epileptic activity. The aim of this study was to morphologically and electrophysiologically characterize cells in pediatric CD tissue... - Full-length human mutant huntingtin with a stable polyglutamine repeat can elicit progressive and selective neuropathogenesis in BACHD miceMichelle Gray
Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, California 90095, USA
J Neurosci 28:6182-95. 2008..In summary, the BACHD model constitutes a novel and robust in vivo paradigm for the investigation of HD pathogenesis and treatment... - Comparative study of cellular and synaptic abnormalities in brain tissue samples from pediatric tuberous sclerosis complex and cortical dysplasia type IICarlos Cepeda
Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California, Los Angeles, California 90024, USA
Epilepsia 51:160-5. 2010..These differences may contribute to variable mechanisms of epileptogenesis in patients with TSC compared with CD type II... - The corticostriatal pathway in Huntington's diseaseCarlos Cepeda
Mental Retardation Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA
Prog Neurobiol 81:253-71. 2007..Finally, as changes in cortical and striatal circuitry are complex and in some cases biphasic, therapeutic interventions should be regionally specific and take into account the temporal progression of the phenotype... - Morphological and electrophysiological characterization of abnormal cell types in pediatric cortical dysplasiaCarlos Cepeda
Mental Retardation Research Center, University of California, Los Angeles, California 90095, USA
J Neurosci Res 72:472-86. 2003..Cytomegalic neurons could play an important role in the generation of epileptic activity... - Human cortical dysplasia and epilepsy: an ontogenetic hypothesis based on volumetric MRI and NeuN neuronal density and size measurementsMarissa Andres
Division of Neurosurgery, University of California, Los Angeles, CA 90005, USA
Cereb Cortex 15:194-210. 2005.... - Location, location, location: contrasting roles of synaptic and extrasynaptic NMDA receptors in Huntington's diseaseMichael S Levine
Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, Los Angeles, CA 90095, USA
Neuron 65:145-7. 2010.... - Dissecting the contribution of individual receptor subunits to the enhancement of N-methyl-d-aspartate currents by dopamine D1 receptor activation in striatumEmily L Jocoy
Intellectual and Developmental Disabilities Research Center, Semel Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA
Front Syst Neurosci 5:28. 2011..The differential contribution of discrete receptor subunits to NMDA responses and dopamine modulation in the striatum has important implications for synaptic plasticity and selective neuronal vulnerability in disease states... - Genetic mouse models of Huntington's disease: focus on electrophysiological mechanismsCarlos Cepeda
Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California Los Angeles, 760 Westwood Plaza, Los Angeles, CA 90095, USA
ASN Neuro 2:e00033. 2010..Mounting evidence points to synaptic abnormalities in communication between the cortex and striatum and cell-cell interactions as major determinants of HD symptoms, even in the absence of severe neuronal degeneration and death... - Epileptogenesis in pediatric cortical dysplasia: the dysmature cerebral developmental hypothesisCarlos Cepeda
Division of Neurosurgery, Department of Neurology, The Brain Research Institute and The Mental Retardation Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Epilepsy Behav 9:219-35. 2006..We propose that local interactions of dysmature cells with normal postnatal neurons produce seizures. This hypothesis will drive future studies aimed at elucidating mechanisms of epileptogenesis in pediatric CD tissue... - Altered Balance of Activity in the Striatal Direct and Indirect Pathways in Mouse Models of Huntington's DiseaseVeronique M Andre
Intellectual and Developmental Disabilities Research Center, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, Semel Institute, University of California at Los Angeles Los Angeles, CA, USA
Front Syst Neurosci 5:46. 2011..These studies provide evidence for differential and complex imbalances in glutamate and GABA transmission, as well as in DA modulation, in direct and indirect pathway MSNs during HD progression... - Assessment and surgical outcomes for mild type I and severe type II cortical dysplasia: a critical review and the UCLA experienceJason T Lerner
Department of Pediatric Neurology, University of California, Los Angeles, California, USA
Epilepsia 50:1310-35. 2009..The authors discuss future challenges to identifying and treating medically refractory epilepsy patients with cortical dysplasia...