Veronique M Andre

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Dopamine and glutamate in Huntington's disease: A balancing act
    Veronique 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
  2. doi request reprint Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoids
    Veronique 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
  3. pmc Differential electrophysiological changes in striatal output neurons in Huntington's disease
    Veronique M Andre
    Department of Psychiatry and Biobehavioral Sciences, University of California, LA, CA 90095, USA
    J Neurosci 31:1170-82. 2011
  4. doi request reprint Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia
    Veronique 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
  5. ncbi request reprint Altered cortical glutamate receptor function in the R6/2 model of Huntington's disease
    Veronique 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
  6. doi request reprint Differential electrophysiological properties of dopamine D1 and D2 receptor-containing striatal medium-sized spiny neurons
    Carlos 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
  7. ncbi request reprint Immature neurons and GABA networks may contribute to epileptogenesis in pediatric cortical dysplasia
    Carlos Cepeda
    Mental Retardation Research Center, David Geffen School of Medicine, University of California, Los Angeles, California 90024, USA
    Epilepsia 48:79-85. 2007
  8. pmc A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease
    Damian 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
  9. ncbi request reprint A hypothesis regarding the pathogenesis and epileptogenesis of pediatric cortical dysplasia and hemimegalencephaly based on MRI cerebral volumes and NeuN cortical cell densities
    Gary W Mathern
    Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA 90095 1769
    Epilepsia 48:74-8. 2007
  10. ncbi request reprint Cytomegalic interneurons: a new abnormal cell type in severe pediatric cortical dysplasia
    Veronique 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

Collaborators

Detail Information

Publications30

  1. pmc Dopamine and glutamate in Huntington's disease: A balancing act
    Veronique 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...
  2. doi request reprint Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoids
    Veronique 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...
  3. pmc Differential electrophysiological changes in striatal output neurons in Huntington's disease
    Veronique 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...
  4. doi request reprint Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia
    Veronique 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
    ....
  5. ncbi request reprint Altered cortical glutamate receptor function in the R6/2 model of Huntington's disease
    Veronique 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...
  6. doi request reprint Differential electrophysiological properties of dopamine D1 and D2 receptor-containing striatal medium-sized spiny neurons
    Carlos 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...
  7. ncbi request reprint Immature neurons and GABA networks may contribute to epileptogenesis in pediatric cortical dysplasia
    Carlos 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...
  8. pmc A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease
    Damian 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
    ....
  9. ncbi request reprint A hypothesis regarding the pathogenesis and epileptogenesis of pediatric cortical dysplasia and hemimegalencephaly based on MRI cerebral volumes and NeuN cortical cell densities
    Gary W Mathern
    Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA 90095 1769
    Epilepsia 48:74-8. 2007
    ....
  10. ncbi request reprint Cytomegalic interneurons: a new abnormal cell type in severe pediatric cortical dysplasia
    Veronique 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
    ....
  11. pmc Age-dependent alterations of corticostriatal activity in the YAC128 mouse model of Huntington disease
    Prasad 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
    ....
  12. pmc Enhanced GABAergic network and receptor function in pediatric cortical dysplasia Type IIB compared with Tuberous Sclerosis Complex
    Carlos 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...
  13. ncbi request reprint NMDA receptor alterations in neurons from pediatric cortical dysplasia tissue
    Veronique 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...
  14. pmc Interneurons, GABAA currents, and subunit composition of the GABAA receptor in type I and type II cortical dysplasia
    Veronique 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...
  15. pmc Multiple Sources of Striatal Inhibition Are Differentially Affected in Huntington's Disease Mouse Models
    Carlos Cepeda
    Intellectual and Developmental Disabilities Research Center, Brain Research Institute, Semel Institute for Neuroscience, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095 and Departments of Bioengineering and Psychiatry and Behavioral Sciences, Stanford University, Stanford, California 94305 2004
    J Neurosci 33:7393-406. 2013
    ..These findings provide strong evidence that both feedforward and to a lesser extent feedback inhibition to MSNs in HD can potentially be sources for the increased GABA synaptic activity of indirect pathway MSNs...
  16. ncbi request reprint Contralateral hemimicrencephaly and clinical-pathological correlations in children with hemimegalencephaly
    Noriko 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...
  17. ncbi request reprint Alterations in N-methyl-D-aspartate receptor sensitivity and magnesium blockade occur early in development in the R6/2 mouse model of Huntington's disease
    Amaal 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...
  18. pmc Full-length human mutant huntingtin with a stable polyglutamine repeat can elicit progressive and selective neuropathogenesis in BACHD mice
    Michelle 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...
  19. pmc Alterations in cortical excitation and inhibition in genetic mouse models of Huntington's disease
    Damian 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...
  20. pmc Comparative study of cellular and synaptic abnormalities in brain tissue samples from pediatric tuberous sclerosis complex and cortical dysplasia type II
    Carlos 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...
  21. ncbi request reprint 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...
  22. pmc The corticostriatal pathway in Huntington's disease
    Carlos 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...
  23. ncbi request reprint Morphological and electrophysiological characterization of abnormal cell types in pediatric cortical dysplasia
    Carlos 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...
  24. pmc Location, location, location: contrasting roles of synaptic and extrasynaptic NMDA receptors in Huntington's disease
    Michael 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
    ....
  25. pmc Dissecting the contribution of individual receptor subunits to the enhancement of N-methyl-d-aspartate currents by dopamine D1 receptor activation in striatum
    Emily 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...
  26. ncbi request reprint Human cortical dysplasia and epilepsy: an ontogenetic hypothesis based on volumetric MRI and NeuN neuronal density and size measurements
    Marissa Andres
    Division of Neurosurgery, University of California, Los Angeles, CA 90005, USA
    Cereb Cortex 15:194-210. 2005
    ....
  27. pmc Genetic mouse models of Huntington's disease: focus on electrophysiological mechanisms
    Carlos 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...
  28. ncbi request reprint Epileptogenesis in pediatric cortical dysplasia: the dysmature cerebral developmental hypothesis
    Carlos 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...
  29. pmc Altered Balance of Activity in the Striatal Direct and Indirect Pathways in Mouse Models of Huntington's Disease
    Veronique 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...
  30. doi request reprint Assessment and surgical outcomes for mild type I and severe type II cortical dysplasia: a critical review and the UCLA experience
    Jason 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...