Michael Levine

Summary

Affiliation: University of California
Country: USA

Publications

  1. 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
  2. pmc Alterations in striatal synaptic transmission are consistent across genetic mouse models of Huntington's disease
    Damian M Cummings
    Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, U S A
    ASN Neuro 2:e00036. 2010
  3. pmc Improvement of neuropathology and transcriptional deficits in CAG 140 knock-in mice supports a beneficial effect of dietary curcumin in Huntington's disease
    Miriam A Hickey
    Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA
    Mol Neurodegener 7:12. 2012
  4. ncbi request reprint Genetic mouse models of Huntington's and Parkinson's diseases: illuminating but imperfect
    Michael S Levine
    Mental Retardation Research Center, The David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Trends Neurosci 27:691-7. 2004
  5. 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
  6. ncbi request reprint Enhanced sensitivity to N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease
    M S Levine
    Mental Retardation Research Center, University of California at Los Angeles, 90095, USA
    J Neurosci Res 58:515-32. 1999
  7. 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
  8. ncbi request reprint NMDA receptor function in mouse models of Huntington disease
    C Cepeda
    Mental Retardation Research Center, University of California at Los Angeles, School of Medicine, Los Angeles, California 90095, USA
    J Neurosci Res 66:525-39. 2001
  9. ncbi request reprint Electrophysiological and morphological changes in striatal spiny neurons in R6/2 Huntington's disease transgenic mice
    G J Klapstein
    Mental Retardation Research Center, University of California, Los Angeles, California 90095, USA
    J Neurophysiol 86:2667-77. 2001
  10. ncbi request reprint Differential sensitivity of medium- and large-sized striatal neurons to NMDA but not kainate receptor activation in the rat
    C Cepeda
    Mental Retardation Research Center and Brain Research Institute, UCLA School of Medicine, 760 Westwood Plaza NPI Room 58-258, Los Angeles, CA 90024, USA
    Eur J Neurosci 14:1577-89. 2001

Collaborators

Detail Information

Publications70

  1. 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...
  2. pmc Alterations in striatal synaptic transmission are consistent across genetic mouse models of Huntington's disease
    Damian M Cummings
    Intellectual and Developmental Disabilities Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, U S A
    ASN Neuro 2:e00036. 2010
    ..The outcomes suggest that the changes are due to the expression of mutant huntingtin and such alterations can be extended to the human condition...
  3. pmc Improvement of neuropathology and transcriptional deficits in CAG 140 knock-in mice supports a beneficial effect of dietary curcumin in Huntington's disease
    Miriam A Hickey
    Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA
    Mol Neurodegener 7:12. 2012
    ..We have examined the ability of life-long dietary curcumin to improve the early pathological phenotype of CAG140 mice...
  4. ncbi request reprint Genetic mouse models of Huntington's and Parkinson's diseases: illuminating but imperfect
    Michael S Levine
    Mental Retardation Research Center, The David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Trends Neurosci 27:691-7. 2004
    ....
  5. 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
    ....
  6. ncbi request reprint Enhanced sensitivity to N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease
    M S Levine
    Mental Retardation Research Center, University of California at Los Angeles, 90095, USA
    J Neurosci Res 58:515-32. 1999
    ..These findings imply that NMDA antagonists or compounds that alter sensitivity of NMDA receptors may be useful in the treatment of HD...
  7. 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
    ....
  8. ncbi request reprint NMDA receptor function in mouse models of Huntington disease
    C Cepeda
    Mental Retardation Research Center, University of California at Los Angeles, School of Medicine, Los Angeles, California 90095, USA
    J Neurosci Res 66:525-39. 2001
    ..These findings indicate that alterations in NMDA receptor function may predispose striatal neurons to excitotoxic damage, leading to subsequent neuronal degeneration and underscore the functional importance of NMDA receptors in HD...
  9. ncbi request reprint Electrophysiological and morphological changes in striatal spiny neurons in R6/2 Huntington's disease transgenic mice
    G J Klapstein
    Mental Retardation Research Center, University of California, Los Angeles, California 90095, USA
    J Neurophysiol 86:2667-77. 2001
    ..These physiological and morphological alterations will affect communication in the basal ganglia circuitry. Furthermore, they suggest areas to target for pharmacotherapies to alleviate and reduce the symptoms of HD...
  10. ncbi request reprint Differential sensitivity of medium- and large-sized striatal neurons to NMDA but not kainate receptor activation in the rat
    C Cepeda
    Mental Retardation Research Center and Brain Research Institute, UCLA School of Medicine, 760 Westwood Plaza NPI Room 58-258, Los Angeles, CA 90024, USA
    Eur J Neurosci 14:1577-89. 2001
    ..These findings help define the conditions that put neurons at risk for excitotoxic damage in neurological disorders...
  11. ncbi request reprint Calcium modulates dopamine potentiation of N-methyl-D-aspartate responses: electrophysiological and imaging evidence
    J C Liu
    Mental Retardation Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
    J Neurosci Res 76:315-22. 2004
    ..The existence of multiple mechanisms leading to a similar outcome allows a certain degree of redundancy in the consequences of DA modulation...
  12. ncbi request reprint Delayed postnatal development of NMDA receptor function in medium-sized neurons of the rat striatum
    R S Hurst
    Mental Retardation Research Center, University of California at Los Angeles, Los Angeles, Calif. 90095-1759, USA
    Dev Neurosci 23:122-34. 2001
    ..Taken together, the present experiments demonstrate that striatal non-NMDA receptor-mediated currents are more mature than NMDA receptor-mediated currents early in development...
  13. ncbi request reprint Metabotropic glutamate receptor activation selectively limits excitotoxic damage in the intact neostriatum
    C S Colwell
    Mental Retardation Research Center, University of California at Los Angeles 90024 1759, USA
    Brain Res 726:223-6. 1996
    ..In contrast, pretreatment with tACPD did not alter the effects of intrastriatal injection of KA...
  14. ncbi request reprint Pediatric cortical dysplasia: correlations between neuroimaging, electrophysiology and location of cytomegalic neurons and balloon cells and glutamate/GABA synaptic circuits
    C Cepeda
    Division of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
    Dev Neurosci 27:59-76. 2005
    ....
  15. ncbi request reprint Ionotropic glutamate receptor expression and dopaminergic modulation in the developing subthalamic nucleus of the rat: an immunohistochemical and electrophysiological analysis
    M K Lobo
    Mental Retardation Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, Calif 90095, USA
    Dev Neurosci 25:384-93. 2003
    ..Correlative electrophysiological studies demonstrated functional GluRs as early as 16 days of age. All neurons tested displayed robust responses to kainate and N-methyl-D-aspartate, and these responses were modulated by dopamine...
  16. ncbi request reprint Modified reperfusion and ischemia-reperfusion injury in human lung transplantation
    Abbas Ardehali
    Division of Cardiothoracic Surgery, Department of Medicine, University of California at Los Angeles, USA
    J Thorac Cardiovasc Surg 126:1929-34. 2003
    ....
  17. pmc Alterations in corticostriatal synaptic plasticity in mice overexpressing human alpha-synuclein
    J B Watson
    Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Neuroscience 159:501-13. 2009
    ..ASOTg mice may recapitulate an early stage in PD during which overexpressed alpha-synuclein dampens corticostriatal synaptic transmission and reduces movement...
  18. ncbi request reprint Glutamate receptor-induced toxicity in neostriatal cells
    C S Colwell
    Mental Retardation Research Center, University of California Los Angeles 90024 1759, USA
    Brain Res 724:205-12. 1996
    ..In conclusion, IR DIC videomicroscopy can be used to follow quantitatively the dynamics of GluR-evoked responses in single cells and should be instrumental in determining the factors capable of modifying excitotoxicity...
  19. ncbi request reprint Neurons recorded from pediatric epilepsy surgery patients with cortical dysplasia
    G W Mathern
    Division of Neurosurgery, University of California, Los Angeles, USA
    Epilepsia 41:S162-7. 2000
    ..In this study, we report initial electrophysiological and morphological observations from normal and dysmorphic cells in pediatric CD patients...
  20. ncbi request reprint Facilitated glutamatergic transmission in the striatum of D2 dopamine receptor-deficient mice
    C Cepeda
    Mental Retardation Research Center, University of California, Los Angeles, California 90095, USA
    J Neurophysiol 85:659-70. 2001
    ..These receptors may function as gatekeepers of glutamate release or of its subsequent effects and thus may protect striatal neurons from excessive excitation...
  21. pmc Extensive early motor and non-motor behavioral deficits are followed by striatal neuronal loss in knock-in Huntington's disease mice
    M A Hickey
    Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine, Reed Neurological Research Center B114, 710 Westwood Plaza, Los Angeles, CA 90095, USA
    Neuroscience 157:280-95. 2008
    ..Accordingly, they provide a useful model to elucidate early mechanisms of pathophysiology and the progression to overt neurodegeneration...
  22. ncbi request reprint Histamine modulates NMDA-dependent swelling in the neostriatum
    C S Colwell
    Mental Retardation Research Center, University of California Los Angeles, 90024 1759, USA
    Brain Res 766:205-12. 1997
    ..Overall, these findings suggest that histamine modulates N-methyl-D-aspartate receptor function in the neostriatum through a H2 receptor-mediated regulation of potassium channels...
  23. ncbi request reprint Postnatal development of glutamate receptor-mediated responses in the neostriatum
    C S Colwell
    Mental Retardation Research Center, University of California, Los Angeles, CA 90024 1759, USA
    Dev Neurosci 20:154-63. 1998
    ..The NMDA receptor subtype displays minimal functional development until PND 14. In contrast, neostriatal AMPA/KA receptor function appears to precede NMDA receptor function...
  24. ncbi request reprint Metabotropic glutamate receptor modulation of excitotoxicity in the neostriatum: role of calcium channels
    C S Colwell
    Mental Retardation Research Center, Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, 760 Westwood Plaza, Los Angeles, CA 90024 1759, USA
    Brain Res 833:234-41. 1999
    ..Again this effect was blocked by omega-conotoxin GVIA. Overall the results suggest that mGluR regulation of voltage-gated calcium channels can limit NMDA toxicity in the neostriatum...
  25. ncbi request reprint Activation, proliferation and commitment of endogenous stem/progenitor cells to the oligodendrocyte lineage by TS1 in a rat model of dysmyelination
    Araceli Espinosa-Jeffrey
    Mental Retardation Research Center, Semel Institute for Neuroscience and Human Behavior and Department of Neurobiology, University of California, Los Angeles, 90095 7332, USA
    Dev Neurosci 28:488-98. 2006
    ..This strategy offers for the first time the possibility of myelin restoration to treat myelin disorders...
  26. ncbi request reprint Modulatory actions of dopamine on NMDA receptor-mediated responses are reduced in D1A-deficient mutant mice
    M S Levine
    Mental Retardation Research Center, University of California, Los Angeles 90024 1759, USA
    J Neurosci 16:5870-82. 1996
    ....
  27. pmc Behavioral effects of dopaminergic agonists in transgenic mice overexpressing human wildtype alpha-synuclein
    S M Fleming
    Department of Neurology and Neurobiology, The David Geffen School of Medicine at the University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095 1769, USA
    Neuroscience 142:1245-53. 2006
    ..In contrast to wild-type mice, Thy1-aSyn mice did not show amphetamine-induced stereotypies. The results indicate that chronic overexpression of alpha-synuclein led to abnormal pharmacological responses in mice...
  28. ncbi request reprint Early behavioral deficits in R6/2 mice suitable for use in preclinical drug testing
    M A Hickey
    Department of Neurology, UCLA David Geffen School of Medicine, RNRC B114, 710 Westwood Plaza, Los Angeles, CA 90095, USA
    Neurobiol Dis 20:1-11. 2005
    ..Furthermore, the data extend the range of behavioral deficits observed in 1-month-old R6/2 mice, an age when synaptic dysfunction can already be detected in the striatum...
  29. ncbi request reprint BMP signaling coordinates gene expression and cell migration during precardiac mesoderm development
    Lionel Christiaen
    Department of Molecular and Cell Biology, University of California, Center for Integrative Genomics, Berkeley, CA, USA
    Dev Biol 340:179-87. 2010
    ..Our observations led us to propose a model for the coordination of cell migration and gene expression based on the temporal unfolding of a gene regulatory sub-network in a relevant developmental context...
  30. ncbi request reprint Liberalization of donor criteria in lung transplantation
    David Whiting
    Department of Surgery, Division of Cardiothoracic Surgery, David Geffea School of Medicine at UCLA, Los Angeles, California 90095, USA
    Am Surg 69:909-12. 2003
    ..The 3-month survival was 97.6 per cent. Selective liberalization of donor lung criteria can decrease the waiting time and is associated with favorable short-term outcome. Utilization of nonstandard lungs can expand the donor pool...
  31. ncbi request reprint Effects of repeated amphetamine treatment on the locomotor activity of the dopamine D1A-deficient mouse
    C A Crawford
    Mental Retardation Research Center, University of California, Los Angeles 90024, USA
    Neuroreport 8:2523-7. 1997
    ..PKA activity also varied depending on genotype, since amphetamine decreased PKA activity in control but not D1A-deficient mice...
  32. ncbi request reprint Striatal potassium channel dysfunction in Huntington's disease transgenic mice
    Marjorie A Ariano
    Mental Retardation Research Center, NPI Room 58 258, 760 Westwood Plaza, University of California, Los Angeles, CA 90095, USA
    J Neurophysiol 93:2565-74. 2005
    ..Attenuation in K+ conductances and channel subunit expression contribute to altered electrophysiological properties of MSNs and may partially account for selective cellular vulnerability in the striatum...
  33. 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
    ....
  34. 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...
  35. ncbi request reprint Development of striatal fast-spiking GABAergic interneurons
    Marie Francoise Chesselet
    Departments of Neurology and Neurobiology, The David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1769, USA
    Prog Brain Res 160:261-72. 2007
    ..These findings point to the need for future research to better understand the functional maturation of this critical population of striatal GABAergic neurons, and the consequences of abnormal maturation of these cells...
  36. ncbi request reprint Altered corticostriatal neurotransmission and modulation in dopamine transporter knock-down mice
    Nanping Wu
    Mental Retardation Research Center, David Geffen School of Medicine, UCLA School of Medicine, Los Angeles, CA 90024, USA
    J Neurophysiol 98:423-32. 2007
    ..These findings have implications for understanding mechanisms underlying attention deficit hyperactivity disorder and Tourette's syndrome and may provide insights into novel therapeutic approaches...
  37. ncbi request reprint Transient and progressive electrophysiological alterations in the corticostriatal pathway in a mouse model of Huntington's disease
    Carlos Cepeda
    Mental Retardation Research Center, University of California at Los Angeles, Los Angeles, California 90095, USA
    J Neurosci 23:961-9. 2003
    ..These alterations are likely to contribute to the selective vulnerability of striatal medium-sized spiny neurons...
  38. 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...
  39. 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...
  40. ncbi request reprint Development and serotonergic modulation of NMDA bursting in rat trigeminal motoneurons
    Chie Fang Hsiao
    Department of Physiological Science, University of California at Los Angeles, 2859 Slichter Hall, Los Angeles, CA 90095 1568, USA
    J Neurophysiol 87:1318-28. 2002
    ....
  41. ncbi request reprint Striatal neurochemical changes in transgenic models of Huntington's disease
    Marjorie A Ariano
    Department of Neuroscience, The Chicago Medical School, North Chicago, Illinois 60064, USA
    J Neurosci Res 68:716-29. 2002
    ..These findings suggest modifications in the striatal DA system and that its downstream signaling through cyclic AMP mechanisms is disrupted severely in HD following onset of motor symptoms...
  42. pmc Repeated exposure to methamphetamine causes long-lasting presynaptic corticostriatal depression that is renormalized with drug readministration
    Nigel S Bamford
    Department of Neurology, University of Washington, Seattle, WA 98105, USA
    Neuron 58:89-103. 2008
    ..These mechanisms might provide a synaptic basis that underlies addiction and habit learning and their long-term maintenance...
  43. 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...
  44. ncbi request reprint Enhanced epileptogenic susceptibility in a genetic model of reactive synaptogenesis: the spastic Han-Wistar rat
    Carlos Cepeda
    Mental Retardation Research Center, University of California, Los Angeles, Calif 90095, USA
    Dev Neurosci 24:262-71. 2002
    ..Our data also underscore the usefulness of this natural model of cell degeneration and reactive synaptogenesis for understanding the mechanisms of neuronal hyperexcitability...
  45. ncbi request reprint Dopamine enhancement of NMDA currents in dissociated medium-sized striatal neurons: role of D1 receptors and DARPP-32
    Jorge Flores-Hernandez
    Mental Retardation Research Center, University of California, Geffen School of Medicine, Los Angeles, California 90095, USA
    J Neurophysiol 88:3010-20. 2002
    ....
  46. doi request reprint Neuronal coupling via connexin36 contributes to spontaneous synaptic currents of striatal medium-sized spiny neurons
    Damian M Cummings
    Mental Retardation Research Center, University of California at Los Angeles, Los Angeles, California 90095, USA
    J Neurosci Res 86:2147-58. 2008
    ..Taken together, the present findings demonstrate that electrical coupling of neuronal populations is important for the maintenance of normal chemical synaptic interactions within the striatum...
  47. 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...
  48. 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...
  49. ncbi request reprint Modulation of AMPA currents by D2 dopamine receptors in striatal medium-sized spiny neurons: are dendrites necessary?
    Elizabeth Hernandez-Echeagaray
    Mental Retardation Research Center, David Geffen School of Medicine, NPI, Room 58 258, 760 Westwood Plaza, University of California at Los Angeles, Los Angeles, CA 90095, USA
    Eur J Neurosci 19:2455-63. 2004
    ..In addition, they indicate that the dendrites and/or the amplitude of the current are important variables for DA modulation of AMPA currents in MSNs...
  50. ncbi request reprint Heterosynaptic dopamine neurotransmission selects sets of corticostriatal terminals
    Nigel S Bamford
    Department of Neurology, University of Washington, Children s Hospital and Regional Medical Center, Seattle, WA 98105 USA
    Neuron 42:653-63. 2004
    ..Thus, dopamine, by filtering less active inputs, appears to reinforce specific sets of corticostriatal synaptic connections...
  51. 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
    ....
  52. 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...
  53. 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...
  54. ncbi request reprint Increased GABAergic function in mouse models of Huntington's disease: reversal by BDNF
    Carlos Cepeda
    Mental Retardation Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
    J Neurosci Res 78:855-67. 2004
    ..In conjunction, both changes will severely alter striatal outputs to target areas involved in the control of movement...
  55. ncbi request reprint Electrophysiological alterations in subthalamic neurons after unilateral dopamine depletion in the rat
    Mahadevan Gajendiran
    Mental Retardation Research Center, UCLA David Geffen School of Medicine, Los Angeles, California 90024, USA
    J Neurosci Res 80:203-10. 2005
    ..These data suggest that unilateral degeneration of DA neurons in the SNc changes firing properties and enhances electrophysiological responsiveness of STN neurons to activation of DA D1 receptors...
  56. ncbi request reprint Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons
    Matthew S Goldberg
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 278:43628-35. 2003
    ..Together these findings provide the first evidence for a novel role of parkin in dopamine regulation and nigrostriatal function, and a non-essential role of parkin in the survival of nigral neurons in mice...
  57. ncbi request reprint Functional and molecular development of striatal fast-spiking GABAergic interneurons and their cortical inputs
    Joshua L Plotkin
    Department of Neurology, The David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1769, USA
    Eur J Neurosci 22:1097-108. 2005
    ....
  58. 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...
  59. ncbi request reprint Changes in expression of N-methyl-D-aspartate receptor subunits occur early in the R6/2 mouse model of Huntington's disease
    Noore J Ali
    Mental Retardation Research Center, The David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA
    Dev Neurosci 28:230-8. 2006
    ..These results support the hypothesis that changes in the composition of postsynaptic NMDARs occur in the R6/2 model of HD and this effect occurs early in the expression of the phenotype...
  60. ncbi request reprint Where do you think you are going? The NMDA-D1 receptor trap
    Carlos Cepeda
    Mental Retardation Research Center, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA 90095, USA
    Sci STKE 2006:pe20. 2006
    ..Together, these mechanisms provide a basis for understanding the increasing complexity of D1-NMDA receptor interactions and their importance in physiological and pathological processes...
  61. 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...
  62. ncbi request reprint Early and progressive sensorimotor anomalies in mice overexpressing wild-type human alpha-synuclein
    Sheila M Fleming
    Department of Neurology, The Mental Retardation Research Center, The David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California 90095 1769, USA
    J Neurosci 24:9434-40. 2004
    ..These behavioral deficits provide a useful way to assess novel drug therapy in genetic models of synucleinopathies...
  63. pmc Genome-wide analysis of clustered Dorsal binding sites identifies putative target genes in the Drosophila embryo
    Michele Markstein
    Department of Molecular and Cell Biology, Division of Genetics and Development, 401 Barker Hall, University of California, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 99:763-8. 2002
    ..These results suggest that bioinformatics can be used to identify novel target genes and associated regulatory DNAs in a gene network...
  64. ncbi request reprint Dopamine reduction of GABA currents in striatal medium-sized spiny neurons is mediated principally by the D(1) receptor subtype
    Elizabeth Hernandez-Echeagaray
    Mental Retardation Research Center, Room 58 258 David Geffen School of Medicine, University of California Los Angeles, 760 Westwood Plaza, Los Angeles, CA 90024, USA
    Neurochem Res 32:229-40. 2007
    ..We conclude that D(1) receptors are the main D1-like receptor subtype involved in the modulation of GABA currents and that D(5) receptors contribute to the normal expression of these currents in the striatum...
  65. ncbi request reprint Age-dependent biphasic changes in ischemic sensitivity in the striatum of Huntington's disease R6/2 transgenic mice
    Gloria J Klapstein
    Mental Retardation Research Center, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    J Neurophysiol 93:758-65. 2005
    ..Although the mechanism for development of ischemic resistance in R6/2 transgenics remains unknown, it correlates with metabolic and biochemical changes described in this model and in HD patients...
  66. 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...
  67. 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
    ....
  68. ncbi request reprint Neurofilament-M interacts with the D1 dopamine receptor to regulate cell surface expression and desensitization
    Ok jin Kim
    Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 1406, USA
    J Neurosci 22:5920-30. 2002
    ..These results suggest that NF-M interacts with the D(1) receptor in vivo and may modify its expression and regulation...

Research Grants36

  1. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2002
    ..abstract_text> ..
  2. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2005
    ..abstract_text> ..
  3. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2002
    ..abstract_text> ..
  4. 2003 Gordon Conference on CAG Triplet Repeat Disorders
    Michael Levine; Fiscal Year: 2003
    ..All participants (except speakers and discussants) will be required to present posters. Priority will be given to women, minorities, and persons with disabilities when selecting participants. ..
  5. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2003
    ..abstract_text> ..
  6. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2007
    ....
  7. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2005
    ..abstract_text> ..
  8. Physiological Modulation by Dopamine in the Neostriatum
    Michael Levine; Fiscal Year: 2005
    ..We possess the unique tools and reagents to perform these studies and they will contribute to development of novel drug strategies to intervene in the treatment of ADHD as well as other diseases involving DA-iGluR interactions. ..
  9. Physiological Modulation by Dopamine in the Neostriatum
    Michael Levine; Fiscal Year: 2006
    ..We possess the unique tools and reagents to perform these studies and they will contribute to development of novel drug strategies to intervene in the treatment of ADHD as well as other diseases involving DA-iGluR interactions. ..
  10. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2000
    ..abstract_text> ..
  11. NMDA RECEPTOR DEVELOPMENT IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2000
    ..The outcomes will provide information necessary to understand the role of these receptors in NS development and provide clues for generating rational strategies to treat GluR dysfunction during development and in the adult. ..
  12. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 1999
    ..abstract_text> ..
  13. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2009
    ....
  14. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2006
    ..abstract_text> ..
  15. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2009
    ..abstract_text> ..
  16. Physiological Modulation by Dopamine in the Neostriatum
    Michael Levine; Fiscal Year: 2007
    ..We possess the unique tools and reagents to perform these studies and they will contribute to development of novel drug strategies to intervene in the treatment of ADHD as well as other diseases involving DA-iGluR interactions. ..
  17. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2009
    ..abstract_text> ..
  18. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2009
    ..abstract_text> ..
  19. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael S Levine; Fiscal Year: 2010
    ....
  20. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2009
    ....
  21. 2005 CAG Triplet Repeat Disorders Gordon Conference
    Michael Levine; Fiscal Year: 2005
    ..All participants will be required to present posters. Priority will be given to women, minorities, and persons with disabilities when selecting participants. ..
  22. NMDA RECEPTOR DEVELOPMENT IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 1999
    ..The outcomes will provide information necessary to understand the role of these receptors in NS development and provide clues for generating rational strategies to treat GluR dysfunction during development and in the adult. ..
  23. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2000
    ..abstract_text> ..
  24. NMDA RECEPTOR DEVELOPMENT IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2001
    ..The outcomes will provide information necessary to understand the role of these receptors in NS development and provide clues for generating rational strategies to treat GluR dysfunction during development and in the adult. ..
  25. NEUROPHYSIOLOGICAL MODULATION BY DOPAMINE IN NEOSTRIATUM
    Michael Levine; Fiscal Year: 2001
    ..abstract_text> ..
  26. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2003
    ..abstract_text> ..
  27. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2004
    ..abstract_text> ..
  28. Transgenic Mouse Models of Huntington's Disease
    Michael Levine; Fiscal Year: 2003
    ..abstract_text> ..
  29. Physiological Modulation by Dopamine in the Neostriatum
    Michael Levine; Fiscal Year: 2004
    ..We possess the unique tools and reagents to perform these studies and they will contribute to development of novel drug strategies to intervene in the treatment of ADHD as well as other diseases involving DA-iGluR interactions. ..
  30. Pathophysiology of Transgenic Mouse Models of Huntington's Disease
    Michael S Levine; Fiscal Year: 2010
    ....