Michael S Levine

Professor, Associate Director, Mental Retardation Research Center Chair, Interdepartmental PhD Program in Neuroscience

Michael S Levine UCLA Intellectual and Developmental Disabilities Research Center
University of California, Los Angeles
Mail Code 175919
NPI, Rm 58-258E
Los Angeles, CA 90024
310-825-7595 (tel)

Biography/Curriculum Vitae:

Research Interests:
Mechanisms of neurodegenerative disorders in basal ganglia and cortex

Narrative of Current Research Efforts:
The primary research interests of the Levine laboratory are directed toward understanding the mechanisms underlying neuronal dysfunction in the basal ganglia and cortex in neurodegenerative disorders. The research consists of a multidisciplinary approach combining neurophysiological, morphological and molecular techniques. This research has evolved into several major projects:
  • Examining the physiological changes in mutant mouse models of Huntington's disease
  • Assessment of neuromodulation in the striatum and subthalamic nucleus in intact preparations and models of Parkinson's disease and
  • Examining cellular cortical electrophysiological and morphological abnormalities occurring in children suffering from intractable pediatric epilepsy.
The first area of research involves using mutant murine models of Huntington's disease to understand how this neurological disorder physiologically affects cellular function. They study different types of mouse models, each with a unique part of the human Huntington's disease gene inserted into the mouse genome. They examine physiological function and morphological changes in striatal and cortical neurons, the two primary areas affected in Huntington's disease.

The studies on neuromodulation have concentrated on examining interactions among receptor subtypes in the striatum and subthalamic nucleus. The ultimate goal of these studies is to learn the rules that guide dopaminergic modulation, to identify their mechanisms and to examine how this modulation is altered in models of Parkinson's disease to help design rational therapies for this disorder.

The third area examines alterations in development of electrophysiological properties of human neocortical neurons. Pathological neocortical tissue is obtained from children suffering from pediatric epilepsy and undergoing surgery to alleviate intractable seizures. These experiments study "abnormal-appearing" neurons and they have shown that a population of neurons with altered voltage-dependent intrinsic currents and in some cases altered ligand-gated currents occurs.

Major Honors and Awards:

Representative Publications:

Andre VM, Cepeda C, Venegas A, Gomez Y and Levine MS (2006) Altered Cortical Glutamate Receptor Function in the R6/2 Model of Huntington's Disease. J Neurophysiol, 95:2108-19.

Starling AJ, Andre VM, Cepeda C, de Lima M, Chandler SH and Levine MS (2005) 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. J Neurosci Res, 82:377-86.

Levine MS, Cepeda C, Hickey MA, Fleming SM and Chesselet MF (2004) Genetic mouse models of Huntington's and Parkinson's diseases: illuminating but imperfect. Trends Neurosci, 27:691-7.

Cepeda C, Hurst RS, Calvert CR, Hernandez-Echeagaray E, Nguyen OK, Jocoy E, Christian LJ, Ariano MA and Levine MS (2003) Transient and progressive electrophysiological alterations in the corticostriatal pathway in a mouse model of Huntington's disease. J Neurosci, 23:961-9.

Flores-Hernandez J, Cepeda C, Hernandez-Echeagaray E, Calvert CR, Jokel ES, Fienberg AA, Greengard P and Levine MS (2002) Dopamine enhancement of NMDA currents in dissociated medium-sized striatal neurons: role of D1 receptors and DARPP-32. J Neurophysiol, 88:3010-20.


Created 7/27/2006 by Evette Mezger
Last modified 8/29/2006 by Dorwin Birt