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Joel Levine

Faculty Profile Levine

Professor Emeritus
John S. Toll Professor

PhD, Washington University
Member, Stony Brook Glial Network

Joel.Levine@stonybrook.edu 

Life Sciences Building
Office: Room 514
Lab: Room 521
Phone: (631) 632-8642
Fax: (631) 632-6661

DR. LEVINE'S LAB IS NO LONGER ACCEPTING STUDENTS. THANK YOU FOR YOUR INTEREST.


Training

Joel Levine attended the University of Pennsylvania and received a B.A. degree in English in 1966. He attended Washington University and received a Ph.D. in Neural Sciences in 1980. He was a Postdoctoral Fellow at The Salk Institute from 1980 to 1983 and a Research Associate in the Molecular Neurobiology Laboratory at the Salk Institute from 1983 to 1984. He joined the Department of Neurobiology and Behavior at Stony Brook in 1984 as Assistant Professor. He was promoted to the rank of Associate Professor with tenure in 1990 and to Full Professor in 1998. From 2001 to 2007 he served as Associate Editor for the Journal of Neuroscience. He has been a member of the Society for Neuroscience since 1984.

Research Interests/Expertise


Glial cells are the most numerous and most poorly understood component of the central nervous system. Traditionally, they have been thought of as a "glue-like" substance providing nutritive and metabolic support to neurons. We know now that glia are a highly diverse and dynamic population of cells actively involved in all aspects of neuronal function ranging from guiding axons to their targets during development to regulating synaptic development, transmission and plasticity in the adult. Glia also play important roles in many diseases. Our research pioneered studies of oligodendrocyte precursor cells (also known as NG2 cells) in developing and adult animals. Recent studies have been aimed at understanding 1) the functions of oligodendrocvte precursor cells in spinal cord injury and repair, 2) how molecules secreted by NG2 cells act to inhibit or prevent axon growth, 3) mechanisms that regulate the differentiation of NG2 cells into myelin-forming cells in animal models of multiple sclerosis, and 4) the epigenetic regulation of cell fate and plasticity in developing and adult oligodendrocytes.

  • Recent Publications

    Rodriguez, JP, Coulter M, Miotke J, Meyer RL, Takemaru K, Levine JM (2014) Abrogation of β-catenin signaling in oligodendrocyte precursor cells reduces glial scarring and promotes axon regeneration after CNS injury. J. Neurosci.,34:10285-10297. PMID: 25080590

    Lee S, Zhang W, Ravi M, Weschenfelder M, Bastmeyer M, Levine JM (2013) Atypical protein kinase C and par3 are required for  proteoglycan-induced axon growth inhibition. J. Neurosci., 33: 2541-2554.

    Petrosyan HA, Hunanyan AS, Alessi V, Schnell L, Levine J, Arvanian VL (2013) Neutralization of inhibitory molecule NG2 improves synaptic transmission, retrograde transport and locomotor function after spinal cord injury in adults rats. J, Neurosci., 33: 4032-4043.

    Kumamoto N, Gu Y, Wang J, Janoschka S, Takemaru KI, Levine J, Ge S (2012) A role for primary cilia in glutamatergic synaptic integration of adult-born neurons. Nat. Neurosci., 15:399-405.

    DeWald L, Rodriquez J, Levine JM (2011) The RE1-binding protein REST regulates oligodendrocyte development. J. Neurosci., 31: 3470-3483.

    Levine, J.M., Reynolds,R., and Fawcett, J.W.(2001)  The oligodendrocyte precursor in health and disease.Trends in Neurosci., 24:39-47.

  • Honors, Awards & Leadership

     Director, Multiple Sclerosis Collaborative Research Center, Stony Brook University, 2007-2013

    Associate Dean, The Graduate School, 2012-2015