Joel Levine attended the University of Pennsylvania and received a B.A. degree in English in 1966. Changing the focus of his research, 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 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. He is currently a member of the graduate programs in Cell and Developmental Biology and Pharmacology. 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
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 now know that glia are a highly diverse population of cells actively involved in all aspects of neuronal function ranging from guiding axons to their targets during development to regulating synaptic transmission and plasticity in the adult. Glia also plays important roles in many diseases.
My lab is interested in the biology and functions of a unique class of glial cells known as oligodendrocyte precursor cells (OPCs), NG2-glia, or polydendrocytes. These cells, which comprise 6-8% of all the cells in the adult brain, are the progenitor cells that give rise to oligodendrocytes, the myelin forming cells of the central nervous system. Several of their properties are inconsistent with them acting solely as oligodendrocyte precursor cells. They are the major dividing cell type in the adult CNS and they proliferate robustly after most types of brain injury. They express proteins and properties usually associated with neurons such as functional neurotransmitter receptors and the ability to fire repetitive action potentials and they are post-synaptic targets in several different brain regions
Our current projects are aimed at understanding 1) the functions of OPCs in spinal cord injury and repair, 2) how the molecules secreted by OPCs act to inhibit or prevent axon growth, 3) mechanisms that regulate the differentiation of OPCs into myelin-forming cells in animal models of multiple sclerosis, and 4) the epigenetic regulation of cell fate and plasticity in developing and adult OPCs.
Selected Publications
- Asher RA, Morgenstern DA, Properzi F, Nishiyama A, Levine JM, Fawcett JW (2005) Two separate metalloproteinase activities are responsible for the shedding and processing of the NG2 proteoglycan in vitro. Mol.Cell. Neurosci., 29:82-96.
- Levine JM, Mendell L (2006) Trophic Factors and Their Influence on Regeneration" in Textbook of Neural Repairand Rehabilitation Eds Selzer,ME , Clarke,S, Cohen, LG, Duncan, PW, and Gage,F. Cambridge University Press, pp.405-420.
- Tan AM, Colletti M, Rorai AT, Skene JHP, Levine JM (2006) Antibodies against the NG2 proteoglycan promote the of sensory axons within the dorsal columns of the spinal cord. J. Neurosci., 26: 4729-4739.
- Tan A, Petruska JC, Mendell LM, Levine JM (2007) Sensory afferents regenerated into dorsal columns after spinal cord injury remain in a chronic pathophysiological state. Expl. Neurol., 206:257-268
- Nolin WB, Zhang Y, Levine JM, Tsirka SE (2008) tPA catalyzed generation of plasmin is enhanced by the core protein of the proteoglycan NG2, Glia, 56: 177-189.
Laboratory Personnel:
- Lisa Evans- graduate student-Graduate Program in Molecular and Cellular Pharmacology
- Justin Rodriguez-MD-PhD graduate student- Program in Neuroscience
- Seong-il Lee- graduate student- Program in Neuroscience
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