After completing undergraduate work in Biopsychology at Wesleyan University in Middletown, Connecticut, Diana Lurie received a Ph.D. in Neuroscience from The University of Pennsylvania in 1989. Following a postdoctoral fellowship at the University of Washington, she moved to the University of Montana as an Assistant Professor in 1995. She was promoted to Associate Professor in 2000.

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INTERESTS OF THE LURIE LABORATORY

Research in the Lurie laboratory focuses on the glial response to central nervous system (CNS) injury and disease. Specifically, Lurie and her co-workers are interested in those cellular cascades that control the proliferation and migration of glial cells following damage, as well as those processes that regulate both the production of, and the glial response to, various growth factors. Recent work has centered on elucidating the role that tyrosine phosphorylation plays in these signal transduction events during CNS injury, including stroke. These studies utilize a wide variety of model systems including the avian auditory system, mouse CNS, and several different tissue culture preparations. Techniques employed in the laboratory include non-radioactive enzyme activity assays, cell proliferation assays, polyclonal antibody development, tissue histology and immunocytochemistry, PCR, gene transduction, and image analysis.

The Lurie laboratory has three major focus areas: 1) the response of the brain to stroke injury, 2) the response of the auditory brainstem to loss of activity in the ear, and 3) the effect of lead exposure on the developing auditory system. We have utilized a mouse mutation model to examine the role of the protein tyrosine phosphatase SHP-1 in regulating the CNS response to injury. In both our stroke and deafness model, the lack of SHP-1 results in both an increase in neuronal cell death as well as a dramatically altered glial response following these injury paradigms. We are currently elucidating those cellular cascades that might be controlled by SHP-1 during CNS damage in order to develop potential therapies that could minimize neuronal death following injury.

The Lurie laboratory is also investigating the effects of lead exposure on the avian auditory brainstem. Early exposure to lead is known to be a risk factor for reading disabilties and attention deficit disorder, and preliminary studies indicate that lead toxicity results in subtle deficits in hearing processing. We have found profound changes in both neuronal and glial cells within the auditory brainstem of animals exposed to very low levels of lead during development. We are currently characterizing these changes and correlating them with the auditory deficits that have been observed in lead-exposed children.

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SELECTED PUBLICATIONS

Ida M. Stone, Diana I. Lurie, Mathew W. Kelley, and David J. Poulsen. ADENO-ASSOCIATED VIRUS MEDIATED GENE TRANSFER TO HAIR CELLS AND SUPPORT CELLS OF THE MURINE COCHLEA. Molecular Therapy 2005 (In Press)

Zhao and Lurie. (2004). Cochlear Ablation in mice lacking SHP-1 results in an extended period of cell death in anteroventral cochlear nucleus neurons. Hearing Res.189:63-75.

Zhao and Lurie. (2004). Loss of SHP-1 phosphatase selectively alters cytokine expression in the mouse hindbrain following cochlear ablation. Cytokine, 28:1-9.

Wishcamper, CA, Brooks DM, Coffin JD, Lurie DI. (2003). Focal ischemia upregulates SHP-1 in non-proliferating reactive astrocytes.  Brain Research, 974:88-98.

Sorbel, J.D. Brooks, D. M. and D.I. Lurie. (2002). SHP-1 expressison in avian mixed neural/glial cultures.  J. of Neurosci. Res.  68:703-715.

Wishcamper, C.A., Coffin, J.D. and D.I. Lurie. (2001). Lack of the protein tyrosine phosphatase SHP-1 results in decreased numbers of glia within the Motheaten (me/me) mouse brain.  J. Comp. Neurol.  441:118-133

Lurie, D.I., F. Solca, E.H. Fischer, E.W Rubel. (2000). Tyrosine Phosphatase SHP-1 immunoreactivity increases in a subset of astrocytes following deafferentation of the chicken auditory brainstem. J.Comp.Neurol. 421:199-214.

Lurie, D.I. and D. Durham. (2000). Neuronal death but not eighth nerve degeneration results in significant gliosis following deafferentation within the auditory brainstem nucleus, n. Magnocellularis in the adult chicken. Hearing Research, 149: 189-198.

Kelley M.S. , D. I. Lurie, E. W Rubel. (1997). Rapid regulation of cytoskeletal proteins and their mRNAs following afferent deprivation in the avian cochlear nucleus. J. Comp. Neurol. 389:469-483.

Oesterle, E.C., D.I.Lurie, E. W Rubel. (1997). Neurofilament proteins in avian auditory hair cells. J. Comp. Neurol. 379:603-616.