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Timothy Schallert, Ph.D.
Professor

VITA Email: TSchallert@mail.utexas.edu or TSchall@umich.edu Phone: 471-3287 Office: SEA 5.232 Lab: ARC Annex 0.222 Schallert Lab See also Behavioral Neuroscience, Clinical Psychology, Behavioral Neuroscience, Institute for Neuroscience, Addiction Science Research and Education Center

Tim Schallert (tschallert@mail.utexas.edu) received his Ph.D. in Behavioral Neuroscience from Arizona State University in 1976. He was a Postdoctoral Fellow at the University of Illinois at Urbana-Champaign and the University of Lethbridge in Alberta, Canada. In 1979 he moved to The University of Texas at Austin, where he is currently a Professor in the Institute for Neuroscience and Departments of Psychology and Neurobiology. He teaches courses on the effects and mechanism of action of psychoactive drugs and brain-behavior interactions. He was elected to the Academy of Distinguished Teachers and has received several other teaching awards, including the President's Associates Teaching Excellence Award and the Amoco Foundation Teaching Award. He has served on the Executive Committee of the Institute for Neuroscience and as the Graduate Advisor for the Neuroscience Ph.D. program. He was Associate Chairman of the Dept of Psychology from 1985-1994. He is currently an Adjunct Professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society. In the past 8 years, he has given over 100 invited talks about his research at universities and scientific meetings around the world. His research, on recovery of function after brain injury and treatment strategies for stroke, Parkinson's disease, brain tumors and spinal cord injury, has been funded by federal grants for over 20 years.

Research Interests

The brain and spinal cord are vulnerable to traumatic injury, stroke, tumors and degenerative diseases, often with devastating functional impairments, but at no time in the history of medicine have scientists been as optimistic as they are now about treatment strategies. Understanding how the central nervous system responds to the loss of nerve cells, and how behavior can influence the mechanisms of brain repair, is a major focus of our research.

We develop rat and mouse models of neurological disorders and strive to improve upon existing models. We have a multidisciplinary approach, with extensive collaborative arrangements with experts in other labs on campus, nationally and internationally. Collaborative research projects include searching for novel treatment interventions.

In Parkinson's disease dopamine cells degenerate, eventually leading to severe impairments of movement. Using a new model of slow degeneration, we have investigated gene therapy, drugs and motor enrichment techniques that increase growth factors in the brain. These growth factors appear to keep the dopamine cells from dying, thereby preventing the behavioral dysfunction.

Whereas skilled motor activity protects neurons, behavioral inactivity is detrimental. In cerebral stroke, Parkinson's disease, and other models of brain injury, physical activity and inactivity hasve only recently been recognized as highly influential. Behavior is often essential for cellular changes, synapse formation and neurogenesis. We look for sensitive periods after brain damage that provide unique opportunities to intervene beneficially.

We have helped to develop a new model of brain cancer. Unlike other models used to examine anti-cancer treatments, our model includes a highly sensitive behavioral analysis of brain function and neural plasticity, which are often adversely affected by traditional anti-cancer interventions. The hope is to use this model to find treatments that can shrink brain tumors without disturbing mechanisms important to optimal brain function. We also want to understand the stealth nature of brain tumors. Tumor cells slowly activate key mechanisms of plasticity which hide their presence despite ever more extensive encroachment on critical brain tissue. In collaboration with investigators at the University of Michigan and Henry Ford Neuroscience Center, we have developed promising chemical interventions that, unlike traditional treatments, appear to stop mitotic activity in tumor cells implanted in the striatum of the brain, without interfering with mechanisms of recovery of function and with a beneficial impact on behavioral outcome due to a positive effect on remaining tissue.

Selected Recent Publications

Day LB, Weisend M. Sutherland RJ & Schallert T. (1999). The hippocampus is not necessary for a place response but may be necessary for pliancy. Behavioral Neuroscience 113: 914-924.

Conner B., Kozlowski D.A., Schallert T., Tillerson J.L., Davidson B.L. & Bohn M.C. (1999) The differential effects of adenoviral vector mediated glial cell line-derived neurotrophic factor (GDNF) in the striatum vs substantia nigra of the aged parkinsonian rat. Gene Therapy, 6: 1936-1951.

Liu Y., Kim D., B. Himes B.T., Chow S.Y., Schallert T., Murray M., Tessler A., & Fischer I. (1999). Transplants of fibroblasts genetically modified to express BDNF promote regeneration of adult rat rubrospinal axons and recovery of forelimb function. Journal of Neuroscience 19: 4370-4387.

Schallert T. & Tillerson J.L. (2000). Intervention strategies for degeneration of dopamine neurons in parkinsonism: Optimizing behavioral assessment of outcome. In Central Nervous System Diseases: Innovative models of CNS diseases from molecule to therapy. (D. F. Emerich, RL Dean III & PR Sanberg Eds.) Totowa, NJ: Humana Press, 131-151.

Bittner GD, Schallert T & Peduzzi JD (2000). Degeneration, trophic interactions and repair of severed axons: A reconsideration of some common assumptions. The Neuroscientist, 6, 88-109.

Schallert T, Fleming S, Leasure JL, Tillerson J & Bland S. (2000). CNS plasticity and assessment of forelimb sensorimotor outcome in unilateral models of stroke, cortical ablation, parkinsonism and spinal cord injury. Neuropharmacology, 39, 777-787.

Schallert T, Leasure JL. & Kolb B. (2000) Experience-associated structural events, subependymal proliferation activity, and functional recovery after injury to the central nervous system: A review. Journal of Cerebral Blood Flow and Metabolism, 20, 1513-1528.

Kozlowski DA, Conner B, Tillerson JL, Schallert T. & Bohn MC (2000) Delivery of a GDNF gene into the substantia nigra after a progressive 6-OHDA lesion maintains functional nigrostriatal connnections. Experimental Neurology, 166: 1-15.

Conner B, Kozlowski DA, Unnerstall JR, Elsworth JD, Tillerson JL, Schallert T, & Bohn MC. (2001) Glial cell line-derived neurotrophic factor (GDNF) gene delivery protects dopaminergic terminals from degeneration. Experimental Neurology, 169: 83-95.

Tillerson JL, Cohen A, Miller G, Zigmond M. & Schallert T (2001). Forced forelimb use effects on the behavioral and neurochemical effects of 6-hydroxydopamine. Journal of Neuroscience, 21: 4427-4435.

Anagnostaras, S, Schallert T & Robinson TE (2002). Memory processes governing amphetamine-induced psychomotor sensitization. Neuropsychopharmacology, 26(6), 703-715

Tillerson JL, Cohen AD, Caudle WM, Zigmond MJ, Schallert T & Miller GW (2002). Forced non-use in unilateral parkinsonian rats exacerbates injury. The Journal of Neuroscience, in press

Cenci MA, Whishaw IQ and Schallert T (2002) Animal models of neurological deficits: How relevant is the rat? Nature Reviews Neuroscience, 3, July 2002, in press.