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Faculty by area of expertise 
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Robert J. Hamm
Professor
www.has.vcu.edu/psy/biopsy/neuro
Contact information
Phone: (804) 828-9822
E-mail: rhamm@vcu.edu
Education
Ph.D. (1974), Southern Illinois University at Carbondale
Program affiliation
Biopsychology
Research interests
In the U.S. there are approximately 2,000,000 head injuries each year with 500,000 requiring hospitalization. Head injury is a leading cause of death and disability for persons under 40 years of age. Using an animal model, the laboratory’s research is focused on understanding the pathobiology of traumatic brain injury, with an emphasis on the receptor-mediated alterations in neuronal signaling that are produced by injury. In collaboration with colleagues in the Departments of Anatomy, Pharmacology, and Neurosurgery, we employ a multidisciplinary neuroscience approach to addressing our research questions. In addition to assessing an intervention’s effects on improving behavioral recovery after injury, we also employ molecular biology techniques (including immunohistochemistry and radioimmunoassay) to investigate changes in neurotrophic factors, neurotransmitter proteins and cell adhesion molecules. The long-term goal of the laboratory is to increase our understanding of how the nervous system responds to injury and to investigate how we can enhance its regenerative capacity in order to reduce the disabilities that follow traumatic brain injury.
Selected publications
Deshpande, L. S., Sun, D. A., Sombati, S., Baranova, A., Wilson, M. S., Attkisson, E., Hamm, R. J., DeLorenzo, R. J. (2008). Alterations in neuronal calcium levels are associated with cognitive deficits after traumatic brain injury. Neuroscience Letters, 441(1), 115-119.
Whiting, M. D., & Hamm, R. J. (2008). Mechanisms of antegrade and retrograde memory impairment following experimental brain injury. Brain Research, 1213, 69-77.
Reid, W. M., & Hamm, R. J. (2008). Post-injury atomoxetine treatment improves cognition following experimental brain injury. Journal of Neurotrauma, 25(3), 248-256.
Sun, D. A., Deshpande, L. S., Sombati, S., Baranova, A., Wilson, M. S., Hamm, R. J., & DeLorenzo, R. J. (2008). Traumatic brain injury causes a long-lasting calcium-plateau of elevated intracellular calcium levels and altered calcium homeostatic mechanisms in hippocampal neurons surviving the brain injury. European Journal of Neuroscience, 27(7), 1659-1672.
Kokiko, O., & Hamm, R. J. (2008). Delayed glucose treatment improves cognitive function following fluid percussion injury. Neuroscience Letters, 436(1), 27-30.
Recent/current courses taught at VCU
- Design and Analysis of Psychological Research, graduate level
- Experimental Design, undergraduate level
| Recent grants |
Lithium as a treatment for traumatic brain injury. Virginia Department of Rehabilitative Services. |
Modulation of hippocapal neurogenesis and cognitive recovery following trauma. N.I.H. |
| The effects of atomoxetine on recovery from traumatic brain injury. Eli Lilly and Co. |
| Evaluation of test compound on outcome after traumatic brain injury, Research Corporation Techologies. |
| Delayed treatment of experimental traumatic brain injury: The role of the AMPA receptor. Virginia Department of Rehabilitative Services. |