Robert F. Berman, Ph.D.

Professor, Department of Neurological Surgery, School of Medicine

University of California, Davis
1515 Newton Court
Davis, CA 95616
E-mail:  rfberman@ucdavis.edu

Dr. Berman, a neuroscientist whose research focuses on cellular mechanisms of brain injury, is currently examining the effects of neonatal toxin exposure on brain development and behavior. His laboratory recently developed a set of behavioral testing procedures for evaluating social behaviors in rodents, an essential step in the development of useful models for the study of neurodevelopmental disorders like autism. Dr. Berman’s research and training activities have been funded by the NIH for the past 20 years, and he is currently funded by the NIEHS, NIAAA and NINDS. He is currently Director of Research for the Neurotrauma Research Laboratories at UC Davis.

Rismanchi N, Floyd C L, Berman RF, Lyeth BG.  Cell death and long-term maintenance of neuron-like state after differentiation of rat bone marrow stromal cells:  A comparison of protocols.  Brain Research 991(1-2), 46-55, 2003.  This project explored the use of stem cells to replaced neurons and glia following brain damage.

Zhao X, Ahram A, Berman RF, Muizelaar JP, Lyeth BG.  Early loss of astrocytes after experimental traumatic brain injury.  Glia 44:140-152, 2003.  This paper describes the interaction between glia and neurons following brain injury, and provides evidence that the loss of supporting glia  may contribute to neuronal degeneration.

Hallam TM, Floyd C L, Folkerts MM, Lee LL, Gong Q-Z, Lyeth BG, Muizelaar JP, Berman RF. Comparison of behavioral deficits and acute neuronal degeneration in rat lateral fluid percussion and weight drop brain injury models.  J Neurotrauma 21(5) 521-539, 2004. This paper describes the neuropathology and neuropsychological deficits seen following either focal or diffuse brain injury.

Aden U, O’Connor WT, Berman RF.  Changes in adenosine metabolites and adenosine receptors in the kindled rat brain.  Neuroreport 15(10), 1585-1589, 2004.  This research describes changes in a major neuromodulatory system in the brain associated with epilepsy.

Examination of neonatal exposure to thimerosal on brain mercury levels and behavior in mice, 21st International Neurotoxicology Conference, Honolulu, HA, February 2004.

Anti-apoptotic pharmacological approaches to in vivo TBI, The 3rd Annual Northern California Neurotrauma Spring Symposium, Univ. Calif. San Francisco, San Francisco, CA, April 2004. 

Lack of evidence for thimerosal neurotoxicity in C57BL/6j mice,  International Meeting for Autism Research (IMFAR).  Sacramento, CA May, 2004.

Developing a Mouse Model to Study Complex Social Behavior,  M.I.N.D. Institute Research Seminar Series, Sacramento, CA., May 2004.

Co-Principal Investigator: Environmental factors in the etiology of autism, NIEHS, 09/01/01 to 08/31/06, $1,000,000 annually. Project 2 – (co-PI: D.G. Amaral) $200,000 annually. The purpose of this program is to investigate environmental risk factors contributing to the incidence and severity of childhood autism.

Co-Principal Investigator: Amelioration of Fetal Alcohol Effects, NIH/NIAAA, 04/00- 3/05, $85,000 annually.  This project examines the effect of prenatal alcohol on brain development and behavior.  It specifically examines the ability of an enriched postnatal environmental to reduce the damaging impact of prenatal alcohol exposure on brain development and behavior.

Chair, National Research Council (NRC) Associateship Programs Life Sciences Review Panel
Member, Associates Program Advisory Committee, National Research Council, Office of Scientific and Engineering Personnel (OSEP). 
National Institutes of Health – Ad hoc review committees
Member, Internal Advisory Committee, Center for Children’s Environmental Health, UC Davis
Master Advisor, Graduate Group in Neuroscience, UC Davis
Research Resources Advisory Committee (RRAC), UC Davis School of Medicine

National Associate of the National Academy of Science (lifetime membership)
Visiting Professor, Pepperdine University