Neurotrauma Research Laboratories


This is a complex of laboratories dedicated to the study of traumatic brain injury with the aim of understanding mechanisms of secondary brain injury. The ultimate goal of this research program is to develop novel clinical therapeutic strategies targeted at reducing the debilitating consequences of traumatic brain injury in patients.


Neurosurgical residents
Postdoctoral fellows
Graduate students
Undergraduate students

Funding Sources

National Institute of Neurological Disease and Stroke
Metabolic Glu Receptors in Traumatic Brain Injury
Bruce G. Lyeth, Ph.D.
Traumatic brain injury is a significant health problem that results in more than 230,000 hospitalization and 50,000 deaths per year in the USA.  The objectives of this research are to determine glutamate-mediate mechanisms of acute neuronal and astrocyte (star-shaped glial cells in the brain) protection following traumatic brain injury.  This research will proved new and important insights into glutamate excitotoxicity and examine important dynamics of neuron-astrocyte interactions in TBI pathophysiology.  It will also provide clinically relevant information about potential pharmacological agents for the treatment of human head injury.

Mouse Models of FXTAS:  Defining Critical Periods and Molecular Targets
PI: Robert F. Berman Ph.D.
Fragile X-associated tremor ataxia (FXTAS) is a hereditary disorder due to a single gene mutation that results in progressive development of tremor, ataxia (gross lack of coordination of muscle movements) and neuropsychological problems.  This project will generate the essential knowledge about the causes and potential treatments for FXTAS that will provide the foundation for the development of treatments that can halt or reverse the disease.

Acute Astrocyte Pathology After Traumatic Brain Injury
Bruce G. Lyeth, Ph.D.
The long-term objective of this research is to examine mechanisms of acute astrocyte damage and death following traumatic brain injury and to develop treatment strategies for attenuating these injury mechanisms.  In in vivo therapeutic studies we measure astrocyte and neuronal viability using anatomical markers, measure brain edema using magnetic resonance imaging, and measure functional outcome using behavioral measures of sensorimotor function and learning and memory following traumatic brain injury in rats. Cell culture studies examine injury-induced changes in intracellular ions such as calcium, sodium, and protons.

Psychogenics, Inc.
NAAG Peptidase Inhibitors for the Treatment of Brain Injury
Bruce G. Lyeth, Ph.D.
Dr. Lyeth performs pharmacological studies of the NAAG peptidase inhibitor prodrugs using an in vivo TBI model: The prodrugs are tested for cellular protection in a well-characterized and clinically relevant rat model of TBI.  Each of the prodrugs is evaluated in a dose-dependent design, in which drugs are administered systemically after TBI.  Drug efficacy for reducing neuronal cell death is evaluated 24 hours after TBI using histofluorescence with advanced stereological cell counting techniques.

Aaken Laboratories, Inc.
Evaluation of Nutritional Supplement and TBI
Bruce G. Lyeth, Ph.D.
Traumatic Brain Injury results in cognitive deficits of learning and memory as well as both primary and secondary cell death.  Animal studies have shown that several products are effective in reducing post-traumatic cognitive deficits and in reducing secondary cell death when they are given prior to the injury.  This study involves pre-injury administration of a proprietary nutritional formula targeted at multiple injury mechanisms to determine improved behavioral function and reduced neuronal cell loss in rats subjected to experimental TBI.

National Institute of Environmental Health Science
UC Davis Center for Children's Environmental Health (CCEH); Project III: Models of Neurodevelopmental Susceptibility
PI: Robert F. Berman Ph.D.
The mission of the University of California-Davis Center for Children's Environmental Health (CCEH) is to promote daily interactions among a multidisciplinary team of scientists whose main research interest is to understand the complex web of etiologic factors that contribute to autism.  Project III is attempting to determine if exposure to environmental toxicants early in development contributes to the etiology of neurodevelopmental disorders such as autism.  The study will provide critical new information on the role of the immune system and its interaction with environmental contaminants in autism and other neurodevelopmental disorders.

Epigenetic Interaction of MECP2 and Organic Pollutants in Neurodevelopment
PI: Janine Lasalle, PhD, Department of Medical Microbiology and Immunology
Co-Investigator: Robert F. Berman Ph.D
This proposal employs a combination of systems and approaches that focus on the central question of the impact of persistent environmental pollutants (POPs) on precise epigenetic changes that occur in neurodevelopmental disorders.  Specific questions addressed are: What specific epigenetic changes to neurodevelopmentally important genes occur as a result of POP exposure? What is the compounding effect of known genetic and environmental factors in the etiology of autism and mental retardation? Can specific epigenetic changes be diagnostic for autism and mental retardation of unknown genetic etiology? Are epigenetic changes affecting neurodevelopment heritable?