The three main research components of his laboratory are focused on the themes of the basic neurobiology of cognition and addiction, neurobehavioral toxicology and the development of novel therapeutic treatments for cognitive dysfunction and substance abuse. Currently, our principal research focus concerns nicotine. We have documented the basic effects of nicotine on learningm memory and attention as well as nicotine self-administration. We are continuing with more mechanistic studies in rat models using selective lesions, local infusions and neurotransmitter interaction studies. We have found that nicotine improves memory performance not only in normal rats, but also in rats with lesions of hippocampal and basal forebrain connections. We are concentrating on alpha7 and alpha4beta2 nicotinic receptor subtypes in the hippocampus, amygdala , thalamus and frontal cortex and how they interact with dopamine D1 and D2 and glutamate NMDA systems with regard to memory and addiction. I am also conducting studies on human cognitive behavior. We have current studies to assess nicotine effects on attention, memory and mental processing speed in schizophrenics, Alzheimer's Disease patients and people with Attention Deficit Hyperactivity Disorder. In the area of neurobehavioral toxicology, I have continuing projects to characterize the adverse effects of prenatal and adolescent nicotine exposure. Our primary project in neurobehavioral toxicology focuses on the cognitive deficits caused by the marine toxins including domoic acid, ciguatera toxin and pfiesteria. We have documented a persistent neurobehavioral effects caused by Pfiesteria and domoic acid exposure. We are determining the neurobehavioral nature and mechanisms of this deficit. The basic and applied aims of our research complement each other nicely. The findings concerning neural mechanisms underlying cognitive function help direct the behavioral toxicology and therapeutic development studies, while the applied studies provide important functional information concerning the importance of the basic mechanisms under investigation.
School DivisionEnvironmental Sciences & Policy
- Ph.D., University of Wisconsin at Madison (1984)
- Using Zebrafish to Help Identify Which Environmental Toxicants Could Increase Autism Risk
- Reinforcing effect of nicotine alone vs. nicotine plus other chemicals in tobacco
- Receptor-type protein in tyrosine phosphatase D (PTPRD) treatment with 7-BIA to reduce nicotine self-adminstration
- HAB toxin exposure and Alzheimer's disease susceptibility
- Study of Novel Treatment to Prevent Acquisition of Opiate Self-Administration in Rats