James Boulter
Dr. Jim Boulter is a Professor in the Department of Psychiatry and Biobehavioral Sciences. He received his doctorate degree in molecular biology from the University of California (Santa Barbara) and obtained postdoctoral training in molecular neuroscience at Dartmouth Medical School, the University of Texas (Houston), the University of California (San Diego), and the Salk Institute for Biological Studies. On the faculty of UCLA since 1996, Dr. Boulter's laboratory uses strains of genetically engineered mice to study the underlying cause of human inherited partial epilepsy and to characterize brain circuits involved in nicotine-induced dependence, tolerance, and withdrawal behaviors among habitual tobacco users. Dr. Boulter is a member of the UCLA Molecular Biology Institute, the Brain Research Institute, and the Hatos Research Center for Neuropharmacology.
| Work Address: |
Office MRL Building, Room 2774 Los Angeles, CA 90095 UNITED STATES |
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| Work Address: |
Laboratory MRL Building, Room 2557 Los Angeles, CA 90095 UNITED STATES |
Research Interests
| One ongoing project in my laboratory seeks to characterize genetically engineered mice, which harbor a mutation in a gene that is expressed in the central nervous system. In humans, this mutation is responsible for a hereditary disorder known as autosomal dominant nocturnal frontal lobe epilepsy. Through an examination of the behavioral and physiological characteristics of these mutant mice, we hope to learn how these mutations elicit seizures and contribute to the epileptic syndrome seen in humans. In addition, research using these mice will provide insight into the mechanism of epilepsy in general, show us how specific brain neurotransmitter systems are involved in epileptic phenomena, and may lead to discovery of new therapies for the treatment of selected epileptic disorders. In a second project, we are examining the physiology and behavior of genetically engineered mice in an effort to understand why abstinence from cigarette smoking evokes such strong somatic (physical) and affective (emotional) withdrawal symptoms. In spite of the obvious detrimental health effects of chronic tobacco use, smokers exhibit extremely high rates of relapse subsequent to a variety of smoking cessation programs. While smoking relapse is certainly a multifaceted and behaviorally complex phenomenon, elevated post-abstinence withdrawal scores are positively correlated with the resumption of tobacco smoking. In our animal studies, we are focused on the role of a single gene in the physiological and behavioral processes leading to the onset of withdrawal symptoms. A principal objective is to identify the brain region and circuits responsible for somatic and affective symptoms of nicotine withdrawal. The results of our experiments could provide a novel molecular target for the pharmacological relief of nicotine withdrawal symptoms, thereby decreasing post-smoking cessation relapse and helping to prevent the 430,000 tobacco-related deaths in the United States each year. |
