Tamara J. Phillips
Research Career Scientist, VAMC
Professor & Vice-Chair, Behavioral Neuroscience, OHSU
e-mail: phillipt@ohsu.edu
Recent Publications
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Tamara J. Phillips)
Major Areas
Behavioral genetics
Quantitative genetics
Drug & alcohol addiction
Previous Positions
Postdoctoral Research Associate, Rutgers University
Assistant Professor, Department of Medical Psychology, OHSU
Associate Professor, Department of Behavioral Neuroscience, OHSU
Education
B.A. (1981) William Paterson College
Ph.D. (1986) State University of New York, Albany
Research Interests
The broad area of interest in my laboratory is the genetic dissection of behavioral traits thought to influence risk for the development of alcoholism and drug abuse. We utilize genetic animal models to study acute and chronic drug and alcohol effects associated with drug reward and behavioral sensitivity. In addition, in collaboration with other investigators, we examine traits thought to co-segregate with potential for addiction, like impulsivity. Mice genetically prone and resistant to the behavioral effects of abused drugs are used in pharmacological and genetic mapping studies to identify specific neurotransmitter systems and chromosomal locations of genes that produce variations in behavior. We are currently focusing most of our attention on two drugs, alcohol and methamphetamine due to my invovlement with both the Portland Alcohol Research Center (PARC) and Methamphetamine Abuse Research Center (MARC).
A primary interest of my lab is in the mechanisms of behavioral sensitization (i.e., the increase in the effect of a drug with repeated exposures). The neuroadaptations associated with behavioral sensitization have been proposed to be determinant factors in the development of drug addiction; they may be associated with the transition from casual use to excessive use and addiction. The genetic studies in my lab have the potential for identifying common and unique genetic and neurochemical mechanisms underlying the motivational and neuroadaptive effects of addictive drugs. Genetic models we use include selectively bred mouse lines, panels of inbred strains, transgenic mice, knockout mice, recombinant inbred strains, and congenic strains.
Pharmacological and molecular genetic approaches are utilized in my laboratory. For example, using mice stereotactically implanted with indwelling cannulae through which drug was infused into the ventral tegmental area (VTA), we have found strong support for the involvement of GABA-B receptors in determining sensitivity to alcohol's stimulant effects. Sensitivity to the behaviorally stimulating effects of alcohol may be predictive of risk for the development of alcoholism. Using recombinant inbred strains, congenic strains and selected lines, we have obtained strong support for a common genetic locus on mouse chromosome 9 that influences alcohol locomotor stimulation and self-administration, as well as methamphetamine-induced stimulation.
Stress activates pathways involved in the behavioral sensitization to alcohol and other drugs of abuse. We are using transgenic and knockout mice with alterations in genes that regulate corticotropin releasing hormone (CRH) and its receptors to explore the role of stress in alcohol self-administration and neuroadaptation. This peptide is the initiator the stress axis response to stressors and drugs of abuse. The 80% homology between the mouse and human genome predicts a high probability of deriving important information about human addiction from the basic rodent research being performed in my laboratory.
Our primary research examining issues important to methamphetamine abuse involve a direct examination of the genetic relationship between sensitization and self-administration. To accomplish this we are using selective breeding methods in combination with gene mapping and microarray gene expression analyses. If high sensitization is found in mice bred for low methamphetamine self-administration, and low sensitization in mice bred for low self-administration, this will indicate that some common genes influence both traits.
Selected Recent Publications
Coste SC , Heard A, McKinnon C, Phillips TJ , Stenzel-Poore MP (2006) Corticotropin-releasing hormone receptor type-2 deficient mice display impaired coping and recovery from stress. Genes Brain Behav 5:131-138.
Mitchell SH, Savelly JM, Li N, Phillips TJ (2006) Delay discounting predicts behavioral sensitization to ethanol in outbred WSC mice. Alcohol Clin Exp Res 30:429-437.
Meyer PJ, Phillips TJ (2007) Behavioral sensitization to ethanol does not result in cross-sensitization to NMDA receptor antagonists. Psychopharmacology, in press.
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Last Updated November 12, 2007