Tamara J. Phillips, Ph.D.
Positions
Senior Research Career Scientist, VA Medical Center
Professor & Vice-Chair, Behavioral Neuroscience
Advisory Council Member, ABMRF/The Foundation for Alcohol Research
Contact
phillipt@ohsu.edu; Phone: 503-220-8262 ext 56674; Lab Phone: 503-220-8262 ext 56672; Fax: 503-721-1029; Office: VA Bldg 101, Rm 427; Mail Code: R&D-32
Research Interests/Major Areas
Behavioral genetics, quantitative genetics, drug and alcohol addiction, neuroscience
Preceptor Rotation Availability
Dr. Phillips might be available for preceptor rotations for upcoming academic terms. Please contact her directly to inquire.
Mentorship Availability
Dr. Phillips might be available for mentorship for the 2012/13 academic year. Please contact her directly to inquire.
Summary of Current Research
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, behavioral sensitivity, and neuroadaptation. We also examine traits that co-segregate with addiction. 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 (MA), due to my involvement with both the Portland Alcohol Research Center (PARC) and Methamphetamine Abuse Research Center (MARC).
A primary interest is 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. Some of our most exciting results are from studies that have focused on the peptide, corticotrophin releasing factor (CRF).
Pharmacological and molecular genetic approaches are utilized in my lab. For example, we used mice stereotactically implanted with indwelling cannulae to infuse drugs into specific brain regions. We have found that GABA-B receptors in the ventral tegmental area are involved 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. We have also obtained strong support for a common genetic locus on mouse chromosome 9 that influences alcohol locomotor stimulation and self-administration, as well as MA-induced stimulation. Finer mapping is currently underway to narrow the region to one containing few genes for further study. Nicotinic receptor genes also appear to play a significant role in some alcohol effects, and we have more recently begun investigations of nicotine-alcohol interactions.
Our primary research examining issues important to MA 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. We have completed the selection of lines that drink high and low amounts of MA and have found that the high line shows increased sensitivity to MA-induced conditioned place preference (a measure of reward) and reduced sensitivity to MA-induced conditioned place and taste aversion. We have recently developed a method to examine operant oral self-administration of MA and have found that the high MA drinking mice operantly self-administer and consume significantly more MA than the low MA drinking line. This represents a powerful and unique genetic animal model for studying MA self-administration.
Recent Publications
Pastor, R., Reed, C., Burkhart-Kasch, S., Li, N., Sharpe, A.L., Coste, S.C., Stenzel-Poore, M.P. and Phillips, T.J. (2011) Ethanol concentration-dependent effects and the role of stress on ethanol drinking in corticotropin-releasing factor type 1 and double type 1 and 2 receptor knockout mice. Psychopharmacology 218:169-177. PMCID: PMC3312392
Shabani, S., McKinnon, C.S., Cunningham, C.L. and Phillips, T.J. (2012) Profound reduction in sensitivity to the aversive effects of methamphetamine in mice bred for high methamphetamine intake. Neuropharmacology 62:1134-1141. PMCID: PMC3297479
Shabani, S., Dobbs, L.K., Ford, M.M., Finn, D.A. and Phillips, T.J. (2012) A genetic animal model of differential sensitivity to methamphetamine reinforcement. Neuropharmacology 62:2168-2176. PMCID: PMC3320769
Education
B.A. (1981) William Paterson College
Ph.D. (1986) State University of New York, Albany
Previous Positions
Postdoctoral Research Associate, Rutgers University
Assistant Professor, Department of Medical Psychology, OHSU
Associate Professor, Department of Behavioral Neuroscience, OHSU
Non-Academic Interests
Tennis
