Deborah A. Finn
Associate Professor, Behavioral Neuroscience, OHSU
Research Pharmacologist, Research Service, VAMC
e-mail: finnd@ohsu.edu
Major Areas
Neuropharmacology; neuroendocrinology of ethanol intake and withdrawal
Previous Positions
NINDS Postdoctoral Research Fellow, University of California, Irvine
Education
B.S. (1978) Loyola Marymount University
Ph.D. (1989) University of Southern California
Research Interests
My research focuses on the physiological significance of neuroactive steroid action. These endogenous modulators can alter brain function by enhancing GABAergic neurotransmission via potent and selective interactions with GABA A receptors. Behaviorally, GABA-agonist steroid metabolites possess anxiolytic, locomotor stimulant, anticonvulsant and sedative-hypnotic properties. In a broad sense, studies are investigating whether drugs or physiological states which produce alterations in endogenous allopregnanolone (ALLO) levels, the most potent neurosteroid, could influence seizure susceptibility, anxiety levels, drug withdrawal hyperexcitability or dysphoria, or patterns of drug intake and the response to drug intake. One funded project is testing the hypothesis that a decrease in endogenous ALLO levels, which alters GABAergic tone, in conjunction with a decrease in GABA A receptor sensitivity, contribute to the increased ethanol withdrawal severity in the selectively bred Withdrawal Seizure-Prone mice. Long-term goals of this research are to gain information that will aid in our understanding of the mechanisms underlying alcohol withdrawal as well as the therapeutic potential of neurosteroid treatment during alcohol withdrawal. A second funded project is utilizing microinjection into discrete brain regions to identify the site(s) of action of ALLO to alter ethanol drinking behavior, measured via lickometers and operant self-administration procedures in male and female mice. One long-term goal of this research is to evaluate the influence of neurosteroids on gender differences in human patterns of alcohol intake and the response to alcohol, since males and females differ in endogenous neurosteroid levels. A third project, through an involvement with the Integrative Neuroscience Initiative on Alcoholism (INIA), is using a combination of environmental and genetic manipulations to generate an animal model of high alcohol intake. Currently, we are pursuing a model whereby chronic intermittent alcohol vapor exposure and withdrawal produces high alcohol intake (termed “withdrawal-induced drinking” or WID). The goal of these studies is to identify pertinent neurotransmitters and begin to discern neural sites that are important for the expression of WID.
Selected Recent Publications
Finn DA, Snelling C, Fretwell AM, Tanchuck MA, Underwood L, Cole M, Crabbe JC, Roberts AJ (2007) Increased drinking during withdrawal from intermittent ethanol exposure is blocked by the CRF receptor antagonist D-Phe-CRF(12-41). Alcohol Clin Exp Res . Jun;31(6):939-949. .
Ford MM, Mark GP, Nickel JD, Phillips TJ, Finn DA (2007) Allopregnanolone influences the consummatory processes that govern ethanol drinking in C57BL/6J mice. Behav Brain Res . May 16;179(2)265-272 .
Finn DA, Douglass AD, Beadles-Bohling AS, Tanchuck MA, Long SL, Crabbe JC (2006) Selected line difference in sensitivity to a GABAergic neurosteroid during ethanol withdrawal. Genes Brain Behav . Feb;5(1):53-63.
Finn DA , Ford MM, Wiren KM, Roselli CE, Crabbe JC (2004) The role of pregnane neurosteroids in ethanol withdrawal: Behavioral genetic approaches. Pharmacol Ther . Feb;101(2):91-112. Review.
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