This proposal will test the hypothesis that acute and chronic changes in the ability to activate PKA dependent phosphorylation underlie addictive behaviors and involves generating two constructs that will allow expression of CRE recombinase in a cell specific and temporal fashion. This recombinase will be used to turn on activating and inhibitory protein kinase A (PKA) mutations in dopamine D1 or D2 receptor expressing cells in order to investigate the effects of altered kinase activity on drug seeking behavior and relapse. We hypothesize that mutations that activate PKA activity in D1 receptor expressing cells will inhibit self-administration and relapse of drug taking behavior while mutations that inhibit PKA activity in D2 expressing cells will enhance drug seeking behavior and induce relapse. A detailed understanding of the molecular changes that occur in specific brain regions during chronic drug exposure that underlie the subsequent behavioral changes may provide novel therapeutic targets for pharmacological intervention.

Agency
National Institute of Health (NIH)
Institute
National Institute on Drug Abuse (NIDA)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32DA018502-03
Application #
7123429
Study Section
Human Development Research Subcommittee (NIDA)
Program Officer
Babecki, Beth
Project Start
2004-09-24
Project End
2007-09-23
Budget Start
2006-09-24
Budget End
2007-09-23
Support Year
3
Fiscal Year
2006
Total Cost
$49,928
Indirect Cost
Name
University of Washington
Department
Pharmacology
Type
Schools of Medicine
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195