Major depression is a common mental illness thought to arise in part from decreased serotonin (5-HT) neurotransmission. Recent evidence suggests that this decrease may arise from increased expression of inhibitory 5-HT1A autoreceptors (5-HT1A-AR) on 5-HT neurons. To model this aspect of the pathophysiology of depression, I have created transgenic mice designed to overexpress 5-HT1A-AR; I hypothesize that these mice will have decreased 5-HT transmission and depressive-like behavior.
Aim 1 : Validate 5-HT1A-AR overexpression in transgenic mice by quantitative autoradiography and immunocytochemistry.
Aim 2 : Determine the effect of 5-HT1A-AR overexpression on 5-HT neurotransmission by in vivo microdialysis and electrophysiology.
Aim 3 : Determine the effect of 5-HT1A-AR overexpression in tests of neurovegetative function and depressive-like behavior. These studies should increase our understanding of the underlying causes of depression and other affective disorders, and may lead to new treatment strategies for patients suffering from these disorders. ? ?

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31MH075708-02
Application #
7119041
Study Section
Special Emphasis Panel (ZRG1-F01 (20))
Program Officer
Curvey, Mary F
Project Start
2005-09-01
Project End
2008-08-31
Budget Start
2006-09-01
Budget End
2007-08-31
Support Year
2
Fiscal Year
2006
Total Cost
$30,061
Indirect Cost
Name
University of California San Francisco
Department
Psychiatry
Type
Schools of Medicine
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
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