Fibroblast growth factor 9 is a novel modulator of negative affect
Abstract
Molecular mechanisms mediating negative emotion and contributing to major depression remain elusive: here, we present evidence implicating fibroblast growth factor 9 (FGF9) as a key mediator. We use whole-transcriptome studies of postmortem human tissue to demonstrate that FGF9 is elevated in depression. Reverse translation animal studies demonstrate that both endogenous and exogenous FGF9 promotes anxiety- and depression-like behavior. Conversely, localized blockade of endogenous FGF9 expression decreases anxiety behavior. To our knowledge, this paper is the first description of hippocampal FGF9 function and the first evidence implicating FGF9 in negative affect. Thus, FGF9 represents a novel target for treating affective disorders. Moreover, our findings suggest that FGF2 and FGF9 work in functional opposition; we hypothesize that the balance between FGF factors may prove critical for optimal regulation of mood.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Sep 08, 2015
- Source ID
- 10.1073/pnas.1510456112
Entities
People
- Alan Schatzberg
- Cortney A. Turner
- Devin Absher
- Edny Gula Inui
- Elyse L. Aurbach
- Huda Akil
- Jack D. Barchas
- Jun Z. Li
- Katherine E. Prater
- Megan H Hagenauer
- Najmul Shah
- Peter Blandino Jr.
- Richard M. Myers
- Stanley J. Watson Jr.
- William E. Bunney
Organizations
- Cornell University
- HudsonAlpha Institute for Biotechnology
- National Eye Institute
- National Institute of Mental Health
- National Institute on Drug Abuse
- Office of Naval Research
- Stanford University
- University of California
- University of Michigan