Abstract

Gene expression changes in the FGF family following chronic FGF9 administration or chronic social defeat.

E. L. GULA; C. A. TURNER; H. AKIL; S. J. WATSON
Society for Neuroscience. 2009.

Abstract

Previously, we have shown that the fibroblast growth factor (FGF) system is dysregulated in post-mortem brains of individuals with major depressive disorder (MDD). In order to understand the complex interaction of this growth factor system in vivo, we have adopted both a behavioral pharmacology and a gene expression profiling approach to assess emotionality in adult Sprague Dawley rats and in animal models of depression. We hypothesize that FGF2 and FGF9 act as physiological antagonists and that the balance between them may be the critical factor in the control of affective behavior. Chronic intracerebroventricular administration of FGF9, 20ng/day for 3 weeks, had effects on depression-like and anxiety-like behavior opposite of FGF2 administration. We have also previously found FGF2 administration to alter gene expression in the FGF system; FGF9 administration had effects opposite of FGF2 on gene expression in the FGF system. In addition, chronic social defeat altered both FGF2 and FGF9 gene expression in opposing direction. Therefore, alterations in gene expression in the FGF family, and more specifically FGF9 and FGF2, may underlie the development of mood disorders.