Abstract

FGF2: A novel antidepressant?

C. A. TURNER; E. GULA; D. O. FROST; N. CALVO; H. AKIL; S. J. WATSON
Society for Neuroscience. 2006.

Abstract

Previous work in our lab has found the FGF system to be altered post-mortem in individuals with major depressive disorder (MDD). Specifically, FGF2 has been shown to be decreased in the hippocampus in individuals with MDD (Evans et al., unpublished observations). To this end, we tested whether administering agents that activate FGF receptors would have antidepressant-like effects in rodents. We microinjected FGF2 (200ng, i.c.v.) or neural cell adhesion molecule (5µg, i.c.v.) into the lateral ventricle of rats and subsequently tested them on the forced swim test (FST). The results support the finding that activating FGF receptors has an antidepressant-like effect, as evidenced by a decrease in percent time immobility. We are also currently assessing gene expression changes of the FGF system (e.g., FGF2, FGFR1) by in situ hybridization in two animal models of depression, namely social defeat and chronic unpredictable stress. Although activating the system can have antidepressant-like effects, it still needs to be determined whether the system is also altered in rodent models of depression. These findings could provide novel targets for the treatment of MDD.